Essential Quick Review PERIODONTICS

Essential Quick Review
PERIODONTICS
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Essential Quick Review
@LibraryEDent ‫ﻣﻛﺗﺑﺔ طب اﻷﺳﻧﺎن‬

PERIODONTICS
Editor-in-Chief
Priya Verma Gupta MDS FPFA
Professor
Department of Pedodontics and Preventive Dentistry
Divya Jyoti College of Dental Sciences and Research
Ghaziabad, Uttar Pradesh, India
Co-Author
Vinita Ashutosh Boloor MDS
Associate Professor
Department of Periodontics
Yenepoya Dental College
Yenepoya University, Derelakatte
Karnataka, Mangalore, India
https://t.me/LibraryEDent
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Essential Quick Review: Periodontics
First Edition: Digital Version 2017
ISBN: 978-93-86056-18-4
Editorial Board

Priya Verma Gupta MDS FPFA
Professor
Divya Jyoti College of Dental Sciences and Research
Modi Nagar, Niwari Road, Ghaziabad
Uttar Pradesh, India
Gunjan Gupta MDS

Assistant Professor
Department of Periodontics
Shree Bankey Bihari Dental College and Research Centre
Hapur Road, Ghaziabad
Nishant Gupta MDS

Assistant Professor
Department of Orthodontics and Dentofacial Orthopedics
Shree Bankey Bihari Dental College and Research Centre
Hapur Road, Ghaziabad
Rishab Malhotra MDS

Assistant Professor
Jaipur Dental College
Jaipur Rajasthan
Preface

I am very pleased to introduce you to the first edition of Essential Quick Review; A series for final year
undergraduate students.
The series will be available in eight subjects. I.e., Periodontics, Pedodontics, Prosthodontics, Endodontics
and Conservative Dentistry, Oral Surgery, Oral Medicine Radiology and Public Health Dentistry covering
essential parts of each subject. It will not only help the student to attain the knowledge, but will also give
an idea how to attempt a question during the examination, covering entire syllabus in a limited period of
time.
The book gives a complete outline for writing an essay type, a short answer type or a viva voce type of
question. The language used is very simple enabling a better understanding with well-illustrated diagrams
wherever possible. Each book also carries a section that contains recently asked questions covering majority
of the universities in India.
What makes it different from other books is, that it is supported with a supplementary booklet for each
subject that contains three sections, i.e., definitions,classifications and viva voce covering the entire syllabus
enabling the student to undergo a quick revision.
The study material provided in this book is an attempt to provide an additional help to students for easy

retention and reproduction of subject in the examination. This book is in no way a replacement to standard
text books.
I thank all my subject matter experts for their valued suggestions and contributions. A very special word
of thanks to my family for being the source of constant encouragement. I profusely thank Shri Jitender P Vij
(CEO), Mr Ankit Vij (Group President), and production team of M/S Jaypee Brothers Medical Publishers (P)
Ltd, New Delhi for their enthusiasm and constant efforts in bringing out this book.
Priya Verma Gupta
Contents

Section 1 Periodontics
1. Gingiva .......................................................................................................................................................................................................... 03-10
2. Periodontal Ligament .............................................................................................................................................................................. 11-14
3. Alveolar Process ......................................................................................................................................................................................... 15-20
4. Cementum ................................................................................................................................................................................................... 21-24
5. Age-related Changes in Periodontium ............................................................................................................................................. 25-27
6. Classification of Periodontal Diseases ............................................................................................................................................... 28-31
7. Epidemiology of Gingival and Periodontal Diseases ................................................................................................................... 32-34
8. Periodontal Microbiology ...................................................................................................................................................................... 35-36
9. Dental Calculus and Iatrogenic Factors ............................................................................................................................................. 47-50
10. Inflammation and Immunity ................................................................................................................................................................. 51-63
11. Microbial Interactions with the Host in Periodontal Diseases .................................................................................................. 64-65
12. Smoking and Periodontal Diseases .................................................................................................................................................... 66-66
13. Host Modulation and Host Modulation Agents ............................................................................................................................. 67-68
14. Influence of Systemic Disorders and Stress on the Periodontium .......................................................................................... 69-74
15. Periodontal Medicine .............................................................................................................................................................................. 75-77
16. Halitosis (Oral Malodour) ........................................................................................................................................................................ 78-79
17. Defence Mechanism of Gingiva ........................................................................................................................................................... 80-81
18. Gingival Inflammation ............................................................................................................................................................................. 82-83
19. Clinical Features of Gingivitis ................................................................................................................................................................ 84-88
20. Gingival Enlargement .............................................................................................................................................................................. 89-94
21. Acute Gingival Infections ....................................................................................................................................................................... 95-100
22. Gingival Diseases in Childhood ...................................................................................................................................................... 101-102
23. Desquamative Gingivitis ................................................................................................................................................................... 103-105
24. Periodontal Pocket .............................................................................................................................................................................. 106-110
25. Bone Loss and Patterns of Bone Destruction ............................................................................................................................. 111-115
26. Trauma from Occlusion ...................................................................................................................................................................... 116-123
27. Chronic Periodontitis .......................................................................................................................................................................... 124-126
28. Necrotising Ulcerative Periodontitis ............................................................................................................................................. 127-127
29. Aggressive Periodontitis .................................................................................................................................................................... 128-132
x
30. AIDS and Periodontium ..................................................................................................................................................................... 133-135

31. Clinical Diagnosis ................................................................................................................................................................................. 136-137

32. Radiographic Aids in the Diagnosis of Periodontal Diseases ............................................................................................... 138-139
33. Advanced Diagnostic Techniques .................................................................................................................................................. 140-142
34. Risk Assessment .................................................................................................................................................................................... 143-144
35. Prognosis ................................................................................................................................................................................................. 145-147
36. Rationale for Periodontal Treatment ............................................................................................................................................. 148-148
37. Periodontal Treatment for Medically Compromised Patients .............................................................................................. 149-151
38. The Treatment Plan .............................................................................................................................................................................. 152-152
39. Phase I Periodontal Therapy ............................................................................................................................................................. 153-154
40. Plaque Control ....................................................................................................................................................................................... 155-159
41. Scaling and Root Planing .................................................................................................................................................................. 160-166
42. Chemotherapeutic Agents ............................................................................................................................................................... 167-168
43. Sonic and Ultrasonic ........................................................................................................................................................................... 169-170
44. Adjunctive Role of Orthodontic Therapy ..................................................................................................................................... 171-172
45. Occlusal Evaluation and Therapy ................................................................................................................................................... 173-174
46. Periodontic-Endodontic Continuum ............................................................................................................................................ 175-176
47. Preparation of the Periodontium for Restorative Dentistry .................................................................................................. 177-178
48. Phase II Periodontal Therapy ............................................................................................................................................................ 179-180
49. General Principles of Periodontal Surgery .................................................................................................................................. 181-183
50. Gingival Surgical Techniques ........................................................................................................................................................... 184-188
51. Treatment of Gingival Enlargements ............................................................................................................................................ 189-189
52. The Periodontal Flap ........................................................................................................................................................................... 190-193
53. Flap Technique for Pocket Therapy ................................................................................................................................................ 194-195
54. Resective Osseous Surgery ............................................................................................................................................................... 196-198
55. Reconstructive Periodontal Surgery ............................................................................................................................................. 199-203
56. Furcation ................................................................................................................................................................................................. 204-206
57. Periodontal Plastic and Aesthetic Surgery .................................................................................................................................. 207-210
58. Recent Advances in Surgical Techniques .................................................................................................................................... 211-212
59. Dental Implants .................................................................................................................................................................................... 213-215
60. Supportive Periodontal Therapy .................................................................................................................................................... 216-217
Section 2 Recently Asked Questions

61. Recently Asked Questions ................................................................................................................................................................ 221-246
1 SECTION
PERIODONTICS

hsipter Gingiva
i
2*
j
o
CD
LONG ESSAYS o
LU
03
Question 1 b. Attached gingiva is separated from the loosely bound
Define gingiva. Enumerate the zones of oral mucosa. What alveolar mucosa by mucogingival junction.
are the different parts of gingiva ? Explain in detail about the c. It is maximum in the incisal region approx. 3.5-4.5 mm
( maxilla) and 3.3-3.9 mm (mandible) and minimum is
microscopic features of gingiva.
the posterior region i.e. 1.9 mm ( maxilla) and 1.8 mm
Answer ( mandible).
3. Interdental gingiva
According to Glickman, gingiva is defined as "that part of
a. It is found between the adjacent teeth, occupying the
oral mucosa that covers the alveolar processes of the jaws
and surrounds the necks of the teeth in a collar-like fashion."
gingival embrasure.
There are Three Zones of Oral Mucosa

Gingival sulcus
1. Masticatory mucosa, e.g. Gingiva and covering of the
Marginal or free gingiva
hard palate. r
Marginal or free gingival groove
2. Specialised mucosa, e.g. dorsum of the tongue.
3. Lining mucosa, e.g. oral mucous membrane lining the
remainder of the oral cavity.
Gingiva is divided into three parts viz. marginal, attached f * \V
Attached gingiva
and interdental ( Fig. 1.1 ). ‘ \\

\
1 . Marginal gingiva * \
\
\ Mucogingival junction
a. It is also called as unattached gingiva, which is loosely
bound and surrounds the teeth in a collar like manner. Alveolar mucosa
\
.
b It is differentiated from the attached gingiva by a
mild/small (shallow) depression, which is called as <x>
free gingival groove. Fig. 1.1: Anatomic landmarks of gingiva. o
LU
c. Gingival sulcus: It is a V-shaped crevice around the
tooth which is bounded by marginal gingiva on one 03
side and tooth on the other side.

e. Normal depth of gingival sulcus is 1.3 mm. In pristine
CD
condition the depth of sulcus is 0 mm.
f. Gingival crevicular, fluid (GCF) is found in the gingival Interdental gingiva
sulcus. Marginal gingiva
2. Attached gingiva Attached gingiva OO
Mucogingival junction
a. It begins after marginal gingiva and is tightly bound
Loose alveolar mucosa
to the underlying periosteum of the alveolar bone
( Fig. 1.2). Fig. 1.2: Diagram depicting attached gingiva.
1

Chapter Gingiva
LONG ESSAYS
Question 1 b. Attached gingiva is separated from the loosely bound

Define gingiva. Enumerate the zones of oral mucosa. What alveolar mucosa by mucogingival junction.
are the different parts of gingiva? Explain in detail about the c. It is maximum in the incisal region approx. 3.5–4.5 mm
microscopic features of gingiva. (maxilla) and 3.3–3.9 mm (mandible) and minimum is
the posterior region i.e. 1.9 mm (maxilla) and 1.8 mm
Answer (mandible).
According to Glickman, gingiva is defined as “that part of 3. Interdental gingiva
oral mucosa that covers the alveolar processes of the jaws a. It is found between the adjacent teeth, occupying the
and surrounds the necks of the teeth in a collar-like fashion.” gingival embrasure.
There are Three Zones of Oral Mucosa

1. Masticatory mucosa, e.g. Gingiva and covering of the
hard palate.
2. Specialised mucosa, e.g. dorsum of the tongue.
3. Lining mucosa, e.g. oral mucous membrane lining the
remainder of the oral cavity.
Gingiva is divided into three parts viz. marginal, attached
and interdental (Fig. 1.1).
1. Marginal gingiva
a. It is also called as unattached gingiva, which is loosely
bound and surrounds the teeth in a collar like manner.
b. It is differentiated from the attached gingiva by a
mild/small (shallow) depression, which is called as
free gingival groove. Fig. 1.1: Anatomic landmarks of gingiva.
c. Gingival sulcus: It is a V-shaped crevice around the
tooth which is bounded by marginal gingiva on one
side and tooth on the other side.
e. Normal depth of gingival sulcus is 1.3 mm. In pristine
condition the depth of sulcus is 0 mm.
f. Gingival crevicular, fluid (GCF) is found in the gingival
sulcus.
2. Attached gingiva
a. It begins after marginal gingiva and is tightly bound
to the underlying periosteum of the alveolar bone
(Fig. 1.2). Fig. 1.2: Diagram depicting attached gingiva.
4
b. It forms a pyramidal shape when the teeth are in close h They are derived from neural crest cells and are
h
contact (Fig. 1.3A), however in cases of diastema the located in stratum basale

pyramidal shape is lost (Fig. 1.3B). h Melanin is produced as melanosomes which is present
h
c. Underneath the facial and the lingual papillae, there is in the cytoplasm of melanocytes and keratinocytes.
a valley like depression known as Col. Langerhans cells: They are dendritic cells seen in

suprabasal region. They play a role in immune
Microscopic Features of Gingiva reaction as they act as antigen presenting cells for
Gingiva is microscopically divided into two parts, viz., lymphocytes. They also have G-specific granules
gingival epithelium and gingival connective tissue. known as Birbeck’s granules
Merkel cells: These are present in deeper layers

Gingival Epithelium containing nerve endings and therefore have a
The epithelium not only provides a physical barrier to sensory function.

various infections but also plays an important role in host The epithelium is connected to the underlying connective

defence mechanisms tissue by a basal lamina which is approximately 300–400
Gingival epithelium protects the deep structures which Å thick

are achieved by proliferation and differentiation of It consists of lamina densa and lamina lucida.

keratinocytes Hemidesmosomes are attached to the lamina lucida
Proliferation occurs by mitosis in basal cell layer composed mainly of glycoprotein laminin. Type IV

Few cells remain in the basal cell layer to act as collagen forms the bulk of lamina densa.

proliferative compartment while majority of the cells Gingival epithelium is of three types:
move towards the surface 1. Oral epithelium.
Differentiation occurs during this movement of the cells to 2. Sulcular epithelium.

the surface, they undergo biochemical and morphologic 3. Junctional epithelium.
changes, thus differentiating into keratinocytes. This
process is called as keratinisation Oral Epithelium
Keratinocytes form the bulk of the gingival epithelium.
It is also known as the outer epithelium that covers the

Other cells like Langerhans cells, Merkel cells and

outer surface of the keratinised gingiva, i.e. the marginal

melanocytes are seen in small numbers. These cells are
gingiva and attached gingiva
together called as non-keratinocytes
Melanocytes: These are specialised cells which
It is composed of four layers viz., stratum basale, stratum

spinosum, stratum granulosum and stratum corneum

synthesize melanin and cause melanin pigmentation
Keratinisation varies in different areas of the oral cavity,
which is occasionally seen on the gingiva

i.e. it is maximum in the palate, gingiva, ventral aspect of
tongue, cheeks in the descending order
The outer epithelium loses its keratinisation if it contacts

a tooth.
Sulcular Epithelium
It is a non-keratinised stratified squamous epithelium

that lines the gingival sulcus
A It extends from the crest of the gingival margin till the

coronal portion of the junctional epithelium. It lacks
stratum granulosum and corneum
It has the capacity to keratinise in certain conditions like:

Upon exposure to oral cavity

Upon complete elimination of inherent bacterial flora.

B Junctional Epithelium
Fig. 1.3A & B: Interdental gingiva : (A) Depicting pyramidal It is also referred to as attachment epithelium which is

shape. (B) Pyramidal shape lost in diastema. stratified, squamous and non-keratinising in nature.
5
Chapter 1 Gingiva
It is found at cemento-enamel junction in healthy

It also acts as a semipermeable membrane as it
conditions. The width of JE is 10–29 cells coronally and allows access of gingival fluid, inflammatory cells and

1–2 cells apically. The length of the junctional epithelium immunologic components of host defence mechanism
is approximately 0.25–1.35 mm to the gingival sulcus

It is formed by confluence of outer epithelium and
It helps in rapid repair of the damaged tissue as cells of
reduced enamel epithelium during tooth eruption junctional epithelium exhibit rapid turnover.

Junctional epithelium exhibits ribosomes, Golgi
bodies and cytoplasmic vacuoles. The junctional Gingival Connective Tissue
epithelium is attached to the tooth by internal basal It is also referred as lamina propria and it consist of two layers:
lamina and to the connective tissue by external basal 1. Papillary layer adjacent to epithelium.
lamina
2. Reticular layer adjacent to the periosteum of the alveolar
The epithelial attachment of junctional epithelium
bone.

consists of internal basal lamina which consists of lamina

densa that is adjacent to the enamel and lamina lucida to
Connective tissue is mainly composed of collagen
which hemidesmosomes are attached fibres which are about 60% by volume, fibroblasts

Hemidesmosomes help in cell-to-cell attachment (5%), and remaining 35% is formed by vessels, nerves
and also take part in gene expression regulation, cell and matrix
proliferation and cell differentiation

It also consists of a ground substance which occupies

The junctional epithelium and the gingival fibres the space between fibres and cells along with high
water content. Ground substance is mainly composed of
together are referred as dentogingival unit because the
proteoglycans like hyaluronic acid, chondroitin sulphate
attachment of the junctional epithelium to the tooth is
and glycoproteins, mainly fibronectin
reinforced by the gingival fibres.

Connective tissue consists of three types of fibres, i.e.
Thus it could be concluded that junctional epithelium collagen, reticular and elastic. Type I collagen is the
has various functions such as: main fibre seen in lamina propria and provides tensile
JE forms an epithelial barrier against plaque bacteria as it

strength. Elastic fibre is composed of elaunin, elastin and
is firmly attached to the tooth surface oxytalan fibres distributed among collagen fibres.
SHORT ESSAYS
Question 1 in this epithelium. There is absence of keratinosomes

which is also referred as Odland bodies and also acid
What is attachment epithelium? What is epithelial
phosphatase is related to lower degree of differentiation ,
attachment?
which reflects weak defence mechanism against bacteria
Answer in d dental plaque
Poly morphonuclear leucocytes (PMN) are commonly
Junctional epithelium is also referred to as attachement

found , but its number increases considerably at the

epithelium which is stratified, squamous and non
time of bacterial attack to fight against infection
keratinizing in nature. It is found at cemento–enamel
(Fig. 1.4).
junction in healthy conditions.
Its width is 10- 29 cells coronally and 1- 2 cells apically.
Epithelial Attachment

The length of the junctional epithelium is approxiametely

0.25 – 1.35 mm
The junctional epithelium is attached to the tooth by
It is formed by confluence of outer epithelium and
internal basal lamina and to the connective tissue by
reduced enamel epithelium during tooth eruption external basal lamina
It can be completely formed after surgery or

The epithelial attachment of junctional epithelium
instrumentation consists of internal basal lamina which consists of lamina
Junctional epithelium exhibits ribosomes, golgi bodies

densa which is adjacent to the enamel and lamina lucida
and cytoplasmic vacuoles. Lysosome- like bodies are seen to which hemidesmosomes are attached
6
Ground substance is mainly composed of proteoglycans

like hyaluronic acid and chondroitin sulphate and

glycoproteins, mainly fibronectin
Connective tissue consists of three types of fibres, i.e.

collagen, reticular and elastic
Type I collagen is the main fibre seen in lamina propria

and provides tensile strength
Elastic fibre is composed of elaunin, elastin and oxytalan

fibres distributed among collagen fibres
Connective tissue is highly collagenous, containing

bundles of fibres known as gingival fibres consisting of
collagen type I. They serve the following functions:
It holds the marginal gingiva tightly against the tooth

Fig. 1.4: Development of junctional epithelium Provides strength to withstand the masticatory forces

and gingival sulcus. Unites the marginal gingiva with the cementum and

attached gingiva of the adjacent tooth.
Hemidesmosomes help in cell-to-cell attachment Group of principal gingival fibres are:

and also take part in gene expression regulation, cell Dentogingival group

proliferation and cell differentiation Alveologingival group

The junctional epithelium and the gingival fibres Dentoperiosteal group

together are referred as dentogingival unit because the Circular group

attachment of the junctional epithelium to the tooth is Transseptal group.

reinforced by the gingival fibres Group of secondary fibres are:

Thus it could be concluded that junctional epithelium Periosteogingival group

has various functions like: Inter-papillary group

It forms an epithelial barrier against plaque bacteria Trans-gingival group

as junctional epithelium is firmly attached to the Inter-circular group

tooth surface Inter-gingival group

It acts as a semipermeable membrane as it Semi-circular group.

allows access of gingival fluid, inflammatory cells
and immunologic components of host defence Cellular Composition of Gingival Connective Tissue
mechanism to the gingival sulcus Fibroblast is the main cell type of gingival connective
It helps in rapid repair of the damaged tissue as cells

tissue. Fibroblasts are responsible for synthesising

of junctional epithelium exhibit rapid turnover.
collagen, elastic fibres, glycoproteins and
Question 2 glycosaminoglycans. They also play an important role in
development, maintenance and repair
Describe in detail about gingival connective tissue.
Mast cells, fixed macrophage and histiocytes are present

Answer in gingival connective tissue
Also seen are adipose cells and eosinophils, which are less
Gingival Connective Tissue

in number. Leucocytes and lymphocytes are also seen.
It is also referred as lamina propria and it consists of two layers:
1. Papillary layer adjacent to epithelium.
Question 3
2. Reticular layer adjacent to the periosteum of the alveolar Explain in detail about gingival sulcus.
bone. Answer
Connective tissue is mainly composed of collagen fibres

which are about 60% by volume, fibroblasts (5%), and Gingival sulcus is also referred to as gingival crevice.
remaining 35% is formed by vessels, nerves and matrix It is a V-shaped shallow crevice around the tooth which is sur-

It also consists of a ground substance which occupies rounded by gingiva on one side and tooth on another side

the space between fibres and cells and has a high-water Normal depth of gingival sulcus is 1–3 mm. In pristine

content condition the depth of sulcus is 0 mm
7
Chapter 1 Gingiva

Depth of the gingival sulcus can be measured with the
It has anti-microbial action.
help of periodontal probe. Gingival crevicular fluid (GCF)
It acts as gingival defence mechanism as it possesses

is found in gingival sulcus. antibody activity.

Various methods of collecting GCF:
Development of Gingival Sulcus Filter paper strips.

Micro-capillary tubes.
When the tooth erupts into the oral mucosa, the reduced

Crevicular washing methods.

enamel epithelium combines with the oral epithelium

Twisted threads.
forming, the junctional epithelium (Fig. 1.4)

GCF samples can be measured on a blotter or a perio

Further this united epithelium becomes condensed

paper on an electronic transducer called as periotron.

along the crown and ameloblasts gradually transform

Ninhydrin staining method.
into squamous epithelial cells

Isotope dilution method.

This transformation moves in an apical direction. This

epithelium continuously renews itself by mitotic activity Dento-gingival Junction

and moves in a coronal direction to the gingival sulcus,
where they are shedded
Attachment of junctional epithelium to the tooth

Gingival sulcus formation takes place when the tooth is reinforced by gingival fibre, therefore junctional
erupts into the oral cavity (Fig. 1.5). epithelium and gingival fibres together is referred to as
dento-gingival unit.
Gingival Crevicular Fluid
The gingival fibres are highly collagenous consisting of
collagen fibres mainly Type I collagen. Principal fibres of
Gingival crevicular fluid can be a transudate or an exudate
gingival connective tissue are:

which contains a wide range of biochemical factors which Dento-gingival group

can be used as a potential diagnostic biomarker of the bio-

Alveolo-gingival group
logic state of the periodontium in health and disease

Dento-periosteal group
Gingival crevicular fluid is mainly composed of

Circular group

epithelium, connective tissue, serum, inflammatory cells

Transseptal group.
and microbial flora

Group of secondary fibres are:

In the state of health GCF is present in small quantities

Periosteoa-gingival group

whereas in inflammation, GCF increases and resembles

Inter-papillary group
an inflammatory exudate.

Trans-gingival group
Functions of GCF are as follows:

Inter-circular group

It has a cleansing action.

Inter-gingival group

It provides adhesion of the gingival epithelium to the

Semi-circular group.

tooth as it contains plasma proteins.

These fibres originate from cementum and are inserted
into connective tissue of gingiva and periosteum of the
alveolar bone.
They provide stabilization and maintain the position of

teeth in the arch by securing them.

Question 4
Correlate various clinical and microscopic features of gingiva.
Answer
Various clinical features of gingiva are:
Colour

Size

Contour

Shape

Consistency

Fig. 1.5: Gingival crevice. Surface texture

8
Position

Colour: Normal colour of gingiva is pink. There are three

factors on which the colour of gingiva is dependent,
i.e. vascularity, degree of keratinisation, and pigment
containing cells.
Vascularity: If the vascularity increases, the colour

of gingiva becomes red. It is seen in cases of
inflammation, but in absence of inflammation the
vascularity is normal, and the colour of gingiva
appears as coral pink.
Degree of keratinisation: More the keratinisation
A B

lesser would be the redness in gingiva. Therefore a
highly keratinized gingiva would appear as pale pink,
whereas if the keratinisation is low, gingiva would
Fig. 1.6A & B: Gingiva : (A) Normal colour of gingiva and.
appear as reddish. Since the attached gingiva and (B) Melanin pigment in gingiva.
marginal gingiva are keratinised, it appears as pink,
whereas alveolar mucosa which is non-keratinised, teeth contacts and shape of teeth. If the teeth are in tight
appears red, smooth and shiny. contact and teeth are narrow mesio-distally, gingiva
Pigmentation containing cells: Melanin is a brown exhibits a pyramidal shape, e.g. in case of anterior teeth,

coloured pigment which is responsible for normal but if the teeth are not in close contact the shape of the
pigmentation. But if these pigment containing interdental gingiva becomes flattened. If the teeth are
cells increase in number, then the gingiva appears wide mesio-distally, that means if the teeth are broad,
brownish-black in colour (Fig. 1.6). e.g. in posterior region, then the interdental gingiva
Size: Size of gingiva depends upon the total amount exhibits a broader shape.

of cellular and intercellular content of gingiva. In cases Consistency: In normal conditions, gingiva is firm and

of gingival inflammation, size is enlarged, otherwise in resilient, but in cases of inflammation it becomes soft
normal conditions it is not enlarged. and oedematous.
Contour: Contour of gingiva is dependent on various Surface texture: In health, gingiva exhibits an orange

factors like alignment of teeth in the arch, shape of the peel-like appearance referred to as stippling. Stippling is
teeth, location, size of the proximal contact and size of an adaptive specialisation or reinforcement of function
the gingival embrasure. In normal conditions the gingiva produced by alternate rounded depressions and
follows a scalloped contour, but in cases of inflammation, protuberances in gingiva. In this state of disease stippling
mostly it becomes a scalloped. In relatively flat teeth, the becomes absent.
gingival contour is flat. If there is pronounced mesio- Position: The normal position of gingiva is at cemento-

distal convexity or if there is gingival recession, the enamel junction (CEJ). In disease, this position is either
scalloping along the teeth becomes more accentuated. above CEJ or below the level of CEJ which is also referred
Shape: Shape of the gingiva depends upon the proximal to as gingival recession.

SHORT NOTES
Question 1 2. Passive eruption is exposure of the crown by the apical

migration of the gingiva. It can be divided into four
What is continuous tooth eruption?
stages:
Answer a. Stage 1: In this the teeth are in the line of occlusion.
There are two types of eruption viz., active and passive The junctional epithelium and the base of the gingival
eruption. sulcus are at the enamel.
1. Active eruption is referred as the eruption of the teeth in b. Stage 2: In this stage there is an apical proliferation
an occlusal direction. of the junctional epithelium such that one part is on
9
Chapter 1 Gingiva
Significance of attached gingiva are as follows:

It helps in protection against microbes and other foreign


bodies as it is tightly bound to the periosteum
Since it is keratinised, it aids in bearing the masticatory

forces
It helps in proper placement of the toothbrush head

It also enhances the aesthetics.

Question 4
Discuss the blood supply, lympatics and nerve supply of
Fig. 1.7: Position of the gingiva in health and disease. gingiva?
cementum while other part is on enamel. Whereas,

Answer
the base of the gingival sulcus is still on the enamel. Blood Supply
c. Stage 3: In this the junctional epithelium completely
rests on the cementum and the base of the sulcus is at
Supraperiosteal arterioles present along the surface of
cemento-enamel junction. the alveolar bone that also pass through surrounding
d. Stage 4: Both junctional epithelium and the base of tissue.
the gingival sulcus are present on the cementum such

Periodontal ligament vessels, which extend into the
that some part of the cementum is exposed (Fig. 1.7). gingiva and anastomose with the capillaries in the
sulcular area.
Question 2
Arteries that emerge from the interdental septa and are
Define is gingival col and what is its significance? extended parallel to the crest of the bone to anastomose
with the vessels of the periodontal ligament.
Answer
It is a valley like depression connecting the facial and lingual Lymphatic Drainage
papillae and conforms to the shape of the interproximal Gingiva brings in the lymphatic vessels of connective tissue
contact. The interproximal space consists of interdental papillae. It progresses to the periosteum of the alveolar
gingiva that occupies the gingival embrasure. process and then to the regional lymph nodes, mainly sub-
Significance of col: Since col is formed of non-keratinised maxillary group.
epithelium, it is very prone to infections and inflammation
and is the most prone site for disease initiation. Nerve Supply
Question 3 Neural system of gingiva is very extensive and is distributed
What is attached gingiva? How is it measured? What is its throughout the gingiva. Neural innervation is derived
significance? from the nerves in the periodontal ligament and from the
labial, buccal and palatal nerves. Nerve structures which are
Answer
present in the connective tissue are:
Meshwork of terminal argyrophilic fibres
It is that part of the gingiva that starts immediately after

Meissner-type tactile corpuscles

marginal gingiva and extends till mucogingival junction.

Temperature receptors, i.e. Krause type end bulbs

It is separated from the marginal gingiva by a very shallow

Encapsulated spindles.
groove known as marginal groove and it is separated

from adjacent loose alveolar mucosa by mucogingival Question 5

junction.
What are clear cells?
It can be measured using a periodontal probe by
subtracting the sulcular depth from the total distance Answer
between the marginal gingiva and the mucogingival Non-keratinocytes (melanocytes, Langerhans cells and
junction. Merkel cells) are referred to as clear cell because in the
It can also be measured using Schiller’s potassium iodide histologic section, the zone around their nuclei appears
solution which stains the keratinised gingiva. lighter than in the zone around the keratin producing cells.
10
Question 6 Quesiton 8
What is the difference between keratinised gingiva and What are McCall’s festoons?

attached gingiva?
Answer
Answer These are rolled thickened margins of gingiva seen near
Keratinised gingiva consists of both loose marginal gingiva the canines when recession reaches upto the mucogingival
and firmly adherent attached gingiva but, attached gingiva junction. These are also called as life preserver-shaped
does not contain any movable mucosa. enlargement. They represent the inflammatory changes
seen in the gingiva.
Question 7
What are Stillman’s cleft? Question 9
What is mucogingival junction?
Answer
According to Carranza, they are defined as apostrophe- Answer
shape indentations extending from and into gingival It is a junction which demarcates the firm attached gingiva
margin of varying distances on facial surface. They are from the loosely bound alveolar mucosa. Its position
narrow V-shaped gingival recessions. remains consistent throughout life.
hsipter Periodontal Ligament
i
2*
j
o
CD
LONG ESSAYS o
LU
03
Question 1 cementum in a coronal direction towards the bone.
Define periodontal ligament (PDL) ? Discuss in detail about They have the capacity to tolerate the masticatory
forces and transform them into tension on the alveolar
periodontal ligament and describe in detail about its
functions. bone.
5. Apical group: These are found at the apex of the tooth
Answer radiating in an irregular manner from the cementum
According to Carranza, PDL is a complex vascular and highly into the bone. They are not present on incompletely
cellular connective tissue that surrounds the tooth root and formed roots.
connects it to inner wall of the alveolar bone. 6. lnter- radiculargroup: Thesearefound in thefurcation
Principal fibres are the most important component of areas of the multi- rooted tooth from the cementum
periodontal ligament. They are collagenous in nature, into the bone.
arranged in the form of a bundle and follow a wavy In the PDL, 2 immature fibres are seen viz. oxytalan and
course. eluanin fibres. The oxytalan fibres in a vertical direction
Sharpey 's fibres are the terminal portions of the principal running parallel to each other and bend to attach to the
fibres whose one end is embedded in to cementum and cementum in the cervical third of the root. They regulate
other end is embedded into the bone. the vascular flow.
There are six groups of principal fibres namely transseptal, Along with these fibres small group of collagen fibres
alveolar crest, horizontal, oblique, apical and lastly the have been found which, run in all direction forming a
interradicular ( Fig. 2.1). plexus known as indifferent fibre plexus.
1 . Transseptal group: They are found in inter-proximal
areas over the alveolar bone crest, embedded into the
.
cementum of adjacent teeth In cases of periodontal
03
destruction, these fibres are reconstructed. Since O
these fibres do not have any osseous attachment, LU
.
they can be considered as a part of gingival fibres Alveolar crest group
CD
.
2 Alveolar crest group: These fibres are extended in c*
an oblique direction from the cementum just below
^
r Horizontal group
% 4
: .4•
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•4
the junctional epithelium into the alveolar bone crest. 03
These fibres resist the lateral tooth movement and K
Oblique
also prevent the tooth extrusion. Bone
A
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A
.
3 Horizontal group fibres: These fibres extend hori- >
•
. .1
Apical 00
zontally at right angles from cementum to the bone. m .
.
4 Oblique group: They are the largest group Interradicular
of periodontal fibres. They extend from the Fig. 2.1: Fibres of Periodontal Liagment.
12
Cellular Elements the elastic deformation of the bony socket. Once

the alveolar bone reaches its limit, the force is then
There are four types of cells:

transmitted to the basal bone.
1. Connective tissue cells. Viscoelastic theory: This theory is based on fluid
2. Epithelial rest cells.

movement, with fibres having just a secondary role.
3. Immune system cells When the force is applied to the tooth, the extracelluar
4. Cells associated with neurovascular elements. fluid is passed from the periodontal ligament into the
Connective tissue cells: e.g. fibroblasts, cementoblasts marrow spaces of the bone through the cribriform plate.

and osteoblasts. Thus the force is transferred to the cancellous portion of
the alveolar bone. Once there is fluid depletion, the fibres
Epithelial rest cells: e.g. epithelial rests of Malassez which
bundles absorb the slack and tighten up which leads to

appear as isolated clusters of cells or interlacing strands.
the stenosis of the blood vessels. This further leads to
Immune system cells: e.g. neutrophils, lymphocytes, ballooning of the vessels and passage of the blood is

macrophages, mast cells and eosinophils. ultrafiltrated into the tissues causing the replenishment
of the tissue fluids.
Ground Substance
It consists of glycosaminoglycans and glycoproteins. Transmission of Occlusal Forces to the Bone

Hyaluronic acid and proteoglycans are the main Whenever a horizontal or a tipping force is applied, two

glycosaminoglycans wheras, fibronectin and laminin are phases of tooth movement can be seen.
the main glycoproteins. First is within the confines of the PDL and second causes

Seventy percent of water content is found in the ground the displacement of the buccal and the lingual plates.

substance. It may also contain calcified mast cells known The tooth would rotate about an axis that may change as
as cementicles. the force is increased. In areas of tension, the periodontal
fibres are taut whereas in areas of pressure, the fibres
Functions of Periodontal Ligament are in a compressed state causing the tooth to displace
Physical. leading to distortion of bone.

Formative and remodelling.
In single-rooted teeth, the axis of rotation is situated in

between the apical-third and middle-third of the root

Nutritional.
whereas in a multi-rooted tooth, the axis of rotation is

Sensory.
situated in the and furcation area.

Physical Functions
Formative and Remodelling Functions
It provides a soft tissue casing which protects the nerves
The periodontal ligament is always in a constant state of

and vessels from injury due to any mechanical force.
It transmits the occlusal force to the bone. remodelling. Old cells and the fibres breakdown at a regular

interval and are replaced by new cells and fibres. The mitotic
It attaches the teeth to the bone.

It maintains the gingival tissues in a proper relationship activity can be seen in fibroblasts and endothelial cells.

with the teeth.
Nutritional and Sensory Functions
It also acts as shock absorber for the occlusal forces.

Periodontal ligament provides the nutrition to gingiva,
Shock Absorber for the Occlusal Forces cementum and bone through the blood vessels. The
There are two theories pertaining to this function: periodontal ligament is also supplied with sensory nerve
fibres which are capable of transmitting tactile, pain
1. Tension theory.
and pressure sensations. There are four types of nerve
2. Viscoelastic theory.
endings seen in periodontal ligament, viz. free endings
Tension theory: Whenever a force is applied to the carrying pain sensation, Ruffini-like mechanoreceptors,

tooth the principal fibres first unfold and then straighten Meissner’s corpuscles and spindle like pressure and
that further transmit the forces to the bone causeing vibration endings.
13
Chapter 2 Periodontal Ligament
SHORT ESSAYS

Question 1 Diagram showing collagen microfibrils, fibrils, fibers and bundle
Discuss the composition and structure of collagen.
Answer
Collagen is a type of protein mainly responsible for
maintaining the framework of the tissues. There are about
19 species of collagen. It is composed of various amino
acids, most importantly are glycine, proline, hydroxylysine
and hydroxyproline. Fibroblasts are the main cell type
responsible for collagen synthesis. Tropocollagen
molecule is formed within the fibroblast which combine
together to form microfibril with a periodicity of 64 nm. Fig. 2.2: Structure of collagen.
These microfibrils are packed together to form fibrils
and they again aggregate to form fibre and these fibres
Functions of Collagen
associate to form a bundle. The principal fibres are
composed mainly of type I collagen. Type III collagen
Provides flexibility and strength to the tissue because of
forms reticular fibres and type IV collagen forms basal its high tensile strength.
lamina (Fig. 2.2).
Responsible for maintaining the framework of tissues.
SHORT NOTES
Question 1 Answer
Write short note on oxytalan fibres.
Sharpey’s fibres are the terminal portions of the principal
fibres which are embedded in to cementum in one end
Answer
and the other end is embedded into the bone.

Oxytalan fibres are one of the immature fibres found
They constitute the bulk of cementum and are mainly
in PDL, other one being the elaunin. composed of type I collagen.

They run in a vertical direction parallel to the root
Once they are embedded into the wall of the alveolus,
surface and bend to attach to the cementum in the they get calcified.
cervical third of the root.

They are also associated with some non-collagenous

These fibres regulate the vascular flow since they are proteins found in bone and cementum, i.e. bone
associated with the blood vessels and nerves of the sialoprotein and osteopontin.
periodontal ligament.
Question 3
There is an elastic meshwork of oxytalan and elaunin
Write short note on indifferent fibre plexus.

fibres in the periodontal ligament.

Oxytalan fibres develop from the beginning in the Answer
regenerated PDL.
Along with the mature and immature fibres of PDL, small
group of collagen fibres have been found which run in
Question 2 all direction forming a plexus known as indifferent fibre
Write short note on Sharpey’s fibres. plexus.
14
Question 4 Question 5
What is the blood supply of periodontal ligament? Enumerate principal fibres of periodontal ligament?

Answer Answer
Main blood supply to PDL is through superior and inferior There are six groups of principal fibres of PDL:

alveolar arteries. 1. Transseptal group.
Apical group of arteries—vessels of the pulp. 2. Alveolar crest group.

Alveolar group of arteries—also known as perforating 3. Horizontal group.

arteries. 4. Oblique group.
Gingival group of arteries—vessels supplying the 5. Apical group.

gingiva. 6. Interradicular group.
hsipter Alveolar Process 1-
i
33
3o
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LONG ESSAYS o
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03
Questiuon 1 Cells and Inter -cellular Matrix

Define alveolar bone. What are the parts and composition Osteoblasts produce the organic matrix of the bone. It is
of alveolar bone? Discuss in detail about remodelling. formed during foetal growth through intra- membranous
ossification and consists of calcified matrix. Osteocytes are
Answer
enclosed in spaces called lacunae. Osteocytes extend their
According to Carranza, it is defined as "the portion of the processes into canaliculi which radiates from the lacuna. The
maxilla and mandible that forms and supports the tooth canaliculi forms an anastomosing system through an inter-
socket ". When the tooth erupts to provide the osseous cellular matrix of bone, which brings oxygen and nutrients
attachment to the forming periodontal ligament (PDL) to the osteocytes through the blood and also removes
that is the time when alveolar process is formed. When metabolic waste products. Blood vessels branch extensively
the tooth is lost, the alveolar process also disappears and traverse through periosteum. The endosteum lies close
gradually. Alveolar processes are the tooth- dependent to the marrow vasculature. The haversian system, also
bony structures, because the alveolar process develops and known as osteons are the internal mechanisms that bring
remodels with the tooth formation and eruption. Therefore, a vascular supply to the bones. They are many found in the
the morphology of alveolar process is dependent upon size, outer cortical plate and alveolar bone proper.
shape, location, and function of the teeth. Parts of alveolar
process are as follows:
Composition of Bone
External cortical bone: It is formed by compact bone Two -third inorganic matter and one -third of organic
lamellae and haversian bone. matter.
Alveolar bone proper: It is the inner socket wall which Inorganic matter
is made up of thin compact bone. It is also known as It consists of minerals like calcium, phosphate, along with
lamina dura in the radiographs. It contains a number of hydroxyl, carbonate, citrate, and trace amounts of other
openings because of the cribriform plate, through which <x>
ions, e.g sodium, magnesium, and fluorine. These salts are O
the neurovascular bundles passes and connects the PDL LU
with the alveolar bone. 03
^ The cancellous bone: Cancellous trabeculae act as

supporting alveolar bone present between two compact
bones. The interdental bone consists of cancellous bone Alveolar bone CD
proper
present between compact bones. (lamina dura)
Besides the above mentioned bones, the jaws also
contain basal bone which is situated apically and is also not Trabecular bone OO
related to teeth ( Fig. 3.1 ).

Compact bone
Most facial and lingual portions of the socket are formed
by compact bone. .
Fig 3.1: Alveolar bone.
16
in the form of hydroxyapatite crystals which are of ultra- The bone consists of 99% of body’s calcium. Therefore,

microscopic size and bone constitute two-thirds of these whenever there is a decrease in the levels of blood

crystals. calcium levels, the bone calcium is released. This process
is monitored by parathyroid gland.
Organic matter There are receptors present on the chief cells parathyroid

Main component of organic matter is type I collagen gland, which get activated in case of decrease in
which is around 90%. Along with it, small amounts of blood calcium levels. These receptors start producing
non-collagenous proteins are present such as osteocalcin, parathyroid hormone (PTH).
osteonectin, bone morphogenic protein, phosphoproteins This PTH stimulates the osteoblasts to produce

and proteoglycans. Some paracrine factors are also present Interleukin-1 (IL-1), and IL-6, which further stimulates
such as cytokines, chemokines and growth factors. monocytes to migrate into the area of bone.
Osteoblasts also secrete leukaemia inhibitory factor
Remodelling

(LIF), which coalesces monocytes into multi-nucleated
Bone remodelling is a process that involves change in osteoclasts, which causes bone resorption, and helps

shape, resistance to forces, repair of wounds and calcium in release of calcium ions from hydroxyapatite into the
and phosphate homeostasis in the body. It also includes blood.
bone formation and bone resorption. Coupling of bone When the blood levels of calcium becomes normal,

deposition and bone resorption constitutes one of the through a feedback mechanism, the secretion of PTH
fundamental principles by which bone is remodelled stops.
throughout life. On the other hand osteoclasts have resorbed the

Bone remodelling includes cells of distinct lineages, i.e. organic as well as inorganic content of bone which

osteoblasts and osteoclasts. Osteoblasts and osteoclasts causes breakdown of collagen. Due to this breakdown,
form and resorb the mineralised connective tissues bone certain osteogenic substrates are released, which bind
respectively. Number of osteoblasts decreases with age, to collagen, and this results in stimulation of osteoblasts,
whereas no change is seen in the number of osteoclasts. which ultimately deposit the bone.
Bone remodelling is a complex process which involves Therefore resorption and deposition of bone goes

hormones and local factors which act in an autocrine side by side. And this interdependency of osteoblasts
and paracrine manner on the production and function of and osteoclasts in bone remodelling is referred to as
differentiated bone cells. “coupling”.
SHORT ESSAYS
Question 1 The cancellous bone: Cancellous trabeculae act as

supporting alveolar bone present between two compact
Discuss alveolar bone in healthy and diseased.
bones. The interdental bone consists of cancellous bone
Answer present between compact bone.
Besides the above mentioned bones, the jaws also
In Health Condition contains basal bone which is situated apically and is also not
Parts of alveolar process are as follows: related to teeth.
Most facial and lingual portions of the socket are formed
External cortical bone: It is formed by compacted bone
by compact bone.

lamellae and haversian bone.
Alveolar bone proper: It is the inner socket wall which Composition of Bone

is made up of thin compact bone. It is also known as Two-third of inorganic matter and one-third f organic matter:
lamina dura in the radiographs. It contains a number
of openings because of the cribriform plate, through Inorganic Matter
which the neurovascular bundles pass and connect the It consists of minerals like calcium, phosphate, along with
periodontal ligament with the alveolar bone. hydroxyl, carbonate, citrate, and trace amounts of other
17
Chapter 3 Alveolar Process
ions, e.g. sodium, magnesium, and fluorine. These salts

Osteoblasts also secrete LIF, which coalesces monocytes
are in the form of hydroxyapatite crystals which are of into multinucleated osteoclasts, which causes bone

ultramicroscopic size and bone constitutes two-thirds of resorption, and helps in release of calcium ions from
these crystals. hydroxyapatite into the blood.
When the blood levels of calcium becomes normal,
Organic Matter

through a feedback mechanism, the secretion of PTH

Main component of organic matter is type I collagen stops.
which is around 90%. Along with it, small amounts of
On the other hand osteoclasts have resorbed the
non-collagenous proteins are present such as osteocalcin, organic as well as inorganic content of bone which
osteonectin, bone morphogenic protein, phosphoproteins causes breakdown of collagen. Due to this breakdown,
and proteoglycans. Some paracrine factors are also present certain osteogenic substrates are released, which bind
such as cytokines, chemokines and growth factors. to collagen, and this results in stimulation of osteoblasts,
which ultimately deposit the bone.
Remodelling
Therefore resorption and deposition of bone goes

Bone remodelling is a process that involve changes in side by side. And this interdependency of osteoblasts
shape, resistance to forces, repair of wounds and calcium and osteoclasts in bone remodelling is referred to as
and phosphate homeostasis in the body. It also includes “coupling”.
bone formation and bone resorption. Coupling of bone
deposition and bone resorption constitutes one of the In Disease Condition
fundamental principles by which bone is remodelled Fenestrations: They are the isolated areas in which
throughout life.

the root is denuded of the bone and the root

Bone remodelling includes cells of distinct lineages, i.e. surface is covered only by the periosteum and the
osteoblasts and osteoclasts. Osteoblasts and osteoclasts overlying gingiva. In these areas the marginal bone is
form and resorb the mineralised connective tissues bone intact.
respectively. Number of osteoblasts decreases with age,
Dehiscence: When the denuded areas extend through
whereas no change is seen in the number of osteoclasts. the marginal bone, such defects are termed as

Bone remodelling is a complex process which involves dehiscence.
hormones and local factors which act in an autocrine
Such kind of defects are seen in approximately in 20%
and paracrine manner on the production and function of
of teeth. These are more commonly seen on facial bone as
differentiated bone cells.
compared to the lingual bone. They are most often found

The bone consists of 99% of body’s calcium. Therefore, on anterior teeth than of posterior teeth and they are
whenever there is a decrease in the levels of blood bilateral frequently. The possible causes for these kinds of
calcium levels, the bone calcium is released. This process defects can be prominent root contours, malposition, and
is monitored by parathyroid gland. labial protrusion of the tooth combines with the thin bony

There are receptors present on the chief cells of plate.
parathyroid gland, which get activated in case of These defects are important because they might
decrease in blood calcium levels. These receptors start complicate the outcome of periodontal surgery.
producing PTH. There are other bony defects also, like one wall defect,

This PTH stimulates the osteoblasts to produce IL-1, and two wall defect, three wall defect, reverse architecture,
IL-6, which further stimulates monocytes to migrate into lipping, ledges, craters, horizontal bone defect, and vertical
the area of bone. bone defects.
18
SHORT NOTES

Question 1 border from which hydrolytic enzymes are secreted,
What are paracrine factors and what are their functions? which digest the organic matter of the bone. The activity
of osteoclasts can be modified by hormones, e.g. PTH and
Answer calcitonin which have the receptors on the osteoclasts
Cytokines, chemokines and various growth factors are membrane.
referred to as paracrine factors. They are responsible for There is another mechanism of bone resorption in which
the local control of mesenchymal condensations that occur an acidic environment is created on the bone surface which
at the start of organogenesis. These factors also play an leads to dissolution of the minerals of the bone. This can
important role in the development of the alveolar processes. be produced by different conditions including a proton
pump through the cell membrane of the osteoclasts, bone
Question 2 tumours, and local pressure which are translated through
What is the function of bone sialoprotein and osteopontin? the secretary activity of the osteoclasts.
Ten Cate has also described sequence of events in the
Answer process of bone resorption, which are as follows:
These are non-collagenous proteins referred to as cell- Attachment of osteoclast to the mineralised bone

adhesion proteins which are responsible for cell to cell surface.
adhesion of both osteoclasts and osteoblasts. Creation of a sealed acidic environment through action

of the proton pump, which demineralises bone and
Question 3 exposes the organic matrix.
What is osteoid? Degradation of the exposed organic matrix to its

Answer constituent amino acids by the action of released
enzymes such as acid phosphatase and cathepsins.
Osteoid is a non-mineralised bone matrix which is laid Sequestering of mineral ions and amino acids within the
down by osteoblasts. As the new osteoid deposits, the older

osteoclasts.
osteoid located below the surface becomes mineralised as
the mineralisation front advances. Question 6
Question 4 What is scalable processor architecture (SPARC)?
What is the origin of osteoclast and how are they formed? Answer
Answer It is a secreted protein, acidic and rich in cysteine. This
protein plays an important role in bone remodelling.
Osteoclast originates from hematopoietic tissue and are
formed by the fusion of mononuclear cells of asynchronous Question 7
populations.
What is bundle bone?
Question 5 Answer
Explain bone resorption. It is the bone adjacent to the periodontal ligaments which
contain a large number of Sharpey’s fibres. It is characterised
Answer by a thin lamella which is arranged in layers parallel to the
Bone resorption is a complex process. It appears as root along with intervening appositional lines. Bundle bone
eroded rough surface referred to Howship’s lacunae is located within the alveolar bone proper or lamina dura.
and also there is involvement of large multi-nucleated Some of the Sharpey’s fibres are completely calcified, but
cells known as osteoclasts. Osteoclasts originate from most contain an uncalcified central core within a calcified
hematopoietic tissue and are formed by the fusion of outer layer.
mononuclear cells of asynchronous populations. When Bundle bone is also found throughout the skeletal
these osteoclasts are active, they develop a ruffled system wherever muscles and ligaments are attached.
19
Chapter 3 Alveolar Process
Question 8 These defects are important because they might

complicate the outcome of periodontal surgery (Fig. 3.2).
What is periosteum and endosteum?

Answer Question 10
Tissue covering the outer surface of the bone is referred to What is the attachment apparatus?
as periosteum whereas the tissue lining the internal bone Answer
cavities in called as endosteum
Cementum, periodontal ligament and alveolar bone all
The periosteum consists of an inner layer and an outer
together form the attachment apparatus.

layer:

The inner layer is composed of osteoblasts which are Question 11
surrounded by osteoprogenitor cells. These cells have What is physiological migration of the teeth.
the potential to differentiate into osteoblasts.

The outer layer is rich in blood vessels and nerves and Answer
is composed of collagen fibres and fibroblasts. Tooth movement continues even after active eruption

The endosteum is composed of a single layer of phase. With time because of the wear and tear, the proximal
osteoblasts and sometimes a small amount of connective contacts of the teeth are flattened and therefore, the teeth
tissue may also be found. The outer layer is the fibrous tend to migrate mesially. This is referred to physiological
layer whereas the inner layer is the osteogenic layer. migration. Alveolar bone remodels in compliance with
the physiological migration of the teeth. Bone resorption
Question 9 increases in the areas of pressure along the mesial surface
What is fenestration and dehiscence? of the tooth and new layers are deposited in the areas of
tension along the distal surface of the tooth.
Answer

Fenestrations: They are the isolated areas in which
Question 12
the root is denuded of the bone and the root surface What is bone remodelling?
is covered only by the periosteum and the overlying
Answer
gingiva. In these areas the marginal bone is intact.

Dehiscence: When the denuded areas extend through

Bone remodelling is a process that involve change in
the marginal bone, such defects are termed as dehiscence. shape, resistance to forces, repair of wounds and calcium
and phosphate homeostasis in the body. It also includes
Such kinds of defects are seen in approximately in 20%
bone formation and bone resorption. Coupling of bone
of teeth. These are more commonly seen on facial bone as
deposition and bone resorption constitutes one of the
compared to the lingual bone. They are most often found on
fundamental principles by which bone is remodelled
anterior teeth than of posterior teeth and they are bilateral
throughout life.
frequently. The possible causes for these kinds of defects
can be prominent root contours, malposition, and labial
Bone remodelling includes cells of distinct lineages, i.e.
protrusion of the tooth combines with the thin bony plate. osteoblast and osteoclasts. Osteoblasts and osteoclasts
form and resorb the mineralised connective tissues
bone respectively. Number of osteoblasts decreases
with age, whereas no change is seen in the number of
osteoclasts.

Bone remodelling is a complex process which involves
hormones and local factors which act in an autocrine
and paracrine manner on the production and function of
differentiated bone cells.

The bone consists of 99% of body’s calcium. Therefore,
whenever there is a decrease in the levels of blood
calcium levels, the bone calcium is released. This process
Fig. 3.2: Fenestrations and Dehiscence. is monitored by parathyroid gland.
20
There are receptors present on the chief cells of to collagen, and this results in stimulation of osteoblasts,

parathyroid gland, which get activated in case of which ultimately deposit the bone.

decrease in blood calcium levels. These receptors start Therefore resorption and deposition of bone goes side

producing PTH. by side. And this interdependency of osteoblasts and os-
This PTH stimulates the osteoblasts to produce IL-1, and teoclasts in bone remodelling is referred to as “coupling”.

IL-6, which further stimulates monocytes to migrate into
the area of bone. Question 14
Osteoblasts also secrete LIF, which coalesces monocytes Discuss the development of alveolar bone.

into multinucleated osteoclasts, which causes bone
Answer
resorption, and helps in release of calcium ions from
hydroxyapatite into the blood. Just prior to mineralisation, matrix vesicles are produced
When the blood levels of calcium becomes normal, by the osteoblasts. These vesicles are rich in enzymes like

through a feedback mechanism, the secretion of PTH alkaline phosphatase that help in jump starting the seeding
stops. of hydroxyapatite crystals. These hydroxyapatite crystals
grow into coalescing bone nodules. These nodules along
On the other hand osteoclasts have resorbed the
with rapidly-developing non-oriented collagen fibres from

organic as well as inorganic content of bone, which
the basic structure of the woven bone and thus first bone
causes breakdown of collagen. Due to this breakdown,
is formed in the alveolus. This woven bone transforms
certain osteogenic substrates are released, which bind
itself into mature lamellar bone by the process of bone
to collagen, and this results in stimulation of osteoblasts,
deposition, remodelling and orientation of collagen fibres
which ultimately deposit the bone.
into layers.
Therefore resorption and deposition of bone goes
In the mature lamellar bone, the hydroxyapatite crystals

side by side. And this interdependency of osteoblasts
align themselves parallel to the collagen fibres along the
and osteoclasts in bone remodelling is referred to as
long axis and are deposited on and within the fibres. This
“coupling”.
kind of layout helps the bone matrix to bear the heavy
Question 13 mechanical stresses and strains during various functions.
It is seen that the alveolar bone develops around the
What is coupling?
dental follicle during the development of a tooth. When a
Answer deciduous tooth is shed, the alveolar bone accompanying
it also gets resorbed and is succeeded by new alveolar
The bone consists of 99% of body’s calcium.Therefore,
bone formation along with the permanent tooth follicle. As

whenever there is a decrease in the levels of blood
the root formation of the permanent tooth occurs and the
calcium levels, the bone calcium is released. This process
surrounding tissue develops, the alveolar bone merges with
is monitored by parathyroid gland.
the basal bone. Thus forming a continuous entity (alveolar
There are receptors present on the chief cells parathyroid bone and the basal bone). Both basal bone and the alveolar

gland , which get activated in case of decrease in blood bone are derived from neural crest ectomesenchyme.
calcium levels. These receptors start producing PTH.
Mineralisation of the mandibular basal bone begins from
This PTH stimulates the osteoblasts to produce IL-1, and

the mental foramen at the exit of the mental nerve whereas

IL-6, which further stimulates monocytes to migrate into
mineralisation of the basal bone of the maxilla starts at the
the area of bone.
exit of infraorbital nerve from infraorbital foramen.
Osteoblasts also secrete LIF, which coalesces monocytes

into multinucleated osteoclasts, which causes bone Question 15
resorption, and helps in release of calcium ions from What is an osteon?
hydroxyapatite into the blood.
When the blood levels of calcium becomes normal, through Answer

a feedback mechanism, the secretion of PTH stops. Osteon is referred as the haversian system which is the
On the other hand osteoclasts have resorbed the internal mechanisms that brings a vascular supply to

organic as well as inorganic content of bone which the bones, specially the bones which are took hick to be
causes breakdown of collagen. Due to this breakdown, supplied by only surface vessels. They are many found in the
certain osteogenic substrates are released, which bind outer cortical plate and alveolar bone proper.
hsipter Cementum 1-
i
33
3o
CD
LONG ESSAYS o
LU
03
Questiuon 1 Acellular afibrillar cementum (AAC): This type of

cementum neither contains cells nor collagen fibres. It
Define cementum ? Discuss in details the types, classification,
consists of mineralised ground substance. It is produced
composition and functions of cementum.
by cementoblasts with a thickness of 1-15 pm.
Answer Acellular extrinsic fibre cementum (AEFC): It consists of
mainly Sharpey's fibres and does not contain any cells. It
According to Carranza, cementum is defined as the calcified,
is produced by fibroblasts and cementoblasts, commonly
avascular mesenchymal tissue that forms the outer covering
found in the apical third of the roots. Its thickness is
of the anatomic root.
around 30-230 pm.
There are basically two types of cementum: Cellular mixed stratified cementum (CMSC): It consists
1. Acellular cementum. of both extrinsic and intrinsic fibres and also consists of
.
2 Cellular cementum. cells. It is produced by fibroblasts and cementoblasts.
It is found in the apical third of the roots, apex and in
Acellular Cementum furcation areas.
It is also known as primary cementum since it is the first- Cellular intrinsic fibre cementum (CIFC): It consists of
formed cementum. It covers cervical third or half of the cells and intrinsic fibres, but does not contain extrinsic
root and as the name suggests, it does not contain cells. fibres. It is formed by cementoblasts.
It is formed before the teeth reaches occlusal plane. Its Intermediate cementum: It consists of cellular remnants
thickness is between 30-230 pm. The main component of of Hertwig's epithelial sheath which is embedded in a
the acellular cementum is Sharpey 's fibres which plays an calcified ground substance. It is seen near the cemento-
important role in supporting the tooth. dentinal junction.
Cellular Cementum Composition of Cementum

<x>
It is formed after the tooth reaches the occlusal plane It consists of an organic portion and an inorganic portion: O
LU
and as name suggests it contains cells, i.e. cementocytes, Organic portion: The organic matrix of cementum is
that are present in individual spaces known as lacunae 03
basically of collagen. Out of which 90% is Type I and 5%
which communicates with each other through a system of Type III collagen. There are two main sources of collagen
anastomosing canaliculi. This cementum is less calcified as in cementum:
CD
compared to acellular cementum. Sharpey 's fibres are found 1. Sharpey 's fibres are also known as extrinsic fibres.
less in number in cellular cementum. They are the embedded portions of the principal
fibres of the periodontal ligament (PDL). They are
Classification of Cementum produced by fibroblasts. oo
According to Schroeder, cementum has been classified as 2. Intrinsic fibres: They belong to the cemental matrix
follows: and are produced by cementoblasts.
22
Sharpey’s fibres form the major bulk of cementum and is The ends of PDL fibres are embedded into the cementum,
composed of Type I collagen. Type III collagen coats the Type which helps in achieving this.

I collagen of Sharpey’s fibres. Ground substance consists of Cementum helps in maintain the occlusal relationships.

proteoglycan, glycoproteins and phosphoproteins. Whenever there is attrition, the incisal or the occlusal
Inorganic portion: It is around 45–50% and is mainly surface gets abraded, because of which the tooth is supra-

composed of hydroxyapatite. Inorganic component of erupted, to compensate for this occlusal discrepancy.
cementum is less than bone, enamel and dentine. Cementum gets deposited at the apex of the tooth, in
such situations.
Functions of Cementum It also maintains the integrity of root surface, by acting as

Cementum provides anchorage to the tooth in its socket. a reparative tissue for the root.

SHORT ESSAYS
What is cemento-enamel junction (CEJ)? What is cemento-dentinal junction (CDJ) ?
Answer Answer
It is that junction where the cementum and enamel meet. The part of cementum, which joins to the internal root

There are three types of CEJ: canal dentine is referred to as CDJ.
1. Cementum overlapping the enamel: It is seen in 60–65% The width of CDJ remains almost constant throughout

cases. life.
2. Edge to edge contact: It is also referred as butt joint. It is It is around 2–3 µm wide.

seen in 30% of cases. It consists significant amount of proteoglycans, and

the fibrils inter-mingle between the cementum and the
3. Gap between cementum and enamel: In this case the
dentine (Fig. 4.1).
cementum and enamel do not meet. It is seen in 5–10%
cases (Fig. 4.1). Question 3
What is cementum attachment protein (CAP)?
Answer
It is a cementum-derived collagenous protein.

It promotes spreading and adhesion of mesenchymal

cell types.
Osteoblasts and fibroblasts shows better adhesion than

keratinocytes and gingival fibroblasts.
Question 4
What is cementum derived growth factor (CGF)?
Fig. 4.1: Normal variations in tooth morphology at cemento-

Answer
enamel junction. (A) Space between enamel and cementum with It is an insulin like growth factor like molecule.
dentin (D); (B) End-to end relationship of enamel and cementum

and (C) cementum overlapping the enamel. It helps in proliferation of PDL cells and gingival fibroblasts.

23
Chapter 4 Cementum
Question 5
Multi-nucleated giant cells and large mononuclear
What are the functions of cementum? macrophages are seen adjacent to cementum

undergoing resorption.
Answer
Several resorption sites coalesce to form large areas of

Cementum provides anchorage to the tooth in its socket. destruction.
The ends of PDL fibres are embedded into the cementum,
Resorption may extend into dentine and pulp, but is
which helps in achieving this. generally painless.

Cementum helps in maintain the occlusal relationships.
Resorption may not always be continuous, but it may
Whenever there is attrition, the incisal or the occlusal alternate with periods of repair, with deposition of
surface gets abraded, because of which the tooth is supra- cementum.
erupted, to compensate for this occlusal discrepancy. The newly formed cementum may be demarcated by a
Cementum gets deposited at the apex of the tooth, in

deeply staining irregular line, referred to as reversal line.

such situations.
Embedded fibres of PDL forms a functional relationship
It also maintains the integrity of root surface, by acting as

with new cementum.

a reparative tissue for the root.

Viable connective tissue is required for cementum repair.
Question 6
Cementum repair can take place in vital as well as non
What is cementum resorption and repair? vital teeth.
Answer Question 7

Cementum of erupted as well as unerupted teeth What are reversal lines?
undergoes some amount of cemental resorption that
may be of microscopic proportion. Answer

There are various local and systemic factors that are
In periods of repair of cementum, the newly formed
responsible for cemental resorption. cementum is differentiated from the root by a

Various local factors responsible for cemental resorption deeply staining irregular line, which is known as
are as follows: reversal line. Reversal line consists of few collagen
Trauma from occlusion

fibrils and a high content of proteoglycans with

Orthodontic tooth movement

glycosaminoglycans.
Pressure from mal-aligned erupting teeth

Fibril intermingling takes place in between reparative
Cysts and tumours

cementum and resorbed cementum or dentin. This takes

Teeth without functional antagonists

place only at few places.
Embedded teeth

Embedded fibres of the PDL re-establishes a functional
Re-planted and transplanted teeth

relationship with the newly formed cementum.
Periapical disease

Periodontal disease.

Question 8

Various systemic factors responsible for cemental What is hypercementosis?
resorption are as follows:
Calcium deficiency

Answer
Hypothyroidism

Hypercementosis is also referred to as cemental
Hereditary fibrous osteodystrophy

hyperplasia.
Paget’s disease.

It is thickening of the cementum.

Microscopically cementum resorption appears as bay
It is mainly an age related process, and it may effect a
like concavities in the root surface. single tooth or the entire dentition.
24
It appears as a nodular enlargement at the apical It is a feature of abnormal repair as it occurs in teeth

one-third or appear as spike like excrescences because with cemental resorption.

of fusion of cementicles to the root or because of After chronic periapical inflammation.

calcification of periodontal fibres which are embedded Tooth replantation.

into cementum. Occlusal trauma

Around embedded teeth.
Causes of Hypercementosis

Diagnostic sign for ankylotic resorption are:

There can be two types of hypercementosis: Lack of physiologic mobility.

Upon percussion, there is usual a metallic sound.
1. Localised: It is seen in teeth without antagonist to

Teeth would be in infra-occlusion, if the ankylotic
keep pace with active eruption. It is believed to be a

compensatory mechanism to counteract the destruction process continues.
of fibrous attachment of the tooth. Proprioception is lost in ankylosed teeth, since PDL is

2. Generalised: It can be due to hereditary reasons or replaced by bone. The pressure receptor in the PDL is
patients having Paget’s disease. Acromegaly, arthritis, deleted or does not function.
calcinosis, rheumatic fever and thyroid goitre are some Also due to absence of periodontium, the physiologic

of the systemic conditions associated with generalized drifting and movement of teeth does not take place.
hypercementosis. Resorption lacunae are filled with bone, and the

periodontal space is absent.
Radiographic Features Treatment options for ankylosed teeth are as follows:

Restorative intervention.
Lamina dura appears radiopaque and periodontal

Surgical extraction of the affected tooth.

appears radiolucent, as it is seen in normal situation.

Periapical cemental dysplasia, condensing osteitis, and Question 10

focal periapical osteoporosis can be differentiated from
Enumerate the various differences between cellular and
hypercementosis that the above mentioned conditions
acellular cementum.
fall outside the shadow of periodontal and lamina dura.
Answer
Clinical Significance
Treatment is not required in cases of hypercementosis Acellular cementum Cellular cementum

Extraction in such conditions can create a problem. • It is also known as primary • It is also known as secondary
cementum. cementum.

In cases of multirooted teeth, sectioning of the tooth
should be done before extraction procedure. • It is formed before the teeth • It is formed after the teeth has
reaches the occlusion. reached occlusion.
Question 9 • It is devoid of cells. • It contains cementocytes.
Define ankylosis? • Sharpey’s fibre make up the • Sharpey’s fibre are found in
bulk. smaller proportions.
Answer • Seen at the coronal portion • Seen at apical portion.
Fusion of cementum with bone with obliteration of PDL • Slow formation. • Rapid formation.

is referred as ankylosis. • Collagen fibres are more • Collagen fibres are irregularly
organised. arranged.
Ankylosis may be seen in following situations.

hsipter Age-related Changes j
in Periodontium 1 -
j
o
CD
LONG ESSAYS o
LU
03
Question 1 There is presence of free radicals because of which there

is an accumulation of waste in the cell.
What are the effects of ageing on periodontium?
There is a decline in the physiologic processes of tissues
Answer because of all these factors.
Maximum changes are because of ageing, but few are
Cellular ageing is the cause for periodontal tissues ageing.
secondary to the physiologic deterioration, for example
Basis for the intrinsic changes are the cellular ageing. Every
loss of elasticity and increase in tissue resistance may
tissue is not affected in the same way in the process of
cause decrease in permeability, decrease in nutrient and
ageing, e.g. epithelial tissue renews very fast which is the
also the accumulation of waste in cells.
primary component of the periodontium, on the other
hand, nerve tissue and muscle tissue undergo very minimal Therefore, vascular peripheral resistance, i.e. decrease in
blood supply may decrease in cellular function.
renewal.
Intrinsic Changes Physiologic Changes

There is a reduction in tissue elasticity because of
In the process of ageing, the regenerative capacity of
decrease in number of collagen fibres.
tissues is slowed down because the cell renewal takes
place at a very slow pace. There is a decrease in production of mucopolysaccharides,
due to decreased vascularity.
There are very few cells left to renew, the dead cells as the
With ageing, alveolar bone shows a decrease in the bone
progenitor cells wear out and die gradually. This effect is
characteristic of the age related changes and biological
density, an increase in resorption of bone, and also a
decrease in vascularity. However, in contrast cementum
changes that occur with ageing.
shows cemental thickness.
The protein synthesis is also slowed down, because of all
these effects, the epithelium becomes thin because of
Functional Changes <x>
reduced keratinisation process. O
There is decrease in mitotic activity of the oral epithelium LU
Stochastic Changes and the periodontal ligament. Also, there is a decrease in
03
the metabolic rate of the tissues.
Stochastic changes occurring within the cells affect the Immune system is also found to be affected. As the
tissues. Morphological and physiological changes occur healing capacity of the tissues also declines. CD
in the process of glycosylation and cross linking. Inflammation, develops very rapidly and more severely.
Structures become stiffer due to reduced elasticity and There is a high susceptibility to fungal and viral infections
increase in mineralisation. because of abnormality in function ofT cells.
Structures become more thermally stable and become 00
Functional changes are associated with reduced efficiency
less soluble as there is a loss of regenerative power. of mastication. This efficacy is lost due to missing teeth,
There are structurally -altered protein and decrease in poorly fitting prosthesis, or non- compliance of the
protein synthesis because of somatic mutations. patient, who may refuse to wear prosthetic appliances.
26
Compensatory Changes soluble collagen, increase in mechanical strength, and

increased denaturing temperature.
Compensatory changes occur, due to ageing or disease.

These changes affect the periodontium in the following Periodontal Ligament

ways:
Bone height is reduced and there is presence of
Fibroblasts are reduced and their structure becomes

irregular.

gingival recessions.
Attrition is also seen as a compensatory change which
Organic matrix production and epithelial cells are

reduced but elastic fibres are increased.

acts as a stabilizer between loss of bony support and
excessive leveraging from occlusal forces imposed on Width of periodontal ligament may increase or decrease.

teeth. The periodontal ligament width is increased because of

There is a reduction in overjet of the teeth, manifesting less number of teeth supporting the entire functional

as an increase in the edge-to-edge contact to the load.
approximal wear of the posterior teeth. The periodontal ligament width is decreased because

There is an increase in food table area, with loss of of reduced strength of the masticatory musculature and

sluiceways and in the mesial migration. continues deposition of cementum and bone.
Effect of Ageing on Periodontal Tissues Cementum

There is an increase in width of cementum, which is a
Gingiva
common finding, since deposition continues after tooth
Gingival Epithelium eruption.
There is thinning and decrease in keratinization of
Because of accumulation of resorption bays, there is an

increase in surface irregularity.

gingival epithelium because of which there is epithelial
permeability to bacterial antigens and a decreased
Alveolar Bone
resistance to functional trauma.
Rete pegs gets flattened and cellular density is also There is decrease in vascularity.

altered. Osteoporosis is seen.

Stippling is reduced or is unchanged. There is a decrease in healing capacity and reduction in

Width of attached gingiva is increased. metabolic rate.

Inter-cellular substances are increased. Rate of bone deposition is decreased, whereas rate of

bone resorption is increased.
Gingival Connective Tissue Alveolar bone facing periodontal ligament shows

Connective tissue becomes coarser and denser due to irregularities. Because of irregular periodontal surface of

increase in rate of conversion of insoluble collagen into bone, there is an irregular insertion of collagen fibres.
SHORT ESSAYS
Question 1 Factors which can modify the relationship between

What is the nature of periodontal diseases in older age group? periodontal disease and age are general health status,
immune status, diabetes, nutrition, smoking, genetics,
Answer medications, mental-healthstatus, salivary flow,
Chronic periodontitis is the disease of periodontal tissues functional deficits, and finances.
Gingival tissues can also be altered by medications
seen mainly in older adults.

prescribed for older adults, e.g. in post-menopausal women
Chronic periodontitis seen in older adults is due to
who are receiving steroids, steroid-induced gingivitis can

accumulation of disease over time. Therefore, it is chronic.
be seen. Drugs like cyclosporins, calcium channel blockers,
One of the theory states that many sites of advanced perio- and anticonvulsants can induce gingival overgrowth. This

dontitis, resulted in tooth loss, early in life, which suggests gingival enlargement can further decrease an individual
that old age is not a risk factor for periodontal disease. ability to maintain proper oral hygiene.
27
Chapter 5 Age-related Changes in Periodontium
Question 2 Answer
What is bruxism and what are its effects on the periodontium? Age changes in periodontal ligament are as follows:

Answer Fibroblasts are reduced and their structure becomes

irregular.
Bruxism can be defined as diurnal or nocturnal Organic matrix production and epithelial cells are

parafunctional activity that includes clenching, bracing, reduced and elastic fibres are increased.
gnashing and grinding of teeth. Width of periodontal ligament may increase or decrease.

The periodontal ligament width is increased because of

Effects of Bruxism on Periodontium

less number of teeth supporting the entire functional load.

They are tooth mobility, tooth fracture, tooth wear, The periodontal ligament width is decreased because

periodontal and muscular pain. Bruxism can be managed of reduced strength of the masticatory musculature and
by a stabilization appliance like a night guard. continues deposition of cementum and bone.
What are the age changes in cementum?
What are the age changes seen in gingiva?
Answer
Answer
Age changes in cementum are as follows:
Gingival Epithelium There is an increase in width of cementum, which is a

There is thinning and decrease in keratinization of common finding, since deposition continues after tooth
gingival epithelium because of which there is epithelial eruption.
Because of accumulation of resorption bays, there is an
permeability to bacterial antigens and a decreased

resistance to functional trauma. increase in surface irregularity.

Rete pegs gets flattened and cellular density is also Question 6
altered.
What are the age changes seen in alveolar bone?

Stippling is reduced or is unchanged.

Width of attached gingiva is increased. Answer

Intercellular substances are increased. Age changes seen in alveolar bone are as follows:
There is decrease in vascularity.
Gingival Connective Tissue

Osteoporosis is seen.

Connective tissue becomes coarser and denser due to There is a decrease in healing capacity and reduction in

increase in rate of conversion of insoluble collagen into metabolic rate.

soluble collagen, increase in mechanical strength, and Rate of bone deposition is decreased, whereas rate of

increased denaturing temperature. bone resorption is increased.

Alveolar bone facing periodontal ligament shows
Question 4

irregularities. Because of irregular periodontal surface of

What are the age changes in periodontal ligament? bone, there is an irregular insertion of collagen fibres.
6 Classification of

Chapter
Periodontal Diseases
LONG ESSAYS
Question 1 Mucocutaneous disorders: Lichen planus, pemphigus,

pemphigoid, etc.
What is the 1999 International workshop for classification of
Allergic reactions:
periodontal diseases and conditions?

h Dental restorative materials—mercury, acrylic, etc.
h
Answer h Reactions attributed to toothpastes/dentifrices,
h
mouth rinses/washes, chewing gum additives,
Gingival Diseases food and additives.
Dental Plaque Induced h Others.
h
Traumatic lesions: Chemical, physical, thermal, factitious,
Associated with dental plaque only with or without other

iatrogenic, accidental.

local contributing factors.
Foreign body reactions.
Gingival diseases modified by systemic factors:

Not otherwise specified (NOS).

Associated with endocrine system: Puberty -

associated gingivitis, menstrual-cycle associated Chronic Periodontitis
gingivitis, pregnancy associated gingivitis, pyogenic
It is based on clinical radiographic, historic and laboratory
granuloma and diabetes mellitus associated gingivitis.
characteristics:
Associated with blood dyscrasias: Leukaemia Localized (< 30% of sites involved)

associated gingivitis and others.

Generalized (> 30% of sites involved).
Gingival diseases modified by medications:

Drug- induced gingival enlargements Aggressive Periodontitis

Drug- influenced gingivitis, e.g. oral contraceptives, etc. Otherwise clinically healthy individuals, rapid attachment

Gingival diseases modified by malnutrition, e.g. vitamin and bone loss, not consistent with local deposits, familial

C and others. aggregation.
Localized (circumpubertal onset, first molar or incisor

Non-plaque-induced Gingival Lesions has proximal attachment loss, robust serum antibody
response to infective agents).
Specific bacterial origin: Neisseria gonorrhoeae,
Generalized (affects below 30 years of age, generalized

Treponema pallidum, streptococcal species and others.

proximal attachment loss, poor serum antibody response
Viral origin: Herpes virus infections and others. to infective agents, episodic nature of periodontal disease).

Fungal origin: Candida species infections, linear gingival

erythema, histoplasmosis and others. Periodontitis as a Manifestation of Systemic
Genetic origin: Hereditary gingival fibromatosis and Disease

others. Associated with haematological disorders: Acquired

Manifestations of systemic conditions: neutropenia, leukaemia, and others.

29
Chapter 6 Classification of Periodontal Diseases

Associated with genetic disorders: Leukocyte adhesion Answer
deficiency (LAD) syndromes and others.

It is based upon clinical, radiographic, historical and
Necrotizing Periodontal Diseases laboratory characteristics, periodontitis can be classified as:
Chronic periodontitis.
NUG, NUP.

Aggressive periodontitis.
Abscesses of the Periodontium
Periodontitis as a manifestation of systemic disease.
Gingival, periodontal, pericoronal abscesses. Chronic Periodontitis

Following characteristics can be seen in a patient of chronic
Periodontitis Associated with Endodontic Lesions periodontitis:
Combined periodontal-endodontic lesion.
Prevalent in adults, but can occur in children.
Amount of destruction consistent with local factors.
Developmental or Acquired Deformities and

Associated with a variable microbial pattern.

Conditions

Subgingival calculus frequently found.

Localized tooth related factors that modify or predispose
Slow to moderate rate of progression with possible
to plaque induced gingival diseases/periodontitis. periods of rapid progression.
Tooth anatomic factors.
Possible modified by or associated with the following:

Dental restorations/appliances.

Root fractures.

Systemic diseases such as diabetes mellitus and
Cervical root resorption and cemental tears.

human immunodeficiency virus (HIV) infection.
Local factors predisposing to periodontitis.
Mucogingival deformities and conditions around teeth

Gingival/soft tissue recession on facial/lingual/

Environmental factors such as cigarette smoking and
interproximal/papillary. emotional stress.
Lack of keratinized gingiva.

Chronic periodontitis may be further subclassified into
Decreased vestibular depth.

localized and generalized forms and characterized as slight,
Aberrant frenum/muscle position.
moderate, or severe based on the common features:
Localized form: Less than 30 % of sites involved.

Gingival excess.
Generalized form: More than 30 % of sites involved.

Pseudo pockets, inconsistent gingival margin, excessive

gingival display, gingival enlargement, abnormal colour,

Slight: 1–2 mm of clinical attachment loss.
mucogingival deformities and conditions on edentulous
Moderate: 3–4 mm of clinical attachment loss.
ridges.
Severe: > = mm of clinical attachment loss.
Vertical and/or horizontal ridges deficiency.

Lack of gingival/keratinized tissue.

Aggressive Periodontitis
Gingival/soft tissue enlargement.

Aberrant frenum/muscle position.

Following characteristics can be seen in the patient suffering
Decreased vestibular depth.

from aggressive periodontitis:
Abnormal colour.

Otherwise clinically healthy patient.

Occlusal trauma
Rapid attachment loss and bone destruction.
Primary occlusal trauma.

Amount of microbial deposits inconsistent with disease
Secondary occlusal trauma.

severity.
Familial aggregation of diseased individuals.
Question 2

What is the American Academy of Periodontology (AAP) The following characteristics are common but not universal:
1999 classification of periodontal diseases? Describe in
Diseased sites infected with Actinobacillus actinomy-
detail. cetemcomitans.
30
Abnormalities in phagocyte function. Periodontitis as a Manifestation of Systemic

Hyper-responsive macrophages, producing increased Disease

prostaglandin E2 (PGE2) and interleukin-1 beta.
Periodontitis may be observed as a manifestation of the
In some cases, self-arresting disease progression. following systemic disease:

Aggressive periodontitis may be further classified into Haematologic disorders:

localized and generalized forms based upon the common Acquired neutropenia.

features described here and the following specific features. Leukaemias.

Others.
Localized Form

Genetic disorders:

Circumpubertal onset of disease. Familial and cyclic neutropenia.

Localized first molar or incisor disease with proximal Down syndrome.

attachment loss on at least two permanent teeth, one of Leucocyte adhesion deficiency syndromes.

which is a first molar. Papillon-Lefevre syndrome.

Robust serum antibody response to infecting agents. Histiocytosis syndromes.

Glycogen storage disease.
Generalized Form

Infantile genetic agranulocytosis.

Usually affecting persons under 30 years of age (however, Chediak-Higashi syndrome.

may be older). Cohen syndrome.

Generalized proximal attachment loss affecting at least Ehlers-Danlos syndrome (types IV and VII AD).

three teeth other than first molars and incisors. Hypophosphatasia.

Pronounced episodic nature of periodontal destruction. Others.

Poor serum antibody response to infecting agents. Not otherwise specified.

SHORT ESSAYS
Question 1 Aberrant frenum or muscle position

What are the various developmental or acquired deformities Gingival excess?

h Pseudopocket
and conditions?
h
h Inconsistent gingival margin
Answer
h
h Excessive gingival display
h
h Gingival enlargement
Various developmental or acquired deformities and
h
h Abnormal colour
conditions are as follows:
h
Localized tooth-related factors that modify or predispose Mucogingival deformities and conditions on edentulous

to plaque-induced gingival diseases or periodontitis. edges.
Tooth anatomic factors Vertical and/or horizontal ridge deficiency

Dental restorations or appliances Lack of gingiva or keratinized tissue

Root fractures Gingival or soft tissue enlargements

Cervical-root resorption and cemental tears.
Aberrant frenum or muscle position

Mucogingival deformities and conditions around teeth. Decreased vestibular depth

Gingival or soft tissue recession
Abnormal colour

h Facial or lingual surfaces

Occlusal trauma.
h

h Interproximal (papillary)

h
Lack of keratinized gingiva Primary occlusal trauma

Decreased vestibular depth Secondary occlusal trauma.

31
Chapter 6 Classification of Periodontal Diseases
Question 2 2. Early-onset periodontitis Age of onset less than 35 years, rapid

(may be prepuber tal, rate of disease progression, defect in
What are the various classifications of various forms of

juvenile, or rapidly host defences, associated with specific
Periodontitis? progressive) microflora
3. Periodontitis associated Systemic disease that predispose to
Answer with systemic disease rapid rates of periodontitis. Diseases
are: diabetes, Down’s syndrome,
Various classifications of various forms of periodontitis are
human immunodeficiency virus (HIV)
as follows: infection, Papillon-Lefevre syndrome

According to American Academy of Periodontology (AAP) 4. N ecrotizing ulcerative Similar to acute necrotizing ulcerative
world workshop in clinical periodontics (year 1989). periodontitis gingivitis but with associated clinical
attachment loss

European Workshop in Periodontology (year 1993).
5. Refractory periodontitis Recurrent periodontitis that does not

According to American Academy of Periodontology respond to treatment
International Workshop for Classification of Periodontal
Diseases (year 1999).
Chronic periodontitis.

Forms of periodontitis Disease characteristics
Aggressive periodontitis.
1. Adult periodontitis Age of onset: 4th decade of life, slow
rate of disease progression, no defects

Periodontitis as a manifestation of systemic disease.

in host response
2. Early-onset periodontitis Age of onset: Before 4th decade of
Forms of periodontitis Disease characteristics life, rapid rate of disease progression,
defect in host defence
1. Adult periodontitis Age of onset more than 35 years, slow
rate of disease progression, no defect 3. Necrotizing periodontitis Tissue necrosis with bone and
in host defences attachment loss
7
Epidemiology of

Chapter Gingival and
SHORT ESSAYS
Question 1 Scoring Criteria

Discuss about the community periodontal index of 0 = negative: There is neither overt inflammation in the
treatments needs (CPITN) PROBE.

investing tissues nor loos of function due to destruction
Answer of supporting tissues
1 = mild gingivitis: There is an overt area of inflammation
It is also termed as WHO probe.

in the free gingiva but this area does not circumscribe
It serves three goals: the tooth.

1. Measures pocket depth.
2 = gingivitis: Inflammation completely circumscribes
2. Detects subgingival calculus.

the tooth, but there is no apparent break in the epithelial
3. Manipulate the sensitive soft tissues around the attachment.
tooth.
6 = gingivitis with pocket formation: The epithelial
The probe has a ball and tip of 0.5 mm diameter that

attachment has been broken and there is a pocket (not

allows detection of subgingival calculus and gingival
merely a deepened gingival crevice caused by swelling
bleeding without causing trauma to the tissues.
in the free gingiva). There is no interference with normal
Probe has a black band beginning at 3.5 mm from the tip masticatory function; the tooth is firm in its socket and

and ending at 5.5 mm [CPITN-E (epidemiological)]. has not drifted.
Probe has two additional markings of 8.5 mm and 11.5
8 = advanced destruction with loss of masticatory

mm [CPITN-C (clinica)].

function: The tooth may be loose, may be drifted, may
Question 2 sound dull on percussion with metallic instrument and
may be depressible in its socket.
What is Russell’s periodontal index?
Russell’s rule: When in doubt assign a lower score.

Answer The value obtained by calculating individual score is

interpreted as follows:
This index was proposed by Russell in 1950s.

0– 0.2—clinically normal supportive tissue.
This index requires a light source, mouth mirror and

0.3–0.9—simple gingivitis.

explore.

1–1.9—beginning of destructive periodontal disease.

Supporting tissues of each tooth has scored according to 2–4.9—established destructive periodontal disease.

progressive scale that gives little importance to gingival

5–8—terminal disease.
inflammation and higher weightage to advanced

periodontal disease. Question 3
An individual score is the sum of the tooth scores divided What is periodontal disease index (given by SP Ramfjord,

by the number of teeth examined. 1959)?
33
Chapter 7 Epidemiology of Gingival and Periodontal Diseases
Answer
Instruments used are mouth mirror, dental explorer and
light source.
In this index six pre-selected teeth in the mouth are

The teeth selected are: 16, 12, 24, 36, 32, 44.

examined, viz.:

Only plaque at the cervical third of the tooth is evaluated

1. Maxillary right first molar.

and no attention is given to the plaque that has extended

2. Maxillary left central incisor above that.
3. Maxillary left first premolar
Scoring criteria:
4. Mandibular left first molar 0 = No plaque in the gingival area

5. Mandibular right central incisor 1 = A film of plaque adhering to free gingival margin at

6. Mandibular right first premolar the adjacent area of tooth. The plaque may be recognized

In this index cemento-enamel junction (CEJ) is used as only after the application of disclosing agent.
a fixed landmark for measuring periodontal attachment 2 = Moderate accumulation of soft deposits within the

loss. gingival pocket on the gingival margin which can be

To begin the assessment, the examiner dries the area seen by the naked eye.
3 = Abundance of soft matter within the gingival
around the six teeth.
pocket and/or on the gingival margin and on the

Then the examiner assesses the severity of gingival
adjacent tooth surface.

inflammation and gives the following scores:

G0 = Absence of inflammation

Plaque index score of each tooth equals to total score of
each tooth divided by four.

G1 = Mild to moderate inflammatory gingival changes,

not extending all around the tooth

Plaque index for individual = total of plaque index of
each tooth divided by number of teeth examined.
G2 = Mild to moderate severe gingivitis extending

around the tooth

Interpretation:
0—excellent
G3 = Severe gingivitis characterized by marked

0.1–0.9—good
redness, tendency to bleed and ulceration.

1.0–1.9—fair

Recording of Pocket 2.0–3.0—poor.

The distance from the CEJ to the bottom of the gingival Question 5
sulcus is the measurement of periodontal attachment What is oral hygiene index-simplified (OHI-S) ?
loss.

If the gingival sulcus does not extend apically to the CEJ, Answer
in any of the measured areas the periodontal disease
It was given by Greene and Vermillion in the year 1964.
index (PDI) score for the tooth is the gingival score.
This index measures the surface area of the tooth that is

If the gingival sulcus extends below the CEJ in any of the covered by debris and calculus.
measured areas by 3 mm or less the PDI score is 4. It consist of two components: (1) debris index-simplified

If the sulcus measurement is between 3 mm and 6 mm (DI-S) and (2) calculus index-simplified (CI-S).
the PDI score is 5. If it is more than 6 mm, the PDI score Scoring criteria for DI-S:
is 6.

0 = No debris or stain present.

If the free gingival margin is on the cementum, it distance

1 = Soft debris covering not more than one-third of the

from CEJ is recorded as a negative number.

tooth surface or the presence of extrinsic stains without

Question 4 other debris regardless of surface area covered.
2 = Soft debris covering more than one-third but not
What is Silness-löe Index?
more than two-third of the exposed tooth surface

Answer 3 = Soft debris covering more than two-thirds of the

This is also known as plaque index. exposed tooth surface.

The purpose of this index is to assess the thickness of

Scoring criteria for CI-S:
plaque only at gingival surface.
0 = No calculus present.
34
1 = Supragingival calculus not covering more than Calculus index simplified scores per person is obtained

one-third of the exposed tooth surface. by totalling the calculus scores per tooth surface and

2 = Supragingival calculus covering more than one- dividing it by the number of surfaces examined.

third but not more than two-third of the exposed The OHI-S scores per person is the sum total of DI-S and

tooth surface or the presence of individual flex of CI-S scores per person.
subgingival calculus around the cervical portion of
Interpretation of DI-S/CI-S scores:
the tooth or both.

0.0–0.6—good
3 = Supragingival calculus covering more than two-

0.7–1.8—fair

third of the exposed tooth surface or a continuous

1.9–3—poor.
heavy band of subgingival calculus around the

cervical portion of the tooth or both. The Interpretation of OHI-S scores:

0.0–1.2—good
Debris index simplified score per person is obtained by

totalling debris scores per tooth surface and dividing it 1.3–3.0—fair

by the number of surfaces examined. 3.1–6.0—poor.

8

Chapter Periodontal
Microbiology
LONG ESSAYS
Question 1 Formation of the Pellicle

Define dental plaque. Explain in detail about plaque as a All surfaces of the oral cavity are coated with a pellicle.
biofilm. Acquired Pellicle
Answer Within nanoseconds after vigorous polishing of the teeth, a
thin saliva derived layer, called the acquired pellicle, covers
Dental plaque is a specific but highly variable structural entity,
the tooth surface.
resulting from sequential colonisation of microorganisms
on tooth surfaces, restorations and other parts of oral cavity,
composed of salivary components like mucin, desquamated
epithelial cells, debris and microorganisms, all embedded in
extracellular gelatinous matrix (WHO, 1961).
Plaque as a Biofilm
Bacteria in a biofilm are not distributed evenly. They are

grouped in microcolonies surrounded by an enveloping
intermicrobial matrix.
Dental plaque biofilm is heterogeneous in structure,

with open fluid-filled channels running through the
plaque mass (act as circulatory system). The matrix is
penetrated by fluid channels that conduct the flow of
nutrients, waste products, enzymes, metabolites, and
oxygen. These microcolonies have micro-environments
with differing pH, nutrient availability, and oxygen
concentrations.
The bacteria in a biofilm communicate with each other

by sending out chemical signals. These chemical signals
trigger the bacteria to produce potentially harmful
proteins and enzymes.
Plaque Formation at an Ultrastructural Level

Process of plaque formation divided into three major phases
(Fig. 8.1):
1. The formation of pellicle on tooth surface.
2. Initial adhesion and attachment of bacteria.
3. Colonisation and plaque maturation. Fig. 8.1: Diagram showing plaque formation
36
Composition of the Pellicle Eighteen genera from the oral cavity show some form

Glycoproteins (mucin). of co-aggregation.

Proline-rich proteins. Co-aggregation is the cell-to-cell recognition of

Phosphoproteins (e.g. statherin). genetically distinct partner cell type.

Histidine-rich proteins.
All oral bacteria possess surface molecules (protein or

Enzymes (α-amylase) and other molecules that can carbohydrate molecules) that foster some type of cell

function as adhesion sites for bacteria. interaction.
Bacteria can colonise tooth surface only when this
Fusobacteria co-aggregate with all other human oral

pellicle is in place for some hours. bacteria; whereas veillonellae, capnocytophage and
prevotella bind to streptococci and actinomyces.
Study of early (2 hourly) enamel pellicle reveal that its
Most co-aggregations among strains of different
amino acid composition differs from that of saliva.

genera are mediated by lectin like adhesins and
Mechanism involved inhibited by lactose and other galactosides.
Electrostatic.
Early Coloniser

Van der waals.

Hydrophobic forces. Each strain of early coloniser is coated with distinct

molecules. Identical cells coated with a specific salivary
Initial Adhesion and Attachment of Bacteria molecule may agglutinate, leading to microconcentration
This situation is very complex. The microbial adhesion to and juxta-positioning of a particular strain.
surfaces in an aquatic environment as a four stage sequence. Secondary colonisers interact with early colonisers,

Phase 1: Transport to the surface: co-aggregation of fusobacterium nucleatum with S.

Random contact may occur through Brownian motion sanguinis.

(40 µm/hr) causing sedimentation of microorganisms, Prevotella loescheii with Actinomyces viscosus.

via liquid flow or chemotactic activity. Capnocytophaga ochracea with Actinomyces viscosus.

Phase 2: Initial Adhesion: Co-aggregation has focussed on interactions among

Reversible adhesion of the bacterium, initiated by the different Gram positive species and between Gram

interaction between the bacteria and the surface from positive and Gram negative species.
a certain distance. Both Actinomycetes and Streptococci are facultative

Phase 3: Attachment: anaerobes, doubling times for microbial populations

After initial adhesion, a firm anchorage between during first 4 hours of development is less than 1 hour.

bacterium and surface will be established by specific
interactions (covalent, ionic or hydrogen bonding). Secondary Coloniser
On rough surface, bacteria are better protected Prevotella intermedia.

against shear forces. P. loescheii.

Each streptococcus and actinomyces strain binds Capnocytophaga.

specific salivary molecules. F. nucleatum.

Streptococcus sanguinis, the principle early coloniser
Porphyromonas gingivalis.

bind to acidic proline-rich proteins and other In the later stages of plaque formation, co-aggregation
receptors in pellicle such as α-amylase and sialic acid. between different Gram negative species is likely to
Actinomyces can also function as primary colonisers.
predominate, e.g. “Corncob” formation. Streptococci adhere

Viscosus possesses fimbriae which contain adhesions
to filaments of Bacterionema matruchotii or Actinomyces

which also bind to the proline rich-layer. specis and the “test tube brush” composed of filamentous
Hidden receptors for bacterial adhesions are referred
bacteria to which Gram negative rods adhere.

to as cryptitopes.
Phase 4: Colonisation of the surface and biofilm Secondary Colonisers fall Into (Fig. 8.2)

formation: Green complex: Eikenella corrodens, Actinobacillus

Firmly attached microorganisms start growing and actinomycetemcomitans serotype A and Capnocytophaga

bacterial clusters are formed, then microcolonies or a species.
biofilm can develop. Orange complex: Fusobacterium, Prevotella, and

Therefore intrabacterial connections occur. Campylobacter.

37
Chapter 8 Periodontal Microbiology

S. sanguinis–hydrogen peroxide lethal to cells of
Actinomycetemcomitans.

C. ochraceus and S. sanguinis are associated with greater
gain in attachment after therapy.
Gingivitis
After 8 hours without oral hygiene, bacteria may be found
at concentrations of 103 to 104/mm2 of tooth surface and
will increase in number by a factor of 100–1,000 in the
next 24-hours period. After 36 hours, the plaque becomes
clinically visible.
The transition to gingivitis is evident by inflammatory
changes and is accompanied first by the appearance of
Gram-negative rods and filaments, spirochetal and motile
microorganisms.
Microbiota of Dental-plaque-induced Gingivitis

(Chronic Gingivitis)
It consist of the following:
Fig. 8.2: Various bacterial complexes. Gram positive (S. sanguis, S. mitis, S. intermedius, S. oralis,

A. viscosus, A. naeslundii, and P. micros).

Red complex: P. gingivalis, Tannerella forsythia and Gram negative (F. nucleatum, P. intermedia, and V. parvula,

Treponema denticola. Haemophilus, Capnocytophaga, and Campylobacter

Yellow complex: Streptococcus specis. species), facultative and anaerobic microorganisms.

Purple complex: Actinomyces odontolyticus.
Question 2 Pregnancy-associated Gingivitis

Describe various microorganisms associated with specific It is an acute inflammation of the gingival tissues associated
periodontal diseases. with pregnancy. P. intermedia is associated with this
gingivitis. It is accompanied by increase in steroid hormones
Answer in crevicular fluid and increases in the levels of growth
The total number of bacteria, determined by microscopic factors.
counts per gram of plaque was twice as high in periodontally
diseased sites than in healthy sites. Chronic Periodontitis
More motile rods and spirochetes are found. Fewer Bacteria seen are:
coccal cells are present.
P. gingivalis, T. forsythia, P. intermedia, C. rectus, E.

corrodens, F. nucleatum, A. actinomycetemcomitans, P.

Periodontal Health micros, Treponema and Eubacterium species.
Bacteria associated with periodontal health are Gram Recent studies shown that presence of subgingival

positive facultative species and members of the genera Epstein-Barr virus type 1 (EBV-1) and human
Streptococcus and Actinomyces (e.g. S. sanguinis, S. mitis, A. Cytomegalovirus (HCMV) are associated with high
viscosus, A. naeslundii). Small proportions of Gram negative levels of putative bacterial pathogens, i.e. P. gingivalis,
species P. intermedia, F. nucleatum, Capnocytophaga, T. forsythia, P. intermedia, and T. denticola.
Neisseria and Veillonella species. Few spirochetes and
motile rods are also present. Microbial Shift during Disease
Species beneficial to host are: Comparing the microbiota in health, gingivitis, and
S. sanguinis, Veillonella parvula and Capnocytophaga

periodontitis, the following microbial shifts can be identified:
ochraceus. From gram positive to gram negative

38
From cocci to rods (and at a later stage to spirochetes) Two gingival tissue responses can be found in the cases of

From non-motile to motile organisms GAP:

From facultative anaerobes to obligate anaerobes One is severe, acutely inflamed tissue, often proliferating,

From fermenting to proteolytic species. ulcerated and fiery red.

Bleeding may occur by slight stimulation
Localised Aggressive Periodontitis

This tissue response occurs in the destructive stage, in

Localised aggressive periodontitis (previously referred to which attachment and bone are actively lost.

as localised juvenile periodontitis) develops around the Patients with the diagnosis of GAP arrested spontaneously
time of puberty, is observed in females more often than or after the therapy, whereas others may continue to
in males and affects. progress inexorably to tooth loss, despite intervention with
The first symptom of localised aggressive periodontitis conventional treatment.

(detectable in deciduous) dentition is periodontal
destruction around canines and second molars. Necrotising Periodontal Disease
Microbiota: Gram negative, capnophilic and anaerobic

rods. Characterised by necrosis of the marginal gingival tissue

A. actinomycetemcomitans compose 90% of the and interdental papillae

microbiota. A. actinomycetemcomitans can be classified Clinically associated with stress or HIV infection

into six distinct serotypes (A to F) based on the surface Accompanied by mal-odour, pain, and systemic

polysaccharides located on the O side chains of symptoms including lymphadenopathy, fever and
lipopolysaccharides. malaise
P. gingievalis, E. corrodens, C. rectus, F. nucleatum, High levels of P. intermedia, and spirochetes are found in

B. capillus, Eubacterium brachy, Capnocytophaga species ulcerative gingivitis lesions
and spirochetes. Spirochetes are found to penetrate necrotic tissue and

Herpes virus, including EBV-1 and HCMV play important unaffected connective tissue.

roles in the aetiopathogenesis of severe types of
periodontitis. Abscesses of the Periodontium
HCMV associated periodontal sites also tend to harbour Acute lesions that result in very rapid destruction of the

elevated levels of bacteria including P. gingivalis, periodontal tissues.
T. forsythia, T. denticola, Campylobacter rectus and Occur in patient with untreated periodontitis or during

A. actinomycetemcomitans. maintenance phase.
A high prevalence of HCMV and EBV type-1 DNA revealed May occur in the absence of periodontitis, associated

in aggressive periodontitis sites compared to healthy sites. with impaction of foreign material.
Mechanical debridement with antibiotics are necessary Clinical symptoms: Pain, swelling, suppuration, bleeding

to control the levels of A. actinomycetemcomitans.

on probing, and mobility of the involved teeth. Systemic
involvement including cervical lymphadenopathy and
Generalised Aggressive Periodontitis
WBC count.
Generalised aggressive periodontitis (GAP) affects Pathogens include: F. nucleatum, P. intermedia, P. micros,

individuals under the age of 30, but older patients may and T. forsythia are present.
be affected.
Characterised by generalised interproximal attachment Periodontitis as Manifestation of Systemic

loss affecting at least three permanent other than first Disease
molars and incisors.
The destruction occurs episodically, with periods of Demonstrates varied immune deficiency, neutrophil

advanced destruction followed by weeks to months or defects and leucocyte adhesion defects.
years. Recent studies: Some cases of severe periodontal

Small amount of plaque associated with the affected destruction are associated with a mutation in the

teeth. cathepsin C gene in affected children.
P. gingivalis, A. acintomycetemcomitans, and T. forsythia Increased host susceptibility resulting from systemic

are detected in the plaque that is present. disease.
39
Peri-implantitis Pathogenicity
It is an inflammatory process that affects the tissues This species produces several proteolytic enzymes that are

around an already osseo-integrated implant and able to destroy immunoglobulin and factors of complement
resulting in loss of supporting bone. system. It also induces apoptotic cell death.
Healthy peri-implant is pocket characterized high
Porphyromonas Gingivalis

proportions of coccoid cells, a low-ratio anaerobic

or aerobic species, a low number of Gram-anaerobic P. gingivalis is a non-motile, pleomorphic rod and Gram −ve
species and low detection frequencies for periodontal obligate anaerobe. Its form based on the capsule type.
pathogens.

Peri-implantitis reveal a complex microbiota. A. Culture Conditions and Identification
actinomycetemcomitans, P. gingivalis, T. forsythia, P. It grows anaerobically with dark pigmentations on blood
micros, Campylobacter rectus, Fusobacterium and agar. L. Porphyromonas gingivalis has a strong proteolytic
Capnocytophaga are isolated from failing sites. activity.

Pseudomonas aeruginosa, enterobacteriaceae, Candida
albicans, and staphylococci are frequently detected Specific Pathogenic Characteristics
around implants.
Aggressive periodontal pathogen. Its fimbriae mediate

High proportions of Staphylococcus aureus and S. adhesion, and its capsule defends against phagocytosis.
epidermidis on oral implants have also been reported.
Produces series of virulence factors, including proteases,
haemolysin and a collagenase.
Question 3
Also inhibit migration of PMNs across an epithelial barrier
What are the various key characteristics of specific and affects the production or degradation of cytokines
pathogens? by mammalian cells.
Answer
P. gingivalis also has the capacity to invade soft tissues.
Actinobacillus Actinomycetemcomitans Prevotella Intermedia and Prevotella Nigrescens

Size varies from 0.4–1 µm. Prevotella group are short, round-ended, non-motile, Gram

Straight or curved rods with rounded ends. negative rods. Its forms P. intermedia and P. nigrescens are

It is non-motile and Gram negative. the most pathogenic.
Forms: Five serotypes (a-e).
Culture Condition and Identification

Culture Condition and Identification Grow anaerobically, with dark pigmentation on blood agar.
Grows as a white, translucent, smooth, non-haemolytic
Special Pathogenic Characteristics

colony on blood agar, because of its low density.

A. actinomycetemcomitans is preferably identified on a Prevotella species are less virulent and less proteolytic than
specific growth medium (with vancomycin and bacitracin P. gingivalis.
as antibiotic to suppress other species) under 5–10%
carbon dioxide where it appears white, translucent Campylobacter Rectus
colony with a star-shaped internal structure.
It is one of the rare motile organisms involved.

It possesses a number of virulence factors including
It is Gram negative, short rod, curved or helical.
lipopolysaccharide (endotoxin), a leucotoxin collagenase
The motility results from the polar flagellum.
and a protease.
Culture Conditions and Identification
Tannerella Forsythia Grows anaerobically with dark pigmentation. Sulphide is
It is a non-motile, spindle shaped, highly polymorphic rod added → FeS, giving a grey stain.
and a Gram negative obligate anaerobe.
Culture Conditions and Identification Produces a leucotoxin.
It grows slowly only under anaerobic conditions and need C. rectus is less virulent and less proteolytic than P.
several growth factors from other species. gingivalis.
40
Fusobacterium Nucleatum Question 4

It is a Gram negative, cigar shaped bacillus with pointed What is the composition of plaque? What is the classification

ends. of plaque?
Its forms are F. nucleatum ss nucleatum, F. nucleatum ss
polymorphum, F. nucleatum ss vincentii, and F. periodonticum.
Answer
Plaque is mainly composed of microorganisms:
Culture Conditions and Identification One gram of plaque approximately contains 1011 bacteria.

Grows anaerobically on blood agar and can easily be Non-bacterial microorganisms like yeast, mycoplasma,

identified on a specific medium. protozoa, and viruses are also present in small amounts.
Cells like host cells, e.g. epithelial cells, macrophages and

leucocytes are also present.
Induc apoptotic cell death in mononuclear and Organic matter of plaque consists of mainly polysaccharide

polymorphonuclear cells and can trigger the release of protein produced by plaque microorganisms. Proteins
cytokines, elastase, and oxygen radicals from leucocytes. such as albumin are present. Levans, glucans, galactose,
Believed to be important bridging organisms. and methyl pentose are some carbohydrates produced

by bacteria. Small amounts of lipids found in plaque are
Peptostreptococcus Micros derived from the disrupted cell walls of gram negative
This is one of the rare cocci in periodontitis. This species is bacteria.
The main inorganic matter of dental plaque consists of
Gram +ve and grows obligate anaerobically.

calcium, and phosphorous along with small amounts of
Eubacterium Species magnesium, sodium and potassium.
Gm positive, obligate anaerobic, small pleomorphic rod.
Classification of Dental Plaque

Forms: E. nodatum, E. brachy, and E. timidum.

Culture Conditions and Identification It is majorly classified as:
Supragingival (Fig. 8.3).
Grow anaerobically, but with difficulty on standard blood

Subgingival.
agar.

Supragingival plaque is further classified as :

Coronal plaque: It is in contact with only the tooth
Spirochaetes

surface.
Represent a diverse group of spiral, motile organisms. Marginal plaque: It is in contact with tooth surface at

They are helical rods 5–15 µm long with a diameter of the margin of gingiva.

0.5 µm. Subgingival plaque is further classified as:

Forms: Treponema denticola, Treponema vincentii, Attached plaque.

Treponema socranskii (often associated with Unattached plaque.

periodontitis), and Treponema pallidum (associated with
secondary syphilis).
Culture Conditions and Identification
Extremely difficult to grow and need strict anaerobic
conditions and a specific medium.

Ability to travel through viscous environments enables

them to migrate within the gingival crevicular fluid and
to penetrate both the epithelium and the connective
tissue.
Degrade collagen and dentin.

T. denticola produces proteolytic enzymes and can Fig. 8.3: Diagram showing supragingival and

destroy (IgA, IgM, IgG) or complement factors. subgingival plaque.
41
Attached plaque is further classified as tooth associated,

This plaque mainly consists of filaments with flagella and
epithelium associated or connective tissue associated. also spirochetes.

This is because of the local availability of blood products
Supragingival Plaque and a low oxidation reduction (redox) potential.

It basically consists of Gram positive cocci and Gram There are three kinds of subgingival plaque (Fig. 8.4):
negative rods and filaments. 1. Tooth associated which is similar to supragingival plaque.

It is adherent to the tooth surface. 2. Tissue associated which is associated with flagellated

It is found at or above the gingival margin. bacteria without a well-defined extracellular matrix and

When it is in contact with gingival margin, it is referred as numerous bristle brush formations. This arrangement is
marginal plaque. also known as test tube brush formation.

It has stratified organisation of a multi-layered 3. Unattached plaque is seen in between the tooth and
accumulation of bacterial morpho-types. tissue associated plaque (Fig. 8.5).

The morphological arrangements of the flora in
supragingival plaque are referred to as “corn cob”
formations.

Corn cob consists of rod-shaped bacterial cells e.g.,
Fusobacterium nucleatum and coccal cells mainly
streptococci.
Subgingival Plaque

This plaque is found below the gingival margin, between
tooth and gingival pocket epithelium. Fig. 8.4: Diagram showing.
SHORT ESSAYS
Question 1 Significance of Biofilms

What is meant by commensal relationship?
Contributing to host-tissue damage:
Sessile bacterial cells release antigens, which results
Answer

in antibodies stimulation which further results in

Bacteria and host cells are the two parties which form immune-complex activation.
a commensal relationship. Generally in this kind of Extracellular

polymeric substances mainly
relationship, both the sides get benefit from each other, polysaccharides are released which cause constant
e.g. the host’s oral epithelial cells produce glucose, which is irritation to macrophages (frustrated macrophages).
utilised by lactobacilli bacteria colonised in the oral cavity, Resistance to antimicrobial agents:

which in turn produces acid. Lowering of pH would prevent 1,000-fold greater than planktonic cells.

the colonisation of many other deleterious effects of other Failure of an agent to penetrate the full depth of the

bacterias. Therefore in this manner both the parties get the biofilm
benefit from each other. Cells in a biofilm experience nutrient limitation and

therefore exist in a slow-growing or starved state

Question 2 Oral biofilms are more resistant to chlorhexidine,

Define biofilm. What is the significance of biofilm? amine fluoride, amoxycillin, doxycycline, and
metronidazole than planktonic cells.
Answer
Potential to spread:
Biofilm: A collection of microorganisms, extracellular Seeding dispersal: Programmed detachment of plank-

polymeric products, and organic matter located at tonic bacterial cells caused by local hydrolysis of the
the interface in solid-liquid, gas-liquid, or liquid-liquid extracellular polysaccharide matrix, and conversion of
biphasic systems. a subpopulation of cells into motile planktonic cells
42
Clumping dispersal: A physical detachment pathway ammonia, which can be further utilised by the bacteria

in which a fragment of a microcolony, simply detaches as the nitrogen source.

from the biofilm and is carried by the bulk until it Breakdown of host haemoglobin results in production

lodges in a new location and initiates a new sessile of haemin, which can be used by P. gingivalis for its
population. metabolism (Fig. 8.5).
Increase in steroid hormone is associated with increase
Question 3

in proportions of P. intermedia present in sub-gingival
What are the physiologic properties of dental plaque? plaque.
Or
Describe the metabolic interactions among different Question 4
species of bacteria in plaque and between host and plaque What are nutritional interdependencies? What is its
bacteria. significance?
Answer Answer
The transition from Gram positive to Gram negative
There are physiologic interactions which occur in between

microorganisms seen in the formation of dental plaque
various species of plaque bacteria and between host and
goes hand in hand with the physiologic transition in the
plaque bacteria. Both release certain by-products which can
developing plaque. For example the initial colonisers, i.e.
be utilised by each other for their growth and metabolism.
streptococci or Actinomyces species utilise the oxygen
This is referred to as nutritional interdependencies. For
and lower the redox potential of the environment, which
example, initial colonisers, i.e. streptococci or actinomyces
in turn makes the anaerobic environment, favouring the
species utilise the oxygen and lower the redox potential
growth of anaerobic bacteria.
of the environment, which in turn makes the anaerobic
The metabolic by-products of actinomycetes and
environment, favouring the growth of anaerobic bacteria.

streptococci are lactate and formate, which can be
The metabolic by-products of actinomycetes and
further utilised by other plaque microorganisms for their
streptococci are lactate and formate, which can be
metabolism.
further utilised by other plaque microorganisms for their
C. ochraceus produces succinate and Campylobacter
metabolism.

rectus produces protoheme, and both succinate and
protoheme are utilised by P. gingivalis for its growth. Capnocytophaga ochraceus produces succinate and

The host can also function as an important source C. rectus produces protoheme, and both succinate and

of nutrients to the bacterial plaque. For example, protoheme are utilized by P. gingivalis for its growth.
the bacterial enzymes which are responsible for the The host can also function as an important source of
degradation of host proteins, causes the release of nutrients to the bacterial plaque. For example, the bacterial
enzymes which are responsible for the degradation of host
proteins, causes the release of ammonia, which can be
further utilised by the bacteria as the nitrogen source.
Breakdown of host haemoglobin result in production of
haemin, which can be used by P. gingivalis for its metabolism.
Increase in steroid hormone is associated with increase in
proportions of P. intermedia present in subgingival plaque.
Significance
These nutritional interdependencies are very important

in the growth and survival of microorganisms present in
dental plaque.
It is responsible for evolution of highly specific structural

interactions among various bacterias (Fig. 8.6).
Question 5
Fig. 8.5: Physiologic properties of dental plaque. What are the various tests done for the microbial analysis?
43
Answer cells of the same species and across species and also
genera.
Various microbial tests are:

Culture methods: Qualitative measurement of all viable
Question 7
microorganisms. Antibiotic sensitivity is determined. But What are the reasons for drug resistance in a biofilm?
costly, time-consuming and difficult.
Immunodiagnostic

methods: Methods like Answer
enzyme-linked immunosorbent assay (ELISA),
Organisms in a biofilm are 1,000–1,500 times more
immunofluorescence etc., less time consuming and less resistant to antibiotics than in their planktonic state.
expensive. Disadvantage is that cross reaction is more.
The mechanism of increased resistance depends upon
DNA probes: It entails segments of single-stranded DNA,

species to species, antibiotic to antibiotic, and for

labelled with an enzyme or radioisotope that can locate biofilms growing in different environment.
and bind to their complementary nucleic acid sequence.
Another reason for increased resistance of bacteria to
No cross reaction seen. antibiotics is slow growth rate of bacteria in a biofilm,
Polymerase chain reaction (PCR): Amplification of a

which makes them less susceptible to many antibiotics.

region of DNA flanked by a selected primer pair specific
Extracellular enzymes such as beta lactamase,
for the target species. More specific real time PCR is an formaldehyde-lyase and formaldehyde dehydrogenase
advanced version where quantitative measurement is may become trapped and concentrated in extracellular
also possible. matrix, thus inactivating some antibiotics.
Question 6
Recently super resistant bacteria have been identified in
What are the special bacterial behaviour in biofilms? a biofilm. These cells have multi-drug-resistant pumps
that can extrude antimicrobial agents from the cell.
Answer
Conjugation (exchange of genes through a direct
The bacteria present in a liquid environment, i.e. planktonic inter-bacterial connection formed by a sex pilus),
state behaves differently as compared to bacteria present transformation (movement of small pieces of DNA
in a biofilm. from the environment into the bacterial chromosome),
Organisms in a biofilm are 1,000–1,500 times more

plasmid transfer, and transposon transfer have all been
resistant to antibiotics than in their planktonic state. seen in a biofilm.
The mechanism of increased resistance depends upon
Question 8

species to species, antibiotic to antibiotic, and for

biofilms growing in different environment. What is corn cob structure and test tube formation?
Another reason for increased resistance of bacteria to

Answer
antibiotics is slow growth rate of bacteria in a biofilm,
which makes them less susceptible to many antibiotics. Marginal plaque has stratified organisation of a multi-
Extracellular

enzymes such as beta lactamase, layered accumulation of bacterial morpho-types (Fig. 8.6).
formaldehyde-lyase and formaldehyde dehydrogenase
may become trapped and concentrated in extracellular
matrix, thus inactivating some antibiotics.
Recently super-resistant bacteria have been identified in

a biofilm. These cells have multi-drug-resistant pumps

that can extrude antimicrobial agents from the cell.
In a biofilm, bacteria have the capacity to communicate

with each other through quorum sensing. This involves

the regulation of expression of specific genes through
the accumulation of signalling compounds that mediate
intercellular communication. When these signalling
compounds reach a threshold level (quorum cell density),
gene expression can be activated.
The high density of bacterial cells in a biofilm also

facilitates the exchange of genetic information among Fig. 8.6: Corn-cob structure.
44
The morphological arrangements of the flora in Question 11

supragingival plaque are referred to as corn cob
What is acquired pellicle?

formations.
Corn cob consists of rod shaped bacterial cells for Answer
example Fusobacterium nucleatum and coccal cells mainly Acquired pellicle is a thin saliva derived layer which covers
streptococci which attach along the surface of the rod the tooth surface and consists of glycoproteins, proline-rich
shaped cells. proteins, phosphoproteins, histidine-rich proteins, enzymes
Tissue associated plaque is associated with flagellated and other molecules which function as adhesion sites for
bacteria without a well-defined extracellular matrix and bacteria
numerous bristle brush formations. This arrangement is This process involves adsorption of positively-charged
also known as test tube brush formation. Large filaments salivary, crevicular fluid and other environmental macromole-
are seen in the test tube brush formation that form the long cules to negatively charged hydroxyapatite surfaces of teeth.
axis, and short filaments or Gram negative rods embedded Various kinds of energies are involved in this process like
in an amorphous matrix (Fig. 8.7). electrostatic force, van der Waals forces and hydrophobic
Question 9 forces.
Pellicle is protective in nature. Along with this it provides
What are the Socransky’s modification of Koch’s postulates?
lubrication and prevents tissue desiccation. It provides a
Answer base for colonisation and proliferation of microorganisms.
Sigmund Socransky gave the criteria by which the Question 12
pathogenicity of microorganisms can be detected. What are the differences between dental plaque and
Socransky’s criteria based on Koch’s postulates are as materia alba?
follows:
A potential pathogen associated with disease should be Answer

increased in number at diseased sites.
After treatment it should be decreased in number at sites
Characteristic Materia alba Dental plaque

that show clinical improvement. Colour White Greyish yellow
It should produce some form of cellular or humoral Removal Easy Difficult

immune response in the host. Organisation Poorly organised Well organised
When experimentally inoculated into animal models, it Bacterial count Less More

should be capable of causing the same disease. Presence of living Less More
organisms
Question 10
Distribution of micro Similar Similar
What is dental pellicle? organisms
Answer Pathogenicity Less More
Within nanoseconds of brushing and polishing of teeth,

Question 13
all the oral surfaces, both hard and soft tissues of the oral-
cavity are coated with a pellicle. What are the methods of detection of plaque?
Pellicle is formed on surfaces of teeth and artificial
Answer

prosthesis and it is an initial organic structure.
Dental pellicle is formed by the adsorption of salivary There are various methods of plaque detection:

proteins to apatite surfaces. Direct vision:

This results from the electrostatic ionic interaction If the plaque is very thin, it will not be visible with

between hydroxyapatite surface which has negative naked eye.
charge that interacts with opposite charged groups in Plaque may acquire extrinsic stain, because of which

the salivary macromolecules. it becomes visible.
Thickness of pellicle varies from 100 nm to 1000 nm. Thick layer of plaque is visible and appears as dull and

Pellicle gets converted into dental plaque quite rapidly. dizzy in colour.

45
5. S h a p e a n d Friction of tongue, Moulded by pocket

size cheeks and lips, limits wall

the size and shape
6. structure Ad h e re n t , d e n s e l y Tooth-attached, tissue
packed microbial layer attached, connective
over pellicle on tooth tissue-associated, un-
surface with intermi- attached plaque
Fig. 8.7: Color of plaque changes upon application of disclosing crobial matrix
soluion.
7. Microorgan- Gram positive cocci, Gram negative, spiro-
isms filamentous chetes
Use of explorer:
8. Source of nu- Saliva and ingested GCF, exudate and leu-

By tactile sensation.

trients food cocytes

By removal of plaque with explorer.
9. Significance Gingivitis and forma- Periodontitis and for-

By use of a curette. tion of supragingival mation of subgingival

Using a disclosing solution: It stains the plaque, because calculus calculus
of which it is easily visualised (Fig. 8.7)
By recording indices and comparing it.
Question 15

Question 14 What are the various plaque hypothesis?

What are the differences between supragingival and sub-
Answere
gingival plaque?
Answer Non-specific Plaque Hypothesis

Supragingival plaque Subgingival plaque
In mid-1900s, periodontal diseases were believed to result
from an accumulation of plaque, along with a lower host
1. Location Located above the Located below the
margin of gingiva margin of the gingiva response and increased host susceptibility with age. This
is referred to as non-specific plaque hypothesis, where
2. Origin Salivary glycoproteins Down growth of bacte-
for acquired pellicle. ria from supragingival the quantity plaque is considered rather than quality of
Microorganisms attach plaque and gingival plaque.
to this pellicle crevicular fluid (GCF)
3. Distribution Prox i m a l s u r f a c e s, Sulcus and periodontal Specific Plaque Hypothesis
cracks, pits, fissures, Pockets
over-hanged margin According to this theory only specific bacteria in plaque are
restoration, artificial responsible for the disease. That means quality of plaque
crowns, orthodontic is more important than quantity of plaque. An increase in
bands etc. the number of specific bacteria would produce the disease
4. Adhesion Acquired pellicle, other Tooth surface, sub-gin- because of release of certain virulent factors. This theory
bacteria, tooth surface gival pellicle, calculus
was given in 1976, by Loesche.
46
SHORT NOTES

What is ecological plaque hypothesis? What is materia alba?
Answer Answer
Environmental perturbations lead to growth and Material alba is a soft deposition of tissue and bacteria,
development of pathologic flora, which is referred to as lacking the organised structure of dental plaque. It can be
ecological plaque hypothesis. easily displaced with a water spray.
This means that any change in the nutrients of pocket or
Question 5
chemical or physical change in the environment can lead
to the overgrowth of pathogens. For example increase in What is the difference between attached, unattached and
levels of gingival crevicular fluid would lead to enrichment tissue-associated plaque?
of proteolytic species, by providing nutrients to the Answer
pathogens.
Attached plaque Unattached Tissue associated
Question 2 plaque plaque
What is quorum sensing? It is attached to the It is present between It is attached to the
tooth surface attached plaque and epithelia of the pock-
Answer tissue-associated et lining
plaque
In a biofilm, bacteria have the capacity to communicate
Gram positive bacte- Variable Variable
with each other through quorum sensing. This involves ria pre-dominate
the regulation of expression of specific genes through
Does not extend to Extend to junctional Extend to junctional
the accumulation of signalling compounds that mediate junctional epithe- epithelium epithelium
intercellular communication. When these signalling lium
compounds reach a threshold level (quorum cell density), Responsible for cal- gingivitis Gingivitis and peri-
gene expression can be activated. culus formation and odontitis
root caries
Question 3
What is conjugation and transformation in a plaque biofilm? Question 6
What is environmental plaque hypothesis?
Answer
Conjugation means exchange of genes through a direct Answer
inter-bacterial connection formed by a sex pilus. In 1991, Haffajee and colleagues suggested that the
Transformation means movement of small pieces of DNA entire subgingival microbial environment is the key to
from the environment into the bacterial chromosome. development of disease.
9 Dental Calculus and

Chapter
Iatrogenic Factors
LONG ESSAYS
Question 1 About two-third of the inorganic component is crystalline

in structure and the four main crystal forms in which they
Describe the structure and composition of calculus. What
exist are:
are the various theories of calculus formation?
1. Hydroxyapatite: 58%, it appears as sand grain or rod like
Answer crystals.
Calculus is defined as an adherent calcified or calcifying 2. Magnesium whitlokite: 21%, hexagonal (cuboidal,
amorphous mass that forms on the surface of natural teeth, rhomboidal) crystals.
restorations and dental prosthesis. 3. Octacalcium phosphate: 21%, they are platelet-like
crystals.
Structure of Calculus 4. Brushite: 9%.
The most important feature of calculus is that its surface Incidence of these crystals varies with age, and location

is covered with a layer of unmineralised plaque. of the calculus, therefore all these crystals do not appear at
Calculus is a very porous structure which contains same frequency.

several spaces within its calcified mass. These spaces
can be uncalcified bacteria, or they may be seen around Hydroxyapatite and octacalcium phosphate are the
individual calcified organisms themselves. most common crystals seen in supragingival calculus, while
Supragingival calculus, microscopically, is heterogeneous brushite is seen commonly in mandibular anterior region,

in nature since it is a layered structure in which the magnesium whitlokite is seen more often in the posterior
degree of calcification varies from layer-to-layer. areas.
On contrary, subgingival calculus is homogeneous as it is

built in layers with almost equal quality of minerals. Organic Components
Composition Mixture of protein polysaccharide complexes, very

little fractions of lipids, desquamated epithelial cells,
Calculus consists of an inorganic matter which accounts for leucocytes and various types of microorganisms.
70–90% and an organic matter that accounts for 10–30%.
Salivary proteins: 5.9–8.2%, includes most of the amino

Inorganic Component acids.
Calcium phosphate: 75.9% Polysaccharides: 1.9–9.1%.These are mainly derived from

Calcium carbonate: 3.1% proteoglycans of bacteria, and salivary glycoproteins,

Magnesium phosphate and other metals: Trace amounts e.g. galactose, glucose, rhamnose, mannose and

Calcium: 39% galactosamine.

Phosphorous: 19% Lipids: 0.2% of neutral fats, free fatty acids, cholesterol,

Magnesium: 0.8% cholesterol esters and phospholipids. These are mainly

Sodium, zinc, bromine, copper, silicon, iron and fluorine: derived from the cell walls of bacteria that present within

Trace amounts. the calculus during the process of mineralisation.
48
Various Theories of Calculus Formation Esterases: Dental plaque, bacteria, leucocytes,

macrophages, desquamated epithelial cells
Various theories of calculus formation are as follows:

hydrolyse fatty esters into free fatty acids. These fatty
Precipitation theory: Booster mechanism.
acids form soap with calcium and magnesium, which

Epitactic concept/heterogeneous nucleation concept.
gets converted into less soluble calcium phosphate

Inhibition theory.
salts.

Precipitation Theory
Epitactic Concept
Due to local rise in degree of saturation of calcium and This is also known as heterogeneous nucleation concept.
phosphate ions, minerals gets precipitated.

Epitactic means formation of crystals of a compound

Booster Mechanism through a seeding mechanism. Formation of the initial
This the most important mechanism of precipitation, in crystal or nucleus is referred to as nucleation.
which local rise in the degree of saturation of calcium and According to this concept, calculus formation can be

phosphate ions results in precipitation of calcium phosphate initiated through epitaxiy by organic complexes in the
salts in the following ways: matrix.
Increase in pH of saliva because of:
An intercellular matrix provides the architectural

template for the initial hydroxyapatite crystal. This focus

Loss of carbon dioxide.
of calcification gets enlarged and coalesces to form a

Production of ammonia from dental plaque. calcified mass.

Precipitation of calcium and phosphate would result Intercellular matrix of plaque, plaque bacteria and lipid

from protein degradation during stagnation by

component of the organic matrix is believed to be the
lowering the precipitation constant.
seeding or nucleating agent in calculus.
Colloidal proteins in saliva bind calcium and phosphate These seeding agents form small foci of calcification.

ions and maintain a super-saturated solution. When These foci get enlarged and coalesce to form calculus,
saliva stagnates in the oral cavity, colloids settle down therefore known as heterogeneous nucleation.
and super-saturated stage is no longer maintained. It
results in the precipitation of calcium and phosphorus Inhibition Theory
salts. According to this theory, there is existence of an inhibiting

Phosphate and esterases are two enzymes that play mechanism present in calculus at non-calcifying site,

a very important role in precipitation of calcium and therefore calcified mass occurs only at specific sites.
phosphate salts. The inhibitors are removed or altered when the

Phosphates: Dental plaque, desquamated epithelial calcification occurs.

cells and bacteria liberate phosphates that hydrolyse The most common inhibiting substance is pyrophosphate

organic phosphates in saliva. Because of this there is which inhibits calcification by preventing the initial
increase in concentration of free phosphate ions that nucleus from growing by poisoning the growth center
initiate the mineralisation of plaque. of the crystal.
SHORT ESSAYS
Question 1 According to this concept, calculus formation can be

What is Epitactic concept in calculus formation? initiated through epitaxiy by organic complexes in the
matrix.
Answer An intercellular matrix provides the architectural
Epitactic means formation of crystals of a compound template for the initial hydroxyapatite crystal. This focus of
through a seeding mechanism. Formation of the initial calcification gets enlarged and coalesces to form a calcified
crystal or nucleus is referred to as nucleation. mass.
49
Chapter 9 Dental Calculus and Iatrogenic Factors
Intercellular matrix of plaque, plaque bacteria and lipid 2. Indirect vision:

component of the organic matrix is believed to be the When the gingival margin is dried either with the


seeding or nucleating agents in calculus. help of a cotton or an air spray, the dark-coloured
These seeding agents form small foci of calcification. subgingival calculus may be seen through the
These foci get enlarged and coalesce to form calculus, marginal tissue.
therefore known as heterogeneous nucleation. With the help of probing or exploring. A fine calculus

probe (WHO 621) can be used to detect calculus

Question 2 subgingivally, also an explorer can be used to explore
What is the classification of dental calculus? Explain in detail. the calculus subgingivally.
Radiographs can also be an important tool for
Answer

diagnosing subgingival calculus.

Calculus can be classified as according to its relation to the Transillumination.

gingival margin as: Fiber optic transillumination probes to detect sub-

Supragingival calculus.
gingival calculus are also available.
Subgingival calculus.
Question 3

Supragingival Calculus Briefly explain inhibition theory of calculus formation.

As the name suggests, supragingival calculus is present Answer
above the level of gingival margin.

It is also referred as salivary calculus as it is derived from According to this theory, there is existence of an inhibiting
the components of salivary secretions. mechanism present in calculus at non-calcifying site,

It is visible in the oral cavity, clinically. therefore calcified mass occurs only at specific sites.

It is can be white or yellowish-white in colour, and can be The inhibitors are removed or altered when the
stained because of tobacco and food pigments. calcification occurs.

It hard and clay-like consistency. The most common inhibiting substance is pyrophosphate

It is more on facial surfaces of maxillary molars and on which inhibits calcification by preventing the initial nucleus
the lingual surfaces of mandibular anterior teeth. from growing by poisoning the growth center of the crystal.

It can be easily detached from the tooth. Question 4
Subgingival Calculus Describe briefly the formation of calculus.

As the name suggests, subgingival calculus is present Answer
below the level of gingival margin.
Mineralised plaque is referred to as calculus.

It is also referred to as serumal calculus or submarginal
It is formed by the precipitation of mineral salts present
calculus as it is derived from gingival exudates.

It is dark brown or green in colour, present as calcified in saliva or gingival crevicular fluid (GCF), which approxi-
deposit on the root surface of the tooth. mately starts between 1st and 14th day of plaque forma-
It is present below the gingival sulcus or within the tion. Within first 2 days plaque can be 50% mineralised

periodontal pocket. and within 12 days 60–90% mineralization can occur.

Within the inner surface of plaque, the process of
It is firmly attached to the tooth surface and is difficult

to remove. calcification starts in form of separate foci, which

It is initially seen on the inter-proximal areas where the gradually increases in size and coalesce to form a solid
supragingival calculus already exists. mass of calculus.
Early plaque of heavy calculus formers contains more

It can also be seen on the dentures, within the narrow
grooves. calcium, thrice more phosphorus and less potassium.

Phosphorous may be more critical than calcium in
It can be diagnosed as by the following methods: plaque mineralisation.
1. Direct vision: Calculus formation continues until it reaches maximum

By the help of an air spray, when the gingival margin is

levels in about 10 weeks and 6 months, after which there
deflected, it can be visualised. is a decline in its formation, due to mechanical wear from
In cases of any gingival surgeries like gingivectomy or

food and from the lips, cheeks and tongue. This process
periodontal surgeries like flap surgeries. is referred to as reversal phenomenon.
50
Question 5 Answer
What are the differences between supragingival and sub- The word iatrogenic is derived from the Greek word, iatro

gingival calculus? which means physician and genic means induced by or
produced by. The factors induced in a patient by a physician’s
Answer manner, activity or therapy, are known as iatrogenic factors.
These are the following differences between supragingival Deficiencies in the quality of dental restorations
and subgingival calculus: or prostheses are contributing factors to gingival
inflammation and periodontal destruction. Inadequate
S. Features Supragingival calculus Subgingival calculus dental procedures that contribute to the destruction of
No. the periodontal tissues are referred to as iatrogenic factors.
1. Location It is seen above the It seen below the level Various iatrogenic factors which lead to poor periodontal
level of gingival mar- of gingival margin
health are as follows:
gin
Locations of margins of restorations: Subgingival

2. Source It is derived from the It is derived from the
components of sali- gingival-fluid exudates,
margins of restorations generally lead to irritation
vary secretions, there- therefore referred to as to the periodontal structures and also favour plaque
fore it is referred to as serumal calculus accumulation. Equigingival or supragingival margins
salivary calculus. should be preferred.
3. Distribution It is arranged sym- It is distributed within Contours/open contacts: It can lead to food impaction.

metrically on teeth, the pocket and more
present more on facial on proximal surfaces Food impaction is the forceful wedging of food into the
surfaces of maxillary periodontium by occlusal forces.
molars and lingual sur-
faces of mandibular This can lead to plaque accumulation and inflammation
anterior teeth subsequently.
4. Visibility It is visible with naked Not visible with naked Materials used in the restorations: Plaque can be

eye in the oral cavity eye or on routine oral formed over the materials used for restoration. And its
examination. Can be
detected by tactile ex-
composition is similar to that formed over natural tooth.
ploration Design of removable partial dentures: Complex

5. Colour It is white, yellow in It can be dark brown designing of removable partial dentures can favour plaque
colour, can be stained or greenish-black in accumulation and further lead to periodontal destruction.
by tobacco and food colour Restorative dentistry procedures: Restorative

pigments
procedures can themselves lead to impingement into
6. Consistency Clay to hard consist- Firm in consistency the periodontal structures.
ency
Potential complications caused due to endodontic

7. Composition Calcium phosphate Calcium phosphate therapy: Endodontic therapy can also lead to
ratio is less than sub- ratio is more than su-
gingival calculus. So- pragingival calculus. periodontal destruction. For example at the time of
dium content is less Sodium increases with biomechanical preparation in Randomized controlled
increase in depth of trial, over instrumentation by an endodontic file can lead
pocket, more magne-
to extension of inflammation into the periodontal space
sium whitlokite and
less of brushite through the apical foramen.
8. Ease of re - Can be easily removed Difficult to remove Other factors could be:
moval Periodontal complications associated with orthodontic

therapy.
Question 6 Extraction of impacted third molars.

What are the iatrogenic factors other than plaque and Chemical irritation.

calculus responsible for periodontal inflammation? Radiation therapy.

10 Inflammation

Chapter
and Immunity
LONG ESSAYS
Question 1 On the other hand chronic inflammation is of longer

duration (days to years) and is manifested by infiltration of
Define inflammation. What are the signs of inflammation?
lymphocytes and macrophages (Fig. 10.1).
Describe the forms of inflammation in detail.
Answer Acute Inflammation

Inflammation can be defined as the local response of living It is the immediate and early response to injury. The function
tissues to injury due to any agent. It is the body’s defence is to deliver leukocytes to the site of injury, where they can
mechanism in order to eliminate or reduce the spread help eradicate the causative agents (or other infectious
of injurious agent as well as to remove the consequent agents) as well as degrade necrotic tissues resulting from the
necrosed cells and tissues. destruction. But, leukocytes themselves may also prolong
inflammation and induce tissue damage by releasing
Agents Causing Inflammation enzymes, chemical mediators and toxic oxygen radicals.
Physical agents like heat, cold, radiation and mechanical Major Compounds

trauma Acute inflammation has three major components:
Chemical agents like organic and inorganic substances 1. Changes in vascular supply that lead to a local increase in

Infective agents and their toxins like from bacteria and blood flow (vasodilation).

viruses 2. Structural changes in the microvasculature that allows
Immunological agents like cell-mediated and antigen- the plasma proteins to leave the circulation.

antibody reactions.
Various Signs of Inflammation
There are five cardinal signs of inflammation:
1. Rubor (redness).
2. Calor (heat).
3. Dolor (pain).
4. Tumour (swelling).
5. Functio laesa (loss of function).
Classification of Inflammation
Inflammation can be classified as acute and chronic.
Acute is of relatively short duration, lasting from a few
minutes to a few days, and is characterized by fluid and
plasma-protein exudation, and by mainly neutrophilic
leukocyte accumulation. Fig. 10.1: Stages of Inflammation
52
3. Emigration of the leukocytes from the microcirculation Exudation of Leukocytes

and accumulation at the site of injury.
The escape of leukocytes from the lumen of

The changes in acute inflammation can be conveniently microvasculature to the interstitial tissue is most important
described in two steps: aspect of inflammatory response. In acute inflammation,
1. Vascular events. polymorphonuclear neutrophils (PMNs) act as the first line
2. Cellular events. of defence, later followed by monocytes and macrophages.
The sequence of events in the extravasation of leukocytes
Vascular Events from the vascular lumen to extravascular space is divided into:
Alteration in the microvasculature (arterioles, capillaries Margination and rolling.

and venules) is the earliest response to tissue injury. These Adhesion and transmigration.

alterations include—haemodynamic changes and changes Migration in interstitial tissues toward a chemotactic

in vascular permeability. stimulus.
Haemodynamic Changes Margination and rolling: In normal blood flow, red blood

cell and white blood cell (WBC) generally travel along the
The initial features of inflammatory response result from
central axis, leaving a cell-poor layer of plasma in I contact
changes in the vascular flow of small blood vessels in the
with endothelium. As vascular permeability increases
injured tissue. The sequence of these changes is as follows:
fluid exits the vascular lumen and blood flow slows. As
In case of mild injury, the blood flow may be re-
a result, the leukocytes settle out of central column,

established in 3–5 seconds. While with more severe
marginating to the vessel periphery. Subsequently, the
injury, the vasoconstriction may last for about 5 minutes.
leukocytes stick to the endothelial surface, along the way
It is the persistent progressive vasodilation, which
and this process is called rolling.

involves mainly the arterioles.
Progressive vasodilation will elevate the local hydrostatic
Adhesion and trans endothelial migration: Eventually

pressure resulting in transudation of fluid into the extra- the leukocytes firmly adhere to the endothelial surface
swelling space. (adhesion) before crawling between the cells and
Next is the slowing or stasis of microvasculature. through the basement membrane into the extravascular

Stasis is followed by leukocytic margination or peripheral space (diapedesis).

orientation of leukocytes (mainly neutrophils) along The adhesion is largely mediated by endothelial
the vascular endothelium. The leukocytes stick to the adhesion molecules of immunoglobulin superfamily,
vascular endothelium briefly, and then move and migrate binding to various integrins found on leukocyte cell
through the gaps between spaces. This process is known surfaces. The endothelial adhesion molecules include
as emigration. intercellular adhesion molecule 1 (ICAM-1) and vascular
cell adhesion molecule 1 (VCAM-1) both of which
Increased Vascular Permeability (Vascular Leakage) have increased surface expression after stimulation of
In the earliest phase of acute inflammation, the vasodilation endothelium by various cytokines (Fig. 10.2).
and increased blood flow increase intravascular hydrostatic Chemotaxis and activation: After extravasation,

pressure, resulting in increased filtration of fluid from the leukocytes emigrate toward the site of injury along a
capillaries, which is known as transudate. Transudate is chemical gradient, in a process called chemotaxis.
basically an ultrafiltrate of blood plasma and little protein. Both exogenous and endogenous substance can act
The movement of protein-rich fluid from the plasma as chemotactic agents for leukocytes.
reduces the intravascular osmotic pressure at the same time
increasing the osmotic pressure of the interstitial fluid. The Chemotactic Agents Include
net result is outflow of matter and ions into the extravascular Soluble bacterial products, particularly peptides with
tissues, which accumulation is called oedema.

N-formylmethionine terminus.
Cellular Events Components of complement system, particularly C5a.

Products of the lipoxygenase pathway of arachidonic
The cellular events of inflammation consist of two processes:

acid (AA) metabolism, particularly leukotriene B4 (LTB4).
1. Exudation of leukocytes. Cytokines especially those of the chemokine family [e.g.

2. Phagocytosis. interleukin 8 (IL-8)].
53
Chapter 10 Inflammation and Immunity
Chemotactic agents bind to specific receptors on the 2. Engulfment with subsequent formation of a phagocytic
leukocyte cell surface and induce an intracellular cascade vacuole.

of phospholipid metabolites, eventually culminating in 3. Killing or degradation of the ingested material.
increased intracellular calcium (Ca++). The increased cytosolic
Ca++ triggers the assembly of cytoskeletal contractile Attachment stage (opsonisation):-
elements necessary for movements. The leukocytes move The phagocytic cells as well as microorganisms to be
by extending pseudopods that anchor themselves to ingested have usually negative charged surface and thus
extracellular matrix and then pull the remainder of the cell they repel each other. In order to establish a bond between
after (Fig. 10.3). bacteria and the cell membrane of phagocytic cell the
Besides stimulating locomotion, chemotactic factors microorganism gets coated with opsonins, which are
also induce other leukocyte responses, generally referred as naturally occurring factors in the serum.
to leukocyte activation.
The two main opsonins present in serum and their
Phagocytosis corresponding receptors on the surface of phagocytic cells
are as under:
Phagocytosis is defined as the processes of engulfment of 1. Immunoglobulin G opsonins and its corresponding
solid particulate material by the cells (cell-eating). The cells
receptor on the surface of polymorphs and monocytes is
performing this function are called phagocytes. There are
Fc fragment of immunoglobulin.
two main types of phagocytic cells.
2. C3b opsonin fragment of complement and its
1. Polymorphonuclear neutrophils, which are also called corresponding receptor for C3b on the surface of
microphages.
phagocytic cells.
2. Circulating monocytes and fixed tissue mononuclear
phagocytes called as macrophages. Engulfment stage:-
The opsonised particles binding triggers engulfment.
Phagocytosis Consists of three Distinct but Interrelated
Pseudopods are extended around the object to be engulfed
Steps
eventually forming a phagocytic vacuole. The lysosome
1. Recognition and attachment of the particle to the of the cell fused with phagocytic vacuole and form
ingesting leukocyte. phagolysosome or phagosome.
Fig. 10.2: Trans-endothelial migration. Fig. 10.3: Chemotaxis.

54
Secretion (Degranulation) Stage Tenton’s Reaction

OH’
The preformed granules stored products of PMNs Haber-Weiss

O2’

are discharged or secreted into the phagosome and
extracellular environment.
H2O2
The ultimate step in phagocytosis of microbes is killing

and degradation.
The microorganisms after being killed by antibacterial
Fenton

substances are degraded by hydrolytic enzymes.
OH’
However, the mechanism fails to kill and degrade same
(Hydroxyl radical)
bacteria like tubercle bacilli.
The antimicrobial agents act by either of following Reactive oxygen metabolites are particularly useful
mechanism: in eliminating microbial organism that grows within
phagocytosis, e.g. Mycobacterium tuberculosis,
Oxygen-dependent bactericidal mechanism. Histoplasma capsulatum.

Oxygen-independent bactericidal mechanism. 2. Oxygen-independent bacterial mechanism: Some

Nitric oxide (NO) mechanism. agents released from granules of phagocytic cell do

not need oxygen for bactericidal activity. These include
Oxygen-dependent mechanism: Phagocytosis lysosomal hydrolases, permeability increasing factors

stimulates an oxidative burst characterised by a defensins and cationic.
sudden increase in oxygen consumption, glycogen 3. Nitric oxide mechanism: In addition to others, the
catabolism (glycogenolysis), increased glucose oxidation nitric oxide is produced by endothelial cells as well as
and production of reactive oxygen metabolites. by activated macrophages. In experimental animals,
The generation of the oxygen metabolites is due to nitric oxide has been shown to have fungicidal and anti-
rapid activation of leukocyte Nicotinamide adenine parasitic action.
dinucleotide (NADH) oxidase, which oxidizes reduced
nicotinamide adenine dinucleotide phosphate (NADPH) Chronic Inflammation
and in the process reduces oxygen to superoxide ion
(O2–). Chronic inflammation can be considered to be inflammation
of prolonged duration (weeks to months to years) in which
2O2 + NADPH 2O2– + NADP+ + H+
active inflammation, tissue injury and healing proceed
Superoxide is then converted mostly by spontaneous simultaneously.
dismutation into hydrogen peroxide.
Chronic inflammation is characterized by
O2– + 2H+ H2O2
Infiltration with mononuclear (chronic inflammatory) cells,

This type of bacterial activity is carried out either via including macrophages, lymphocytes and plasma cells.
enzymes myeloperoxidase (MPO) present in granules of Tissue destruction largely induced by inflammatory cells.

neutrophils or independent of enzyme MPO.
Repair involving new vessel proliferation (angiogenesis)

a. MPO-dependent killing: (H2O2-MPO-halide system): In and fibrosis.
this mechanism the enzyme MPO acts on H2O2 in the
presence of halides (Cl–, Br–, I–) to form hypohalous acid Causes
(HOCl, HOI, HOBr), which is more potent antibacterial Chronic inflammation following acute inflammation:

agent than H2O2. When the tissue destruction is extensive or the bacteria
MPO survive and persist in small numbers at the site of acute
H2O2 HOCl + H2O
Cl–, Br–, I– (Hypochlorous acid) inflammation.
Recurrent attacks of acute inflammation.

b. MPO-dependent killing: Mature macrophages lack the
enzyme MPO and they carry OH– ions and superoxide
General Features
singlet oxygen (O’) from H2O2 in presence of O2’ (Haber- Mononuclear cell infiltration: Chronic inflammation

Weiss reaction) or in Fe++ (Fenton reaction). lesions are infiltrated by mononuclear inflammation
55
cells like phagocytes and lymphoid cells. Macrophages Arachidonic Acid Metabolism
compromise the most important cells in chronic Product derived from the metabolism of AA affect a

inflammation. variety of biologic processes including inflammation and

Tissue destruction or necrosis: These are common and haemostasis.
are brought about by activated macrophages by release Arachidonic acid is a 20-carbon polyunsaturated fatty acid
of variety of biologically-active substance. (four double bonds) derived primarily from dietary linoleic

Proliferative changes: As a result of necrosis, proliferation acid and present in the body only in esterified form as a
of small blood vessels and fibroblasts is stimulated component of cell membrane phospholipids. arachidonic
resulting in formation of inflammation granulation acid metabolism proceeds along one of the two major
tissue. pathways, named for the enzymes that initiate the reactions.
Question 2 1. Cyclooxygenase pathway.
2. Lipoxygenase pathway.
What are the various chemical mediators of inflammation?
Answer 1. Cyclooxygenase Pathway

These include prostaglandin E2 (PGE2), PGD2, PGF2a,
The substances acting as chemical mediators of
PGI2 (prostacyclin), and thromboxane (YTXA2), each of
inflammation can be released from the cells, the plasma or
which is derived by these enzymes has a restricted tissue
damaged tissue itself. They are broadly classified into two
distribution. For example, platelets contain the enzyme
groups:
thromboxane synthesis, and hence TXA2, a potent platelet-
1. Mediators released by cells. aggregating product in these cells. Endothelium, on the
2. Mediators originally from plasma. other hand, lacks thromboxane synthetase but possess
prostacyclin synthetase, which leads to the formation
Cell-Derived Mediators of PGI2, a vasodilator and a potent inhibitor of platelet
Vasoactive Amines aggregation. Both TXA2 and PGI2 have an opposing action.
Prostaglandin D2 is the major metabolic product of the
Histamine is widely distributed in tissues, particularly
cyclooxygenase (COX) pathway in most cells, along with
in mast cells adjacent to vessels, as well as in circulating
PGE2 and PGI2a (which are more widely distributed), it causes
basophils and platelets. Performed histamine is present in
vasodilation and potentiates oedema formation.
mast cell granules that are released in response to a variety
Aspirin and non-steroidal anti-inflammatory drugs (NSAIDS)
of stimuli.
such as ibuprofen inhibit all PG synthesis. Lipoxygenase
Physical injury such as trauma or heat.
however is not affected by these (NSAIDS).

Immune reaction involving binding of Ig E antibodies to

Recent studies have revealed that there are two forms of

Fc receptors on mast cells. COXs called COX-1 and COX-2 that are of interest, COX-1 but
C3a and C5a fragments of complement so called

not COX-2 are expressed in the gastric mucosa. At this site

anaphylatoxins. the mucosal PG generated by action of COX-1 are protective
Leukocyte-derived histamine releasing proteins. because they prevent acid-induced damage.

Neuropeptides. (e.g. substance P).

2. Lipoxygenase Pathway

Certain cytokines. (e.g. IL-1 and IL-8).

5-lioxygenase is the predominant AA-metabolising

In humans, histamine causes arteriolar dilation and is enzyme in neutrophils. 5-hydroperoxy derivative of AA,
the principle mediator of the immediate phase of increased 5-hydroperoxyeicosatetraenoic acid (5-HPETE) is quite
vascular permeability, causing endothelial contraction and unstable and is either reduced to 5-HETE (chemotactic
widening of the inter-endothelial cell junctions. Soon after for neutrophils) or converted into a family of compounds
its release, histamine is inactivated by histaminase. collectively called leukotrienes. The first leukotriene
Serotonin (5-hydroxytryptamine) is also a vasoactive generated from 5-HPETE is called leukotriene A4 (LTA4),
mediator with effects similar to histamine. It is found which in turn gives rise to LTB4 by enzymatic hydrolysis or
primarily within platelet-dense body granules (along with LTC4 and its subsequent metabolites LTD4 and LTE4, cause
histamine, adenosine diphosphate and calcium) and release vasoconstriction, bronchospasm and increased vascular
is stimulated by platelet aggregation. permeability.
56
Lysosomal Components Interleukin-1 and TNF a and b induce endothelial

The inflammatory cells—neutrophils and monocytes effects in the form of increased leukocytes adherence,

contain lysosomal granules, which on release elaborate a thrombogenicity, elaboration of other cytokines,
variety of mediators of inflammation. These are as under: fibroblastic proliferation and acute phase reactions.
Granules of neutrophils:
IF-a causes activation of macrophages and neutrophils

and is associated with synthesis of nitric acid synthase.

Specific or secondary.

Azurophil or primary. Nitric Oxide and Oxygen Metabolites

The specific (secondary) granules—contain lactoferrin, Nitric oxide plays the following role in inflammation:
lysozyme, alkaline phosphatase and collagenase while
Vasodilation.
the large azurophil granules have myeloperoxidase,

Anti-platelet activating agent.
acid hydrolases and neutral proteases such as elastase,

collagenase and proteinase.
Possibly microbicidal action.

Oxygen-derived metabolites are released from
Acid proteases act within the cell to cause destruction

activated neutrophils and macrophages, their action in
of bacteria in the phagolysosome while neutral proteases
inflammation is:
attack on the extracellular constituents such as basement
Endothelial cell damage and thereby increased
membrane, collagen, elastin, cartilage, etc.

vascular permeability.
Granules of monocytes and tissue macrophages:
Activation of protease and inactivation of antipro-

These cells on degranulation also release mediators

tease causing tissue matrix damage.
of inflammation like acid proteases, collagenases and
Damage to other cells.
plasminogen activator. However, they are more active in

chronic inflammation than acting as mediators of acute
Plasma-derived Mediators (Plasma Proteases)
inflammation.
Platelet Activating Factor These include the various products derived from activation
and interaction of four interlinked systems:
It is released from immunoglobulin E (IgE)-sensitized 1. Kinin
basophils or mast cells, other leukocytes endothelium and 2. Clotting
platelets. Apart from its action on platelet aggregation and 3. Fibrinolytic
release, the actions of platelet activating factor (PAF) as 4. Complement.
mediator of inflammation are: Hageman factor (factor XII) of clotting system plays a key
Increased vascular permeability.
role in interactions of four systems.

Vasodilatation in low concentration and vasoconstriction

otherwise. Kinin System
Bronchoconstriction. This system on activation is factor XIIa generates

Adhesion of leukocytes to endothelium. bradykinin, so named because of the slow contraction of

Chemotaxis. smooth muscle it induces. First, kallikrein by the action of

pre-kallikrein activator, which is a fragment of factor XIIa.
Cytokines
Kallikrein then acts on high molecular weight kininogen to
Cytokines are polypeptide substances produced by form bradykinin.

activated lymphocytes (lymphokines) and activated
monocytes (monokines). Bradykinin effects include:
Cytokines can act on the same cell that produces them Smooth muscle contraction.

(autocrine effect) on other cells in the immediate vicinity Vasodilatation.

(paracrine) or systemically (endocrine effect). Increased vascular permeability.

Currently main cytokines acting as mediators of Pain.

inflammation are:
Clotting System
Interleukin-1 (IL-1), tumour necrosis factor a (TNF-a) and

b, interferon-a (IF-a) and chemokines [IL-8, platelet factor Factor XIIa initiates the cascade of the clotting system
4 (PF4)]. The actions of various cytokines as mediator of resulting in formation of fibrinogen to form fibrin and
inflammation are as under: fibrinopeptides or fibrin split products.
57
Actions of fibroblast-specific protein (FSP) in inflammation inflammatory response by increasing vascular permeability
are: and leukocyte chemotaxis.

Increased vascular permeability

Complement components (numbered C1–C9) are
Chemotaxis for leukocyte

present in plasma in inactive forms. Briefly the most inactive
Anticoagulant activity.
step in the elaboration of the biological functions of
complement is the activation of third complement C3. C3
Fibrinolytic System cleavage can occur:
This system is activated by plasminogen activator. It acts on Via classic pathway, triggered by fixation of C1 to antigen-

plasminogen present as component of plasma protein to antibody complexes or

form plasmin. Further breakdown of fibrin by plasmin forms Through the alternative pathway, triggered by bacterial

fibrinopeptides or FSP. polysaccharides or aggregated IgA. Alternative pathway

involves distinct set to serum components, including
Actions of plasmin are: properdin and factors B and D.

Activation of factor XII to form prekallikrein activator that Whichever pathway is involved, C3 convertase cleaves
stimulates the kinin system to bradykinin. C3 to C3a and C3b.C3b then binds to C3b to C3 convertase

Splits off complement C3 to form C3a, which is a complex to form C5 convertase, this complex cleaves C5 to
permeability factor. generate C5a and initiate the final stages of assembly of the

Degrades fibrin to form fibrin split product which to form C5 to Ca MAC.
fibrin split product which increase vascular permeability
Phenomenon in acute inflammation
and are chemotactic to leukocytes.

Vascular effect: C3a and C5a (called anaphylaxins)
Complement System increase vascular permeability and cause vasodilation by
Complement system consists of cascade of plasma inducing mast cells to release their histamine. C5a also
protein that plays an important role in both immunity activates the lipoxygenase pathway of AA metabolism
and inflammation. They function in immunity primarily in neutrophils and monocytes causing further release of
by generating a pore like membrane attack complex inflammatory mediators
(MAC) that effectively punches holes in the membranes of
Leukocyte activation, adhesion and chemotaxis
invading microbes. In the process of generating the MAC, a
Phagocytosis: With fixed to a microbial surface C3b and
number of complement fragments are produced, including C3bi act as opsonins, augmenting phagocytosis by cells
C3a opsonins, as well as fragments that contribute to the bearing C3b receptors (neutrophils and macrophages).
SHORT ESSAYS
Question 1 Cytokines
What are the systemic effects of inflammation?
Interleukin-1, IL-6, and TNF are most important in acute-
Answer phase reaction. These are produced by leukocytes in
response to infection, or to immune and toxic injury and
Various systemic effects of inflammation are defined below:
are released systemically frequently in a short of cytokine
Pyrexia cascade.
Fever is only one of the more common obvious of the Tumour necrosis factor can induce production of IL-1
systemic effects of inflammation called as acute phase in turn induces production of IL-6 that stimulates the
reaction. hepatic synthesis of several plasma proteins, most notably
fibrinogen.
These include slow-wave sleep, anorexia, and accelerated
degradation of skeletal muscle hypotension, hepatic synthesis Elevated fibrinogen levels cause erythrocytes to
of acute-phase proteins (e.g. complement or coagulation agglutinate more readily. So higher erythrocyte sedi-
protein) and alterations in the circulating WBC pool. mentation rate is associated with inflammation.
58
Leukocytosis eventually forming a phagocytic vacuole. The lysosome

Especially in bacterial infection, it results from the release of of the cell fused with phagocytic vacuole and form

cells from the bone marrow (caused by IL-1 and TNF) and is phagolysosome or phagosome.
associated with an increase number of relatively immature
neutrophils in the blood. Secretion (Degranulation) Stage
Neutrophilia—increase in polymorphonuclear cells. The preformed granules stored products of PMNs are

Eosinophilia—in parasitic infection and allergic reactions. discharged or secreted into the phagosome and extracellular

Lymphocytosis—in viral infection, such as mumps, and environment.

rubella. The ultimate step in phagocytosis of microbes is killing
and degradation.
Question 2
The microorganisms after being killed by antibacterial
What is phagocytosis? Explain in detail with diagrams?
substances are degraded by hydrolytic enzymes. However,
Answer the mechanism fails to kill and degrade same bacteria like
Phagocytosis is defined as the processes of engulfment of tubercle bacilli.
solid particulate material by the cells (cell-eating). The cells The antimicrobial agents act by either of following
performing this function are called phagocytes. There are mechanism:
two main types of phagocytic cells: Oxygen-dependent bactericidal mechanism.

1. Polymorphonuclear neutrophils, which are also called Oxygen-independent bactericidal mechanism.

microphages. Nitric oxide (NO) mechanism.

2. Circulating monocytes and fixed tissue mononuclear
phagocytes called as macrophages. Oxygen-dependent Mechanism
Phagocytosis consists of three distinct but interrelated steps:
Phagocytosis stimulates an oxidative burst characterised
1. Recognition and attachment of the particle to the
by a sudden increase in oxygen consumption, glycogen
ingesting leukocyte.
catabolism (glycogenolysis), increased glucose oxidation
2. Engulfment with subsequent formation of a phagocytic and production of reactive oxygen metabolites. The
vacuole. generation of the oxygen metabolites is due to rapid
3. Killing or degradation of the ingested material. activation of leukocyte NADH oxidase, which oxidizes
Attachment Stage (Opsonisation) reduced NADPH and in the process reduces oxygen to
superoxide ion (O2–).
The phagocytic cells as well as microorganisms to be
ingested have usually negative-charged surface and thus 2O2 + NADPH 2O2– + NADP+ + H+
they repel each other. In order to establish a bond between
bacteria and the cell membrane of phagocytic cell the Superoxide is then converted mostly by spontaneous
microorganism gets coated with opsonins, which are dismutation into hydrogen peroxide.
naturally occurring factors in the serum.
O2– + 2H+ H2O2
The two main opsonins present in serum and their
corresponding receptors on the surface of phagocytic cells This type of bacterial activity is carried out either via
are as under: enzymes myeloperoxidase (MPO) present in granules of
1. Immunoglobulin G opsonins and its corresponding neutrophils or independent of enzyme MPO.
receptor on the surface of polymorphs and monocytes is
Fc fragment of immunoglobulin. MPO-dependent Killing: (H2O2-MPO-halide system)
2. C3b opsonin fragment of complement and its In this mechanism the enzyme MPO acts on H2O2 in the
corresponding receptor for C3b on the surface of presence of halides (Cl–, Br–, I–) to form hypohalous acid
phagocytic cells. (HOCl, HOI, HOBr), which is more potent antibacterial agent
Engulfment Stage than H2O2.
The opsonised particles binding triggers engulfment. MPO
H2O2 HOCl + H2O
Pseudopods are extended around the object to be engulfed Cl–, Br–, I– (Hypochlorous acid)
59
MPO-dependent Killing not need oxygen for bactericidal activity. These include
lysosomal hydrolases, permeability increasing factors
Mature macrophages lack the enzyme MPO and they carry

defensins and cationic.
OH– ions and superoxide singlet oxygen (O’) from H2O2 in
presence of O2’ (Haber-Weiss reaction) or in Fe++ (Fenton Nitric Oxide Mechanism
reaction).
in addition to others, the nitric oxide is produced by
Fenton’s Reaction endothelial cells as well as by activated macrophages. In
experimental animals, nitric oxide has been shown to have
OH’ fungicidal and anti-parasitic action but its role is bactericidal
– Haber-Weiss activity in human being is yet not clear.
O2
Question 3
H2O2
What are the cells of inflammation and immunity?
Answer
Fenton
OH’ Various cells of immunity and inflammation are as follows:
(Hydroxyl radical) Mast cells.

Dermal dendrocytes.

Reactive oxygen metabolites are particularly useful Peripheral dendritic cells.

in eliminating microbial organism that grows within Neutrophils and monocytes/macrophages.

phagocytosis, e.g. M. tuberculosis, H. capsulatum. Lymphocytes.

T-cells.
Oxygen-independent Bacterial Mechanism

B-cells.

Some agents released from granules of phagocytic cell do Natural killer cells (NK cells) (Fig. 10.4).

Fig. 10.4: Various cells of inflammation.

60
Mast Cells receptors 1, 3 and 4 (CR1, CR3, CR4) and C5 (C5aR). They also
possess receptors for IgG antibody (fcy R).
Mast cells are mainly present in the connective tissue around

These receptors enable:
the blood vessels and also in the junctional epithelium.
Their most prominent feature is that there is a presence Neutrophils to be recruited from the blood.

of cytoplasmic granule known as lysosomes, eosinophil Locate offending agents and.

chemotactic factor, neutrophil chemotactic factor and Ingest (phagocytose) and kill the offending agents.

heparin. They also contain receptors for IgE antibodies
which are found in the gingiva. These cells can synthesise Monocytes: When macrophages leave the blood, they
inflammatory mediators like the slow-reacting substances form monocytes. They complete their differentiation
of anaphylaxis (SRS-A), TNF a, IL-6 and leukotriene C4. in local tissues and may become greater than 22 µm in
diameter because macrophages differentiate and live
Mast cells are important in mediating inflammatory
in the local tissues; they suited for communicating with
process and they also possess toll like receptors, which allow
lymphocytes and other surrounding cells. Macrophages
the innate immune system to adapt which is transitory.
live along enough to present antigen to T cells. Monocytes
Stimulation of these receptors can lead to activation
and macrophages possess CR1, CR3, CR4, C5aR receptors
and secretion of vasoactive substances that increase the
several classes of Fcy receptors (FcyRI, FcyRII, FcyRIII) and
vascular permeability and dilation.
molecules important in antigen presentation (MHC class II
receptor CD1).
Dermal Dendrocytes
They are also known as histiocytes and are widely distributed Lymphocytes
and form a large system of collagen associated dendritic cells Three main types of lymphocytes are distinguished on
(DCs) of myeloid origin. These cells are distributed near the the basis of their receptors for antigens: T lymphocytes, B-
blood vessels and possess receptors for the complement C3a lymphocytes, and NK cells.
by which they participate in immediate inflammation. They
express the major histocompatibility complex (MHC) class II T cells
molecules. They can express the matrix metalloproteinases
T cells recognise diverse antigens using a low affinity
(MMPs) in response to the bacterial challenge and help in
trans-membranous complex, the T cell antigen receptor
periodontal tissue destruction.
(TCR). T cells are subdivided based on whether they
Peripheral Dendritic Cells possess the co-receptors CD4 or CD8. The CD4 co-receptor
reversibly binds MHC class II molecules that are found
They are leukocytes with dendrites or cytoplasmic DCs, macrophages and B cells. CD4+ T cells initiate and
projections, Langerhans cells are dendritic Cells that help with immune responses by providing proliferation
reside in suprabasilar portions of squamous epithelium. and differentiation signals. The CD8 co-receptor scans for
They ingest the antigen locally and transport the antigen MHC, class I molecules, which are found on all cells. The
to the lymph nodes through the afferent lymphatics. They CD8+ T cells are predominantly cytotoxic T cells involved
express high levels of MHC II molecules and CD1, as well as in controlling intracellular antigens (e.g. certain bacteria,
intercellular adhesion molecules (e.g. ICAM-1, lymphocyte
hyphal fungi, viruses).
function-associated antigen 3 (LFA-3) and co-stimulatory
factors. B cells
B cells recognise diverse antigens using the B cell antigen
Neutrophils and Monocyte/Macrophages
receptor (BCR), which is a high affinity antigen receptor. The
Neutrophils are closely related to phagocytic leukocytes antigen is tightly bound not scanned. Ingested antigen is
neutrophils and macrophages are of the same size. degraded and presented to T cells. Before antigen exposure,
Neutrophils, also known as polymorphonuclear leukocytes B cells express immunoglobulin M (IgM) as part of the BCR.
(PMNLs), are the predominant leukocyte in blood, After antigen exposure, some B cells differentiate to form
accounting for about two-thirds of all blood leukocytes plasma cells dedicated to the production and secretion of
(1,000–8,000 cells/mm3). antibodies of IgM isotype. Memory B cells give rise to plasma
Neutrophils possess receptors for metabolites of the cells on secondary exposure to antigen and produce high
complement molecule C3, designated complement affinity antibodies of the appropriate isotype.
61
Natural Killer Cells Eventually, the combined efforts of lymphatic drainage

and macrophages lead to clearance of the oedema fluid,
Natural killer cells (NK cells) recognise and kill certain

inflamed cells and necrotic debris from the battlefield.
tumour and virally-infected cells possess several classes of
antigen receptors including killer inhibitory receptors (KIRs) Scarring or Fibrosis
and killer activating receptor (KAR). Normal cells possess
MHC class I molecules that present antigens recognised as This results when inflammation occurs in tissues that do not
self; these interact with KIRs and protect the cells from NK regenerate or after substantial tissue destruction.
cell mediated killing. Alterations in antigens presented by In addition, extensive fibrous exudates that cannot
the MHC class I molecules, occurring in tumour-infected be completely absorbed are organised by ingrowth of
and virally-infected cells, may result in NK cell activation connective elements, resulting in the formation of a mass of
because the KIRs do not detect sufficient self-antigens. KAR fibrous tissue.
activation can override KIR inhibition and cause the NK cells Abscess Formation
to kill the target cell.
It may occur in the setting of certain bacterial or fungal
Question 4 infections (pyogenic).
Write short notes on mast cells. Progression to Chronic Inflammation
Answer This may follow acute inflammation.
Mast cells are mainly present in the connective tissue around the Question 6
blood vessels and also in the junctional epithelium. Their most What are cytokines? What are their roles in inflammation?
prominent feature is that there is a presence of cytoplasmic
granule known as lysosomes, eosinophil chemotactic factor, Answer
neutrophil chemotactic factor and heparin. They also contain Cytokines are the peptides or protein mediators or
receptors for IgE antibodies which are found in the gingiva. intercellular messengers which regulate immunological,
These cells can synthesise inflammatory mediators like the inflammatory and reparative host responses.
SRS-A, TNF α, IL-6, and leukotriene C4. They are released by wide variety of cells like lymphocytes,
Mast cells are important in mediating inflammatory macrophages, platelets, and fibroblasts.
process and they also possess toll like receptors, which allow Cytokines can include interleukins, growth factors,
the innate immune system to adapt which is transitory. chemokines and interferons. They act on various cells like
Stimulation of these receptors can lead to activation macrophages, fibroblasts, keratinocytes, PMNLs.
and secretion of vasoactive substances that increase the Various roles of cytokines are as follows:
vascular permeability and dilation.
To initiate and maintain immune and inflammatory

Question 5 response.
Interleukins forms a link between leukocytes, endothelial
What are the various outcomes of acute inflammation?

cells, fibroblasts and epithelial cells.

Answer Interleukin-6, IL-1 and TNF α are important for periodontal

destruction.
Various outcomes of acute inflammation are mentioned Cytokines mainly associated with periodontal diseases

below: are IL-1, IL-2, IL-4, IL5, IL-6, IL-8, IL-10, TNF, PGE2.
Complete Resolution Question 7
When the injury is limited or short lived, when there has What are the functions of various cytokines?
been little tissue destruction, and when tissue is capable
of regeneration, the most usual outcome is restoration to Answer
histological and functional normalcy. Functions of various cytokines are as follows:
This resolution involves neutralisation or removal of
Interleukin-1: It is produced mainly by macrophages
chemical mediators, with subsequent normalisation of and lymphocytes. Fibroblasts, platelets, keratinocytes
vascular permeability and halting of leukocyte emigration. and endothelial cells may also produce IL-1. IL-1, triggers
62
the release of PGE2 in large quantities. It also stimulates h Secretory IgA has increased concentrations in
h
the secretion of MMPs. saliva.

h Secretory IgA protects mucosal surfaces and
Interleukin-2: Monocytes and T lymphocytes produce IL-
h

2. It stimulates T cells and enhances clonal expansion of prevents adhesion of bacteria to tissue surfaces
beta cells into plasma cells. especially in the early stages of periodontal
Interleukin-4, IL-5, and IL-10: They all are produced by diseases.

TH2 cells and also help in the activation of beta cells into Immunoglobulin M

h Responsible for early antibody response and
plasma cells and downregulate monocytic response.
h
Interleukin-6: It is produced by lymphocytes, fibroblasts complement fixation.

and monocytes. It is responsible for conversion of blood Immunoglobulin E

h It causes immediate hypersensitivity reactions.
monocytes into osteoclasts.
h
Interleukin-8: Monocytes, keratinocytes and fibroblasts
Immunoglobulin D

h The functions of IgD are not known.

are responsible for releasing IL-8. It is a strong chemo-
h
attractant of PMNLs at low concentrations. Question 9
Tomour necrosis factor: It is produced by macrophages
What is transendothelial migration?

and release lymphotoxins. It stimulates the proliferation
of osteoclast precursor cells and also activates the mature Answer
osteoclasts to resorb bone.
Trans-endothelial migration is selective interaction between
Prostaglandin E2: PGE2 is produced by macrophages and
leukocytes and endothelium that result in the leukocyte

fibroblasts, but IL-1 also induces its production. It is a
pushing its way between endothelial cells to exit the blood
responsible for osteoclastic resorption.
and enter the tissues.
Question 8 In a local inflammatory response, trans-endothelial
What are immunoglobulins? migration occurs in the following sequential phases:
Step 1: Rolling.
Answer

Step 2: An insult to local tissue.

Immunoglobulins are gamma globulins produced by Step 3: Signalling the endothelium.

plasma cells in response to antigens with which they can Step 4: Increased rolling.

react in a specific way. Step 5: Signal for rolling arrest.

They can be found in blood, tissues, secretions, and are Step 6: Strong adhesion.

effectors of the humoral response. Step 7: The zipper phase.

These molecules are composed of two light chains (l, k) Leukocytes use the lectin (a non-enzymatic carbohydrate

and one of the five types of heavy chains (g, a, d, m, e). The binding protein) designated L-selectin to interact with
class of the Ig molecules is donated by the heavy chain. carbohydrate molecules known as vascular adhesion (CD
Basic structure of this molecule resembles the letter Y, 34) on the luminal surface of endothelial cells. This brief

where the tail of the Y contains the ends of the heavy- interaction manifests itself as the rolling of the leukocyte
chains Fc fragments and complement-binding site. The
along the luminal surface of the endothelium.
remaining area is the heavy chains antibody binding site.
A local insult triggers the release of a variety of
Functions of immunoglobulins: inflammatory signals (e.g. IL-1, IL-1b, TNF α) from cells in the

Immunoglobulin G. tissue, especially from resident leukocytes such a mast cells.

h Complement fixation. Mast cells are crucial in initiating neutrophil recruitment
h
h Delayed antibody response. against bacteria and responding to anaphylatoxins such as
h
h Opsonisation. C3a and C5a.
h
h Cross placental barrier. Interleukin-1b, TNF a, C5 and lipopolysaccharides
h
h Increased concentration in gingival crevicular fluid. can stimulate endothelial cells to express P-selectin and
h
Immunoglobulin A. E-selectin in their luminal surfaces.

There are two types of IgA: serum IgA and secretory IgA. The stimulated endothelium also releases chemokines
h Serum IgA helps in complement fixation by which small peptide cytokines, first recognised for their
h
alternate pathway. chemo-attractant activities.
63
Chemokines function as a signal for rolling arrest. gradient across its cell body and migrates in the direction of
The interaction of a chemokine, IL-8, with the leukocyte increasing concentration.

receptor CXCR2 causes the leukocyte to shed L-selectin The phagocyte senses only a limited number of
and upregulate the integrins leukocyte function–– chemicals: chemotaxins for which it has receptors and
associated antigen-1(LFA-1). Integrins are transmembrane chemotaxis receptors.
adhesions, some of which have been adapted for use by The receptors for chemotaxis belong to a family called
the immune system. LFA-1 binds intercellular adhesion the G-protein coupled family. This family of receptors also
molecule-2 (ICAM-2), which is expressed constitutively by includes the various light receptors in our retains; thus in
endothelium. some ways, leukocytes “see” a chemotactic gradient much
Because leukocytes differ with respect to their chemokine as we see light. The only class of chemotaxins derived
receptors, the chemokines dictate which leukocytes (e.g. directly from bacteria are formyl-methionyl peptides.
neutrophils, macrophages, lymphocytes, eosinophils, and To migrate toward a target leukocyte, assume an
basophils) dominate the leukocyte infiltrates. Different asymmetric or polarized shape rather than the rounded
stimuli (e.g. cytokines, tissue injury, viral or microbial insults) morphology evident in blood.
can lead to expression of different chemokines.
Chronic inflammatory leukocytes (monocytes and Question 11
lymphocytes) possess integrins that are not expressed by
What are the various defects in leukocyte function?
neutrophils. One such integrin, very late antigen-4 (VLA-
4), binds endothelial vascular cell adhesion molecule-1 Answer
(VCAM-1). Endothelium expresses VCAM-1 after prolonged
Various defects in leukocyte function are mentioned in
inflammation, thus providing a mechanism for the selection
(Table 10.1):
of chronic inflammatory cells.
CD31 (platelet-endothelium cell adhesion molecule-1)
is a 130-kD trans-membrane glycoprotein present at the Table 10.1: Various defects in leukocyte function
intercellular borders of endothelial cells facing into lumen Disease Defect
and on all leukocytes. CD31 is a homophilic adhesion Genetic
molecule because CD31 molecules bind to one another. Leukocyte adhesion Beta chain of CD11/CD18 integrins
Once the leukocyte locates the inter-endothelial junction, Deficiency 1
Leukocyte adhesion Sialyl-Lewis X (selectin receptor)
it uses its own CD31 as a zipper effect has been proposed
as a mechanism of minimizing the leakage of fluid. As the Deficiency 2
Neutrophil-specific Absence of neutrophil-specific
endothelium unzips its CD31, the leukocyte rapidly “zips”
granules
between the endothelial cells.
Granule deficiency
Leukocytes possess several proteases including urokinase Chronic granulomatous disease Defective chemotaxis
plasminogen activator receptor (mPAR). The mPAR leads to decrease oxidative burst NADPH
the activation of collagenase which then may degrade the oxidase (Membrane component)
basement membrane and enable the leukocyte to enter the X-linked
connective tissues. Autosomal recessive NADPH oxides (c ytoplasmic
component)
Defects in trans-endothelial migration are associated
Myeloperoxidase deficiency Absent MPO-H2O2 system
with aggressive periodontitis reflecting are importance in
Chediak-Higashi syndrome Membrane protein involved in
periodontal diseases. organelle trafficking
Question 10 Acquired
1. T hermal injury, diabetes, Chemotaxis
What is chemotaxis? sepsis, etc.
2. Hemodialysis, diabetes Adhesion
Answer 3. Sepsis, diabetes, malnutrition, Phagocytosis and microbicidal
etc. activity
Chemotaxis is leukocyte’s ability to sense a chemical
11
Microbial Interactions

Chapter with the Host in
LONG ESSAYS
Question 1 Bacterial byproducts can disturb the host system which

may lead to tissue destruction. These products can also lead
Explain in detail host microbial interactions. to bone resorption and inhibit other host immune cells.
Answer
Immunologic Aspects
There are two aspects of host microbial interaction:
Bacteria are responsible for causing periodontal disease and
1. Microbiologic aspect. can directly interact with the host tissues leading to tissue
2. Immunologic aspect. destruction. If the destruction exceeds the reconstruction
rate, it leads to periodontal disease.
Microbiologic Aspect There is a major role of immune system in periodontal
Bacterial colonisation and the survival in the periodontal pathogenesis.

region. There are three important paradigms involved in this
Bacterial adherence in the periodontal environment: process.

The bacteria get attached to tooth or root surfaces, 1. Innate factors like complement system, resident
tissue surfaces and pre-existing plaque mass. leucocytes like mast cells play an important role in
Host tissue invasion: Many bacterial species initiating inflammation.

have been recognised which are capable of tissue 2. Neutrophils which are the acute inflammatory cells
invasion. These species are responsible for producing protect the tissue by controlling the periodontal
periodontal diseases. There localisation into the microorganisms.
tissues provide a position from where they can release 3. Macrophages and lymphocytes which are the chronic
toxic substance into the host tissue which further lead inflammatory cells protect the entire host from within the
to tissue destruction.
subjacent connective tissues and do all that is necessary
Bacterial evasion of host defence mechanisms: Bac- to prevent local infection into a systemic one, including

teria produce substances which help them in evading the sacrifice of local tissues.
the host defence mechanisms for its survival, e.g. bac-
teria produce immunoglobulin degrading proteases Question 2
which counteract the effect of immunoglobulins Which are the various mediators of inflammation?
which forms an important host defence constituent.
Microbial mechanisms of host tissue damage.
Answer

There is a number of bacterial products which can retard The various mediators of inflammation are:
the growth and alter the metabolism of host tissue cells. 1. Proteinases: Primary proteinases are the matrix
For example, ammonia, fatty acids, volatile sulphur, metalloproteinases (MMPs) which are responsible for
collagenase and matrix metalloproteinases, etc. tissue destruction.
65
Chapter 11 Microbial Interactions with the Host in Periodontal Diseases
These are produced by neutrophils, macrophages, The effect of IL-1 and TNF-α include:
fibroblasts, osteoblasts, osteoclasts and epithelial cells. Stimulation of endothelial cells to express selectins,

Other proteinases which are associated with perio- which facilitate recruitment of leucocytes.
dontitis are elastase, cathepsin G, and neutrophil serine Activation of macrophage IL-1 production.

proteinases. Induction of prostaglandin E2 (PGE2) by macrophages

and gingival fibroblasts.

2. Cytokines: There are three important pro-inflammatory
cytokines which play an important role in tissue 3. Prostaglandins:
destruction viz. interleukin 1 (IL-1), interleukin 6 (IL-6)
They are arachidonic acid metabolites which are
and tissue necrotic factor (TNF). released by cyclooxygenases.

Interleukin: 1 is produced by macrophages and
Macrophages and fibroblasts are primarily responsible
lymphocytes. for production of prostaglandins.

TNF-α is also produced by macrophages.
PGE2 is responsible for bone resorption.
12 Smoking and

Chapter
LONG ESSAYS
Question 1 There is an increase in the enzymes collagenase and

elastase.
Explain the association of smoking and periodontal disease?
Impact of smoking on periodontal diseases are as follows:
Answer Gingivitis: There is a decreased gingival inflammation

and bleeding on probing.
Smoking has a widespread effect on health of gingival and
periodontal tissues like: Periodontitis:

Smoking is associated with increased incidence of
Physiological effects:

pocket depth, attachment loss and bone loss.

There is decreased flow of gingival crevicular fluid Rate of periodontal destruction is hastened.

(GCF).
The prevalence on severity of periodontal destruction

Altered bleeding on probing. is increased.

There is a decrease in sub-gingival temperatures. Chances of prevalence of severe periodontitis are

Microbiological effects: It has been seen that smoking seen in smokers as compared to non-smokers.

is closely associated with increased levels of periodontal Chances of tooth loss are commonly associated with

pathogens specially in deep pockets. smoking.
Immunological effects: The frequency of cigarette smoking per day is directly

There is an alteration of the processes of neutrophil proportional to the all the above-mentioned points.

chemotaxis, oxidative bursts and phagocytosis. Patients who have stopped smoking show decrease

There is an increase in the concentration of tumour ne- in the prevalence and severity of periodontal

crosis factor alpha (TNF-α), and prostaglandin E2 (PGE2). diseases.
13 Host Modulation and

Chapter
Host Modulation Agents
LONG ESSAYS
Question 1 protective or regenerative response and is used for treating

the host side of the host-bacteria interaction.
What is the modulatory therapy? Discuss various host
A variety of agents acts as host modulating agents. They
modulating agents?
are mentioned below.
Answer
Systemically Administrered Agents
According to carranza host is defined as the organism from
which a parasite obtains its nourishment and modulation is Non-steroidal anti-inflammatory drugs (NSAIDs).

defined as the alteration of function or status of something Bisphosphonates.

in response to a stimulus or an altered chemical or physical Sub-antimicrobial dose doxycycline (SDD).

environment.
Locally Administered Agent
Host modulatory therapy (HMT) is a treatment concept
that aims to reduce tissue destruction and stabilize or 1. Non-steroidal anti-inflammation drugs.
regenerate periodontics by modifying or down-regulating 2. Enamel matrix proteins.
destructive aspects of the host response and up-regulating 3. Growth factors, and bone morphogenic proteins.
Fig. 13.1: Diagram showing how doxycycline inhibits connective tissue break down.
68
Non-steroidal Anti-inflammatory Drugs ketorolac have been found very effective in reducing the
GCF leves of PGE2.
They inhibit the formation of prostaglandins, released

2. Enamel matrix proteins, growth factor, and bone

by neutrophils, macrophages, fibroblasts, and gingival
morphogenic proteins: These have been shown to be
epithelial cells.
very effective as HMTs.
Inflammation is reduced by administering NSAIDS, as it

inhibits the production of prostaglandin.
NSAIDs are given for the treatment of pain, acute SHORT ESSAYS

inflammation and a variety of chronic inflammatory
conditions. Question 1
Bisphosphonates What is best comprehensive periodontal management?
These drugs inhibit osteoclastic activity, there by Answer

inhibiting bone resorption. The best clinical improvement can be achieved by
They also have anti-collagenous properties. combination of various treat more treatment (Fig. 13.2).

Sub-antimicrobial Dose Doxycycline
It is a 20 mg dose of doxycycline (periostat) that is

indicated as an adjacent to SRP for the treatment of
chronic periodontitis.
It is taken for 3 months, twice only.

It can be taken maximum for 9 months continuously.

It acts by inhibiting the action of enzyme, cytokines

and osteoclasts, rather than by exerting any antibiotic
effect.
The rationale for using Sub Antimicrobial dose
doxycycline (SDD) as an Host modulatory therapy (HMT) in
the treatment of periodontitis is that doxycycline inhibits
the activity of MMP’s by a variety of mechanisms including
reduction in cytokine levels and by stimulating osteoblastic
activity and new bone formation by promoting collagen
production (Fig. 13.1).
Locally Administered Agents

1. NSAIDs: Topical Mouthrinse containing NSAIDs for eg Fig. 13.2: Diagram showing best clinical improvement.
14
Influence of Systemic

Chapter Disorders and Stress
on the Periodontium
LONG ESSAYS
Question 1 Periodontal disease is more severe in persons having

Describe the relationship between diabetes and periodontal diabetes. Indeed the periodontal signs and symptoms are
diseases. Discuss the management of a diabetic patient now recognized as the “sixth complication”.
having periodontitis. Relationship between Diabetes and Periodontitis
Answer Pathogenesis
Diabetes is defined as clinically and genetically The various factors which lead to increased prevalence of
heterogeneous group of metabolic disorders manifested by periodontitis in diabetic patients are as follows:
high levels of glucose in blood. Vascular changes.

Functions of polymorphonuclear neutrophils (PMNs).
It can be classified into two types:

Biochemistry of crevicular fluid.
1. Type I: It is also known as insulin-dependent diabetes.

Changes in plaque microflora.
2. Type II: It is also known as non-insulin dependent

diabetes. Vascular Changes
The most common clinical signs of diabetes are: There are certain vascular changes observed in diabetic
Polydipsia which means excessive thirst patients such as:

Polyuria which means excessive urination Thickening and hyalinization of vascular walls.

Polyphagia which means excessive hunger, which can be Diastase resistant thickening of capillary basement

associated with loss in weight. membranes.
Various oral manifestations of diabetes mellitus are as Swelling and occasional proliferation of the endothelial

follows: cells.
Cheilosis Splitting of capillary basement membrane.

Mucosal drying and cracking All these diabetes induced vascular changes can lead to

Burning mouth and tongue inhibitory effect on the transport of oxygen, white blood

Decreased salivary flow cells, immune factors and waste product, which further

Abscess formation leads to impaired tissue repair and regeneration. This results

Change in the oral flora with predominance of Candida in greater chances of having periodontitis.

albicans, haemolytic streptococci and staphylococci.
Functions of PMNs
Complications of Diabetes Mellitus Functional impairment of PMNs is a classic feature of
There are five classic complications of diabetes mellitus: periodontitis.
1. Retinopathy. There are various disorders of PMNs which can be
2. Nephropathy. observed in diabetic patients. They are:
3. Neuropathy. Reduced phagocytosis and intracellular killing.

4. Altered wound healing. Impaired adherence.

5. Macrovascular disease. Impaired chemotaxis.

70
There is also inhibition of the glycolytic pathway with In the patients having uncontrolled diabetes, periodontal

PMNs, abnormal cyclic nucleotide metabolism, which can treatment is contraindicated.

lead to a disturbance in the organization of microtubules Diabetic patients with periodontitis, should receive

and microfilaments, and also a decrease in leukocyte oral hygiene instructions, mechanical debridement to
membrane receptors. remove the local factors and regular maintenance.
All these factors cause increased prevalence of In case of periodontal conditions, which require

periodontitis. immediate care, prophylactic antibiotics should be given.
If there is a patient of brittle diabetes, optimal periodontal
Biochemistry of Crevicular Fluid

health is necessary. Glucose levels should be monitored
There has been observed a change in the composition of continuously and periodontal treatment should be
gingival crevicular fluid (GCF) in patients having diabetes. performed, when the disease is in a well-controlled state.
This change favours the growth of periodontogenic Prophylactic antibiotic treatment should be started and

bacteria which leads to increase rate of periodontitis. penicillin is the drug of choice.
Also levels of cyclic AMP also reduce in patients having
diabetes.
Guidelines for a Diabetic Patient Receiving
Periodontal Therapy
Changes in Plaque Microflora
Early morning appointments should be scheduled

In the plaque of diabetic patients, there is a decreased because of less stress and insulin levels are optimal.
activity of hyaluronidase. Post-operative dose of insulin should be altered, after

There is a shift in the flora, with a greater prevalence any surgical procedure.
of Candida albicans, haemolytic streptococci, and Tissues should be handled as minimally and as a

staphylococci. traumatically as possible.
Because of the earlier reasons, it has been concluded Preoperative sedation is necessary if the patient is

that patients having diabetes are more susceptible to anxious.
periodontitis, which is mainly characterized by widening Not more than 1:100,000 concentrations of epinephrine

of periodontal ligament, increase in tooth mobility, should be used.
suppuration, abscess formation, and bone loss. In case of extensive therapy, antibiotics are recommended.

Recall appointments and meticulous home oral care
Laboratory Diagnosis of Diabetes

should be prescribed.
Diabetes can be diagnosed by any of the laboratory Question 2
methods:
What is the role of vitamin C/ascorbic acid in aetiology of
Random blood glucose: Less than 200 mg/dL.
periodontal diseases. Discuss the oral manifestations of

Fasting plasma glucose: Normal fasting glucose is
scurvy?

70–100 mg/dL.
2-hours post-prandial glucose: Normal 2-hours Answer

post-prandial glucose is Less than 140 mg/dL. Scurvy is caused due to the severe deficiency of vitamin C,

Glycosylated haemoglobin assay (HbA1c): Normal is which is characterised by haemorrhagic diathesis and

4–6%; Less than 7% good diabetes control; 7–8% suggests delayed wound healing.
moderate diabetes control; >8% action suggested to It may be seen both in infants and adults.

improve diabetes control. It may be seen in infants in their first year of life if the

formulate are not fortified with vitamins and in adults
Treatment because of malnutrition.
If the patient is suspected to be diabetic, following Malnutrition associated with alcoholism may predispose

procedures should be performed: an individual to scurvy.
Patients physician should be consulted.
Role of Vitamin C in Aetiology of Periodontal Disease

Laboratory tests should be analysed like fasting blood

glucose, post-prandial blood glucose, HbA1c and urinary Vitamin C plays an important role in periodontal diseases

glucose. through—for the maintenance of epithelial barrier,
71
Chapter 14 Influence of Systemic Disorders and Stress on the Periodontium
function to bacterial products, optimal level of vitamin C Periodontitis

are required. Vitamin C is also required to maintain the Deficiency of Vitamin C can result in swelling and

integrity of periodontal vasculature, also the vascular haemorrhage in the periodontal ligament.
response to bacterial plaque and wound healing.
Vitamin C deficiency can cause osteoporosis in the

Metabolism is affected with low levels of vitamin C due to alveolar bone which can cause increase in the tooth
which there is deficient ability of the tissue to regenerate mobility.
and repair itself.
Deficiency of Vitamin C alone does not cause periodontitis

Bone formation is also impaired leading to periodontal since it requires bacterial factors are required for
support in the deficiency of ascorbic acid. In the deficient attachment loss to occur.
state of vitamin C, there is a failure of osteoblasts to form
Decrease in Vitamin C can aggravate the pre-existing
osteoid. periodontitis.
In the presence of vitamin C, both the chemotactic and
Question 3

the migratory action of are enhanced without influencing

their phagocytic activity. Discuss the pathogenesis of diabetes and periodontal

There is an increase in the pathogenicity of the bacterial disease.
plaque because of the interference of the ecologic
equilibrium because of the decreased vitamin C
Answer

Deficiency of vitamin C results in scurvy which further The various factors which lead to increased prevalence of
leads to defective formation and maintenance of periodontitis in diabetic patients are as follows:
collagen, impaired osteoid formation and osteoblastic
Vascular changes.
function.
Functions of PMNs.
There is an increased capillary permeability, traumatic
Biochemistry of crevicular fluid.

haemorrhages susceptibility, hyporeactivity of the

Changes in plaque microflora.

contractile elements of the peripheral blood vessels,

and sluggishness of blood flow in the deficient state of

Vascular Changes
vitamin C.
There are certain vascular changes observed in diabetic
Clinical Manifestation of Scurvy patients such as
Thickening and hyalinization of vascular walls.
Bleeding, swollen gingiva and loosened teeth.

Diastase resistant thickening of capillary basement

Haemorrhagic lesions into the muscles of extremities,

membranes.

joints, nail beds and sometimes hair follicles.

Swelling and occasional proliferation of the endothelial
Petechial haemorrhages can also be seen.

cells.

There is impaired wound healing.

Splitting of capillary basement membrane.

There is increased susceptibility to infections.

All these diabetes induced vascular changes can lead to

Gingivitis inhibitory effect on the transport of oxygen, white blood
cells, immune factors and waste product, which further

There is enlarged haemorrhagic bluish-red gingiva seen leads to impaired tissue repair and regeneration. This results
in deficiency of Vitamin C.
in greater chances of having periodontitis.

Patients having Vitamin C deficiency do not always have
gingivitis. Functions of Polymorphonuclear Neutrophils

Vitamin C deficiency does not cause gingivitis, but it can
increase its severity. Functional Impairment of PMNs is a classic feature of
periodontitis.

Deficiency of Vitamin C can aggravate the gingival
response to plaque and can increase enlargement and There are various disorders of PMNs which can be
bleeding. observed in diabetic patients. They are:

If the levels of Vitamin C become normal then there would
Reduced phagocytosis and intracellular killing.
be reduction in the severity of the disorder but gingivitis
Impaired adherence.
will remain as long as the bacterial plaque persists.
Impaired chemotaxis.
72
There is also inhibition of the glycolytic pathway with Also levels of cyclic AMP also reduce in patients having
PMNs, abnormal cyclic nucleotide metabolism, which can diabetes.

lead to a disturbance in the organization of microtubules
and microfilaments, and also a decrease in leukocyte Changes in Plaque Microflora
membrane receptors.
In the plaque of diabetic patients, there is a decreased
All these factors cause increased prevalence of activity of hyaluronidase
periodontitis. There is a shift in the flora, with a greater prevalence of
Candida albicans, haemolytic streptococci, and staphylococci.
Biochemistry of Crevicular Fluid
Because of the above reasons, it has been concluded

There has been observed a change in the composition of that patients having diabetes are more susceptible to
GCF in patients having diabetes periodontitis, which is mainly characterized by widening
This change favours the growth of periodontogenic of periodontal ligament, increase in tooth mobility,
bacteria which leads to increase rate of periodontitis. suppuration, abscess formation, and bone loss.
SHORT ESSAYS
Question 1 Post-operative dose of insulin should be altered, after

What is the treatment of diabetic patients having any surgical procedure.
periodontitis and what are the treatment guidelines? Tissues should be handled as minimally and as a

traumatically as possible.
Answer Pre-operative sedation is necessary if the patient is

anxious.
Treatment Not more than 1:100,000 concentrations of epinephrine

If the patient is suspected to be diabetic, following should be used.
procedures should be performed: In case of extensive therapy, antibiotics are recommended.

Patients’ physician should be consulted. Recall appointments and meticulous home oral care

Laboratory tests should be analysed like fasting should be prescribed.

blood glucose, post-prandial blood glucose, glycated
haemoglobin and urinary glucose.
Question 2
In the patients having uncontrolled diabetes, periodontal What is the management of periodontal diseases in

treatment is contraindicated. pregnant patients?
Diabetic patients with periodontitis should receive
Answer

oral hygiene instructions, mechanical debridement to
remove the local factors and regular maintenance. Periodontal therapy aims to minimise the potential
In case of periodontal conditions, which require exaggerated inflammatory response related to pregnancy-

immediate care, prophylactic antibiotics should be given. associated hormonal alterations, in pregnant females.
If there is a patient of brittle diabetes, optimal periodontal
The second trimester of pregnancy is considered as the

health is necessary. Glucose levels should be monitored most safest period for performing dental procedures. But
continuously and periodontal treatment should be still long, stressful appointments and surgical procedures
performed, when the disease is in a well-controlled state. should be delayed until the period of post-partum.
Prophylactic antibiotic treatment should be started and The non-emergency periodontal procedures performed

penicillin is the drug of choice. in pregnant patients are meticulous plaque control,
scaling, root planning and polishing.
Guidelines for a Diabetic Patient Receiving Periodontal Appointments should be short and patient should be
Therapy

allowed to change positions frequently.
Early morning appointments should be scheduled In an ideal condition no medicines should be prescribed

because of less stress and insulin levels are optimal. but based on the needs of the pregnant female they
73
Chapter 14 Influence of Systemic Disorders and Stress on the Periodontium
should be reviewed for the potential adverse effects on periodontitis, all these conditions may be collectively
the foetus before prescribing drugs such as analgesics, referred to as necrotizing gingivostomatitis.

antibiotics, local anaesthetics and other drugs.

Dental radiographs should be avoided during pregnancy. Staging of Necrotizing Gingivostomatitis
The American Dental Association has stated that normal
Staging of necrotizing infections was proposed by Pindborg,
radiographic guidelines do not need to be altered during
who described four stages:
pregnancy, use of a properly positioned lead apron is an
absolute requirement. 1. Only the tip of the interdental papilla is affected.
2. Marginal gingiva was affected, with punched out papilla.
Question 3 3. Attached gingiva is also affected.
What are the periodontal manifestations of HIV infection? 4. Exposure of bone.
Answer Question 5
What are the periodontal findings of AIDS?
Periodontal manifestations of an HIV infection are as follows:

Linear gingival erythema Answer
Necrotising ulcerative gingivitis
All HIV infected patients may not know that they are

Necrotising ulcerative periodontitis. infected when they report for dental treatment. Individuals
with known HIV infection may not admit their status on the
Linear Gingival Erythema medical history.

It is characterised by reddish to bluish-red, oedematous Thus, every patient receiving dental treatment should

gingival tissue. be managed as a potentially infected person, using

There is usually presence of swollen interdental papilla universal precautions for all therapy.
and tendency to bleeding in increased. Extensive

periodontal treatment plans must be

There are significantly more bleeding sites and considered in regard to the patients’ systemic health,
destruction of interdental papilla is seen. prognosis, and survival time.
Large variations in progression of HIV disease exist among

Necrotising Ulcerative Gingivitis individuals, and selection of an appropriate treatment

plan depends on the state of the patients overall health.

It is characterised by red and swollen gingiva with a Although there appears to be few contraindications to
yellowish-grey marginal areas of necrosis.

routine dental treatment for many HIV infected patients,

Loss of interdental papilla is also seen. the periodontal treatment plan is influenced by the

It has an extremely rapid progression and there is patients overall systemic health and coincident oral
increased destruction of the periodontal ligament and infections or diseases.
alveolar bone which is usually accompanied by severe An awareness of oral disorders associated with HIV

pain. infection allows the clinician to recognise previously

undiagnosed disease or to modify treatment protocols
Necrotising Ulcerative Periodontitis appropriately.
It is characterised by severe attachment loss and bone
Question 6

loss with increased tooth mobility.

There is severe gingival bleeding. Describe in detail the periodontal manifestations of
leukaemia

There is also deep seated along with tooth mobility and
halitosis. Answer
Question 4 The leukaemias are the malignant neoplasias of WBC
What is necrotising gingivostomatitis? precursors characterised by:
Diffuse replacement of the bone marrow with
Answer

proliferating leukaemic cells.

The three conditions, i.e. linear gingival erythema, Abnormal numbers and forms of immature WBCs in the

necrotizing ulcerative gingivitis and necrotizing ulcerative circulating blood.

74
Widespread infiltrates in the liver, spleen, lymph nodes, Periodontal infections:

and other body sites. Infections of the periodontal tissues secondary to

leukaemia can be of two types:
Periodontal Manifestations in Leukaemic Patients h An exacerbation of an existing periodontal disease.
h
Oral and periodontal manifestations of leukaemia consist h Through an increased susceptibility of the
h
of leukaemic infiltration, bleeding, oral ulcerations and periodontium to fungal, viral or bacterial infections.
infections. Oral ulcerations and infections :

Gingival enlargements: The response to bacterial plaque and other local

The enlargements are primarily the result of a irritation is altered, the cellular component of the

massive leukemic cell infiltration into the gingival inflammatory exudates differs both quantitatively
connective tissue. When present, it is usually a feature and qualitatively from that in non-leukaemic
of acute monocytic leukaemia, although it has been individuals.
reported as a feature of other forms, including chronic Granulocytopenia results from the displacement of

lymphocytic leukaemia. normal bone marrow cells by leukaemic cell, which
The enlarged gingiva hinders mechanical plaque increases the host susceptibility to opportunistic

removal, and hence there is an inflammatory microorganisms and leads to ulcerations and
component enhancing this enlargement. infections.
Gingival bleeding: These lesions occur in sites of trauma such as buccal

Gingival bleeding can be seen as an early sign of mucosa in relation to the line of occlusion or on the

leukaemia and is secondary to thrombocytopenia palate.
that accompanies the leukaemia. Discrete, punched-out ulcers penetrating deeply into

It is specially marked when the platelet count drops the sub-mucosa and covered by a firmly-attached

below 10,000/mL and is compounded by poor oral white slough can be found on the oral mucosa.
hygiene. The gingival appearance is peculiar bluish-red. It is

Gingival haemorrhage is a common finding in sponge-like and friable and bleeds persistently on

leukaemic patients, even in the absence of clinically slightest provocation or even spontaneously.
detectable gingivitis. There are a variety of changes seen in the epithelium.

Bleeding tendency can also manifest in the skin and It may be thinned or hyperplastic. Common findings

throughout the oral mucosa, where the petechiae are include degeneration associated with intercellular
often found, with or without leukaemic infiltrates. More and intracellular oedema and leukocytic infiltration
diffuse submucosal bleeding manifests as ecchymosis. with diminished surface keratinisation.
Bleeding can also be a side effect of the drugs used to A gingival bacterial infection can be seen as a result of

treat leukaemia. an exogenous bacterial infection.
15

Chapter Periodontal Medicine
LONG ESSAYS
Question 1 with Streptococcus sanguinis (plaque), Porphyromonas

Which are the various systemic diseases which can be gingivalis with help of platelet aggregation-associated
effected by periodontitis? Explain in detail. protein (PAAP) resulting formation of thromboemboli.
Atherosclerosis: Focal thickening of arterial intima and

Answer media of the vessel.
Various systemic diseases which can be effected by
periodontitis are as follows: Pathological Changes
Cardiovascular system (CVS) and Cerebrovascular system: Circulating monocytes adhere to endothelium via

Atherosclerosis. adhesion molecules. Intercellular adhesion molecule-1,

Coronary artery disease (CAD) and stroke. endothelial leukocyte adhesion molecule-1, vascular

Myocardial infarction. cell adhesion molecule-1, that are triggered by

Endocrine system: prostaglandins, bacterial LPS, cytokines. Complex

Diabetes mellitus. penetrates the endothelium, ingests LDL and form foam

Reproductive system: cells significant of atheromas.

Pre-term low birth weight (PLBW). Monocytes, macrophages liberating pro-inflammatory

Pre-eclampsia. cytokines (IL-1, TNF, PGE2) that proliferate lesion.

Respiratory system: FGF, PDGF mitogenic factors stimulate collagen

Chronic obstructive pulmonary disease. formation, arterial thickening, narrow lumen and less

Acute bacterial pneumonia. blood supply.

Systemic inflammatory markers, i.e. acute phase reactant
Cardiovascular and Cerebrovascular System proteins (CRP and fibrinogen) serve as a proven risk
Daily oral-hygiene activity, e.g. mastication/tooth assessment tool for cardiovascular disease. Serum CRP and
fibrinogen is elevated in periodontitis.

brushing creates greater bacteremia than from dental
procedures. Periodontal disease has two-fold effects systemically:
Periodontal disease predisposes the patient to bacte- 1. Direct effects on Blood vessels (atheroma formation).

remia via the virulent Gram-negative periopathogens. 2. Indirect effects stimulating CVS changes (elevation of
8% of infective endocarditis cases are associated systemic inflammatory responses) (Figs 15.1 to 15.6).

with periodontal disease even in absence of dental
procedures. Stroke and Periodontal Disease
American Heart Association (AHA) recommendations: Studies reveal that poor dental health is a significant risk

Importance of establishing and maintaining best factor for stroke (25%).
possible oral health to reduce potential sources of Periodontitis is a severe risk factor than smoking.

bacterial seeding. Longitudinal study states that the periodontal patients

Thrombogenesis: Platelet aggregation is the primary with more than 20% bone loss at baseline were three

cause for, periopathogens involved in coronary times more likely to develop stroke versus those with less
thrombogenesis especially platelets selectively bind than 20% bone loss (Fig 15.7).
76
Periodontitis increases individual’s risk factor by threefold

to develop stroke.

Diabetes and Periodontal Disease
Complications of diabetes mellitus are as follows:
Retinopathy.

Nephropathy.

Neuropathy.

Macrovascular disease.

Fig. 15.4: Pathogenesis of atherosclerosis.
Fig. 15.1: Acute and chronic pathways to ischemic

heart disease.
Fig. 15.5: Influence of periodontal infection on atherosclerosis.

Fig. 15.2: Factors affecting blood viscosity in health.
Fig. 15.6: Cardiovascular and periodontal consequences of

Fig. 15.3: Effect of infection on blood viscosity. hyper-responsive monocyte/macrophage phenotype.
77
Chapter 15 Periodontal Medicine
Aetiology for Low Birth Weight

In Pre-term labour, premature rupture of membrane. Risk

factors are smoking, drug use, hypertension, diabetes,
low socioeconomic status, genitourinary tract infections
(bacterial vaginosis), etc.
Periodontitis primarily a Gram negative infection,

plays a role in low birth weight (LBW) infants chiefly by

stimulation of host cytokine production.
Fig. 15.7: Mechanism of stroke.
Studies state high levels of Tannerella forsythia, P.

gingivalis found in subgingival plaque of women with

Altered wound healing. LBW infants.

Periodontal disease. Women with higher PGE2 and IL-1 levels in gingival

Diabetes mellitus type 2 and severe periodontitis at crevicular fluid (GCF) are more prone to pre-mature
baseline resulted in worsened glycemic control over births.
time. Pre-eclampsia (hypertensive disorder) acts as risk in

Periodontal therapy along with systemic antibiotics presence/severity of periodontal disease (2.5%).
significantly improves glycemic levels in cases with Maternal

infection raises prematurely the pro-
severe periodontitis with poor metabolic control. inflammatory cytokines and prostaglandin levels in

Antibiotics act as adjunct to periomechanical therapy. amniotic fluid premature labour (Fig 15.9).

Mode of action of doxycycline 20 mg (tetracycline).

Eliminates residual microorganisms. Periodontal Disease and COPD
Anticollagenase property reduces the MMP’s activity
COPD is characterized by airflow obstruction resulting

and protein glycation henceforth suppressing the AGE

from chronic bronchitis/emphysema.

complex formation and improving metabolic control Pathogenic mechanisms are similar to periodontal
(Fig 15.8).

disease, i.e. host response aggravated by bacteria in

periodontal disease and smoking in COPD.
Periodontitis and Pregnancy
Correlation is still in an infancy stage.
Low birth weight infants less than 2,500 g at birth have high
risk for death in neonatal period or on survival increased risk
for congenital defects, respiratory disorders, etc.

Fig. 15.8: Potential effects of periodontal infection and
periodontal therapy on glycemic control in patients with Fig. 15.9: Mechanisms by which infection may induce preterm
diabetes labor
16 Halitosis

Chapter
(Oral Malodour)
LONG ESSAYS
Question 1 Dry Mouth

Define oral malodour/halitosis/breath malodour. Give its In patients with xerostomia, large amount of plaque are

aetiology, diagnosis and management. found on teeth, prosthesis and tongue surface.
This plaque causes increase in the microbial load thus

Answer producing a lot of VSC and thus breath malodour.
Breath malodour can be defined as the unpleasant Extra-oral Causes (Ear-Nose-Throat)
subjective perception after smelling someones breath due
to some pathological cause.
In patients with acute pharyngitis, purulent sinusitis,

Breath malodour should not be confused momentarily chronic sinusitis or regurgitation oesophagitis, strong
disturbing odour caused by food intake or smoking. breath malodour is commonly seen.
Bronchi and lungs: Breath malodour is commonly

Aetiology seen in cases of chronic bronchitis, bronchiectasis, and
bronchial carcinoma.
The unpleasant smell of breath is due to the presence of
volatile sulphide compound (VSC) specially hydrogen Diabetes
sulphide, methyl mercaptan and dimethyl sulphide. Accumulation of ketone bodies in type 1 diabetes causes
alteration of breath malodour and may prove useful in
Intra-oral Causes diagnosis.
Dentition Diagnosis
In deep carious lesions with food impaction and
Self-examination

putrefaction, extraction wounds filled with blood clots,
purulent discharge or any other factor causing food Smelling metallic or plastic spoon after the scraping of

back of the tongue.
impaction.
Acrylic dentures when worn overnight or are not Smelling a tooth pick after introducing it in interdental area.

regularly cleaned. Smelling saliva.

Periodontal Infections Organoleptic Rating
Bacterias associated with gingivitis or periodontitis It is considered gold-standard.

like porphyromonas gingivalis, prevotella intermedia, In this, a trained judge sniffs the expired air and rates the

prevotella nigrescens, Campylobacter rectus, fusobacterium intensity from 0 to 5:
nucleatum, peptostreptococcus micros, tannerella 0—no odour present.

forsythia, spirochetes, etc. produce VSC, thus causing 1—barely noticeable odour.

breath malodour. 2—slight but clearly noticeable odour.

Anaerobic conditions, deep periodontal pockets help in 3—moderate odour.

the decarboxylation of lysine and ornithine to cadaverine 4—strong offensive odour.

and putrescine which are malodourous in nature. 5—extremely foul odour.

79
Chapter 16 Halitosis (Oral Malodour)

The judge smells a series of different air samples:
Dark-field or phase-contrast microscopy.
1—oral cavity odour: Judge places his or her nose

Saliva intubation test.

close to the mouth opening while the patient refrains
Electronic nose.
from breathing and counts from 1 to 20.
2—breath odour: The subject expires through the
Treatment
mouth, while the judge smells both at the beginning Mechanical reduction of intra-oral nutrients and
and at the end.

microorganisms: Tongue cleaning, tooth-brushing,

3—tongue coating: The judge smells the tongue
interdental cleaning, scaling.

scraping. Chemical reduction of oral microbial load:

4—nasal breath odour: The judge places his nose near

Chlorhexidine, triclosan-based mouthwashes, chlorine

the nostrils while the patient expires through the nose

dioxide, two-phase oil water rinses, Listerine rinses,
keeping the mouth closed.
amino fluoride/stannous fluoride, 3% hydrogen peroxide
Specific Characteristics of Breath Malodour rinses, oxidizing lozenges.

Conversion of malodourous gases into non-

Rotten-egg smell indicates the presence of VSC. volatile compounds: Metal salt solutions metal

A dead mice smell is associated with liver insufficiency, salts like zinc ions, combined with sulphur making
VSC, aliphatic acids. volatile sulphide compound into non-volatile sulphide

Rotten-apple smell indicated type I diabetes. compounds.

Fish odour indicates kidney insufficiency.
Toothpastes: Baking soda based dentifrices have been
shown to be effective by reducing VSC levels.
Technology to Detect Oral Malodour
Masking the malodour: Mouth rinses, mouth sprays,

Portable volatile sulphide monitor. and lozenges contain pleasant odour which mask the

Gas chromatography. breath malodour for a short duration.
17 Defence Mechanism

Chapter
of Gingiva
LONG ESSAYS
Question 1 Organic compounds: Glucose hexose amine and

Describe in detail defence mechanism of gingiva? hexuronic acid are commonly seen.
Glucose concentration in GCF is three to four times than

Answer serum.
Metabolic and bacterial products commonly seen in
Sulcular Fluid or Gingival Crevicular Fluid
GCF are lactic acid, urea, hydroxyproline, endotoxins,
Gingival crevicular fluid (GCF) is an inflamtmatory hydrogen sulphide and antibacterial factors.

exudate and not a continuous transudate. Many enzymes are also seen.

In normal gingiva little or no fluid can be collected.
Clinical Significance of GCF:

Methods of collection of GCF:

GCF is an inflammatory exudate whose presence in

Brill Technique: In this a filter-paper strip is inserted sulci gives an indication of inflammation even in the

into the pocket till resistance is encountered. sulcus which appears normal to naked eye.
This method introduces irritation of sulcular The amount of GCF is proportional to the severity of

epithelium which can trigger the low of fluid, therefore inflammation.
this gives an inaccurate picture.
Factors that influence the amount of GCF are:
Loe and Holm-Pedersen technique: In this method

they place the filter-paper strip at the entrance of the Circadian periodicity: Between 6 am to 10 pm

pocket to minimise the irritation. a gradual increase in GCF amount is seen which
In this method fluid seeping out of the pocket is decreases post 10 pm.
picked up by the strip but sulcular epithelium does Sex hormones: Females sex hormones enhance

not come in contact with the paper. vascular permeability thus enhancing GCF flow.
Weinstein method: In this method they use pre- Mechanical stimulation: Chewing and vigorous

weighed twisted threads which are placed in the gingival brushing stimulates the increases of GCF flow.
gingival crevice along the tooth and the amount of Smoking: Smoking produces an immediate but

fluid collected is estimated by re-weighing the thread. transient increase in GCF flow.
Micropipette: In this method micropipettes are used, Periodontal therapy: GCF production is increased

which are placed in the pocket. during the healing period after periodontal surgery.
These collect the fluid by the capillary action.
Composition of GCF: Leucocytes in Dentogingival Area

Cellular elements: Bacteria, desquamated epithelial Leucocytes which are predominantly polymorphonuclear

cells, leucocytes [polymorphonuclear neutrophils neutrophils (PMNs) are found in clinically healthy gingival
(PMNs)], lymphocytes, monocytes/ macrophages. sulci.
Electrolytes: Potassium, sodium and calcium ions are These appear in small numbers extravacularly in

seen in GCF. connective tissue adjacent to the bottom of the sulcus.
81
Chapter 17 Defence Mechanism of Gingiva

From here these travel across the epithelium into the
Lacto peroxidase -thiocyanate system: It is
gingival sulcus. bactericidal to some strains of Lactobacillus and

91.2–91.5% PMNs and 8.5–8.8% mononuclear cells Streptococcus.
together form the leucocyte population.
Lactoferrin: It is effective against Actinobacillus

Mononuclear cells are composed of 58% B lymphocytes, species.
18% mononuclear phagocytes and 24% T lymphocytes.
Myeloperoxidase: This enzyme is released by

Leucocytes form a major protective mechanism against leucocytes and is bactericidal towards Actinobacillus
plaque in the gingival sulcus. and also inhibits attachment of actinomyces to
hydroxyapatite.
Saliva
Salivary Antibodies:
Saliva in oral cavity performs following functions:

Lubrication with the help of glycoproteins and

Saliva contains IgG, IgM and IgA immunoglobulins.
muccoids.
However out of these, IgA has the highest
Physical protection with glycoprotein and muccoids.

concentration in the saliva while IgG is seen more
Cleansing with the physical flow.

in GCF.
Buffering action with the help of bicarbonate and

Salivary Enzymes:
phosphate action. Most common enzyme is parotid amylase; however,
Anti-bacterial action.

in periodontal diseases, following enzymes are also

Anti-bacterial Factors seen: hyaluronidase, lipase, beta glucuronidase,

chondroitin sulphatase, amino acid decarboxylase,

Inorganic Factors: catalase, peroxidase and collagenase.
Ions and gases, bicarbonate , sodium, potassium,

Saliva also contains anti-proteinases, which inhibit
phosphates, calcium, fluorides, ammonium and cysteine proteinases like cathepsin and anti-
carbon dioxide. leucoproteases which inhibit elastase.

Organic Factors:
Tissue inhibitor of matrix metalloproteinase
Lyzozyme: It is a hydrolytic enzyme which works on
(TIMP) inhibits the activity of collagen degrading
both Gram-negative and Gram-positive organisms. enzymes.
18

Chapter Gingival Inflammation
LONG ESSAYS
Question 1 This process starts in about one week after the beginning

of plaque accumulation.
What are the various stages of gingivitis? Explain in detail This stage shows erythema due to the proliferation of
with histopathology.

capillaries and increase formation of capillary loops
Answer between rete pegs or ridges.
Bleeding on probing also becomes evident.
There are four stage of gingivitis:

Between 6 and 12 days after the onset of clinical gingivitis,

1. Stage I gingivitis: The initial lesion. the gingival fluid flow and the number of leucocytes
2. Stage II gingivitis: The early lesion. reach to the maximum level.
3. Stage III gingivitis: The established lesion. About 70% of collagen is destroyed around the cellular

4. Stage IV Gingivitis: The advanced lesion. infiltrate.
The polymorphonuclear leukocytes (PMNs) are now
Stage I Gingivitis: The Initial Lesion

evident in the gingival epithelium, since they leave the
Clinically, this initial response to bacterial plaque is blood vessels and through chemotactic stimuli from
plaque, migrate to the epithelium.

not apparent and therefore referred to as subclinical
gingivitis.
Process of phagocytosis occurs, in which the PMNs

It is the first manifestation of gingival inflammation. engulf the bacteria.
There is a decreased capacity of collagen production,

There are vascular changes in this stage consisting of

and fibroblast shows cytotoxic alterations.

dilated capillaries and an increase in blood flow.
If the host respose is good, the initial lesion would resolve Histologically

rapidly, leaving the tissue to the normal state. Seventy-five percent lymphocytes, mainly T lymphocytes

But if the host does not responds well, then the lesion are found in the connective tissue, just beneath the

might take up a chronic form and there might be junctional epithelium.
infiltration of macrophages and lymphoid cells. Neutrophils, macrophages and some amount of plasma

cells and mast cells are also seen within the connective
Histologically
tissue.
There is increase in the number of leucocytes. Rete pegs may be seen in the Junctional epithelium.

There is increase in the gingival crevicular fluid (GCF) The features of initial lesion aggravate in early lesions.

flow, due to increased accumulation of leucocytes within
the gingival sulcus. Stage III Gingivitis: The Established Lesion
Leucocytes increase within the junctional epithelium This lesion is predominated by plasma cells and B

and the connective tissue.

lymphocytes.
There is widening of the blood vessels. B lymphocytes are mainly of immunoglobulin G1 (IgG1)

and G3 (IgG3) subclasses.
Stage II Gingivitis: The Early Lesion This stage occurs around 2–3 weeks of plaque

Early lesion evolves form the initial lesion. accumulation.

83
Chapter 18 Gingival Inflammation

There is presence of localised gingival anoxemia which is
Intercellular spaces are filled with granular debris, along
due to engorged and congested blood vessels, impaired with lysosomes derived from disrupted neutrophils,

venous return and sluggish blood flow. lymphocytes and monocytes.

Anoxemia leads to bluish hue on the reddened gingiva.
Tissue components can be destroyed, because of acid

Colour of the gingiva can deepen due to extravasation hydrolases released by lysosomes.
of erythrocytes and into the connective tissue and break
Rets ridges can be seen in the Junctional epithelium that
down of haemoglobin into its component pigments. protrude into the connective tissue.

Collagenase is an enzyme which is normally present in
Collagen fibres are also destroyed within the connective
gingival tissue it is produced by PMNs and also by some tissue, around, the infiltrate disrupted plasma cells,
bacteria. neutrophils, lymphocytes, monocytes and mast cells.
The activity of this collagenase is increased in inflamed
Stage 4 Gingivitis: The Advanced Lesion

gingival tissue which causes destruction of the gingival

connective tissue.
These lesion evolves from stage three gingivitis.

In the chronically inflamed gingiva there is also increased
It is characterised by extension of inflammation into the
levels of acid phosphatase, alkaline phosphatase, alveolar bone.
b-glucuronidase, b-glucosidase, b-galactosidase,
Therefore, it is referred to as phase of periodontal break
esterases, aminopeptidase and cytochrome oxidase. down.
Histologically Histologically

There is presence of a chronic inflammatory reaction.
Extensive inflammation and immunopathologic tissue

There is increase in the number of plasma cells and B damage is seen.
lymphocytes.
Plasma cells continue to dominate the connective tissue.

Intercellular spaces within the Junctional epithelium
PMNs dominate the Junctional epithelium and crevice.
widens.
Gingiva becomes fibrotic.
19 Clinical Features

Chapter
of Gingivitis
LONG ESSAYS
Question 1 Clinical features of gingivitis are as follows:

A. Gingival bleeding on probing.
What is gingivitis? Describe gingivitis. Discuss clinical
B. Colour changes in the gingiva.
features of gingivitis in detail.
C. Changes in consistency of gingiva.
Answer D. Changes in surface texture of gingiva.
E. Changes in position of the gingiva.
Inflammation of gingiva is refrred to as gingivitis.
F. Changes in gingival contour.
It can occur as a sudden onset for short duration can be

painful. A. Gingival Bleeding on Probing
Gingivitis which reappears even after having been
Bleeding on probing is one of the clearest signs of gingival

eliminated by treatment is referred to as recurrent

inflammation seen before the gingivitis is established,
gingivitis.
other being the increase in gingival crevicular fluid
Gingivitis which is slow in onset and is for longer duration
production rate.

is inferred to as chronic gingivitis. It is most commonly It may vary in severity duration and case of provocation.
found.

It has been seen that bleeding on pooling appears
Gingivitis which is confined to the gingiva of a single

before visual signs of inflammation, thus it is a more

tooth or group of teeth is referred to as localised gingivitis.
Gingivitis, involving the margin of the gingiva and may
objective sign that requires less subjective estimation by
the examiner.

include a portion of the contiguous attached gingiva is
Presence of bleeding is not a definite indicator of clinical
referred to as marginal gingivitis.

Gingivitis involving the interdental papillae and may extend
attachment loss, but its absence definitely indicates an
excellent negative predictor of future attachment loss.

to the gingival margin, is referred to as papillary gingivitis.
Gingivitis affecting the gingival margin, the attached
Factors causing gingival bleeding could be local or

gingiva and the interdental papillae is referred to as. systemic
Diffuse gingivitis.
Gingival disease can be described as follows:
Local factors causing gingival bleeding:

Other than plaque, there are various other
Localised marginal gingivitis: It is confined to one or

more areas of the marginal gingiva. contributing factors for gingivitis. They can be
Localised diffuse gingivitis: It extends from margin to anatomic and developmental tooth variations, caries,

the mucobucccal fold in a small area. frenum pull, iatrogenic factors, malposition of teeth,
Localised papillary gingivitis: It is seen in one or more mouth breathing, overhangs, partial dentures, lack of

interdental regions in a small area. attached gingiva and recession.
Generalised marginal gingivitis: It is seen in the gingival Chronic and recurrent bleeding:

margin in relation to all the teeth. Chronic inflammation is the most common cause of

Generalised diffuse gingivitis: It involves the complete abnormal gingival bleeding

gingiva that includes the interdental, marginal and Mechanical trauma can provoke gingival bleeding,

the attached gingiva. either chronic or recurrent
85
Chapter 19 Clinical Features of Gingivitis

Mechanical trauma could be from tooth brushing B. Colour Changes in Gingiva
tooth picks, food impactions or biting into solid foods
Colour of the gingiva is dependent on three factors

for example apples

The severity of bleeding and the ease of its provocation

vascularity, degree of keratinisation and pigments within
depends upon the intensity of inflammation the epithelium.
Once the vessels are ruptured and damaged,

Colour change is a very important clinical sign of
mechanism of hemostasis starts, which include gingivitis.
contraction of the vessel wall, decrease in blood

The normal colour of gingiva is coral pink, and is because
flow, platelets adhere to the edges of the tissue of vascularity and overlying epithelial layers.
forming a fibrous clot which contracts, resulting in

If the vascularity increase, the colour changes to reddish
approximation of the edges of the injured area pink.
But when this area is irritated, bleeding starts again

Thus, in chronic periodontitis, the colour changes to
Bleeding on probing is a sign of active tissue

reddish pink due to increased proliferation of blood
destruction vessels and reduced keratinisation. Bluish hue may be
Injury can lead to active episodes of gingival

seen in later stages due to venous.
inflammation
The colour change starts from the interdental and
Injury could be laceration of gingiva during tooth

the marginal gingiva and may extend to the attached
brushing or by sharp pieces of hard food, gingival gingiva.
burns from hot foods or chemicals
Colour changes in acute gingivitis differs in both
Spontaneous bleeding is also seen in acute necrotising

distribution and nature from those in chronic
ulcerative gingivitis as the inflamed connective tissue gingivitis.
consists of engaged blood vessels, which get enrobed
The colour change may be marginal, diffuse or patch like,
by ulceration due to necrotic surface epithelium. depending upon the acute condition.

Systemic factors causing bleeding:

For example in acute necrotising ulcerative gingivitis,
Certain conditions have common feature of a
the marginal gingiva is involved. In herpetic
gingivostomatitis the involvement is diffuse and in acute

haemostatic mechanism failure which result in

reaction to chemical irritation can be diffuse or patch
abnormal bleeding in the skin, internal organ and
like.
other tissues including oral mucosa.
In such condition, the bleeding is spontaneous.

If the condition does not worsen, the colour remains
red and may revert back but if the condition worsens

Haemorrhagic disorders, in which there is abnormal

in acute inflammation, then the colour changes to dull,

gingival bleeding is seen are as follows: Vascular

whitish grey.
abnormalities like vitamin C deficiency or allergy like
Schonlein-Henoch purpura, platelet disorders like Metallic Pigmentation
thrombocytopenic purpura, hypoprothrombinemia
like vitamin K deficiency, other coagulation defects
Systematic absorption of heavy metals like bismuth,
such as haemophilia, leukaemia or Christmas disease, arsenic, mercury, lead and, from therapeutic was or
deficient platelet thromboplastic factor (PF3) resulting occupational or household environment might discolour
from uraemia, multiple myeloma and post rubella the gingiva and other areas of the oral mucosa.
purpura.
A black or bluish line is present in the gingiva due to
There are certain other . They can be effects of

these metals.
hormonal replacement therapy, oral contraceptives,
Colour Changes Associated with Systemic Factors
pregnancy and the menstrual cycle.
Fluctuation in certain hormones such as androgonic

There are certain systemic factors which may influence
hormones have been associated in modifying the colour of the gingiva.
gingivitis, especially during puberty.
There could be endogenous or endogenous source of
Certain medications also alter the gingivitis like,
pigments.
anticonvulsants antihypertensive calcium-channel
Endogenous oral pigments are melanin, bilirubin and
blockers and the immunosuppressant drugs, cause iron which can cause oral pigmentation.
gingival enlargements, which cause gingival bleeding,
Melanin pigmentation is a normal physiologic process
secondarily. which is found in highly-pigmented ethnic groups.
86
Following are the diseases in which there is increase in Chronic Gingivitis

melanin pigmentation:

Addison’s disease: Isolated patches of discolouration Clinical Changes Microscopic Features

are seen in this disease, which is of varying degree Saggy and puffiness that pits It is because of infiltration by fluid
from bluish-black to brown. on pressure. and cells of inflammatory exudate.
h It is basically caused due to adrenal dysfunction.
H ighly sof t and friable Degeneration of the connective
h
Peutz- syndrome: This disease causes intestinal gingiva which readily gets tissue and epithelium associated

polyposis. fragmented on exploration with injurious substances that
with a probe and pinpoint provoke the inflammation and
h Melanin pigmentation is seen in oral mucosa and lips.
surface areas of redness and inflammatory exudate.
h
Albright syndrome: (fibrous dysplasia) and von desquamation are seen. There is a change in the connective

reckling hausen’s disease (neurofibronatosis) tissue and epithelium relationship,
produces areas of oral melanin pigmentation. with inflamed, engorged connective
tissue expanding to within a few
h Bile pigments can also stain the skin and the
epithelial cells of surface.
h
mucous membrane. Thinning of the epithelium and
h Iron deposition seen in case of haemochro-matosis degeneration is associated with
h
also produces a blue-grey pigmentation of the oral oedema and leucocyte invasion,
separated by areas in which rets
mucosa. pegs are elongated.
h Disorders related to blood can produce colour
h
Firm Leathery Consistency It is because of fibrosis and due to
changes of the oral mucosa such as anaemia,
epithelial proliferation associated
polycythaemia or leukaemia. with long-standing chronic
h Disorders related to endocrine system and inflammation.
h
metabolic disturbance can also produce colour
change such as diabetes and pregnancy. Acute Gingivitis
h Exogenous factors which are responsible for colour
h
changes in gingiva are as follows: Clinical Changes Microscopic Features
» Irritants such as coal, metal dust and colouring Diffuse puffiness and It is because of diffuse oedema of
»
agents in food and lozenges. softening. acute inflammatory origin.
» Tobacco leads to increase in melanin
»
pigmentation and hyperkeratosis of the gingiva. Sloughing with greyish There is necrosis with formation of
flake like particles of debris pseudo membrane which can be
» Amalgam implantation in the mucosa can lead
adhering to eroded surface. composed of bacteria, PMNs and
»
to localised bluish black areas of pigmentation. degenerated epithelial cells in a
If a patient wants to get his gingiva depigmented fibrous meshwork.

because of aesthetic concern, procedure known as Vesicle formation There is intercellular and intracellular
gingival depigmentation can be performed. oedema with degeneration of
There are various ways of gingival depigmentation such nucleus and cytoplasm and rupture

and with the help of scalpels, chemicals, electrocautery of cell wall.
and lasers.
D. Changes in Surface Texture of the Gingiva
C. Changes in Consistency of Gingiva The normal surface of gingiva is usually stippled.

Both the acute and chronic form of gingiva produces Stippling, basically refers to an orange peel appearance of

changes in the consistency of gingiva. gingiva which is caused by numerous small depressions
In chronic gingivitis, both the forms, i.e. destructive and elevations.

which is oedematous and reparative which is fibrotic, It is seen in interdental gingiva and attached gingiva.

coexists and the form which is predominated, will define Surface of gingiva can be either smooth and shiny or

the consistency of gingiva. firm and nodular depending whether the changes are
The various clinical and histopathological changes seen exudative or fibrotic.

in the gingival consistency in chronic and acute form of Nodular texture is seen in cases of drug-induced gingival

gingivitis are as follows: overgrowth.
87
Chapter 19 Clinical Features of Gingivitis
E. Changes in Position Gingiva

Normal position of gingiva is usually at cementoenamel

junction (CEJ)

In cases of inflammation the gingiva can be above CEJ,
due to increase in the size of gingiva

Also in cases of gingival enlargement, the gingiva will be
above CEJ, most of the times covering the clinical crowns
as well

In case of attachment loss, there can be shift in the
position of gingiva apical to CEJ

This is referred to as gingival recession

Recession is exposure of the root surface by the apical
shift in the position of gingiva Fig. 19.1: Diagram showing apparent and actual position of the

There can be two positions of gingiva in recession Gingiva along with visible and hidden recession.

First is the actual position, which is the level of the
epithelial attachment on the tooth
It can cause hyperaemia of pulp and associated symptoms

Second is the apparent position which is the level of the may result from excessive exposure of the root surface
crest of the gingival margin
Oral hygiene can be a problem in cases of interproximal

Actual position of the gingiva would determine the recession, resulting in plaque accumulation.
severity of the recession and not the apparent position
(Fig. 19.1). F. Changes in Gingival Contour

Causes of recession are as follows:
Change in the contour of gingiva is mainly seen in cases
Faulty tooth brushing techniques (gingival abrasion)

of gingival enlargement
Tooth malposition

Normal contour of the gingiva is scalloped
Friction from soft tissues (gingival ablation)

In cases of disease, the contour of gingiva becomes
Gingival inflammation

scalloped
Abnormal frenum attachment

Inflammatory changes is in the marginal gingiva can lead
Iatrogenic dentistry

to formation of and clefts

Trauma from occlusion

Some suggest they occur because of traumatic occlusion
Orthodontic treatment

and the treatment would be occlusal adjustments clefts

and narrow, triangular shaped gingival recession
Clinical Significance of Recession
As the recession progression apically, the cleft becomes
Gingival recession can lead to: broader, causing exposure of the root cementum
Root caries

McCall festoons are rolled, thickened band of gingiva
Recession can causes abrasion or erosion of the

which is generally seen along the canines, when the
cementum leading to hypersensitivity of dentin recession approaches the muco gingival junction.
SHORT ESSAYS
Question 1
Thickening of alveolar bone.
It has been seen in various studies that tooth brushing incre-
What is the effect of tooth brushing on the consistency of

ases the proliferative capacity of the functional epithelium.

the gingiva?
Therefore, it means that the tooth brushing can increase
Answer the turnover rate and desquamation of junctional
epithelial surfaces.
There are various effects of tooth brushing on the
This process holds an important clinical significance
consistency of gingiva such as: as it prevents direct access to the underlying tissue by
It promotes keratinisation of oral epithelium.

periodontal pathogens and may repair small breaks in
Capillary gingival circulation is enhanced.

the junctional epithelium.
88
Question 2 These calcified masses are removed from the tooth and

displaced into the gingiva during scaling root remnants,
What is the significance of calcified masses in gingiva?

cementum fragments or cementicles.
Answer These masses leads to chronic inflammation and fibrosis

and sometimes foreign body giant cell activity.
Calcified masses in gingiva can be found as alone or in groups. Sometime they can be enclosed within an osteoid like

They may vary in size, location, shape and structure. matrix.

20

Chapter Gingival Enlargement
LONG ESSAYS
Question 1 Generalised: Involving the gingiva throughout the

mouth.
What is gingival enlargement and its classification and
Marginal: Confined to the marginal gingiva.
grades? Discuss in detail about drug-induced gingival

Papillary: Confined to the interdental papilla.
enlargement?

Diffuse: It involves the marginal, attached gingiva and

Answer papilla.
Gingival enlargement is the increase in the size of gingiva.
Discrete: It an isolated sessile or pedunculated tumor

like enlargement.
It is also referred to as gingival over growth.
Classification of gingival enlargements are as follows: Degree of gingival enlargement are as follows:
(According to Carranza) Grade 0: No signs of gingival enlargement

I. Inflammatory enlargement Grade I: Enlargement confined to interdental papilla.

A. Chronic Grade II: Enlargement involving papilla and marginal

B. Acute gingiva.
II. Drug induced enlargement Grade III: Enlargement covering three quarters or more

III. Enlargements associated with systemic disease or of the crown.
conditions
A. Conditioned enlargements Drug-induced Gingival Enlargement
h Pregnancy
Few drugs are responsible for causing clinical
h

h Puberty

enlargements.
h
h Vitamin C deficiency
These include anti-consultants, immuno suppressants
h

h Plasma cell gingivitis

and calcium-channel blockers.
h
h Non-specific conditioned enlargements (pyogenic
h
granuloma) Enlargement can creates problem in speech, mastication,

B. Systemic diseases causing gingival enlargements tooth eruption and problems with esthetics.
h Leukaemia Clinical and microscopic features of different drugs are

h
h Granulomatous diseases (e.g. Wegener’s almost similar.
h
granulomatosis, sarcoidosis)
IV. Neoplastic enlargement (gingival tumors) Clinical Features
A. Benign tumors Enlargement starts as a painless, beadlike enlargement

B. Malignant tumors of the interdental papilla and extends to the facial and
V. False enlargements. lingual gingival margins.
Depending upon the location and distribution, gingival As the enlargement progresses the growth from the

enlargement can be given the following designations: marginal and papillary gingiva unites and converts into
Localized: Limited to gingiva adjacent to a single a massive tissue fold covering a considerable portion of

tooth or group of teeth. crowns, which may interfere with occlusion.
90
The enlargement appears as pale pink, firm, resilient and Epithelium shows acanthosis.

resembles the shape of a mulberry with a small lobulated There is presence of enough amount of ground

surface with no bleeding. substance.
The enlargement appears beneath the gingival margin, Enlargement starts as a hyperplasia of the connective

from which it is separated by a linear groove. tissue core of the marginal gingiva and is increased due
Because of the enlargement, the plaque control becomes to proliferation and expansion beyond the crest of the

difficult. gingival margin.
Because of poor plaque control, a secondary Enlargements which reoccur, appears as granulation

inflammatory process starts, which complicates the tissue, composed of several new capillaries and
gingival enlargement caused due to drug. fibroblasts and irregularly arranged collagen fibrils with
Because of the above reasons, the enlargement few lymphocytes.

becomes a combination of overgrowth due to drugs and Sometimes, the connective tissue is more vascularized

inflammation caused by bacteria. along with chronic inflammatory cells at the foci, specially
Secondary inflammatory changes produce a red or a plasma cells in case of cyclosporine enlargements.

bluish-red discoloration, increases the bleeding tendency In a phenytoin enlargement, there is an equal ratio of

and obliterates the lobulated surface demarcations. fibroblast to collagen, which is seen in a normal gingiva
Enlargement can be generalized in the mouth, but is of normal individuals. This shows that at some point, the

more commonly seen in the maxillary and mandibular development of the lesion must have abnormal high
anterior regions. fibroblastic proliferation.
Enlargement is not seen in edentulous areas. It is always There are numerous oxytalan fibres seen beneath the

seen in areas, where teeth are present. epithelium and in the areas of inflammation.
Enlargement gets disappeared from the area where the Along the sulcular surfaces of the gingiva, inflammation

teeth are extracted. is common.
In very few cases, hyperplasia of edentulous sites have

been reported. 1. Anti-convulsants
Drug induced gingival enlargements, may be absent in
Anti-convulsants are the drugs used to treat epilepsy.

mouths with excessive plaque and calculus and it may be

present in mouth with little or no plaque.
Phenytoin (Dilantin) is the first drug inducing gingival

Maintaining the oral hygiene using toothpaste, enlargement.
Phenytoin is a hydantoin introduced by Merritt and

toothbrush, floss or mouthwash can reduce the

inflammation, but not the overgrowth. Putman is the year 1938.
It can recur, even after it is surgically excised.
Clinical Features

Enlargement is chronic and increases slowly in size.

If the causative drug is discontinued, there is a Fifty percent of the patients receiving the drug, suffer

spontaneous disappearance within a few months. from gingival enlargement.
Enlargement begins as a hyperplasia of the connective It is more commonly seen in young patients.

tissue core of the marginal gingiva. After a threshold level has been exceeded, the occurrence

It increases by its expansion and proliferation beyond and severity of the enlargement are then not related to

the crest of the gingival margin. the dosage.
There is presence of an inflammatory infiltrate at the
Pathogenesis

bottom of sulcus or the pocket.
Proliferation of fibroblast like cells and epithelium are
Histopathology

proliferated by phenytoin.
There is a pronounced hyperplasia of the connective There are two analogues of phenytoin the have similar

tissue and the epithelium within the enlargement. effect on fibroblast like cells and two analogues are:
Rete pegs become elongated and go deep inside the 1. 1-allyl-5-phenylhydantoinate.

connective tissue. 2. 5-methyl-5-phenylhydantoinate.
There are densely arranged collagen bundles within the There is an increased synthesis of glycosaminoglycan

connective tissue, with an increase in the number of by fibroblast from a phenytoin induced gingival
fibroblasts and new blood vessels. overgrowth.
91
Chapter 20 Gingival Enlargement

There is also a reduction in collagen degradation because
They act by blocking the intracellular mobilization of
of phenytoin. It is due to production of an inactive calcium, by inhibiting the calcium ion influx across the

fibroblastic collagenase. cell membrane of heart and smooth muscle.

Gingival enlargement may result from the genetically
Because of this the coronary arteries and arterioles are
determined ability or inability of the host to deal dilated, due to which the oxygen supply to the heart
effectively with prolonged administration of this drug. muscle gets improved.

It has been seen that fibroblasts in a non inflamed
It also dilates the peripheral vasculature due to which the
gingiva, are less active and do not respond to phenytoin. hypertension is reduced.

But fibroblasts in an inflamed tissue are active and
Examples of some of these drugs are amlodipine,
respond to phenytoin. feladipine, nifedipine, verapamil, cardizem.

Therefore it can be concluded, that the pathogenesis
Nifedipine is the most common drug which induces
of phenytoin-induced gingival enlargement is not very gingival enlargement.
specific and clear but three factors, i.e.,
Isradipidine is a dihydropyridine derivative which can
1. Specific genetically predetermined subpopulations of act as a substitute for nifedipine and would not cause
fibroblast. gingival enlargement.
2. Inactivation of collagenase and
Nifedipine along with cyclosporine is given in kidney
3. Plaque induced gingival inflammation are thought transplant recipients.
to be important in causing and accelerating the This combination of drugs causes more gingival
phenytoin-induced gingival enlargement.

enlargement.
2. Immunosuppressants Question 2

Immunosuppressants are the drugs which are given What are conditioned gingival enlargements?
to several autoimmune diseases and to prevent organ
transplant rejections. Answer

Most commonly used drugs are immunosuppressants. Conditioned gingival enlargements are the enlargements

These drugs inhibit the function of helps T cells, which that occurs when there is exaggerated systemic condition
play an important role in cellular and humoral immune of the patient or when it distorts the usual gingival response
responses. to dental plaque.

Dosage of greater than 500 mg/day have been reported Initiation of this type of enlargement requires dental

to induced gingival overgrowth. plaque, but dental plaque is not the sole determinant of

Vascularisation is more in cyclosporine induced gingival the nature of the clinical features.
enlargement as compared to phenytoin enlargement. There can be three kinds of conditioned gingival

Microscopic examination reveals that the enlargement enlargements:
is a hypersensitivity response to cyclosporine as there is 1. Hormonal that include pregnancy and puberty.
presence of abundant amorphous extracellular substance. 2. Nutritional that include vitamin C deficiency.

It is more commonly seen in children. 3. Allergic.
Patients who are medicated both with cyclosporine and

Non-specific conditioned enlargement can also be seen.

calcium-channel blockers, are more like to have greater

gingival enlargement.

Cyclosporine has other side effects also, other than
1. Enlargements in Pregnancy
gingival enlargement, they are nephrotoxicity,
These enlargements can be marginal or generalised or
hypertension and hypertrichosis. can occur as single or multiple tumor like masses.

Tacrolimus, is another immunosuppressive drug that can
There is an increase in the level of progesterone and
be used as an substitute for cyclosporine and has very estrogen at the time of pregnancy, which reaches up to
less side effects as compared to cyclosporine. 10 and 30 times the levels during menstrual cycle during
the end of third trimester respectively.
3. Calcium-Channel Blockers
There is a change in the vascular permeability due to the

These drugs are given to treat cardiovascular problems change in the hormonal levels, because of which there is
such as angina pectoris, hypertension, coronary artery gingival edema and an increased inflammatory response
spasms, and cardiac arrhythmias. to the dental plaque.
92
There is also a shift in the subgingival microbiota. There is 2. Enlargement in Puberty

an increase in prevotella intermedia. It is seen both in male and female adolescents at the time

Marginal enlargement: This enlargement does not occur of puberty.
without the presence of dental plaque. It is generally seen in plaque retentive areas.

This enlargement results from aggravation of the It is seen on the marginal and interdental gingiva mainly,

previous inflammation. which peculiar bulbous interdental papilla.
It is more prominent on the interproximal surfaces, than The size of the enlargement far exceeds the enlargement

on the facial or lingual surface. caused by local factors.
The enlargement is generally generalised. Because of the mechanical action of the tongue and

It appears as bright red in color, friable, soft and has a the excursion of food, the enlargement is less on lingual

shiny, smooth surface. side as compared to labial or buccal, since this action
Bleeding or slight provocation is seen. prevents a heavy accumulation of local irritants on the

lingual surface.
Tumour-Like Gingival Enlargement The clinical features of puberty enlargement are almost

It is usually seen after the 3rd month of pregnancy, similar to that of chronic inflammatory gingival disease.

though earlier incidences have also been reported. There is a spontaneous reduction in the enlargement

This is an inflammatory response to the plaque and is after puberty, but does not disappear completely until

modified by the patients condition. the local causative factors are removed.
Enlargement is mushroom like, discrete, flattened

Microscopically, there is presence of chronic inflammation

spherical mass that protrudes from the gingival margin. with prominent oedema and associated degenerative
It can be attached to sessile or a pedunculated base. changes.

It is magenta or dusky red in colour.
3. Enlargement Due to Vitamin C Deficiency

It has a tendency to expand laterally, its flattened

appearance is perpetuated by pressure from the tongue Gingival enlargement due to vitamin C deficiency in

and cheeks. referred to as scurvy.
It has a smooth, shiny surface and often exhibits Vitamin C deficiency itself does not cause inflammation,

numerous deep red, pinpoint markings. it also requires bacterial plaque.
It does not invade the bone, as it is a superficial lesion. Acute vitamin C deficiency causes haemorrhage,

The consistency is semi-firm and may have various collagen destruction and oedema of the connective

degrees of softness and friability. tissue, all of which modify the response of gingiva to
It is painless. dental plaque to an extent that the normal defensive
reaction of gingiva is limited.

If its size and shape foster accumulation of debris under
Because of this inflammation also exaggerates.

its margins or interferes which occlusion, in which,

painful ulceration may occur.
Massive gingival enlargement is produced as a combined

If proper plaque control is performed, many gingival effect of acute vitamin C deficiency and the inflammation.

diseases during pregnancy can be avoided. Clinical Features
Histopathology Marginal gingiva is most commonly involved

Gingiva is bluish red in color.
Angiogranuloma is the term given to gingival

It is soft, friable and has a shiny, smooth surface.

enlargement during pregnancy.

There is haemorrhage on spontaneous or on slight
There is presence of central mass of connective tissue,

provocation.

with numerous diffusely arranged, newly formed, Surface necrosis is seen, with pseudomembrane
and engorged capillaries which are lined by cuboidal

formation.
endothelial cells.
There is a moderately fibrous stroma, with varying Histopathology

degrees of oedema, and chronic inflammatory infiltrates. Gingiva consists of chronic inflammatory cellular

There is thickening of stratified squamous epithelium. infiltration with a superficial acute response.

Rete pegs become prominent. Scattered areas of haemorrhage is seen, with engorged

There is some amount of intra-cellular and extra-cellular capillaries.

oedema, prominent intercellular bridges, and leucocyte There is collagen degeneration, marked diffuse oedema

infiltration. of scarcity of collagen fibrils or fibroblasts.
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Chapter 20 Gingival Enlargement
4. Plasma Cell Gingivitis 5. Non-specific Conditioned Enlargement

It can also be referred as Atypical Gingivitis or Plasma Cell (Pyogenic Granuloma)

Gingivostomatitis.
It is a tumour-like enlargement.

Enlargements starts from the marginal gingiva and
It is an exaggerated conditioned response to minor trauma.
extends up to the attached gingiva.

Plasma cell Granuloma– It is a small lesion which is Clinical Features
localised can also be present.
The lesion varies from a discrete spherical, tumor like
mass with a pedunculated attachment to a flattened,
Clinical Features
keloid like enlargement having a broad base.

Gingiva is red, friable, and sometimes granular and can
It colour ranges from red to purple, can be either friable
bleed easily. or firm.

There is generally no loss of attachment.
In most of the cases, if presents with surface ulceration

This is located in the oral aspect of the attached gingiva and purulent exudation.
and thus differs from plaque induced gingivitis.
The lesion can convert into a fibro-epithelial papilloma

Cheilitis and glossitis can be seen. or may remain unchanged.

Aetiology of plasma cell gingivitis is usually allergic
Removal of the lesion and elimination of local irritating
specially to substances like churning gum, dentifrices factors is the treatment option for pyogenic granuloma.
and various other diet components.
Fifteen percent is the recurrence rate.
Histopathology

Clinical and microscopic features of pyogenic granuloma
is similar to that of enlargement seen during pregnancy.

There is spongiosis and infiltration with inflammatory
cells in the oral epithelium. Histopathology

Spinous layers and basal layers are damaged.
It appears as a mass of granulation tissue, with chronic

There is a dense infiltrate of plasma cells in the connective inflammatory cellular infiltration.
tissue which can extend into the epithelium.
Prominent features of pyogenic granuloma are

It there is cessation of the allergen, the condition would endothelial proliferation and the formation of numerous
be normal. vascular spaces.

In a very few cases, rapidly progressive periodontitis can
Atrophic surface epithelium can be seen in some areas
be seen due to presence of marked inflammatory gingival and hyperplastic in others.
enlargements with a predominance of plasma cells.
Surface ulceration and exudation are common features.
SHORT ESSAYS
Question 1
The adjacent teeth are generally sensitive to percussion.
What is gingival abscess?
Aetiology
Answer
It is caused because of bacteria carried deep into tissues
when any foreign substance such as toothbrush bristle,
It is a localised, painful and rapidly expanding lesion that is
piece of apple, or a lobster shell, fragment, etc are
generally of sudden onset.
forcefully embedded into the gingiva.
It is usually limited to marginal gingiva and the interdental

The lesion is confined to gingiva and does not extend to
papilla. the periodontal ligament.
Appears as a red swelling with a smooth, shiny surface.

The lesion becomes fluctuant and pointed with a surface

Histopathology
orifice from which a purulent exudate is expressed,
Gingival absence consists of purulent focus in connective
within 24-48 hours. tissue.
If the lesion continues to expand, it can rupture

It is surrounded by a diffuse infiltration of PMNs
spontaneously. oedematous tissue and vascular engorgement.
94
There is varying degrees of intracellular and extracellular The enlargement are physiologic and does not causes

oedema and invasion by leucocytes over the surface any problem.

epithelium. When such enlargements have inflammation then it

Surface epithelium sometimes shows ulceration. looks like an extensive gingival enlargement.

Treatment of inflammation is the treatment of choice in
Question 2

such cases.
What are false enlargements?
Question 3
Answer What is a gingival cyst?
These enlargements are not the true enlargements of the
Answer

gingival tissue.
They appear because of increase in the size of underlying It is benign tumour of gingiva.

bony of dental tissue. When they reach a clinically significant size, they appear

There are no abnormal clinical features seen over the as localised enlargements, which involve the marginal

gingiva, except the massive increase in size of the area. and the attached gingiva.
They are most commonly seen in the lingual areas of
Underlying Osseous Lesions

mandibular canine and premolar area.
Tori and exostosis are the most common bony They are generally painless, but if they expand, they

enlargements, subjacent to the gingival area. might cause erosion of the surface of alveolar bone.
It can also be seen in Paget’s disease, fibrous dysplasia, Gingival cyst can be differentiated from a lateral

central giant cell granuloma, cherubism, ameloblastoma, periodontal cyst as it arises within the alveolar bone,
osteoma and osteosarcoma. adjacent to the root and is developmental in origin.
The gingival tissues appear normal. Gingival cyst develops from odontogenic epithelium

They might have unrelated inflammatory changes. or from surface or sulcular epithelium traumatically

implanted in the area.
Underlying Dental Tissue Its treatment include its removal which is followed by

uneventful recovery.
At the time of eruption, especially the primary dentition,

the labial gingiva may show a bulbous marginal
distortion caused by superimposition of the bulk of the
Histopathology
gingiva on the normal prominence of the enamel in the Gingival cyst cavity is lined by a thin flattened epithelium

gingival half of the crown. with or without localised areas of thickening.
This kind of enlargement has been termed as Epithelium like unkeratinised stratified squamous

development enlargement. epithelium, keratinised stratified squamous epithelium
If often persists until the junctional epithelium has migrated and parakeratinized epithelium with palisading basal

from the enamel to the cemento-enamel junction. cells can be found.
21 Acute Gingival

Chapter
Infections
LONG ESSAYS
Question 1 Pre-existing gingivitis, deep periodontal pockets, and

pericoronal flaps which favour the proliferation of
Discuss in detail about the aetiology, clinical features,
anaerobic fusiform bacilli and spirochaetes.
differential diagnosis and treatment options for acute
necrotising ulcerative gingivitis. Systemic Factors
Answer Immunodeficient patients

Nutritional deficiencies like vitamin C and B2 deficiencies

It is also referred to as Vincent’s infection. Chronic sleep deficiency leading to fatigue

Acute necrotising ulcerative gingivitis (ANUG) is rapid in Habits like alcohol or drug above

onset, painful microbial disease of the gingiva. Systemic diseases like diabetes

Its main causative microorganism is fusobacterium Other debilitating diseases like syphilis, cancer, severe

species, along with spirochaetes. gastrointestinal tract disorders, anaemia, leukaemia and
ANUG has been renamed as necrotising ulcerative acquired immune deficiency syndrome.

gingivitis (NUG)
It is also referred to as trench mouth, because of its Psychosomatic Factor

prevalence in the soldiers working in trenches during This disease is related to stressful situations like patients
World War I. with depression or any emotional disturbances, patients
The disease is known as Vincents angina because this feeling inadequate at handling life situations.

disease was first described by Vincent.
Clinical Features
Aetiology It presents as an acute disease and symptoms are sudden

It is mainly caused by fusobacterium and spirochaetes, in onset.

therefore it is a fusospirochaetal infection. In some cases, it can resolve on its own, and shows milder

The complex of microorganisms consists of following symptoms which lead to subacute stage.

bacteria– Treponema microdentium, intermediate Some common predisposing factor could be debilitating

spirochaetes, vibrios, fusiform bacilli and filamentous disease or acute respiratory tract infection, psychological
organism- Borrelia species. stress, nutritional deficiencies use of tobacco, smoking
and continuous work without rest.
Predisposing Factors
It can be divided into three factors: Characteristics Clinical Signs are as follows
1. Local factors. This infection shows punched out, crater like depressions

2. Systemic factors. at the crest of the interdental papillae and it might
3. Psychosomatic factor. involve the marginal gingiva. Attached gingiva and oral
mucosa are rarely involved
Local Factors A slough which is grey in colour and pseudomembranous

Smoking and use of tobacco in nature, cover the gingival craters.

96
It can be demarcated from the healthy gingiva by a Zone 3 (Necrotic Zone)

pronounced linear erythema. It consists of disintegrated tissue cells, fibrillar material,

In some cases lesions may be denuded of the remnants of collagen fibres, and many intermediate and

pseudomembrane, exposing red, shiny and large types of spirochaetes with few other bacteria.
haemorrhagic gingival surface.
Zone 4 (Zone of Spirochaetes Infiltration)
Lesion bleeds even on slightest provocation.

Fetid odour. This zone contains well preserved tissues infiltrated

Increased salivation. with intermediate and large spirochaetes without other

Pasty saliva. organisms.

Metallic foul taset.
Diagnosis

Generally patient complains off a constant radiating,

gnawing pain that is aggravated upon taking hot and Diagnosis can be made by clinical picture of the patient

spicy food and upon chewing. which include gingival pain, bleeding and ulceration.
Extraoral and systemic sign and symptoms are local Biopsy specimen, or a microscopic examination of a

lymphadenopathy and mild fever. bacterial smear, would not give a clear diagnosis.
In very severe cases following signs can be seen: High Necrotising ulcerative gingivitis can be differentiated

fever, increased pulse rates, leukocytosis, loss of appetite, from other infections such as tuberculosis through a
and general lassitude. biopsy specimen.
These signs and symptoms are more severe in children.
Treatment for Necrotising Ulcerative Gingivitis

Clinical Courses Treatment objectives of NUG are as follows:
Resolution of acute phase.
If NUG is untreatued, it may progress to necrotising

Treatment of chronic disease either underlying the acute
ulcerative periodontitis.

involvement or elsewhere in the oral cavity.
The staging of NUG given by Horning and Cohen is as Alleviation of generalized symptoms such as fever and

follows: malaria.
Stage 1: Necrosis of the tip of the interdental papilla (NUG). Correction of systemic aetiological factors such as

Stage 2: Necrosis of the inertia papilla (either NUG or NUP). smoking and stress.

Stage 3: Necrosis of the marginal gingiva (NUP). Necrotising ulcerative gingivitis can be treated in thee

Stage 4: Necrosis extending to the marginal gingiva (NUP). clinical visits:

Stage 5: Necrosis involving the buccal and labial mucosa First Visit

(necrotising stomatitis). Primary goal of this visit is the treatment of acute lesion.
Stage 6: Necrosis exposing alveolar bone (necrotising

Complete medical history and history of present illness

stomatitis).

should be recorded.
Stage 7: Necrosis perforating skin of check (NOMA). Dietary history and smoking history should be taken.

Human immunodeficiency virus risk factor and
Various Zones of the Lesion

psychological factors should be evaluated.
Various zones in the lesion, described by Listgarten, may Vitals signs should be recorded, along with palpation of

overlap one another, and all zones may not be present at lymph nodes, mainly submaxillary and segmental lymph
the same time. nodes.
Any skin lesion present, should be evaluated.
Zone 1 (Bacterial Zone)

After all these basic evaluations and recordings, the

This is the most superficial zone. pseudomembrane and surface debris should be gently

It consists of various bacterias and few spirochaetes removed with a moist cotton and a topical anaesthetic

which can be of small, medium and large types. should be applied over the affected area.
Supra-gingival scaling, using an ultrasonic instrument
Zone 2 (Neutrophil Rich Zone)

should be done.
This zone contains numerous leukocytes, mainly Sub-gingival scaling and curettage are contraindicated

leukocyte with bacteria, including spirochaetes of at this stage, since it can lead to extension of the infection
various types interspersed in between the leukocytes. and bacteremia.
97
Chapter 21 Acute Gingival Infections

Any kind of periodontal surgery or extractions are
All the local irritants like faulty restorations etc should be
postponed, until the patient becomes symptom free. removed.

And it usually takes about 4 weeks for a patient to
Chronic gingivitis, periodontal pockets should be treated
become symptom free. well.

Patient should be prescribed the following antibiotics:
After a period of 1 month, the patient is re-evaluated for
Amoxicillin 500 mg orally every 6 hours for 10 days.

oral hygiene maintenance, habits, psychosocial factors
If patient is allergic to penicillin, then in that case,

and determination of the need for reconstructive or
erythromycin 500 mg every 6 hours, or metronidazole aesthetic surgery.
500 mg twice daily for 7 days.
Other than this treatment, some additional treatment
Analgesics such as non-steroidal anti-inflammatory drugs should also be given to the patient such as:
Contouring of gingival margin (gingivoplasty).
(NSAIDs) can be prescribed to the patient, so as to get relief

Nutritional supplements.
from pain.

Instructions to be given to the patient on first visit are as Contouring of gingival margin (gingivoplasty)
follows: The normal gingival architecture is spoiled in cases of NUG
Patient should avoid habits such as tobacco, smoking,
because there is severe loss of interdental gingiva and bone.
alcohol and condiments. This can be restored by a procedure known as gingivoplasty
Patients are advised to rinse with 3% hydrogen peroxide

or gingivectomy in which the normal gingival architecture

mixed with equal amount of warm water every 2 hours, is obtained.
or twice daily with 0.2% chlorhexidine mouth wash.
Overzealous tooth brushing and interdental cleaning

Nutritional supplements
device should be avoided.
Patient is unable to take food because of pain, therefore
For tooth brushing, an ultra-soft toothbrush should be

nutritional supplements should be indicated with the
used. local treatment.
Adequate rest should be taken by the patient.

A standard multivitamin preparation should be given to the
patient, along with therapeutic dose of vitamins B and C.
Second Visit

One to two days after the first visit, the second visit
Question 2
should be scheduled. Describe in detail about the aetiology, clinical features,

All the systemic signs and symptoms should be checked histopathology and differential diagnosis of acute herpetic
if they have resolved or not. gingivostomatitis.
The lesion would be still erythematous but with marked
Answer

reduction of necrotic tissue.

Scaling can be performed during their visit.
Acute herpetic gingivostomatitis mostly affects infants

All the instructions given during the first visit, should be and children younger than 6 years of age
followed by the patient.
The causative organisms is herpes simplex virus type-1
(HSV-1)
Third Visit

The patient is recalled after a prised of 5 days, after the Clinical Features
second visit, to check for resolution of the symptoms.
This infection is mostly seen in children and young adult.

Complete protocol for the periodontal management is
Males and females are equally affected.
planned, during this visit.
There are vesicular lesions which are painful and develop

Patient advised to discontinue the hydrogen peroxide on all mucosal surfaces and rupture to produce foul
rinse and continue with chlorhexidine mouth wash for smelling ulcers.
2 or 3 weeks.
Patient is usually febrile, drools and has significant

Scaling and root planning can be repeated if required. malaise and will have tender cervical lymphadenopathy.

Patient should be reinforced to follow proper plaque
Acute illness and lesions lasts about 10 days and resolve
control measurements. with scar formation.

The patients is counselled on nutrition, smoking
Herpes simplex virus type-1 has access to the patient
cessation and other associated habits, to prevent further through direct or airborne water droplet transmission
possible recurrence. from an infected individual.
98
The mucous membrane lesions represent direct viral Constitutional signs and symptoms are as follows:

infection at the site of inoculation. High grade fever.

After primary infection, the virus ascends through Generalized malaise.

sensory and autonomic nerves and persists as latent HSV Cervical adenitis.

in the neuronal ganglia that innervates the sites.
Herpes simplex virus type-1 mostly resides in the Diagnosis

trigeminal ganglion. Diagnosis is made mainly by taking a detailed history

Various stimuli such as sunlight, trauma, fever and stress and performing a proper clinical examination

can result in secondary manifestation. Virus culture and immunologic tests should be performed

using monoclonal antibodies or deoxyribonucleic acid
Oral Signs
hybridization techniques to confirm the diagnosis.
Gingiva and oral mucosa, both are involved.

In the initial stage, the characteristic feature is the Differential Diagnosis

presence of discrete, spherical grey vesicles on the Necrotising ulcerative gingivitis
gingiva, labial and buccal mucosa, soft palate, pharynx,

Recurrent aphthous stomatitis

lingual mucosa and the tongue. Erythema multiforme

The vesicles rupture after 24 hours and form painful, Stevens Johnson syndrome

small ulcers with a red, elevated, halo like margin and a Bullous lichen planus.

depressed, yellowish or greyish white central portion.
The ulcers may occur in dust as or can be widely Treatment

separated. Earlier the treatment only consisted of supportive care
In a few cases, the lesion may be diffuse, erythematous,

but recently an antiviral therapy with 15 mg/ kg of an

shiny discoloration and oedematous enlargement of the acyclovir suspension is given 5 times daily for 7 days. But
gingiva with a tendency to bleed. this therapy is effective only if the patient reports or is
The lesion wound resolve by 7–10 days, or its own. being diagnosed within 3 days of onset.

It heals without scarring. Patients reporting after 3 days of onset should be given

a palliative care which includes removal of plaque and
Symptoms
food debris, administrations of NSAIDs and nutritional
Soreness of the mouth associated with difficulty in supplements.

drinking and chewing food. Periodontal therapy should be postponed until the acute

Lesions are painful and sensitive to touch. symptoms subsides.

SHORT ESSAYS
Clinical Features
Question 1
What is pericoronitis? What are its types and clinical features? The pericoronal flap or the operculum is markedly

Explain in detail about the management of pericoronitis. swollen and red along with presence of exudate.
Answer Patient complains of pain radiating to the ear, throat and

floor of the mouth.
Pericoronitis is an acute infection in which there is
Because of inability to open the jaws, the patient is

inflammation of gingiva and surrounding soft tissues of

an incompletely erupted tooth. extremely uncomfortable.
It is most common in lower third molars. Patient would complain of foul taste.

Types of Pericoronitis Swelling of the cheek may also be seen in the region of

the angle of the jaw.
Acute.
There may be presence of lymphadenitis.

Subacute.

Chronic. Fever, malaise and leukocytosis are also present.

99
Chapter 21 Acute Gingival Infections
Complications of pericoronitis are as follows: Clinical Diffuse erythema and A necrotising condition

Pericoronal abscess. features vesicular lesion which with punched out gingival

Peritonsillar abscess, cellulitis and ludwig’s angina, are
rupture leaving slightly margins covered by a
depressed area of ulcer. pseudomembrane.

the potential sequelae of acute pericoronitis. Diffuse involvement of the Only marginal gingiva
gingiva. involved.
Treatment Age Children and adolescents. In children it is rare.
Treatment of pericoronitis is dependent on three factors. Course Course of 7–10 days. No definite duration.
They are as follows: Contagion Contagious. Non contagious.
1. Severity of inflammation
2. Systemic involvement Question 3
3. Possibility of retaining the tooth
Treatment can take more than one visit:

What is gingival abscess?
Answer
First Visit

Debris, irritants and exudate should be removed with Gingival abscess is a localised, acute inflammatory lesion
gentle irrigation of area with warm saline. that can arise due to various number of sources such as

Occlusion has to be evaluated. One should check for the microbial, trauma, foreign body impactions.
occlusion of the opposing tooth with the pericoronal
flap.
Aetiology

Occlusal adjustment should be done in case of opposing It can be caused due to impingement by any foreign body
tooth traumatizing the flap. like dental floss, food particle or impression material in

In cases with lymph node involvement, antibiotics are previously healthy sites.
prescribed.

A 15 no. blade can be used for drainage for a fluctuant Clinical Findings
swelling, if present. Gingival is red, swollen and painful.
Patient should be prescribed hourly warm saline rinses.

Impacted foreign object may still be embedded into the

Second Visit gingiva.

After the resolution of acute symptoms the pericoronal
Treatment

flap should be surgically excised using the periodontal

knives.
Scaling and root planing are completed to establish

The surgical produce which is done for removal of drainage and any foreign body present is removed.
operculum is referred to as operculectomy. Scaling can be done with or without local anaesthetic.

It can be performed using scalpel, knives, cautery or
The area is irrigated with warm water and covered with
lasers. moist gauze under light pressure.
An easily maintainable site should be created for the Once bleeding is arrested, the patient is dismissed with

patient which can be achieved by removing the flap. instructions to rinse with warm saline and gargle every 2
hours for the rest of the day.
Question 2
After 24 hours the area is re-evaluated.
What are differences between primary herpetic gingivo
stomatitis and necrotising ulcerative gingivitis? Question 4
Enumerate various acute lesions of gingiva.
Answer
Answer
Table 21.1: Differences between primary herpetic gingivo
stomatitis and necrotising ulcerative gingivitis. According to Manson, acute gingival lesions can be
Primary herpetic Necrotising classified as follows:
gingivo stomatitis ulcerative gingivitis Traumatic lesions of gingiva

Aetiology Caused by virus herpes Fusospirochaetal Physical injury

simplex virus type-1. complex. Chemical injury

100
Viral infections Tuberculosis

Acute herpetic gingivostomatitis Syphilis

Herpangina Fungal disease

Measles Candidiasis

Herpes varicella/zoster virus infections Gingival abscess

Glandular fever Aphthous ulcers

Bacterial infections Erythema multiform

Acute necrotising ulcerative gingivitis Drug allergy and contact hypersensitivity.

22 Gingival Diseases in

Chapter
Childhood
LONG ESSAYS
Question 1 Chronic Marginal Diseases

What are the changes seen in gingiva during tooth eruption? It is the most common type of gingival change seen in
childhood.
Answer
Changes in colour, size, texture and consistency resembling
During the transition phase of dentition, gingival changes chronic inflammation are seen.
are seen. It is important to differentiate between these In some cases fiery red discolouration may also be noticed.
physiological changes from gingival diseases.
These changes in children are commonly caused due to
Various changes seen during tooth eruption are: gingivitis and should not be associated with bleeding and
Pre-eruption bulge: A gingival bulge is seen at the site of increase in pocket depth.

crown eruption. The gingiva in this bulge is firm, slightly Aetiology
blanched and is in confirmation with the underlying
shape of crown. Plaque.

Formation of gingival margin: As the crown erupts into Materia alba.

the oral cavity penetrating through the oral mucosa,
Poor oral hygiene.

development of marginal gingiva and sulcus is seen.
Calculus is mainly seen in age group of 7–15 years.

During eruption, the marginal gingiva appears
Tooth eruption associated gingivitis due to accumulation

of plaque around erupting tooth.

oedematous, rounded and erythematous.
Normal prominence of gingival margin: During mixed Partially exfoliated deciduous teeth are a common site of

dentition stage, the gingiva around the newly erupted plaque accumulation and thus cause gingivitis.
teeth, specially in the anterior region appears quite Gingivitis occurs more commonly in children with increased
prominent. over bite and over jet, nasal obstruction and mouth-
breathing habits.
This prominence is due to the fact, that gingiva is still
attached to crown due to which it gets superimposed on High prevalence and intensity of gingivitis is seen in patients
the bulk of underlying enamel. who are in circumpubertal period and this type of gingivitis
is termed as pubertal gingivitis. Bleeding from interdental
Question 2 sites is commonly seen and this condition autoresolves
after puberty.
What are the types of gingival diseases seen in childhood?
Answer Localised Gingival Recession

Gingival recession in childhood is generally seen in teeth,
Types of gingival diseases seen in childhood are:

which are labially placed in the arch.
Chronic marginal diseases. It is also seen in teeth that are excessively tipped, rotated

Localised gingival recession. due to which there roots project labially, thus making

Acute gingival infections. them prone to gingival recession.

102
Local irritants may also cause gingival recession. occurs as a sequela to upper respiratory tract

Gingival recession is also seen in teeth which are near infection.

highly attached fraenum. Candidiasis: Fungal infection caused by Candida

The gingival recession due to positioning of teeth may albicans.

autocorrect with growth of the arches or may have to be Necrotising ulcerative gingivitis (NUG): Incidence is

treated orthodontically. generally low in children.
Seen more commonly in malnourished children and
Acute Gingival Infections children with Down syndrome.
Primary herpetic gingivostomatitis: Most common Primary herpetic gingivostomatitis can be sometimes

acute gingival infection in childhood and generally erroneously diagnosed as NUG.
23 Desquamative

Chapter
Gingivitis
LONG ESSAYS
Question 1 h This form present as a patchy distribution of bright,
h
red and grey areas involving the marginal and
Define desquamative gingivitis. Discuss about its aetiology, attached gingiva.
clinical features, pathogenesis and management. h Gingival surface exhibits pitting on pressure and
h
Answer appears soft, smooth and shiny.
h Epithelium not firmly attached to the underlying
h
Desquamative gingivitis is a clinical term to describe connective tissue. It pulls off on massaging with
red, painful, glazed and friable gingiva, which may be a finger, which leads to exposure of the connective
manifestation of some mucocutaneous conditions such as tissue.
lichen planus or the vesiculobullous disorders. h Patients complain of burning sensation in the mouth.
h
It is characterised by intense redness and desquamation h Tooth brushing may lead to denudation of the
h

of the surface epithelium of the attached gingiva. gingival surface, which can cause pain. Because
Initially, it was referred to as “gingivosis” as it was of this, patient is not able to brush properly, which

considered to be degenerative condition. leads to deposition on the teeth, which in turn
In 1960, McCarethy et al. said that desquamative gingivitis causes the gingival inflammation.

is not a specific entity, instead it is a non-specific gingival Severe form:

h It is characterised by irregularly-shaped areas
manifestations of many systemic disturbances.
h
which are denuded from the gingiva.
Clinical Features h The area is bright-red in colour and scattered all
h
over the gingival surface.
It is an oral manifestation of dermatosis like lichen planus, h This form is very painful and it is constantly dry and

mucous membrane pemphigoid, bullous pemphigoid or
h
there is burning sensation.
pemphigus. h There is presence of Nikolskys sign in which the
h
Based upon clinical manifestation, it can be mild, epithelium can be easily peeled off.

moderate or severe. h Oral mucosa is smooth and shiny.
h
Mild form: h Patients having severe form, cannot tolerate coarse

h
h It is usually seen in females between the age of 17 food, condiments or changes in temperature.
h
years and 24 years.
h Characterised by diffuse erythema of the marginal, Histopathology
h
interdental and attached gingiva. The lesions may be of lichenoid or bullous types.

h It is generally painless.
The lichenoid type resembles lichen planus, whereas
h

h Patient would generally complain of discolouration
bullous type has the features of mucous membrane
h
of gingiva. pemphigoid.
Moderate form: There is separation of collagen fibres because of which

h Individuals between 30 years and 40 years are there is a separation of epithelium from underlying
h
mainly affected. connective tissue.
104
There is also a decrease in number of anchoring fibrils. Question 2

Epithelium is atrophic, keratinisation is reduced.
Explain in detail about mucous membrane pemphigoid.

There is infiltration of the connective tissue with

inflammatory cells. Answer
Diagnosis Mucous membrane pemphigoid is also referred to as
cicatricial pemphigoid, which is a group of putative
Diagnosis is very important to form a line of treatment. autoimmune, chronic inflammatory, subepithelial blistering

Oral cavity should be inspected carefully for any lesions. disease predominantly affecting mucous membrane, with

In case of lichen planus, gingiva as well as other parts of or without clinically observable scarring.

the oral mucosa may be affected. It is most commonly seen in women in their 5th decade
Papular skin lesions are present on wrist and ankles.

of life.

A detailed history should be taken. Young children are rarely affected.

Conjunctivitis, burning sensation on urination, vaginal

It is characterised by an auto immune reaction involving

irritation, etc. are suggestive of mucous membrane

auto-antibodies, directed against basement membrane
pemphigoid.
zone, followed by complement activation and
Hormonal aetiology has also been suggested specially in
subsequent leucocyte recruitment.

cases of menopause or hysterectomy.
Proteolytic enzyme release and dissolve the basement
Biopsy helps in confirmation of diagnosis of lichen
membrane zone.

planus, mucosa membrane pemphigoid and rare
bacterial conditions, such as candidiasis. Cicatricial pemphigoid involves the oral cavity,

conjunctiva and mucosa of the nose, vagina, rectum,
Management oesophagus and urethra.
It is essential to reduce the gingival inflammation, which Clinical Features of Oral Lesions

can be achieved by improvement in oral hygiene.
Soft tooth brushes should be prescribed to patients, Oral lesions are characterised by erosive or desquamative

for routine plaque control. Care should be taken not to gingivitis.
injure the gingival tissues. Vesicles and ulceration may be seen on the gingiva.

Hydrogen peroxide (3%) diluted with two part of warm Attached gingiva is erythematous.

water can be used as mouth wash, twice daily. Bullae rupture in about 2–3 days forming irregular

Topical corticosteroid ointment can be used many times shaped ulcers.

in a day. Before application, gingiva should be gently Healing of the ulcers is generally delayed and takes up
dried with sterile sponge.

to 3 weeks.
Triamcinolone acetonide (0.1%), fluocinonide (0.05%), or

desonides (0.05%) may be used for topical application. Histopathology
Systemic corticosteroids can also be given. It should

Lesion shows sub-epithelial vesiculation.
be given only after complete evaluation of the general

health of the patient and the physicians consent. Epithelium is separated from the connective tissue.

Mucous membrane pemphigoid responds favourably Basement membrane shows a split, under electron

to systemic steroid therapy. Prednisone 30–40 mg daily microscope.
or on alternate days to begin and gradually should
be reduced to 5–10 mg daily or on alternate days as Treatment
maintenance dose may be used.
It is generally treated with systemic corticosteroids.
Nutritional supplements should also be given.

The patient should have patience, since the lesion
Oral hygiene should be maintained.

takes long time to heal. And also patient should not Use of hydrogen peroxide mouthwash should be

discontinue the treatment before the lesion heals and to recommended.
patiently wait for the results. Soft brush should be used.

105
Chapter 23 Desquamative Gingivitis
SHORT ESSAYS

Question 1
Mucous membrane pemphigoid.
What is the classification of desquamative gingivitis lesions?
Bullous pemphigoid.
Pemphigus vulgaris.
Answer

Chronic ulcerative stomatitis.

Classification of disease that clinically present at

desquamative gingivitis is as follows:

Linear IgA disease.
Lupus erythematosus.
Dermatological:

Lichen planus.

24

Chapter Periodontal Pocket
LONG ESSAYS
Question 1 Suprabony pocket: Also referred to as supracrestal/

h
h
supra-alveolar pocket. It is present above the crest
Define periodontal pocket. What are its classifications and
of alveolar bone, i.e. the bottom of the pocket is
clinical features? Discuss the pathogenesis in detail.
coronal to the underlying alveolar bone.
Answer h Infrabony pocket: Also referred to as intrabony/
h
subcrestal pocket (Fig. 24.1). It is present below the
According to Carranza, periodontal pocket is defined as
crest of alveolar bone, i.e. the bottom of the pocket
a pathologically deepened gingival sulcus. It is a very
is apical to the level of adjacent alveolar bone. The
important feature of periodontal disease.
lateral pocket wall lies between .the tooth surface
Classification and the alveolar bone (Fig. 24.2).
Based on the number of surfaces involved:

It can be classified as: Simple pocket: In this pocket involves one tooth

Based on morphology and their relationship to adjacent
surface.

structures: Compound pocket: In this pocket, two tooth surfaces

Gingival pocket: It is also referred as false or
are involved.

relative pocket. It is formed by gingival enlargement Complex pocket: It is spiral pocket which originates

without destruction of the supporting tissues of the on one tooth surface and on some other tooth surface
periodontium. of the same tooth. These types of pockets are most
Periodontal pocket: It is also referred to as true
commonly seen in furcation areas (Fig. 24.3).

pocket. It is formed by pathologic deepening of the
gingival sulcus due to apical proliferation of epithelial Clinical Features
attachment. It can be further classified as:
Clinical features are as follows:
Bluish-red, thickened marginal gingiva.

Fig. 24.1: Diagram showing Gingival pocket and Periodontal Fig. 24.2: Diagram showing Subrabony pocket and Intra bony
pocket. pocket.
107
Chapter 24 Periodontal Pocket

Immediately apical to this, is a zone of partial destruction
and then an area of normal attachment. There are two

mechanisms involved for collagen destruction:
1. Collagenases and other lysosomal enzymes from
polymorphonuclear leukocytes (PMNLs) and
macrophages become extracellular and destroy
collagen.
Fig. 24.3: 2. Fibroblasts phagocytize collagen fibres by extending
cytoplasmic process to the ligament interface and by

A bluish-red, vertical zone from the gingival margin to resorbing the inserted collagen fibrils and fibrils of the
the alveolar mucosa. cementum matrix.

Gingival bleeding and suppuration.
Because of the loss of collagen, the apical portion of

Tooth mobility. the junctional epithelium proliferates along the root.

Diastema. Extension of junctional epithelium along the root

Localised pain or deep pain in pockets. requires the presence of healthy epithelial cells.
Pathogenesis of periodontal pocket:
Marked degeneration or necrosis of the junctional
periodontal pockets occur because of the micro-
epithelium retards rather than accelerates pocket
formation because of lack of healthy epithelial cells.

organism and their by-products that produce pathologic

changes which lead to deepening of the gingival sulcus.

As the apical portion migrates, the coronal portion
Deepening of gingival sulcus may be because of either

of the junctional epithelium detaches from the root.
migration of the junctional epithelium apically and It occurs because of cohesiveness of the junctional
its separation from the tooth surface, or because of epithelium as a result of rapidly proliferating bacteria,
movement of the gingival margin in the direction of the bacterial enzymes and the relative volume of PMNs.
crown resulting in a pocket or it could be due to both the
Therefore, the gingival sulcus shifts in an apical direction
reasons. from the base and the sulcular epithelium is replaced by
Changes which are involved in the transition from the

pocket epithelium.
gingival sulcus to the pocket are due to increase in
Because of this transformation from the gingival sulcus to
number of spirochetes and motile rods. a periodontal pocket, the plaque accumulation increases
This transition involves several zones of inflammatory

and becomes even more difficult to clean, increasing the
changes, along with destruction of connective tissue severity of disease.
attachments in the connective tissue wall of the sulcus.
Therefore, with continued inflammation, crest of the
Apical to the junctional epithelium an area of destroyed
gingival margin extends coronally and junctional
collagen fibres develops and is occupied by inflammatory epithelium extends apically along the root, separating
cells and oedema. from it.
SHORT ESSAYS
Question 1
Connective tissue also shows proliferation of the
endothelial cells with newly formed capillaries, fibroblasts
Describe the histopathology of pocket formation.
and collagen fibres.
Answer
The junctional epithelium at the base of the pocket is
usually much shorter than that of a normal sulcus.

The connective tissue is oedematous and densely
The corono-apical length of the junctional epithelium is
infiltrated with plasma cells and lymphocytes and 50–100 mm.
scattered PMNLs.
The most severe degenerative changes in the periodontal

Blood vessels are increased in number, they become pocket occur along the lateral wall.
dilated and engorged, single or multiple necrotic foci are
Epithelial buds or interlacing cords of epithelial cells
occasionally present. project from the lateral wall into the adjacent inflamed
108
connective tissue and frequently extend further apically penetrate into the intercellular spaces which get
than the junctional epithelium. enlarged. The main bacteria which are seen are: Cocci,

Progressive degeneration and necrosis of the epithelium rods and filaments along with few spirochetes. These

leads to ulceration of the lateral wall, exposure of the under- bacteria are covered with a loose, intercellular, fibrillar
lying marked inflamed connective tissue and suppuration. substance.
The epithelium at the gingival crest of a periodontal

pocket is generally intact and thickened with prominent Areas of Emergence of Leukocytes
rete pegs.
Filaments, rods and coccoids organisms with pre- Holes are located in the intercellular spaces, through which

dominant gram-negative cell walls have been found in leukocytes appear.
the intercellular space initially under exfoliating epithelial
cells, but they are also found between deeper epithelial Areas of Leukocytes-bacterial Interaction
cells and accumulating on the basement lamina. Many leukocytes are present which are covered with
Few bacteria can traverse the basement lamina and bacteria, during the process of phagocytosis.

involve the sub-epithelial connective tissue.
Question 2 Areas of Intense Epithelial Desquamation

What are the contents of a pocket? They appear as semi-attached and folded epithelial squames
in which one end in generally attached to the pocket wall
Answer and the other is free towards the pocket space.
Periodontal pockets consists of debris, mainly containing
microorganisms and their products, for example, enzymes, Areas of Ulceration with Exposed Connective
endotoxins and other metabolic products, dental plaque, Tissue
gingival fluid, food remnants, salivary mucin, desquamated
epithelial cells and leukocytes. Haemorrhage is seen occasionally in this area. Bottom of
In the exudate, living, degenerated and necrotic PMNLs, ulcer shows exposed collagen fibres and various connective
living and dead bacteria, serum and some amount of fibrin tissue cells.
is seen.
Areas of Haemorrhage with Numerous
Question 3 Erythrocytes
Describe the microtopography of the gingival wall of the Several erythrocytes are seen in this area.
pocket.
Question 4
Answer
What are the differences between suprabony and infrabony
Soft tissue wall in the periodontal pockets in scanning pockets?
electron microscopy (SEM), shows following areas:
Areas of relative quiescence. Answer

Areas of bacterial accumulation.

Areas of emergence of leukocytes.
Supra-bony pockets Infra-bony pockets

Areas of leukocytes-bacterial interaction.
In this, the base of the pocket is In this, the base of the pocket is

Areas of intense epithelial desquamation.
coronal to the alveolar crest. apical to the alveolar crest.

Areas of ulceration with exposed connective tissue.

Areas of haemorrhage with numerous erythrocytes.
There is a horizontal pattern of There is a vertical or angular
bone loss. pattern of bone loss.

Interproximally, the trans-septal Interproximally, the trans-septal
Areas of Relative Quiescence fibres are restored horizontally fibres are restored, obliquely,
It is relatively flat surface with minor depression and wounds in the space between the base from cementum beneath the
of the pocket and alveolar bone. base of pocket over the crest of
and occasional shedding of cells.
the cementum of adjacent tooth.
On the facial and lingual surfaces, On the facial and lingual surfaces,
Areas of Bacterial Accumulation the peridontal ligament fibres the periodontal fibres beneath
On the epithelial surface, depressions are seen, along beneath the pocket follow their the pocket follow the angular
normal course pattern of adjacent bone.
with enough debris and bacterial clumps which
109
Chapter 24 Periodontal Pocket
Question 5 Clinical features Histological feature

What are the root surface wall changes during pocket 1. Gingival wall of pocket shows:

formation? • Various degrees of blu- • This discoloration is caused due to
ish red discolouration circulatory stagnation
Answer • Flaccidity • It is because of destruction of gingival
• Smooth and shiny sur- fibres and surrounding tissues

Significant changes are seen in root surface wall of a face • It is caused due to atrophy of epithe-
periodontal pocket. • Pitting on pressure lium and oedema

These changes can increase the periodontal infection, • It is because of oedema and degen-
cause pain and may complicate the periodontal therapy. eration

Many changes are seen in the root cementum which 2. Gingival wall may be • When fibrotic changes predominate
could be structural, chemical or cytotoxic. pink and firm over exudative changes, specially in
the outer wall of the pocket, the wall

New tissues are formed in the continuous effort of repair, becomes pink and firm. Also degenera-
but they are degenerative due to cellular exudates tion and often ulcerations is seen in the
released during the changes in the root surface wall. inner wall of the pocket

Features, such as colour, consistency and surface texture 3. Upon slightest • Easy bleeding is because of increase
of the pocket wall are determined by the balance probing, bleeding occurs in vascularity, degeneration and thin-
between the destructive and reparative changes. ning of epithelium and proximity of
engorged vessels to inner surface
Question 6 4. Inner part of pocket is • It is because of ulceration of inner
What are the clinical signs and symptoms of the pocket? generally painful aspect of pocket wall
5. Upon digital pressure, • Pus occurs because of suppurative
Answer puss may be expressed inflammation of inner wall
Clinical signs are:
Enlarged, bluish red marginal, gingiva with a blunt edge.
Question 8

Shiny, discoloured and puffy gingiva associated with

exposed root surface. Write short note on periodontal cyst.

Break in the continuity of the interdental gingiva.

Answer
Gingival bleeding, purulent exudate from the gingiva.

Extrusion, mobility and migration of teeth

A periodontal cyst is a localised destruction of the
Development of diastema.

periodontal tissues along a lateral root surface, most
commonly mandibular canine premolar area.
Symptoms are:
Localised pain or a sensation of pressure in the gingiva

Aetiology of periodontal cyst could be:
Proliferation of epithelial rests of malassez.
after eating which diminishes gradually
Foul taste

Lateral dentigerous cyst retained in this jaw after tooth

Radiating pain deep inside the bone

eruption.
Growing feeling in the gums

Primordial cyst of supernumerary tooth germ.

Sensitivity to hot and cold

Stimulation of epithelial rests of the periodontal ligament

Pain in the absence of caries

by infection from a periodontal abscess or the pulp
Urge to dig a pointed substance like a tooth pick into the

through an accessory root canal.
gums Its clinical features are as follows:
Patient would generally complain that food sticks to the
Asymptomatic

teeth upon eating. Localised, tender swelling.

Question 7 Radiographic features would be:

Periodontal cyst appears on the interproximal side, on
What are the correlation of clinical and histopathological
features of periodontal pocket? the side of the root.

It appears as a radiolucent area bordered by a radiopaque

Answer line.
Correlation of clinical and histopathological features of Radiographically it is very difficult to differentiate it from

periodontal pocket are as follows: a periodontal abscess.

110
Its microscopic features are as follows: Pus is formed, which is basically formed by the PMNLs

The cystic epithelium is non-keratinised, thickened, which liberate enzymes that digest the cells and other

loosely arranged and proliferating epithelium. tissue structures, forming the pus.
The purulent area is surrounded by an acute inflammatory
Question 9

reaction.
Write short note on periodontal abscess. The epithelium overlying it, exhibits extracellular and

intracellular oedema and invasion of leukocytes.
Answer
Periodontal abscess is a localised purulent inflammation in Question 10
the periodontal tissues. It is also referred to as lateral abscess Describe the surface morphology of tooth wall of
or a parietal abscess. periodontal pocket.
Aetiology Answer
The following zones can be seen on the surface of tooth wall:
Periodontal abscess may be formed in the following ways:
Extension of infection from a periodontal pocket deeply
Cementum covered by calculus.

Attached plaque: It covers the calculus and extends

into the supporting periodontal tissues and localisation

apically from it to a variable degree around 100–500 µm.
of the suppurative inflammatory process along the
Zone of unattached plaque: It surrounds attached
lateral aspect of the root.

When the inflammatory process extends laterally
plaque and extends apically to it.
Zone of attachment of junctional epithelium to the

from the inner surface of a periodontal pocket into

tooth: The extension of this zone, which in normal, sulci
the connective tissue of the pocket wall and when the
is more than 500 µm, is usually reduced in periodontal
drainage into the pocket space is impaired, it result in
zocket to less than 100 µm.
localisation of abscess.
Zone of semi destroyed connective tissue fibres: They
A periodontal abscess may form in the cul-de sac, the

may be apical to the junctional epithelium.

deep end of which is shut off from the surface.
Zones 3, 4, and 5 form the plaque free zone (Fig. 24.4)
Because of incomplete removal of calculus from the

periodontal pocket, may result in periodontal abscess.
Trauma to the tooth or with perforation of the lateral wall

of the root during endodontic therapy.
Classification of Periodontal Abscess

Periodontal abscess can be classified as:
Abscess in the supporting periodontal tissues along the

lateral aspect of the root. In this situation generally a
sinus is seen in the bone which extends laterally from the
abscess to the external surface.
Abscess in the soft tissue wall of a deep periodontal

pocket.
Microscopic Features
There is accumulation of viable and non-viable PMNLs Fig. 24.4: Diagram of the area at the bottom of a pocket;

within the periodontal pocket wall. C.T = connective tissue.
25 Bone Loss and Patterns

Chapter
of Bone Destruction
LONG ESSAYS
Question 1 Various factors for bone destruction are:

Local
Explain in detail about mechanism of bone destruction,

Systemic.
along with histopathology and diagrams.

Answer Local Factors
Inflammation has been the most common cause of bone
Bacterial: Various bacterial products and inflammatory

mediators act on osteoblasts or their progenitors,
destruction, which spreads from marginal gingiva into the
inhibiting their action and reducing their numbers.
supporting periodontal tissues. “Periodontitis is always
Host factors: Various host factors produced by
caused by gingivitis but not all gingivitis progresses to

inflammatory cells are responsible for bone resorption
periodontitis”.
and periodontal destruction. Various host mediator
The transformation of gingivitis to periodontitis is associated
factors which can produce their effect are prostaglandins
mainly with two changes, i.e.
and their precursors, interleukin-1a (IL-1a), IL-1B and
1. Bacterial composition change.
tumour necrosis factor alpha (TNF-a). Non-steroidal
2. Cellular composition chance. anti-inflammatory drugs (NSAIDs) can inhibit PGE2
Other than this, there are various factor associated with production thus reducing bone resorption.
bone destruction and they are: Trauma from occlusion can induce bone destruction in

Local factor
presence as well as absence of inflammation. Bone loss

Systemic factor
can be seen lateral to the root surface.

Bacterial factors

Host-mediated factor Systemic Factors

Trauma from occlusion (TFO) Local and systemic factors regulate the physiologic

Bacterial composition change: In cases of gingivitis, more equilibrium of bone.
of gram-positive microorganisms are observed, but in case When there is a generalised tendency towards bone

of severe inflammation and destruction, the number of resorption, bone loss initiated by local inflammatory
gram-negative microorganisms increase along with motile processes can be magnified.
organisms and spirochete, whereas the number of coccoid A strong relationship exists between periodontal bone

rods and straight rod decreases. loss and osteoporosis. Osteoporosis is a physiologic
condition of post-menopausal women, which leads to
Cellular composition change: In the initial stage of
bone loss and structural bone changes.
gingivitis, fibroblasts and lymphocytes are seen. But as the Periodontitis and osteoporosis share a number of risk
disease progresses, the cellular composition is changed and

factors such as ageing, smoking, diseases, medication
more of plasma cells and blast cells are seen. that interferes with healing.
A fibrin-fibrinolytic system has also been seen in advancing Periodontal bone loss may also occur in generalised

lesion which is been mentioned as “walling off” the skeletal disturbances such as hyperparathyroidism,
advancing lesion. leukaemia, Langerhans cell histiocytosis (LCH).
112
Histopathology of Bone Destruction

Gingival inflammation extends along the collagen fibre

bundles and follows the course of the blood vessels
through the loosely arranged tissues around them into
the alveolar bone (Fig. 25.1)
Along its course from gingiva to the bone, there is

destruction seen in the gingival and transseptal fibres.
However there is continuous tendency of transseptal

fibres to recreate themselves. Therefore, even in cases
of extreme periodontal bone loss, transseptal fibres are
present.
After reaching to the bone, the inflammation spreads

into the marrow spaces.
A B
The marrow is replaced with leukocytic and fluid exudate,

new blood vessels and proliferating fibroblasts. Fig. 25.1: Pathways of inflammation from gingiva into the
There is an increase in the number of multinuclear supporting periodontal tissues in periodontitis
[(A) Interproximally, from the gingiva into the bone (1), from

osteoclasts and mononuclear phagocytes and Howship
the bone into the periodontal ligament (PDL) (2), and from
lacunae lines the bone surfaces. the gingiva into the PDL (3); (B) Facially and lingually, from the
The amount of inflammatory infiltrate correlates with the gingiva along the outer periosteum (1), from the periosteum into
degree of bone loss but not with the number of osteoclasts. the bone (2), and from the gingiva into the PDL (3)]
SHORT ESSAYS
Question 1 autopsy specimen, that there is a range of about 1.5–2.5

What are the factors determining bone morphology in mm within which bacterial plaque can induce bone loss.
Beyond 2.5 mm there is no bone loss.
periodontal disease?

Large defects exceeding a distance of 2.5 mm from the

Answer tooth surface (as seen in aggressive types of periodontitis)
Various factors that determine bone morphology in may be caused by the presence of bacteria in the tissues.
periodontal disease are as follows: {Note to operator: Kindly insert “Discuss the rate of bone
The thickness, width, and crestal angulation of the loss” from page 6 of Bone loss 1 file.}

interdental septa. Question 3
The thickness of the facial and lingual alveolar plates.
Explain in detail how bone destruction is caused by trauma

The presence of fenestration and dehiscence.
from occlusion?

The alignment of the teeth.

Root and root trunk anatomy.
Answer

Root position within the alveolar process.
Bone destruction mechanism from trauma from occlusion

Proximity with another tooth surface.
(TFO) occurs in following ways:

Question 2 TFO can produce bone destruction in the presence as

What is radius of action? well as absence of inflammation.
In the absence of inflammation the changes caused by

Answer TFO varies from increased compression and tension of
Locally produced bone resorption factors may need to be the PDL and increased osteoclasts of alveolar bone to
present in the proximity of bone surface, to produce their necrosis of the PDL and bone and resorption of bone and
effect tooth structures.
It has been postulated by Page and Schroeder on the These changes are reversible and can be repaired if the

basis of Waerhaug’s measurements made on human offending forces are removed.
113
Chapter 25 Bone Loss and Patterns of Bone Destruction

Continuous TFO, can result in funnel-shaped widening Horizontal Bone Loss
of the crestal portion of the PDL, with resorption of the
It is the most common pattern of bone loss.

adjacent bone.

The height of the bone is reduced, but the bone margins

These changes which may cause the bony crest to have

remains nearly perpendicular to the surface of the tooth.

an angular shape represent adaptation of the PDL tissue

It can occur at different degree around the same tooth.
aimed at cushioning, increased occlusion forces, but the

modified bones shape may weaken tooth support and

cause tooth mobility.
Vertical Bone Loss

In presence of inflammation, TFO aggregates the bone The bone is lost in an oblique direction leaving a

destruction and can lead to bizarre bone patterns. hollowed-out trough in the bone along side the root.
The base of the defect is apical to the surrounding bone.
Question 4

These defects are generally accompanied with infrabony

What are periods of destruction? pocket.

These defects can be classified as one wall two walls or
Answer

three wall defects on the basis of the number of osseous

Periodontal destruction is not always occurring or is wall.
continuous, instead, it occurs in an episodic, intermittent 1. Three wall defect: This defect has three walls. It has
manner. This destructive period results in loss of collagen the best prognosis.
and alveolar bone with an increase in the depth of 2. Two wall defect: This defect has two osseous walls.
periodontal pocket. 3. One wall defect: This defect has one osseous wall
Aetiology for onset of destructive periods have been (Fig. 25.2)
summarised by following four theories: Sometimes, the numbers of osseous walls are greater

Bursts of destructive activity are associated with

in the apical portion of the defect than in its occlusal

subgingival ulceration and an acute inflammatory portion. This type of defect is termed as combined
reaction, resulting in rapid loss of alveolar bone. osseous defect.
Burst of destructive activity coincide with the conversion

Surgical exposure of the defect is the only sure way

of a predominantly T-lymphocyte lesion to one with a to determine the presence and configuration of vertical
predominantly B-lymphocyte plasma cell infiltrate. osseous defect.
Periods of exacerbation are associated with an increase

Three wall defects are also referred as intrabony defects,

of the loose, unattached, non-motile, gram-negative, whereas one wall defects are referred as hemiseptum
anaerobic pocket flora and periods of remission coincide originally.
with the formation of dense, unattached, non-motile,
gram-positive flora with a tendency to mineralize. Osseous Craters
Tissue invasion by one or several bacterial species is
They are the concavities seen in the crest of the

followed by an advanced local host defence that controls interdental bone, confined within facial and lingual walls.
the attack.
Craters form around 35.2% of all defects and occur twice
Question 5 as often in posterior segments as in anterior segments.
What are the various bone destruction patterns in Reasons for the high frequency of interdental craters are
periodontal disease? as follows:
1. The interdental area collects plaque and is difficult to
Answer clean.
Various bone destruction patterns in periodontal disease 2. The normal flat or even concave faciolingual shape of
are as follows: the interdental septum in lower molars may favour crater
1. Horizontal bone loss formation.
2. Vertical or angular defects 3. Vascular patterns from the gingiva to the centre of the
3. Osseous craters crest may provide a pathway for inflammation (Fig. 25.3).
4. Bulbous bone contours
5. Reversed architecture Bulbous Bone Contours
6. Ledges Bulbous bone contours are bony enlargement caused
7. Furcation involvements. because of exostosis, adaptation to function, or buttressing
114

A
Fig. 25.3: Diagrammatic representation of an osseous crater in

a faciolingual section between two lower molars—left, normal
bone contour and right, osseous crater
C
Figs 25.2A to C: (A) Three wall defect, three bony walls B
present—distal, lingual and facial; (B) Two wall defect, two bony Figs 25.4A and B: (A) Normal architecture, where interdental
wall present—buccal and lingual; (C) One wall defect, one bony bone is higher than radicular bone; (B) Reverse architecture
wall present—distal wall only. where interdental bone is lower than radicular bone
bone formation. They are seen more commonly in the Furcation Involvements
maxilla than in the mandible. It refers to invasion of the bifurcation and trifurcation of

multirooted teeth by periodontal disease.
Reversed Architecture The furcation can either be visible or may be covered

It is found due to loss of interdental bone, both in facial and with a pocket wall.
lingual plates, without the simultaneous loss of radicular There are four grades of furcation:

bone. Because of this, the normal architecture (i.e. radicular Grade I: In this, there is incipient bone loss.

bone at a lower height, than the interproximal bone) is Grade II: Partial bone loss (cul-de-sac).

reversed. It is seen more commonly in maxilla (Fig. 25.4). Grade III: Total bone loss, with through-and-through

opening of furcation but covered with the pocket wall.
Ledges Grade IV: Complete bone loss (similar to Grade III),

They are plateau-like bone margins caused by resorption of but accompanied with gingival recession, exposing
thickened bony plates. the furcation.
115
Chapter 25 Bone Loss and Patterns of Bone Destruction
Furcation involvement represents progressive perio-

This types of bone formation is referred to as buttressing
dontal destruction and has the same cause as periodontitis. bone formation.

Sometimes, plaque removal becomes difficult from the
It can be of two types: Central and peripheral.
furcation area, which may aggregate the disease process.
When it occurs within the jaw it is referred to as central
buttressing bone formation.
Question 6

When it occurs on the external surface of the jaw, then it
What are Exostoses? is referred to as peripheral buttressing bone formation.
Answer It may cause bulging of the bone which can be termed
Exostoses are outgrowth of bone of varied size and shapes. as lipping.
They can be seen as small nodules, large nodules, sharp

Question 8
ridges, spike like projections, or combination of any of
What is the role of the food impaction in bone loss?
these.
Exostoses have been reported rarely, in areas where free

Answer
gingival grafts have been placed.
Whenever proximal contacts are abnormal or absent,
Question 7 interdental bone defects can be seen. It is generally due to
What is buttressing bone formation? pressure and irritation from food impaction.
Poor proximal relationship can also result from shift in

Answer the position of the teeth, because of which there is food

It is also referred to as lipping. impaction, leading to bone loss.
Sometimes bone formation occurs in an attempt to butt-

Therefore, food impaction is a complicating factor than

ress bony trabeculae, which are weakened by resorption. the cause of bony defects.
26

Chapter Trauma from Occlusion
LONG ESSAYS
Question 1 Acute Trauma from Occlusion

Define trauma from occlusion. What are the various clinical Acute TFO results from an abrupt occlusal impact which

and radiographic features? Discuss in detail the classification can result from biting over a hard object such as stone or
of trauma from occlusion. Discuss the treatment of traumatic an olive pit
occlusion.
It can also result from restorations or prosthetic
appliances that may interfere with or alter the direction
Answer of occlusal force.
Definition Various features of acute TFO are:
Tooth pain
When the forces exceed the adaptive capacity of the tissues,

tissue injury results. The resultant injury is termed as trauma Sensitivity to percussion

from occlusion. Increased tooth mobility

If this abrupt force can be corrected by shifting the
Clinical features are as follows:

position of the tooth or by wearing away or correction of
Mobility
the restorations, the injury can heal and symptoms can

Occlusion
subside. But if this does not happen, then the periodontal

Fremitus
injury might worsen and develop into necrosis, which

Prematurities
can be accompanied by periodontal abscess formation

Wear facets
or persist as a symptom free chronic condition

Tooth migration
Cemental tears can also lead to acute trauma from

Fractured teeth or tooth

occlusion.

Thermal sensitivity.

Radiographic indicators of trauma from occlusion (TFO) are Chronic Trauma from Occlusion
as follows: Chronic trauma from occlusion is more common than

Thickening or discontinuity of lamina dura
acute trauma from occlusion and has more clinical

Widened periodontal ligament space
importance

Bone loss
It results from gradual changes in occlusion produced

Root resorption.

by tooth wear, drifting movement and extrusion of

teeth combined with a para-functional habit such as
Classification
bruxism and clenching, rather than as a sequel of acute
It can be classified as: periodontal trauma
Acute Chronic trauma from occlusion can be divided into

Chronic primary and secondary:

117
Chapter 26 Trauma from Occlusion
Primary Trauma from Occlusion Question 2

Primary trauma from occlusion may be caused by What are the various stages of trauma from occlusion?

alterations in occlusal forces, reduced capacity of the

periodontium to withstand occlusal forces or both Answer

When TFO results from alteration in occlusal forces, it is Tissue response from trauma can be in three stages. They
referred to as primary TFO. are as follows:
The main aetiological factors in primary TFO are the local 1. Stage 1: Injury.
alterations in the occlusion due to the following reasons: 2. Stage 2: Repair.
Because of insertion of a high filling or a prosthetic
3. Stage 3: Adaptive remodelling of the periodontium.
replacement that creates excessive force on the
abutment and antagonist teeth Stage 1: Injury
The extrusion or the drifting movement of the teeth

In this stage there is tissue injury resulting from excessive
into spaces created by unreplaced missing teeth or occlusal force
the orthodontic movement of teeth into functionally
In this the body attempts to repair the injury and restore
unacceptable position the periodontium
Changes produces by primary trauma do not alter the

This can occur if the forces are diminished or if the tooth
level of connective tissue attachment and do not initiate drifts away from them
pocket formation because supracrestal gingival fibres
If the offending force is chronic, the periodontium
are not affected and therefore prevent apical migration is remodelled to cushion its impact. This ligament is
of the junctional epithelium. widened at the expense of the bone, resulting in an
angular bone defects without periodontal pockets and
Secondary Trauma from Occlusion
the tooth becomes loose

Secondary TFO occurs when the adaptive capacity of the
Slightly excessive pressure stimulates resorption of
tissues to withstand occlusal forces is impaired by bone the alveolar bone, with a resultant widening of the
loss resulting from marginal inflammation periodontal ligament space

This diminishes the periodontal attachment area and
Slightly excessive tension can cause elongation of
alters the leverage on the remaining tissues the periodontal ligament fibres and apposition of the

The periodontium becomes more vulnerable to injury alveolar bone
and previously well-tolerated occlusal forces become
In the areas of increased pressure there are numerous
traumatic (Fig. 26.1). blood vessels but reduced in size, while in areas of
increased tension they become elongated
Combined TFO
A gradation of changes is produced with increase in
When the injury results from abnormal occlusal forces pressure in the periodontal ligament starting from
applied to teeth or teeth with inadequate periodontal compression of fibres, which can produce areas of
support. hyalinization
Fibroblasts and other connective tissue cells get injured

subsequently, leading to necrosis of the areas of ligament

Vascular changes may also be seen

Within 30 minutes, retardation and stasis of blood flow
occurs

At 2–3 hours, blood vessels appear to be packed with
RBCs starts to fragment

Between 1 and 7 days disintegration of blood vessels
walls and release of contents to surrounding tissue

In addition to this, there is increased resorption of
A B C alveolar bone and resorption of tooth surface occur
Fig. 26.1: Can occur on; (A) Normal periodontium with normal
Severe tension may cause widening of periodontal
height of bone (B) Normal periodontium with reduced height of ligament, thrombosis, haemorrhage, tearing of the
bone (C) Marginal periodontitis with reduced height of bone. periodontal ligament and resorption of alveolar bone
118
Severe pressure can force the root against the bone, is remodelled in an effort so as to create a structural

which can lead to necrosis of the periodontal ligament relationship in which the forces are no longer injurious

and bone to the tissues
The bone gets resorbed from the viable periodontal This would result in a thickened periodontal ligament,

ligament adjacent to necrotic areas and from marrow which is funnel shaped at the crest with vertical defects
spaces, and this process is known as undermining in the bone, and no formation of pockets
resorption The affected teeth becomes loose along with increased

The areas of periodontium most susceptible to injury vascular supply

from excessive occlusal forces are the furcations The injury phase has increased bone resorption, and

Injury to the periodontium produces a temporary decreased bone formation. Repair phase shows increased

depression in mitotic activity and rate of proliferation bone formation and decreased bone resorption. After
and differentiation of fibroblast, in collagen formation adaptive remodelling of the periodontium, resorption
and in bone formation and formation of bone return to normal.
This would return to normal levels after dissipation of the
Question 3

forces.
Explain in detail about the concept of trauma from occlusion
Stage II: Repair in periodontal diseases. Discuss about the physiological and
Repair is a constant phenomenon that is seen normally pathological tooth mobility observed in teeth having TFO.

in the periodontium. TFO further stimulates increased Answer
reparative capacity
The tissue that has been destroyed are removed and new There are various concepts of trauma from occlusion in

connective tissue cells and fibres, bone and cementum periodontal disease. They are as follows:
are formed in an attempt to restore the injured
periodontium
Glickman’s Concept
When the damage produced, exceeds the reparative According this concept, given by Glickman and Smulow

capacity of the tissues, till then the forces remain in the year 1965 and 1967, if the forces of an abnormal
traumatic magnitude are acting on teeth harbouring sub-gingival
When the bone is resorbed by excessive occlusal forces, plaque, then the pathway of spread of a plaque associated

the body attempts to replace the thinned bone with gingival lesion can be altered
new bone. This attempt to compensate for the lost bone According to Glickman, instead of an even destruction

is referred to as buttressing bone formation and it is an of the periodontium and alveolar bone, i.e. suprabony
important feature of the reparative process associated pockets and horizontal bone loss, which occurs at the
with TFO. sites with uncomplicated plaque associated lesions,
Buttressing bone formation can be of two types: sites which are exposed to abnormal occlusal force will
1. Central buttressing: It occurs within the jaws. In this form develop angular bony defects and infra bony pockets.
of buttressing, endosteal cells deposit new bone, which The periodontal structure can be divided into two zones:
restores the bony trabecula and reduces the size of the 1. The zone of irritation and
marrow spaces. 2. The zone of co-destruction.
2. Peripheral buttressing: It occurs on the surface of the
bone. It can occur on either or facial or lingual surfaces of The Zone of Irritation
the alveolar bone. Peripheral buttressing may be seen as This zone consists of marginal and interdental gingiva.

a shelf-like thickening of the alveolar margin of the bone, The soft tissue of this zone is bordered by hard structure
in severe cases, which is referred to as lipping. It basically on one side, i.e. tooth on one side and is not affected by
looks lies a pronounced bulge in the contour of the facial forces of occlusion. Therefore, it means that inflammation
and lingual bone. of gingiva cannot be induced by TFO but is because of
microbial plaque irritation
Stage III: Adaptive Remodelling of the Periodontium Such plaque associated lesion at a non-traumatised

If the repair process does not keep pace with the tooth propagates in apical direction firstly by involving

destruction caused by occlusion, the periodontium the alveolar bone and later the periodontal area.
119
The advancement of this lesion results in an even or

According to the concept of Waerhaug, because of
horizontal bone destruction. the inflammatory lesions associated with sub-gingival

plaque, the periodontal destruction occurs. He said
The Zone of Co-destruction that the angular or vertical defects occur when the sub-
This zone includes the periodontal ligament, the root

gingival plaque of one tooth has reached more apically,
cementum and alveolar bone, and is demarcated than the microbiota of the neighbouring tooth, also
coronally by the trans-septal fibres, i.e. interdental and when the volume of the alveolar bone around the roots
the dentoalveolar collagen is comparatively large.
The tissue in this zone might become the seat of lesion
Therefore to conclude, whenever there is gingival

caused by TFO inflammation in a tooth, exposed to trauma, four possibilities

The fibre bundles that separate the zone of co-
can be seen:

destruction from the zone of irritation can be affected

TFO may alter the pathway of extension of gingival
from two different directions:

inflammation to the underlying periodontal tissues.

1. From the inflammatory lesion maintained by the
Inflammation may proceed into the periodontal ligament
plaque in the zone of irritation
2. From trauma induced changes in the zone of co- rather than to the alveolar bone and the resulting bone
destruction. loss would be angular with infra bony pockets.
It may favour the environment for the formation
Because of this exposure from two different directions the

fibre bundles become oriented to some other direction and attachment of plaque and calculus and may be
which is parallel to the root surface (Fig. 26.2). responsible for development of deeper lesions.
If the tooth is tilted orthodontically or migrates into

Waerhaug’s Concept an edentulous space, then supra-gingival plaque can

become sub-gingival, resulting in formation of a supra
This concept is supported by Prichard in 1965 and
bony pocket into an infra bony pocket.

Manson in 1976
There might be a pumping effect on plaque metabolites
From his similar studies he came to a conclusion that

increasing their diffusion, due to increased tooth mobility

angular defects and infra bony pockets occur more often

at periodontal sites of teeth not affected by TFO associated with trauma to the periodontium.

In other words the Glickman’s concept/hypothesis that Physiologic Adaptive Capacity of the Periodontium
TFO played a role in spread of inflammation into the zone
to Occlusal Forces
of co-destruction

Adaptive capacity is referred to as the dynamics of the
periodontium to accommodate the forces exerted on
the crown

This can vary in different persons and in the same person
at different times. This can be explained by four factors
which affect the occlusal forces on the periodontium:
Magnitude: When the magnitude of occlusal forces

increases the periodontium shows the following:

h Thickening of the periodontal ligament
h
h An increase in the number and width of periodontal

h
ligament fibres
h An increase in the density of the alveolar bone.
h
Direction:

Changes in the direction cause a
reorientation of the stresses and strains within the
periodontium
Duration: Constant pressure on the bone is more

injurious than intermittent forces

Frequency: The more frequent the application of
Fig. 26.2: The reaction between dental plaque and the host

takes place in the gingival sulcus region. Trauma from occlusion an intermittent force, the more injurious to the
appears in the tissues supporting the tooth. periodontium.
120
Pathologic Migration Unreplaced Missing Teeth

Pathologic migration refers to tooth displacement that The spaces created by unreplaced missing teeth lead to

results when the balance among the factors that maintain drifting of adjacent teeth
physiologic tooth position is disturbed. Drifting does not result from destruction of the

periodontal tissues. But it usually creates conditions
Pathogenesis that lead to periodontal diseases and thus, the initial
The normal position of the teeth is maintained by two major tooth movement is aggravated by loss of periodontal
factors: support.
1. The health and normal height of the periodontium
2. The forces exerted on the teeth. Failure to Replace Tirst Molars
Tilting of the second and the third molars causing a
Health and Normal Height of the Periodontium

decrease in the vertical dimension
A tooth with weakened periodontal support is unable to Movement of premolars distally and the mandibular

withstand the forces and moves away from the opposing incisors tilting lingually
force Increased anterior overbite

When the periodontal support is reduced, forces that are Pushing the maxillary incisors labially and laterally

acceptable to an intact periodontium become injurious. Extrusion of the anterior teeth due to disappearance of

Pathologic migration may continue even after a tooth no incisal apposition
longer contacts its antagonist.

Diastema of the anterior teeth.
Forces Exerted on the Teeth Other Causes
The changes in the forces may occur as a result of: Pressure from the tongue may cause drifting of teeth in

Unreplaced missing teeth normal conditions

Failure to replace first molars When the periodontium is sufficiently weakened, these

Other causes.
forces cause pathologic migration

If the periodontium is sufficiently weakened, these forces Pressure from the granulation tissue of the periodontal

do not have to be abnormal to cause pathologic migration. pocket also causes pathologic migration.
SHORT ESSAYS
Question 1 Answer
What is trauma from occlusion and what is traumatic It can be classified as:
occlusion? Acute

Chronic
Answer

When occlusal forces exceed the adaptive capacity of the Acute Trauma from Occlusion

tissues, tissue injury results. The resultant injury is termed Acute TFO results from an abrupt occlusal impact which

trauma from occlusion can result from biting over a hard object such as stone or
Therefore, trauma from occlusion refers to the tissue an olive pip

injury, not the occlusal force It can also result from restorations or prosthetic

An occlusion that produces such injury is called a appliances that may interfere with or alter the direction

traumatic occlusion. of occlusal force.
Question 2 Various features of acute TFO are
What is the classification of trauma from occlusion? Tooth pain

121

Sensitivity to percussion
The periodontium becomes more vulnerable to injury

Increased tooth mobility and previously well-tolerated occlusal forces become

If this abrupt force can be corrected by shifting the traumatic.
position of the tooth or by wearing away or correction of
the restorations, the injury can heal and symptoms can Question 3
subside. But if this does not happen, then the periodontal What are the clinical and radiological signs of trauma from
injury might worsen and develop into necrosis, which occlusion?
can be accompanied by periodontal abscess formation
Answer
or persist as a symptom free chronic condition

Cemental tears can also lead to acute trauma from occlusion. Clinical features are as follows:
Mobility
Chronic Trauma from Occlusion

Occlusion

Chronic trauma from occlusion is more common than Fremitus

acute trauma from occlusion and has more clinical Prematurities

importance. Wear facets

It results from gradual changes in occlusion produced Tooth migration

by tooth wear, drifting movement and extrusion of Fractured teeth or tooth

teeth, combined with a para-functional habit such as Thermal sensitivity.

bruxism and clenching, rather than as a sequel of acute Radiographic features of TFO are as follows:
periodontal trauma. Thickening or discontinuity of lamina dura

Chronic trauma from occlusion can be divided into Widened periodontal ligament space

primary and secondary: Bone loss

Root resorption.
Primary Trauma from Occlusion

Primary trauma from occlusion may be caused by Question 4
alterations in occlusal forces, reduced capacity of the What is bone buttressing?
periodontium to withstand occlusal forces or both

When TFO results from alteration in occlusal forces, it is Answer
referred to as primary TFO When the bone is resorbed by excessive occlusal forces,

The main aetiological factors in primary TFO are the local the body attempts to replace the thinned bone with new
alterations in the occlusion due to the following reasons:
bone. This attempt to compensate for the lost bone is
Because of insertion of a high filling or a prosthetic
referred to as buttressing bone formation and it is an

replacement that creates excessive force on the

important feature of the reparative process associated
abutment and antagonist teeth
with TFO.
The extrusion or the drifting movement of the teeth

into spaces created by unreplaced missing teeth or Buttressing bone formation can be of two types:
the orthodontic movement of teeth into functionally 1. Central buttressing: It occurs within the jaws. In this
unacceptable position form of buttressing, endosteal cells deposit new bone,
Changes produces by primary trauma do not alter

which restores the bony trabecula and reduces the size
the level of connective tissue attachment and do of the marrow spaces.
not initiate pocket formation because supracrestal 2. Peripheral buttressing: It occurs on the surface of the
gingival fibres are not affected and, therefore prevent bone. It can occur on either or facial or lingual surfaces of
apical migration of the junctional epithelium. the alveolar bone. Peripheral buttressing may be seen as
a shelf-like thickening of the alveolar margin of the bone,
Secondary Trauma from Occlusion
in severe cases, which is referred to as lipping. It basically

Secondary TFO occurs when the adaptive capacity of the looks like a pronounced bulge in the contour of the facial
tissues to withstand occlusal forces is impaired by bone and lingual bone.
loss resulting from marginal inflammation

This diminishes the periodontal attachment area and Question 5
alters the leverage on the remaining tissues What is the Glickman’s concept of trauma from occlusion?
122
Answer Answer
According this concept, given by Glickman and Smulow This concept is supported by Prichard in 1965 and

in the year 1965 and 1967, if the forces of an abnormal Manson in 1976.
magnitude are acting on teeth harbouring sub-gingival From his similar studies, he came to a conclusion that

plaque, then the pathway of spread of a plaque associated angular defects and infra bony pockets occur more often
gingival lesion can be altered. at periodontal sites of teeth not affected by TFO
According to Glickman, instead of an even destruction In other words the Glickman’s concept/hypothesis that

of the periodontium and alveolar bone, i.e. supra bony TFO played a role in spread of inflammation into the zone
pockets and horizontal bone loss, which occurs at the of co-destruction
sites with uncomplicated plaque associated lesions, According to the concept of Waerhaug, because of

sites which are exposed to abnormal occlusal force will the inflammatory lesions associated with sub-gingival
develop angular bony defects and infra bony pockets. plaque, the periodontal destruction occurs. He said
The periodontal structure can be divided into two zones: that the angular or vertical defects occur when the sub-

1. The zone of irritation. gingival plaque of one tooth has reached more apically,
2. The zone of co-destruction. than the microbiota of the neighbouring tooth, also
when the volume of the alveolar bone around the roots
The Zone of Irritation is comparatively large.
This zone consists of marginal and interdental gingiva. The Therefore to conclude, whenever there is gingival
soft tissue of this zone is bordered by hard structure on one inflammation in a tooth, exposed to trauma, four possibilities
side, i.e. tooth on one side and is not affected by forces of can be seen:
occlusion. Therefore, it means that inflammation of gingiva Trauma from occlusion may alter the pathway of

cannot be induced by TFO but is because of microbial extension of gingival inflammation to the underlying
plaque irritation. periodontal tissues. Inflammation may proceed into the
Such plaque associated lesion at a non-traumatised periodontal ligament rather than to the alveolar bone
tooth propagates in apical direction firstly by involving and the resulting bone loss would be angular with infra
the alveolar bone and later the periodontal area. The bony pockets.
advancement of this lesion results in an even or horizontal It may favour the environment for the formation

bone destruction. and attachment of plaque and calculus and may be
responsible for development of deeper lesions.
The Zone of Co-Destruction If the tooth is tilted orthodontically or migrates into

This zone includes the periodontal ligament, the root an edentulous space, then supragingival plaque can

cementum and alveolar bone and is demarcated become sub-gingival, resulting in formation of a supra
coronally by the trans-septal fibres, i.e. interdental and bony pocket into an infra bony pocket.
There might be a pumping effect on plaque metabolites
the dentoalveolar collagen.

The tissue in this zone might become the seat of lesion increasing their diffusion, due to increased tooth mobility
associated with trauma to the periodontium.

caused by TFO
The fibre bundles that separate the zone of co- Question 7

destruction from the zone of irritation can be affected
What is pathologic migration? Explain with examples.
from two different directions:
1. From the inflammatory lesion maintained by the Answer
plaque in the zone of irritation Pathologic migration refers to tooth displacement that
2. From trauma induced changes in the zone of co- results when the balance among the factors that maintain
destruction. physiologic tooth position is disturbed.
Because of this exposure from two different directions
the fibre bundles become oriented to some other direction Pathogenesis
which is parallel to the root surface. The normal position of the teeth is maintained by two major
factors:
Question 6 1. The health and normal height of the periodontium.
What is Waerhaug’s concept of trauma from occlusion? 2. The forces exerted on the teeth.
123
Health and Normal Height of the Periodontium

This can vary in different persons and in the same person
A tooth with weakened periodontal support is unable to at different times. This can be explained by four factors

withstand the forces and moves away from the opposing which affect the occlusal forces on the periodontium.
force
Magnitude: When the magnitude of occlusal forces

When the periodontal support is reduced, forces that are increases the periodontium shows the following:
acceptable to an intact periodontium become injurious. a. Thickening of the periodontal ligament.
Pathologic migration may continue even after a tooth no b. An increase in the number and width of periodontal
longer contacts its antagonist. ligament fibres.
c. An increase in the density of the alveolar bone.
Forces Exerted on the Teeth

Direction: Changes in the direction cause a reorientation
The changes in the forces may occur as a result of: of the stresses and strains within the periodontium.
Unreplaced missing teeth

Duration: Constant pressure on the bone is more
Failure to replace first molars

injurious than intermittent forces.

Other causes.

Frequency: The more frequent the application
If the periodontium is sufficiently weakened, these forces of an intermittent force, the more injurious to the
do not have to be abnormal to cause pathologic migration. periodontium.
Unreplaced Missing Teeth Question 9

The spaces created by unreplaced missing teeth lead to What is the test done for trauma from occlusion. Explain.
drifting of adjacent teeth.

Drifting does not result from destruction of the Answer
periodontal tissues. But it usually creates conditions that
lead to periodontal diseases and thus, the initial tooth The test done for trauma from occlusion is referred to as
movement is aggravated by loss of periodontal support. Fremitus Test.
It is a measurement of the vibratory pattern of the teeth
Failure to Replace first Molars

when the teeth are placed in contact with each other and

Tilting of the second and the third molars causing a in moving positions.
decrease in the vertical dimension It is mainly seen in maxillary teeth, but in cases of edge
Movement of premolars distally and the mandibular

to edge contact or when there is overlap of teeth,

incisors tilting lingually

mandibular teeth can also be checked.
Increased anterior overbite
In performing this test, the Index finger is placed on the

Pushing the maxillary incisors labially and laterally

Extrusion of the anterior teeth due to disappearance of maxillary teeth at the cervical third, and the patient is
incisal apposition asked to click the posterior teeth several times.
There are various grades of fremitus:

Diastema of the anterior teeth.
Class I: Mild vibrations or movements are detected.

Other Causes

Class II: Easily palpable vibrations but no visible

Pressure from the tongue may cause drifting of teeth in movements.

normal conditions Class III: Movements are visible with naked eye.

When the periodontium is sufficiently weakened, these
forces cause pathologic migration Question 10

Pressure from the granulation tissue of the periodontal What are the treatment options for TFO?
pocket also causes pathologic migration.
Answer
Question 8
The treatment for TF O depends on what the cause is. TFO is
What are the physiologic adaptive capacities of the
usually treated with one or more of the below procedures:
periodontium to occlusal forces?
Occlusal adjustments

Answer Coronoplasty

Adaptive capacity is referred to as the dynamics of the Occlusal bite planes

periodontium to accommodate the forces exerted on Orthodontics

the crown Permanent or temporary splint.

27

Chapter Chronic Periodontitis
LONG ESSAYS
Question 1 Diagnosis
Define chronic periodontitis, what are in clinical features, It can be diagnosed by detecting the chronic

how can it be diagnosed? Describe the disease severity, inflammatory changes in gingiva like pocket formation,
disease distribution, symptoms and disease progression? attachment loss.
Radiographically, bone loss can be detected.
Answer

In some cases, suppuration may be seen.

According to Carranza, chronic periodontitis is defined In advanced cases, mobility is present.

as infections disease resulting in inflammation within the
supporting tissues of the teeth, progressive attachment loss Disease Distribution
and bone loss.
Chronic periodontitis is site-specific, that means a site
The main aetiological characteristics of the disease are: harbouring chronic microbial plaque would show signs of
Microbial plaque formation chronic periodontitis, while other sites would be normal.

Periodontal inflammation
Other than this, chronic periodontitis can be localised or

Loss of attachment and alveolar bone.
generalised.

Its clinical features are as follows: Localised periodontitis is when there are less than 30% of

Supragingival and sub-gingival plaque accumulation sites involved with attachment loss or bone loss.

Gingival inflammation Generalised periodontitis is when there are more than

Pocket formation 30% of sites involved with attachment loss or bone loss.

Loss of periodontal attachment

Loss of alveolar bone Disease Severity

Suppuration can be seen occasionally
Disease severity can be described as mild, moderate or

Gingiva can be slightly to moderately swollen and

severe.

exhibits alterations in colour ranging from pale red to
Mild (slight) periodontitis when attachment loss is not
magenta

Stippling is lost
more than 1–2 mm.
Moderate periodontitis when attachment loss is around

Blunt or rolled out gingival margins

3–4 mm.

Flattened or cratered papillae
Severe periodontitis when attachment loss is 5 mm or

Inflammation related exudates of crevicular fluid and

more than 5 mm.

suppuration from the pocket may be seen
Because of long standing, low-grade inflammation,
Symptoms

thickness, fibrotic marginal tissue may obscure the
underlying inflammatory changes Patient complains of bleeding gums white brushing or

Both horizontal or vertical bone loss may be found eating.

Tooth mobility can be present Spacing between teeth because of mobility.

Attachment loss and bone loss seen in severe cases. Loosening of teeth

125
Chapter 27 Chronic Periodontitis

Usually, there is no pain, but in some cases patient may Prior History of Periodontitis
complain of pain because of exposure of roots due to
Patients are at a greater risk if they have a prior history of

recession or due to pocket formation.

periodontitis.
Localised dull pain, sometimes radiating deep into the
If a patient is not successfully treated he or she will

jaws have been reported.

continue pocket formation, attachment and bone loss.

Areas of food impaction.
This reason makes it necessary for continuous monitoring

Gingival tenderness or itchiness may be present in some

and maintenance of periodontitis patients so that the

cases.
recurrence of the disease could be prevented.
Disease Progression
Local Factors
Various models have been described which are related to
Plaque is considered to be the main cause of chronic

disease progression.

periodontitis.
Progression is measured by attachment loss during a
Increase in Gram –ve microorganisms is associated with

given period.

bone loss and attachment loss.

Following models have been prepared.
Calculus is considered to be the most important plaque

The Continuous Model retentive factor.

Other plaque retentive factors are as follows: Sub-gingival
It suggests that the disease progression is slow and

and overhanging margins of restorations, carious lesions

continuous.
that extend sub-gingivally, furcation, malalinged or
Affected sites show a constantly progressive rate of
crowded teeth, root grooves or concavities.

destruction throughout the duration of the disease.
The Random Model Systemic Factors

According to it, the periodontal disease progresses by
When chronic periodontitis occurs in patients who have
short bursts of destruction followed by periods of no a systemic disease which may influence the effectiveness
destruction. of host response, then the rate of periodontal destruction

This pattern of disease is random with respect to the may be high significantly. For example, if a diabetic
tooth sites affected and the chronology of the disease patient encounters periodontitis, then the rate of disease
process. progression would be much higher as compared to non-
diabetic person having periodontitis.
Asynchronous, Multiple-burst Model
Synergistic effect of plaque and modulation of host

It suggests that periodontal destruction occurs around response because of effect of diabetes leads to severe
affected teeth during defined periods of life. and extensive periodontal destruction, which can be

These bursts of activity are interspersed with periods of very difficult to manage.
inactivity or remission.

Chronology of these bursts of disease is asynchronous Environmental Behavioural Factors
for individual tooth or groups of teeth.
Smoking increases the extent and severity of periodontal
Question 2 disease.
When smoking combines with plaque induced chronic
What are the various risk factors for chronic periodontitis?

periodontitis, there is an increase is the rate of periodontal

Answer destruction.
Various risk factors for chronic periodontitis are as follows:

Also emotional stress has also been seen to influence the
Prior history of periodontitis

extent and severity of chronic periodontitis.
Local factors
Genetic Factors

Systemic factors

Environmental and behavioural factors

There is no clear genetic determinant to describe chronic
Genetic factors.

periodontitis, but still a genetic predisposition to more
126
aggressive periodontal breakdown in response to plaque aggressive form of chronic periodontitis.

and calculus accumulation might exist. Therefore, with increased characterisation of genetic

A genetic variation or polymorphism in the genes polymorphisms that may exist in other target genes,

encoding interleukin 1 alpha (IL-1a) and IL-1b is a complex genotype is likely to be identified for many
associated with an increased susceptibility to a more different clinical forms of periodontitis.
28 Necrotising Ulcerative

Chapter
Periodontitis
LONG ESSAYS
Question 1 This lesion when extends into vestibular area and palate

Describe necrotising ulcerative periodontitis (NUP). is termed as necrotising ulcerative stomatitis.
Answer Aetiology
When acute necrotising ulcerative gingivitis (ANUG) Predisposing factors: Poor oral hygiene, pre-existing

progresses into the underlying periodontal structures periodontal disease, smoking, viral infections,
leading to the loss of attachment level and bone, it is termed immunocompromised status, psychosocial stress and
as necrotising ulcerative periodontitis (NUP). malnutrition.
Microbial flora: Candida albicans, P. intermedia, P.
Clinical Presentation

gingivalis, Fusobacterium nucleatum, Campylobacter
Ulceration and necrosis of interdental papilla and spp.

gingival margin. Immunocompromised status: NUP lesions are more

Painful bright red marginal gingiva, that bleeds easily. prevalent in patients with compromised or suppressed

Periodontal attachment and bone loss. immune system.

Deep interdental osseous craters. Psychological stress: Studies have shown that emotional

Advanced lesions can lead to severe bone loss, sensitivity, stress leads to the development of NUP.

tooth mobility and tooth loss. NUP patients having anxiety, higher depression scores

Absence of conventional deep periodontal pockets under emotional or physical stress are more prone and

as the ulcerative and necrotising nature destroys the predisposed to development of NUP.
marginal epithelium and connective tissue.
Oral malodour, fever, malaise and lymphadenopathy is Treatment

also seen. Thorough medical history and examination to rule out

any underlying systemic disease.
Necrotising Ulcerative Periodontitis In HIV/AIDS Administration of local anaesthesia in the affected area.
Patients

Removal of necrotic hard and soft tissues with scaling,

This disease is much more destructive and causes root planning and curettage procedures.

complications that are rarely seen in a non-HIV/AIDS Ultrasonic instrumentation with 10% povidone-iodine

patient. solution irrigation.
Periodontal attachment and bone loss is extremely rapid Anti-microbial therapy to reduce Gram-negative

and patients can loss 90% of periodontal attachment anaerobes
and 10 mm bone in 3–6 months. Anti-fungal agents in cases of fungal infection.

Other complications include progression of lesion Home care procedures: Brushing and interdental flossing,

involving large areas of soft tissue necrosis which leads to chlorhexidine rinses, systemic follow-up when the lesion
exposure of bone and sequestration of bone fragments. is resolved.
29 Aggressive

Chapter
Periodontitis
LONG ESSAYS
Question 1 Other characteristics that are common to patients with

aggressive periodontitis are
Discuss in detail about the classification, clinical
Otherwise clinically healthy patient
characteristics, epidemiology, risk factors, radiographic

Rapid attachment and bone loss
findings, diagnosis and treatment options for aggressive

Amount of microbial deposits inconsistent with
periodontitis.

disease severity
Answer Familial aggregation of cases.

Some characteristics are common but not universal in
Classification of Aggressive Periodontitis
aggressive periodontitis patients:
Aggressive periodontitis may be classified into localised Diseased sites infected with Actinobacillus actinomy-
aggressive periodontitis (LAP) and generalised aggressive

cetemcomitans (A.a.)
periodontitis (GAP) forms. Abnormalities in phagocyte function

Localised Form
Hyper-responsive macrophages, producing increased

prostaglandin E2 (PGE2) and interleukin-1 beta (IL-1b)
Localised form is characterised by In some cases self-arresting disease progression.

Circumpubertal onset of disease

Localised first molar or incisor involvement on at least Epidemiology

two permanent teeth one of which is a first molar
Prevalence of Aggressive Periodontitis
Robust serum antibody response to infecting agents.

Most of the prevalence and incidence data available are

Generalised Form from studies done in the US
Usually affects persons under 30 years of age (however
Prevalence and incidence of aggressive periodontitis in

India is not known clearly due to lack of epidemiological

may be older)
Generalised proximal attachment loss affecting at least studies
In the US and other countries prevalence of LAP is

three teeth other than first molars and incisors

Pronounced episodic nature of periodontal destruction estimated at 1%.

Poor serum antibody response to infecting agents
Localized Aggressive Periodontitis

The distinction between localised and generalized

form is mainly based on the distribution of periodontal Clinical Characteristics
destruction in the mouth LAP has an age of onset around puberty

Clinically, it is characterised as having localised first molar/
Clinical Characteristics

incisor presentation with interproximal attachment loss
The primary characteristic of aggressive periodontitis on at least two teeth one of which is a first molar, and

that differentiates it from chronic periodontitis is the involving no more than two teeth other than first molars
rapid progression of attachment loss and bone loss. and incisors
129
Chapter 29 Aggressive Periodontitis

This localised distribution is characteristic but Microbiologic aspects of LAP:
unexplained
Microbiologic studies of LAP have provided clear evidence

Possible explanations for this have been suggested—
of a strong association between disease and a unique

After initial colonisation of the first permanent teeth

bacterial microbiota predominated by A.a.

to erupt, i.e. first molars and incisors, A.a. evades

host defences by different mechanisms including Other organisms that have been associated with LAP
production of PMN chemotaxis inhibiting factor, include P. gingivalis, E. corrodens, C. rectus, F. nucleatum, B.
endotoxin, collagenase and leucotoxin and other capillus and Capnocytophaga spp. and spirochetes.
factors that allow the bacteria to colonise the However, research shows a primary aetiologic role for
pocket and initiate destruction of the periodontal A.a. in LAP.
tissues. After this initial attachment adequate Evidence supporting A.a.’s role in LAP are
immune defences are stimulated to produce opsonic Humoral immune response to this organism is elevated

antibodies to enhance clearance and phagocytosis in patients with LAP. A.a. has been isolated in 97% of
of the invading bacteria and neutralise leucotoxic LAP patients compared with 21% of adult periodontitis
activity. This prevents colonisation of other sites. A patients and 17% of healthy patients. The prevalence of
strong antibody response to infecting agents is one A.a. is six times greater in LAP than in healthy patients.
characteristic of LAP Serotype B is the most common compared to serotype A.
Bacteria antagonistic to A.a. may colonise periodontal

Incidence of A.a. is greater in younger LAP patients than

tissues and inhibit A.a. from further colonisation of in older patients. Younger patients have more destructive
periodontal sites in the mouth. This would localise A.a. activity. The presence of this organism correlates with
infection and tissue destruction. disease activity.
A.a. may lose its leucotoxin producing ability for

A large number of A.a. organisms occur in lesions in LAP

unknown reasons. If this happens the progression patients but they are absent or occur in low numbers in
of the disease may be retarded or arrested and healthy sites.
colonisation of new periodontal sites averted. A.a.

can be identified by electron microscopy,
Defect in cementum formation may be responsible

immunofluorescence and culture from LAP lesions

for localisation of the lesions. Root surfaces of teeth within the gingival connective tissues.
extracted from patients with LAP have been found A.a. is quite virulent and produces a leucotoxin,

to have hypoplastic or aplastic cementum. This collagenase, phosphatase and bone resorbing factors
was found not only on root surfaces exposed to and other factors important in invasion of host tissue
periodontal pockets but also on roots still surrounded cells, evasion of host defences, immunosuppression and
by the periodontium. destruction of periodontal tissues.
Elimination of this organism from the sub-gingival flora
Other Features

results in successful clinical treatment of LAP.

Another striking feature of LAP is the lack of clinical
inflammation despite the presence of deep pockets. Also in Immunologic Considerations in Lap
many cases the amount of plaque seems to be inconsistent Numerous mechanisms of serum mediated killing
with amount of destruction. are available to kill bacteria. These include lysis by
LAP progresses rapidly. Baer et al. have shown that the the membrane attack complex of complement and
rate of bone loss is about 3–4 times faster than in chronic antimicrobial substances such as lysozyme
periodontitis. There is a decrease in the chemotactic response to
Other features of LAP include distolabial migration of chemotactic agents like C5a, N-formylmethionyl-leucyl-
maxillary incisors with diastema formation. phenylalanine and leucotriene B4.
Increased mobility of first molars
In LAP the main collagenase found in tissues and gingival
Sensitivity of denuded root surfaces to thermal and
crevicular fluid (GCF) is matrix metalloproteinases-1 (MMP-1)
tactile stimuli as opposed to MMP-8 in chronic periodontitis. LAP patients
Deep dull radiating pain during mastication

have elevated antibodies to A.a. In LAP the dominant
Periodontal abscesses may form and regional lymph

serum antibody isotype is immunoglobulin G2 (IgG2). Some
node enlargement may occur. individuals possess a variant of the Fc receptor on neutrophils
130
that do not bind efficiently to IgG2. To compensate for this Other Features
inefficient binding more serum antibody is present resulting
Some patients with GAP may have systemic manifestations

in a robust serum antibody response. This increase in serum
such as weight loss, mental depression and general malaise.
antibody limits the progression of the disease.
Patients with a presumptive diagnosis of GAP should have
Radiographic Findings their medical histories updated and reviewed to rule out
systemic involvement.
Vertical loss of alveolar bone around first molars and incisors
As with LAP, GAP may be arrested spontaneously or
beginning around puberty in otherwise healthy teenagers
after therapy, while some cases may continue to progress
is a classic diagnostic sign of LAP. Radiographic findings
inexorably to tooth loss despite intervention with
may include an arc-shaped loss of alveolar bone extending
conventional treatment.
from distal surface of second premolar to mesial surface of
second molar. Radiographic Findings
Burn out phenomena—the property of LAP to resolve by it. Radiographic picture can range from severe bone loss
The lesion stops progressing. associated with minimal number of teeth to advanced bone
loss affecting majority of teeth in the dentition.
Generalised Aggressive Periodontitis—Clinical
Characteristics Page et al. have described sites in GAP patients that
demonstrated osseous destruction of 25–60% during a
Generally affects individuals under the age of 30, but older 9-week period.
patients may also be affected. Despite this extreme loss, other sites in the same patient
They produce a poor antibody response to the pathogens showed no bone loss.
present.
Characterised by “generalised interproximal attachment Prevalence and Distribution by Age and Sex
loss affecting at least three permanent teeth other than first In a study of untreated periodontal disease conducted in
molars and incisors”. Sri Lanka by Loe and colleagues, 8% of the population had
Destruction occurs episodically with periods of advanced rapid progression of the disease characterised by yearly loss
destruction followed by stages of quiescence. of attachment of 0.1–1 mm.
As in LAP, GAP patients often have small amounts of In the US a national survey of adolescents revealed a
plaque associated with the affected teeth. prevalence of 0.13%. Blacks were at much higher risk than
Quantitatively amount of plaque inconsistent with whites for all forms of aggressive periodontitis. Males were
amount of periodontal destruction. more likely to have GAP than females.
Qualitatively P. gingivalis, A.a. and B. forsythus are
Risk Factors for Aggressive Periodontitis
frequently detected in the plaque that is present.
Microbiologic Factors
Tissue Responses in GAP
Although several specific microorganisms frequently are
Two gingival tissue responses can be found in cases of GAP. detected in patients with LAP such as A.a., Capnocytophaga,
One is a severe acutely inflamed tissue often proliferating, E. corrodens, Prevotella intermedia and Campylobacter rectus.
ulcerated and fiery red. Bleeding may occur spontaneously A.a. has been implicated as the primary pathogen.
or with slight stimulation. Suppuration may also be present. The link between A.a. and LAP is based on evidence
This tissue response is considered to occur in the destructive summarised by Mombelli and Tonetti—
stage in that attachment and bone are actively lost. A.a. is found in about 90% of lesions characteristic of LAP.

In other cases the second gingival response occurs where Sites with evidence of disease progression often show

the gingival tissues may appear pink, free of inflammation elevated levels of A.a.
and occasionally with some degree of stippling. But LAP patients have increased serum antibody levels to A.a.

despite the mild clinical appearances, deep pockets can be Clinical studies show a correlation between reduction

demonstrated on probing. in sub-gingival load of A.a. during treatment and a
Page and Schroeder have considered this tissue response successful clinical response.
to coincide with periods of quiescence in that the bone level A.a. produces virulence factors that contribute to the

remained stationary. disease process.
131
Chapter 29 Aggressive Periodontitis
Immunologic Factors
Microbiologic—sub-gingival plaque samples to culture
microorganisms; antibiotic sensitivity testing.
Some immune defects have been implicated in aggressive

Immunological—done to test antibodies against A.a.
periodontitis. Human leucocyte antigens (HLA) that regulate
immune responses have been evaluated as candidate Treatment
markers for aggressive periodontitis. HLA-A9 and B15 have
been consistently associated with aggressive periodontitis. Based on whether disease is localised or generalised and the
Secondly several studies have shown that patients with degree of destruction present. If diagnosed early respond to
aggressive periodontitis display functional defects of PMNs standard periodontal therapy.
monocytes or both. These defects can impair chemotaxis The following treatment modalities have been considered:
and phagocytosis.
A hyper-responsiveness of monocytes from LAP
Extraction
patients with respect to production of PGE2 in response to
Teeth with hopeless prognosis have to be extracted.
lipopolysaccharide (LPS) has also been seen. This leads to
Transplantation of developing third molars to the sockets
increase connective tissue and bone loss. Poorly functional of previously extracted first molars has been attempted.
inherited forms of FcrRII which is the receptor for human
Standard Periodontal Therapy
IgG2 antibodies have been found in patients with LAP.
Possible immune mechanisms include increased It includes scaling, root planing, and flap surgery with
expression of MHC type II, HLA-DR4 altered helper or or without bone grafts, root amputation, hemi-sections,
suppressor T-cell function, polyclonal activation of B cells by occlusal adjustments and strict plaque control.
microbial plaque and genetic predisposition.
Antibiotic Therapy
Genetic Factors
In the late 1970s and 1980s the identification of A.a. as
a major culprit and the discovery that this organism
Several studies have shown that all individuals are not penetrates tissues has formed the basis for therapy.
equally susceptible to aggressive periodontitis. Authors
LAP can be treated with scaling root planing (SRP) and
have shown a familial pattern of alveolar bone loss and tetracycline 250 mg four times for 14 days, every 8 weeks
have implicated genetic factors in aggressive periodontitis. for up to 18 months.
Specific genes have not yet been identified, but segregation
If surgery indicated systemic tetracycline should be
and linkage studies suggest the involvement of a major prescribed to be taken 1 hour before surgery.
gene that is transmitted through an autosomal dominant
Chlorhexidine mouth rinses to aid mechanical plaque
pattern. control.
Also there is a genetic basis for immunologic defects. But
Local delivery systems can be used in the localised form
it is unlikely that all patients with aggressive periodontitis of the disease.
have the same genetic defect.
Advantages of this are the smaller dosage required
and the reduced side effects associated with systemic
Environmental Factors antibiotic therapy.
Amount and duration of smoking are important variables
Antibiotic sensitivity testing is required for cases which
that can influence extent of destruction. Patients with GAP are refractory to treatment.
who smoke have more affected teeth and more loss of

Based on cultured organisms the antibiotic regimen can
clinical attachment than non-smokers with GAP. However, be given.
smoking may not have the same impact on attachment

When the microflora consists of Gram positive organisms:
levels in patients with LAP. Augmentin (Amoxicillin 250 mg and K clavulanate 125
mg) is given TID for 14 days along with SRP.
Diagnosis
This can be combined with intrasulcular full mouth
lavage with 10% povidone-iodine solution.

Clinical diagnosis based on probing pocket depth,
Patient’s positive for bacteroides in the absence of A.a.
attachment loss, mobility and E. corrodens can be treated with metronidazole 500

Radiographic—LAP arc-shaped bone loss, around mg 3 times a day for 7 days.
first molars; GAP serial radiographs to assess rate of
Clindamycin HCl 150 mg QID for 7 days with SRP can also
destruction of bone. be used.
132
It should be used with caution due to the possibility of Occlusal Adjustments

occurrence of pseudomembranous colitis. Migration and drifting of teeth is a late characteristic of

Azithromycin can be used for patients positive for

aggressive periodontitis.

P. gingivalis.
Combination antibiotic therapy can be used and has been
Premature contacts should be relieved using selective

grinding.

shown to be more effective since no single antibiotic is
bactericidal to all microorganisms. After successful periodontal therapy when the condition

Combinations of metronidazole/augmentin is stable gentle orthodontic retraction of labially drifted

Metronidazole/ciprofloxacin for treatment of recurrent incisors can be considered.

cases.
Amoxicillin/doxycycline also used. Prosthetic Management

Another approach is the use of host modulation therapy Any partial dentures should be carefully designed to

using sub-antimicrobial doses of non-steroidal anti- avoid further gingival irritation.
inflammatory drugs (NSAIDs) in conjunction with Abutment teeth should be loaded as near axially as
conventional therapy.

possible.
Low dose doxycycline controls the activity of MMPs.
Chrome cobalt dentures are usually indicated.

Other agents such as flurbiprofen, indomethacin and

naproxen may reduce inflammation. Acrylic dentures should be used only in the immediate

replacement phase.
Other Adjuncts
Other than Scaling and Root Planing, Oral Hygiene Maintenance
Instructions, antibiotic therapy both local and systemic Patients should be recalled every 3 months for Oral Hygiene
other treatment requirements would include reinforcement and scaling.
30 AIDS and

Chapter
Periodontium
LONG ESSAYS
Question 1 Below parakeratotic surface, acanthosis and balloon cells

resembling koilocytes are seen.
What are the oral manifestations of human immuno-
These cells contain virus particles of herpes group and
deficiency syndrome (HIV) infection?

Epstein-Barr virus.
Answer Differential Diagnosis
Oral lesions in HIV infected patients are very common. Dysplasia, lichen planus, carcinoma, tobacco-related
Commonly associated oral manifestation seen in HIV

leucoplakia, frictional and idiopathic keratotis,
infected patients are: psoriasiform lesions and hyperplastic candidiasis.
Oral hairy leucoplakia. Microscopic confirmation of oral hairy leucoplakia serves

Oral candidiasis. as an indicator that patient will develop AIDS.

Kaposi’s sarcoma. Severity of lesion is not correlated with chances of

Bacillary (epithelioid) angiomatosis. developing AIDS, thus small as well as extensive lesion

Oral hyperpigmentation. are diagnostically significant.

Atypical ulcers and delayed healing.
Oral Candidiasis

Oral Hairy Leucoplakia It is a fungal infection which is associated with Candida

It is commonly seen in patients with HIV infection. albicans.

Site of infection is generally lateral borders of tongue, It is the most common oral lesions and is seen in 90% of

commonly bilaterally distributed and sometimes may AIDS patients.
extend to the ventrum. Sometimes it also affects dorsum It is of four types:

of tongue, buccal mucosa, floor of mouth, retromolar 1. Pseudomembranous candidiasis: It is also known as
area and soft palate. oral thrush. It is a white lesion that can be easily scraped
Characterised clinically by asymptomatic, poorly and removed from oral mucosa. Commonly seen on

demarcated keratotic areas ranging from few millimetres hard and soft palate, and buccal and labial mucosa.
to several centimetres. Often, vertical striations are seen 2. Erythematous candidiasis: It is a pseudomem-
which give it a corrugated appearance. Sometimes. branous type lesion. Appears as red patches on
surface is shaggy and gives a hairy appearance. buccal and palatal mucosa. May be associated with
The lesion does not rub off and resembles other keratotic depapillation of the tongue.

oral lesions. 3. Hyperplastic candidiasis: Least common form.
Candidal infections are secondary to this and colonies Seen on tongue and buccal mucosa. It is resistant to

can be seen on surface of the lesion. removal.
Microscopically, hyperkeratotic surface with projection 4. Angular cheilitis: Commissures are erythematous

that resemble hair. with crusting and fissuring of surface.
134
Microscopically, smear of lesion is obtained by scraping Oral Hyperpigmentation

the lesion and viewed in a microscope. The lesion shows
There is an increased incidence of oral hyperpigmentation

hyphae and yeast forms of organisms.

in HIV affected individuals. Pigmented areas appear as
Candidiasis in HIV infected patients respond to antifungal
spots or striations on buccal mucosa, gingiva, palate or

treatment but is refractory and recurs within 4 weeks to
3 months due to the decrease in immunocompetency of tongue.
the individual. Pigmentation can be due to prolonged use of drugs,

such as zidovudine, ketoconazole or clofazimine.
Kaposi’s Sarcoma
Atypical Ulcers and Delayed Healing
Kaposi’s sarcoma is generally a rare, multifocal, slow-

growing malignant vascular neoplasm. Atypical ulcers in HIV infected individual are commonly

However, in AIDS patient, it is an aggressive lesion and associated with neoplasms, lymphoma, Kaposi sarcoma,

is reported in almost 70% of the patients affecting oral squamous cell carcinoma, neutropenia.
mucosa mainly palate and gingiva. Klebsiella pneumoniae, Enterobacter cloacae and

In early stages, the oral lesions are painless, reddish Escherichia coli have been seen causing ulcers in oral

purple macules of the oral mucosa. mucosa.
As the lesion progress, they become nodular. It manifests Herpes simplex virus, varicella zoster virus, Epstein-Barr

as modules, papules, or non-elevated macules generally virus or cytomegalovirus have been retrieved from oral
brown, blue or purple in colour. ulcers.
Microscopically, formed of four components—
Management

(1) endothelial cell proliferation with atypical vascular
channels, (2) extravascular haemorrhage with hemo- Neutropenia can be treated with recombinant human

siderin deposition, (3) spindle-cell proliferation with granulocyte colony stimulating factor.
atypical vessels and (4) mononuclear inflammatory Prolonged oral ulcers can be managed using prednisone

infiltrate formed mainly of plasma cells. or thalidomide.
Viral infection can be treated with zidovudine,
Differential Diagnosis

trimethoprim-sulphamethoxazole or ganciclovir.
Pyogenic granuloma, atypical hyperpigmentation, sarcoid-
osis, angiosarcoma, haemangioma, bacillary angiomatosis, Question 2
pigmented nevi and cat scratch disease. What are the periodontal manifestations of HIV infection?
Bacillary (Epithelioid) Angiomatosis Answer

Bacillary angiomatosis (BA) is an infectious vascular Periodontal manifestation of HIV infections are:
proliferative disease similar to Kaposi’s sarcoma clinically Linear gingival erythema:

and histologically. This is characterised by persistent, linear, easily

bleeding erythematous gingivitis.
Aetiology
May serve as precursor to rapidly progressing

Rickettsia-like organisms, Bartonella henselae, Bartonella necrotising ulcerative periodontitis (NUP).

quintana, etc. May be localised or generalised.
Clinically, BA appears as red, purple or blue oedematous

May be limited to marginal tissue.

soft tissue lesion which causes destruction of periodontal

Extends into attached gingiva in a punctuate or
ligament and bone.

diffuse erythema.
Differentiation of BA from Kaposi sarcoma is done by
Extends into alveolar mucosa.

biopsy, which shows an epithelioid proliferation of

angiogenic cells with acute inflammatory cell infiltrate. Necrotising ulcerative gingivitis (NUG):

Warthin-Starry silver stain reacts with causative Some reports have shown increase in incidence of

organisms in the biopsy specimen. NUG in HIV-infected patients.
135
Chapter 30 AIDS and Periodontium

Necrotising ulcerative stomatitis (NUS):
Lesions are seen anywhere in dental arches and are
It is characterised by necrosis of oral soft tissue and

generally localised to a few teeth.

underlying bone.
Generalised NUP can be seen after marked CD4+ cell
It can occur alone or in conjunction with NUP.

depletion.
Severe depression of CD4 immune cells is seen.

Exposed bone undergoes necrosis and subsequent

Necrotizing ulcerative periodontitis (NUP): sequestration.
Characterised by soft tissue necrosis, rapid periodontal

It is a severely painful condition and requires
destruction and inter-proximal bone loss. immediate treatment.
31

Chapter Clinical Diagnosis
LONG ESSAYS
Question 1 Answer
Define wasting diseases. Discuss various wasting diseases. Grades of tooth mobility are:
Answer Normal mobility.

Grade I mobility: Slightly more than normal.

According to Carranza “wasting is defined as any gradual Grade II: Moderately more than normal.

loss of tooth substance characterised by deformation of Grade III: Severe mobility faciolingually and mesiodistally

smooth, polished surfaces, without regard to the possible along with vertical depressibilty.
mechanism of this loss”.
Various wasting diseases are as follows: Mechanism of Tooth Mobility
Erosion: It is also known as corrosion. Tooth mobility occurs in two stages:

It is a wedge-shaped depression which is sharply 1. In the initial stage the tooth moves within the confines of

defined in the cervical area of the facial region of the the periodontal ligament. It is due to viscoelastic distortion
tooth. of the periodontal ligament (PDL) and redistribution of
It is caused due to intake of acidic or citrous foods.
the PDL fluid, interbundle content, fibres.

Abrasion: it is caused due to mechanical wear other than 2. In the secondary stage, there is elastic deformation of the

that of the mastication. alveolar bone in response to horizontal force.
It causes saucer-shaped depression with a smooth

shiny surface. Factors of Tooth Mobility
Most common cause is toothbrushing with an
Loss of tooth support.

abrasive paste in a horizontal direction.

Trauma from occlusion.
It is also caused by holding objects like pins in

Extension of inflammation.

between the teeth.

Periodontal surgery.
Attrition: It is the occlusal wear caused due to functional

During pregnancy.

contacts with opposite teeth.

Pathologic processes of the jaws.
It is most commonly seen in bruxism patient.

Abfraction: It is caused due to occlusion loads because Question 3

of tooth flexure and mechanical microfractures and Discuss periodontal screening and recording system (PSR).
tooth substance loss in the cervical area.
Answer
Question 2 It is a method of periodontal screening developed by

What are the grades of tooth mobility? Discuss the American Academy of Periodontology and American
mechanism of tooth mobility and what are the factors Dental Association.
causing tooth mobility? It is a simple and fast method of periodontal screening.

137
Chapter 31 Clinical Diagnosis

It is done with the help of a probe which has a 0.5 mm
Code 2: The colour band is completely visible,
ball tip and is colour coded from 3.5–5.5 mm. there is bleeding on probing, supragingival or

Patient’s mouth is divided into six sextants and each tooth is subgingival calculus and defective margins are
probed and examined at least six points around each tooth. found.

The deepest finding is recorded in each sextant, along
Code 3: Colour band is partially submerged.
with other findings, according to the following codes: h This suggests there is need of comprehensive
h
Code 0: In the deepest sulcus of the sextant the

periodontal examination.
probes colour band remains completely visible.
Code 4: Colour band completely disappears.
h Gingiva is healthy and no calculus is found.
h h Comprehensive
h
examination, charting and
Code 1: The colour band is completely visible.

treatment planning are required.
h No calculus but slightly bleeding on gentle probing
h
Code * : There is furcation involvement, tooth mobility,
is seen. mucogingival problem or gingival recession.
32 Radiographic Aids

Chapter in the Diagnosis of
LONG ESSAYS
Question 1 There is an increase in bone resorption along the

endosteal margins of the medullary spaces because
What are the various radiographic changes in periodontitis?
of inflammatory cells and fluid, proliferation of
Answer connective tissue cells and increased osteoclasis.
There are composite images of the partially eroded
Radiographic changes in periodontitis are as follows:

bony trabeculae which separates the radiopaque
1. Fuzziness and a break in the continuity of the lamina projection from the radiolucent spaces.
dura: The break in the continuity of the lamina dura Because of extension of inflammation and the

either on the mesial or the distal aspect of the crest of resorption of bone, the height of the interdental
the intendental septum are considered to be the earliest septum gets reduced.
radiographic changes in periodontitis.
It is caused due to extension of gingival inflammation
Radiographic Appearance of Interdental Craters

into the bone which causes reduction in calcified
tissue at the margin of the septum and also causes Craters generally cannot be sharply demarcated from the

widening of the vessel channel. rest of the bone, with which they blend gradually.
These changes depend a lot on the radiographic They can be seen as irregular areas fo reduced

technique like angulation of the tube or placement radioopacity on the alveolar bone crests.
of the film and on the anatomical variation such as Depth or morphology of the interdental craters cannot

thickness and density of the interdental bone and be depicted accurately on the radiograph.
position of the adjoining teeth. They sometimes appear as vertical defect.

Therefore it can be concluded that the intact crestal

lamina dura might be an indicator of periodontal Radiographic Appearance of Furcation Involvement
health, whereas its absence lacks diagnostic relevance.
Naber’s probe makes the correct diagnosis of the

2. A wedge shaped radiolucent area is seen either on the

furcation involvement.
mesial or distal aspect of crest of the septal bone.
Following radiographic diagnostic criteria have been
This is caused due to resorption of the bone of the

suggested to assist in the radiographic furcation

lateral aspect of the interdental septum, with an
associated widening of the periodontal space. detection :
3. Height of the interdental septum is reduced: when the 1. If there is bone loss, specially adjacent to roots, then this
destruction process extends across the crest of the slightest change in the furcation should be investigates
interdental septum, the height of the bone is reduced. clinically.
4. Finger like radiolucent projection extend from the crest 2. Diminished radio-density in the furcation area, in which
into the septum. outlines of bony trabeculae are visible suggests furcation
When there is deep extension of the inflammation involvement.

into the bone, there is appearance of radiolucent 3. Furcation might be involved, if there is marked bone loss
projection into the interdental septum. in relation to a single molar.
139
Chapter 32 Radiographic Aids in the Diagnosis of Periodontal Diseases
Radiographic Appearance of a Periodontal Radiographic Appearance of Localized Aggressive

Abscess Periodontitis

There is discreet area of radiolucency along the lateral
Bone loss may be seen in the maxillary and mandibular
aspect of the root. incisor and or first molar areas, usually bilaterally and

But, the radiographic picture is not very typical because result in vertical, arc like destructive pattern.
of the following reasons:
Loss of alveolar bone may be generalized, but is seen
more in molars and incisors and less in premolar area.
1. Stage of the lesion: Early stages of acute periodontal
abscess is extremely painful but there are no radiographic Radiographic Changes of TFO
changes. Injury phase: In this phase, there is a loss of lamina dura

2. The extent of bone destruction and the morphologic along the apex, furcation marginal areas.
changes of the bone. Widening of PDL space is seen.

3. The location of abscess: Lesion in soft tissue wall of Repair phase: There is widened PDL space which can be

periodontal pocket shows less radiographic changes localized or generalised.

as compare to lesions which are present deep into the Advanced traumatic lesion can lead to angular bone loss,

supporting tissues. along with marginal inflammation may lead to intrabony

Therefore a clinical diagnosis is important along with pocket formation.
a radiographic diagnosis, especially for a periodontal Root resorption can be seen in cases of excessive forces
abscess. like force by orthodontic appliances.
33 Advanced Diagnostic

Chapter
Techniques
LONG ESSAYS
Question 1 Lack of bleeding indicates periodontal stability;

What are the advancements in diagnostic techniques? however, this may not be true in heavy smokers.
Answer Advances in Radiographic Assessment

Advancements in diagnostic techniques can be divided into
Conventional radiographs lack sensitivity and show
the following: positive readings only when about 30% of bone mass
Advances in clinical diagnosis.
has been lost.

Advances in radiographic assessment.
Newer techniques of radiography are more sensitive and

Advances in microbiological analysis.

give a clear picture:

Advances in characterization of host response.
Digital radiography: This technique of radiography

has an advantage over conventional radiographs
Advances in Clinical Diagnosis
as the radiographic image can be digitally stored or
Gingival temperature: Periotemp probe enables processed and enhanced thus, providing us real or

the calculation of the temperature differential with a almost real images.
sensitivity of .1 degree centigrade between the probed Subtraction radiography: Relies on conversion of

pockets and subgingival temperatures. serial radiographs into digital images:
Periodontal probing: Florida probe system—this is an h These images then can be superimposed and the

h
automated probe system consisting of probe handpiece, resultant composite can be reviewed.
computer interface , foot switch, computer and digital h Studies have shown:
read out:
h
» A high degree of correlation between changes
The probe tip is .4 mm in diameter.
»
in alveolar bone, determined by subtraction

The measurements are made electronically and
radiography and clinical attachment level

transferred to the computer when the foot-control
changes in periodontal patients after therapy.
switch is pressed.
This method combines the advantage of constant
» Small osseous lesions can be easily detected as
»
compared to conventional radiographs.

probing with precise electronic measurements, thus
eliminating the potential errors. » It facilitates both qualitative and quantitative
»
This method has the disadvantage of lack of tactile visualisation of minor density changes in bone.

h Computer assisted densitometric image analysis
sensitivity and underestimation of the probing
h
depths. (CADIA).
Gingival bleeding: Bleeding on probing is an indicator In this technique, grey scale images are formed by

for the presence of an inflammatory lesion in the converting the light transmitted through a radiograph
connective tissue: with a help of a video camera.
Severity of bleeding increases within increase in size This technique has shown higher sensitivity and a high

of inflammatory infiltrate. degree of reproducibility and accuracy.
141
Chapter 33 Advanced Diagnostic Techniques
Advances in Microbiological Analysis

Evalusite is a chair-side clinically diagnostic aid in which
there is a linkage between antigen and membrane bound
Bacterial Culturing

antibody to form an immunocomplex. This complex can
In this technique, the plaque samples are cultivated in be later revealed by a colorimetric evaluation.
anaerobic conditions with the use of selective or non- Latex Agglutination: This is a simple immunologic

selective media along with several biochemical and physical assay based on binding of protein to latex.
tests, allowing the identification of different putative
pathogens. DNA Probes
Advantage Probe are basically the nucleic acid molecule obtained
from a specific microorganism, artificially synthesized and
Clinician can obtain relative and absolute count of
labelled for detection when placed with plaque sample.

cultured species. Hybridization is done for the production of a double

Clinician can also assess antibiotic susceptibility.

stranded nucleic acid by pairing of complementary DNA

Disadvantage strands.

This method can only grow live bacteria; therefore, This method is highly specific and can accurately detect the
careful sampling and transport are essential. presence of target microorganism.
Checker board DNA DNA hybridization: This technology

Some pathogens are fastidious (Treponema pallidum and
Treponema forsythus), which are difficult to culture. uses whole genomic, digoxigenin-labelled DNA probes

These require sophisticated equipment and experienced and facilitates rapid processing of large number of
personnel and is time consuming and expensive. plaque samples with multiple hybridization up to 40
species of microorganisms in a single test.
Immunodiagnostic Methods
Polymerase Chain Reaction

Immunologic assays employ antibodies that recognise
specific bacterial antigens to detect microorganisms. Polymerase Chain Reaction (PCR) is the most powerful tool
Direct Immunofluorescent Assays (IFA): These
for the amplification of genes and their RNA transcripts.
The conventional PCR methods only provided qualitative

employ both monoclonal and polyclonal antibodies.

information and therefore were of limited clinical use.

These antibodies are then conjugated to a fluorescein
Because of this drawback, newer methods have emerged
marker which binds with bacterial antigen to form a

which give quantitative information as well.

fluorescent immune complex which can be detected
under a microscope. Advances in Characterising Host Response
Indirect

Immunofluorescent Assays IFA: This
technique employs a secondary fluorescence Assessment of host response is the study of immunologic or
conjugated antibody that reacts with primary antigen biochemical mediators and methods that are recognised as
antibody complex. part of individuals response to periodontal infections.
Cytoflorography or flow cytometry: This technique
Sources of Samples

helps in rapid identification of oral bacteria.

In this technique bacterial cells are labelled from the Potential sample sources are saliva gingival crevicular fluid
patient’s plaque sample with both species specific (GCF), gingival crevicular cells, blood serum, blood cells and
urine.
antibody and fluorescein-conjugated antibody.
Components of GCF have been studied and can be
This suspension is then introduced into the flow
divided into:

cytometer which will separate the bacterial cells into

1. Host derived enzymes
single-cell suspension with the help of laminar flow
2. Tissue break-down products
through a narrow tube.
3. Inflammatory mediator
Enzyme-linked

Immunosorbent Assa: In this
technique enzymatically derived colour reaction is Host-Derived Enzymes
substituted as the label. Various enzymes are released from host cells during

The intensity of the colour is dependent on the initiation and progression of periodontal disease:
concentration of the antigen and is red photometrically Aspartate aminotransferase (AST): This enzyme is

for quantification. released from dead cells from a variety of tissues.

142
Marked elevation is seen in AST levels from GCF Tissue Breakdown Products

samples which are collected from the sites with severe Analysis of GCF, obtained from sites with periodontal

gingival inflammation. infection, shows higher levels of hydroxyl proline
Periogard is a commercially available chair side test kit
(collagen breakdown) and glycosaminoglycans (matrix

for measuring AST levels. degradation).
Alkaline phosphatase (ALP): Studies have shown that Presence of osteocalcin and type I collagen peptides are

concentration of this enzyme in GCF is significantly seen when there is loss of alveolar bone.
higher in diseased sites as compared to normal one.
Beta glucuronidase: Studies have shown an elevated Inflammatory Mediators

level of beta glucuronidase at sites with severe Presence of cytokines like TNF alpha, IL-1 alpha, IL-1 beta, IL-
periodontal disease. 6, and IL-8 in GCF are potential diagnostic markers.
Elastase: GCF collections from the sites with periodontitis Increased PGE2 in GCF indicates active phase of

have shown higher elastase activity. periodontal destruction.
34

Chapter Risk Assessment
LONG ESSAYS
Question 1 Risk Determinants (Background Characteristics)

What is risk assessment? Discuss in detail its various This term is used for those risk factors that cannot be
components. modified.
Genetic factors: Some periodontal diseases show familial
Answer

aggregation, e.g. localised and generalised aggressive
Risk is the probability that an individual will develop a periodontitis.
Age: Prevalence and severity of periodontal disease
specific disease in a given period. There are numerous

components which define risk assessment. increase with age.
Gender: Various studies have shown that males have
Various risk elements are:

more loss of attachment than females because of higher
Risk factors. levels of plaque and calculus.

Risk determinants. Socio-economic status: It has been seen that poor oral

Risk indicators. hygiene is related to lower socio-economic status.

Risk markers. Stress: Incidence of necrotising ulcerative gingivitis

increases during the period of stress. Studies have shown
Risk Factors that emotional stress interferes with normal immune
They are the factors which when present increase the function and result is increased circulating hormone
levels which have an effect on periodontium.
likelihood of development of a disease. They can be
environmental, behavioural or biologic. Risk Indicators
Exposure to risk factors can occur at a single point in time
They are referred as probable or putative risk factors that
over multiple, separate points in time, or continuously.
have been identified in cross-sectional studies but not
Various risk factors are: confirmed through longitudinal studies.
Tobacco smoking: There is a direct relationship between HIV/AIDS: It has been reported that there is an increased

smoking and development of periodontal disease. susceptibility in periodontal diseases in patients having
Smoking has a negative impact on response to therapy. HIV/AIDS.
Osteoporosis: It has been suggested that reduced bone
Smokers show greater attachment loss.

Diabetes: It is a well-established risk factor for mass in osteoporosis may aggravate the progression of

periodontitis. Prevalence of periodontitis is significantly periodontal disease.
Infrequent dental visits: Infrequent visits to the dentists
higher in patients with diabetes.

Pathogenic bacteria and microbial tooth deposits: It can increase the risk for periodontitis.

has been well proven that accumulation of microbial
plaque leads to periodontal diseases and if oral hygiene
Risk Markers/Predictor
measures are taken properly then this situation can be These do not cause the disease but still they are associated
reversed. with increased risk for disease.
144
Previous history of periodontal disease: It has been Medical History

seen that patients with most severe existing loss of
Diabetes.

attachment are at the greatest risk for future loss of

attachment. Tobacco smoking.

Bleeding on probing: It is the best clinical indicator of HIV/AIDS.

gingival inflammation. Absence of bleeding on probing Osteoporosis.

is an excellent indicator of periodontal health. Stress.

Question 2 Dental History
Enumerate the various clinical risk assessment for Family history of early tooth loss.
periodontal disease.

Genetic predisposition to aggressive disease.

Answer Previous history of periodontal disease..

Frequency of dental care.
Demographic Data

Age Clinical Examination

Duration of exposure to risk elements
Plaque accumulation.

Post-menopausal women

Microbial sampling for putative periodontal pathogens.

Evidence of aggressive disease

Male gender

Calculus.

Preventive practices Bleeding on probing.

Frequency of care Extent of loss of attachment.

Socio-economic status Plaque retentive areas in tooth.

Dental awareness Anatomic factors in tooth.

Frequency of care. Restorative factors in tooth.

35

Chapter Prognosis
LONG ESSAYS
Question 1 maintain areas, doubtful patient cooperation and

What is the definition of prognosis? What are various types presence of systemic/environmental factors.
of prognosis? Explain the factors that help in determining
Hopeless prognosis: The following factors suggest

overall prognosis of a patient. hopeless prognosis:
Advanced bone loss, non-maintainable areas,

Answer extraction indicated, presence of systemic or
According to Carranza “prognosis is defined as the prediction environmental factor.
of the probable course, duration and outcome of a disease
Questionable prognosis: The following factors suggest

based on the general knowledge of the pathogenesis of questionable prognosis:
Advanced bone loss, grades I and II furcation
the disease and the presence of risk factors for the disease

and the likelihood of its response to treatment.” Prognosis is involvements, tooth mobility, inaccessible areas and
divided as follows: presence of systemic/environmental factors.
Overall prognosis (concerned with entire dentition). Factors for determination of prognosis are as follows:

Individual tooth prognosis (determined after overall 1. Overall clinical factors.

prognosis and is affected by it). 2. Systemic/environmental factors.
There are various kinds of prognosis: 3. Local factors.
Excellent prognosis: In this type of prognosis, there is 4. Prosthetic restorative factor.

no bone loss, excellent gingival conditions, good patient 1. Overall clinical factors:
cooperation, no systemic/environmental factors. Patient age.

Good prognosis: Any one or more of the following Disease severity.

factors could determine good prognosis: Plaque control.

Adequate remaining bone support, possibilities Patient compliance and cooperation.

to control aetiological factors and establish a 2. Systemic/environmental factors:
maintainable dentition and adequate patient Patient habits like smoking.

cooperation with no systemic/environmental factors. Systemic disease/condition.

Fair prognosis: Any one or more of the following factors Genetic factors.

could suggest fair prognosis: Stress.

Less than adequate remaining bone support, some 3. Local factors.

teeth mobility, grade I furcation involvement, Plaque/calculus.

acceptable patient cooperation and existence of Sub-gingival restorations.

limited systemic/environmental factors. Anatomic variations/factors.

Poor prognosis: One or more of the following suggests h Short tapered roots with short curves.

h
poor prognosis. h Cervical enamel projections (CEP).
h
Moderate to advanced bone loss, tooth mobility, h Enamel pearls.

h
grades I and II furcation involvement, difficult to h Bifurcation ridges.
h
146
Root concavities.
h are favourable, chances of regeneration of bone after
h
Development groves.
h therapy to approximately the level of alveolar crust exist.
h
h Furcation involvement. When there is greater bone less on one tooth surface,

h
h Tooth mobility. the bone height on the less involved surfaces should be
h
4. Prosthetic/restorative factors: considered when determining prognosis.
Abutment selection.
Plaque Control

Caries.

Non-vital teeth. Active removal of plaque by the patient on a daily basis is

Root resorption. critical to the success and prognosis of periodontal therapy.

1. Overall Clinical Factors Patient Compliance and Cooperation
The prognosis of patients with gingival and periodontal
Patient Age

involvement is critically dependent on the patient’s
In two patients with comparable connective tissue attitude and desire to retain the natural teeth and

attachment and alveolar bone, prognosis is better in the willingness and ability to maintain good oral hygiene.
older of the two. If patients are unwilling to perform adequate plaque

When compared within the older patient, the reparative control, or follow justification and receive timely

process in a younger individual is more, the amount of periodic, maintenance check-ups, then the dentist can
bone loss in a span of few years is also more than the refuse to accept the patient for treatment or extract
bone formed. teeth that have a poor prognosis and perform routine
The younger patient would normally be expected to oral prophylaxis on remaining teeth.

have a greater reparative capacity, but the occurance of
destruction is so much in a relatively short period, would 2. Systemic and Environmental Factors
exceed any naturally occurring periodontal repair.
Genetics
Disease Severity Detection of genetic factors can influence the prognosis in
Patients with a history of previous periodontal disease several ways:

may be indicative of their susceptibility for future Early implementation of preventive and treatment

periodontal breakdown. measures for these patients.
During the course of treatment, it can influence treatment
Prognosis is affected by following factors:

recommendations.
Level of attachment.
Identification of young individuals at risk can lead to the

Pocket depth/endo-perio-relationship.

development of interventional strategies.

Height of remaining bone.

Types of defect. Patient Habits: (Smoking)

1. Level of attachment: It means base of the pocket. Level It is one of the most important environmental risk factors

of clinical attachment reveals the clinical extent of root putting an impact on the development and prognosis of
surface devoid of periodontal ligament. periodontal disease.
2. Pocket depth: A tooth with deep pockets and little Systemic effects of smoking are inhibition of

attachment loss has better prognosis compared with peripheral blood and oral neutrophil function, reduced
one with shallow pockets and more attachment loss. antibody production and alteration of peripheral
3. Height of remaining bone: Prognosis is poor in case of immunoregulatory T-cells.
teeth with severe bone loss where there is no sufficient Patients who smoke, respond very poorly to the

bone to support the tooth. periodontal therapy.
4. Type of defect (horizontal or angular): In case of Cessation of smoking can affect the treatment outcome

horizontal bone loss, the prognosis depends upon and also the prognosis.
the exciting bone because it is unlikely to regenerates
significant amount of bone. Systemic Disease and Condition
In case of angular or infrabony defects, if the contour Patients systemic background can affect overall

of the existing bone and the number of osseous walls prognosis in several ways for e.g. in diabetes mellitus,
147
Chapter 35 Prognosis
the prognosis is questionable when surgical treatment is hh

Commonly seen in maxillary third molars and
required. rarely on the permanent molars.

Diseases which affect the motor functions like Parkinson’s h They also lead to plaque accumulation causing
h
disease limit these oral hygiene performances adversely periodontitis.

affecting prognosis.
Bifurcation ridges
h These
h
bifurcation ridges interfere with the
Stress attachment apparatus and prevent regenerative
Stress can be physical or emotional and may alter the procedures from achieving their potential.
patient’s ability to respond to the periodontal treatment
Root concavities
performed. h Root concavities creates areas which are difficult to
h
maintain and cause plaque accumulation leading

3. Local Factors to inflammation.

Plaque/calculus.

Developmental grooves
h Palatogingival groove is a developmental groove
Sub-gingival restorations.
h

Anatomic variations/factors. seen most commonly on maxillary lateral incisors
and maxillary central incisors.

Plaque/calculus: Plaque and calculus are the factors h These grooves start from enamel and extend to
h
which cause periodontal disease. A good prognosis in some distance of the root, making it a plaque
most of cases depends on the ability of both patient and retentive area.
the clinician to remove these factors. h Attachment apparatus is absent in the region
h

Sub-gingival restorations: Supragingival margin of the of developmental grooves, therefore a zone is
restorations are always better than sub-gingival margins, created for bacterial entry and also periodontal
as sub-gingival margins may contribute to increased regenerative procedures are difficult to perform.
plaque retention, which further causes inflammation
Tooth mobility
and bone loss. h Pockets in a non-mobile tooth responds well as
h
Therefore supragingival margins have good prognosis compare to pocket in a mobile tooth.
than sub-gingival margins. h If the mobile teeth are splinted, they may have
h

Anatomic factors: a beneficial effect on the overall and individual
Short tapered roots with short crowns:

prognosis of the tooth.

h Prognosis is very poor in such cases because of
h
poor periodontal health as there is a very less 4. Prosthetic/Restorative Factors

available root surface.
CEPs (Cemento enamel projections):

Abutment selection.
h They are ectopic enamel projections extending
h

Caries.
beyond the normal cementoenamel junction

Non-vital teeth.
(CEJ).

Root resorption.
h Most commonly seen on the mandibular molars Abutment selection: If the bone levels and attachment
h

and rarely on maxillary premolars. levels of the tooth are adequate then the prognosis of
h Tooth having CEPs also have a poor prognosis as
h
that tooth is good.
they can be sources of plaque accumulation.
Caries, non-vital and root resorption: Carious, non-vital
Enamel pearls

and teeth with root resorption have poor prognosis.
h Enamel peals are round, large enamel deposits that
h
Therefore, these teeth should be treated before any
are present in the furcation areas. periodontal therapy.
36 Rationale for

Chapter
Periodontal Treatment
SHORT ESSAYS
Question 1 Bacteria and plaque hinders regeneration process

Explain healing after periodontal therapy. whereas their removal would be beneficial for
regeneration process.
Answer Repair: It restores the continuity of the diseased marginal

Healing processes are almost same for all the forms of gingiva and re-establishes a normal gingival sulcus at the
periodontal therapy, which consist of removal of diseased same level on the roots as the base of the pre-existing
tissue and replacement of destroyed tissue. periodontal pocket.
It can halt the disease process but will not form new
Various techniques to gain attachment and bone level are

as follows: bone or periodontal ligament.
Regeneration: It is the natural renewal of a structure, New attachment: It is the formation of new periodontal

produced by growth and differentiation of new cells and ligament into cementum and the attachment of gingival
intercellular substances to form new tissues. epithelium to a tooth surface previously denuded by
Regeneration is part of healing and it is a continuous diseases.

physiologic process. Reattachment: It means repair in areas not previously

It happens by growth from the same type of tissue. exposed to disease, e.g. surgical attachment of tissues.

37 Periodontal Treatment

Chapter
for Medically
Compromised Patients
LONG ESSAYS
Question 1 Newer pacemakers—bipolar, electrical.

Dental equipment should not interfere with the
What is the management of a patient with cardiovascular

functioning of cardiac pacemakers. For example, in cases
diseases?
of ultrasonic scalars.
Answer
Infective Endocarditis
Hypertension It is caused by Streptococcus viridans, Capnocytophaga, etc.
Epinephrine concentration with local anaesthesia (LA) American Heart Association Guidelines

t1 : 1,000,000 should be given.
If blood pressure (BP) extending more than180/110, then Antibiotic prophylaxis should be given for procedures
associated with bleeding from soft/hard tissues, periodontal

only emergency care should be given prior consultation
with physician. surgery, scaling and professional tooth cleaning.
Frequent change of position should be done to avoid
Indications for Prophylaxis

postural hypertension.
High-risk Patients:
Ischeamic Heart Diseases Previous history of endocarditis.

Prosthetic heart valves.
Angina pectoris—stress induced, nitroglycerine should

Congenital heart disease.

be administered as an emergency.

Myocardial infarction (MI) n frequent episodes of MI, Moderate-risk Patients:

dental treatment should be deferred for 6 months. Rheumatic heart disease.

Mitral valve prolapse .

Congestive Heart Failure Prophylaxis not recommended.

Mitral valve prolapses without valvular or regurgitation.
Uncontrolled disease not ideal for treatment.

Coronary artery bypass graft (CABG) surgery.

In case of orthopnoea (inability to breathe unless in

Cardiac pacemaker and implanted defibrillator.

upright position), chair position should be adjusted.

Patent ductus arteriosus (PDA)/ventricular septal defect
Short stress free visit should be made.

(VSD).

Profound anaesthesia should be given.
Standard regimens.

Cardiac Pacemakers and Cardioverter Oral
Defibrillators Amoxicillin 2 g 1 hour before procedure

Dental consultation should check the underlying cardiac Clindamycin/azithromycin/cephalexin 600 mg/500 mg/

status. 2 g 1 hour before V
Older pacemakers—unipolar/unshielded. Ampicillin 2 g IM/IV within 30 minutes before procedure.

150
Preventive Measures for Infective Endocarditis Good ora l hygiene, frequent recall, poor prognosis teeth

Careful history should be taken to be extracted.

Meticulous oral hygiene maintenance (gentle brushing Avoid nephrotoxic drugs/those metabolised by kidney,

and oral rinses) should be advocated so as to avoid e.g. tetracycline, aminoglycoside, etc.
bleeding and bacteraemia A dialysis patient should be screened for Hepatitis B and C.

Heparin anticoagulation given prior to dialysis, hence
Antibiotic prophylaxis to be alternated with other

antibiotic for periodontal therapy wait for periodontal treatment.
Renal transplant patients who are on
Reduce the number of visits and avoid developing

resistant bacteria plan multiple procedures immunosuppressive drugs have reduced resistance to
7–14 days interval should be there between two visits infection, hence teeth with septic focus/periodontally

Absorbable sutures should be used involved should be extracted.

Recall visits are very important. Question 4

Stroke What is the management of a patient having bleeding
disorder?
Post-stroke Management
Answer
No periodontal therapy should be given for 6 months

Short stress-free appointments should be kept with Firstly, history of bleeding should be recorded, past and

1:100,000 concentration of epinephrine with anaesthetic. present drug history and family history, etc. should be done.
Adjust oral anticoagulant doses with physician if any
Clinical Examination

procedure is to be performed involving bleeding,
Regular BP monitoring should be done. Jaundice, haemarthrosis, ecchymosis, petechiae, sponta-

neous gingival bleeding, gingival hyperplasia should be
Question 2
checked.
What are the steps in managing a patient with diabetes? Laboratory tests like BT, CT, tourniquet test, complete
Answer blood count (CBC), PT, PTT should be done.
Bleeding disorder can be coagulation disorder (heredity/
Steps in managing a patient with diabetes:
acquired), thrombocytopenic purpura (TCP).
If possible surgical treatment should be done at

glycosylated less that 10%. Heredity Defect
In office blood glucose evaluation should be performed.
Haemophilia A (factor 8)

Long procedures should be avoided.
Factor 8 levels = 30%, are desirable to prevent surgical

Long procedures demand checking for hypoglycaemia.
haemorrhage.

If symptoms of hypoglycaemia arise, then oral
(Desmopressin) increases levels 2–3 folds.

carbohydrate/IV (20–30 mL of 50% dextrose)/IM/IV 1 mg

Haemophilia B (factor 9) desirable levels 30–50%.
glucagon should be given immediately.

Factor 9 concentrates or purified prothrombin

Question 3 concentrates are given.
Von Willebrands disease (vWf factor).
What is the management of a patient with renal disease?

Factor 8 concentrates/cryoprecipitate, desmopressin.

Answer Probing, scaling may be undertaken but local anaesthesia

In a patient with renal disease following should be done: administration, surgery demands medical modification.
Physician consent. Complete wound closure is extremely important.

Blood pressure (BP). Pressure application, anti-haemostatic agent administra-

Laboratory values for partial thromboplastin time tion, anti-fibrinolytic (EACA/tranexamic acid).

(PTT), prothrombin time (PT), bleeding time (BT), CT,
haematocrit. Acquired Coagulation Defect
No treatment if blood urea is less than 60 mg/dL, serum Liver disease (chronic alcoholics, chronic hepatitis).

creatinine < 1.5 mg/dL. Vitamin K deficiency (anticoagulants—warfarin vitamin

Remove oral infection focus. K antagonist)

151
Chapter 37 Periodontal Treatment for Medically Compromised Patients

Look for:
Blood profile (BT, CT, PT, platelet count)
Physician consent.

Antibiotic cover should be given prior to treatment

Laboratory test—PT, BT, CBC, PTT.

hopeless teeth extract 10 days prior to chemotherapy
Prefer nonsurgical periodontal therapy.

Routine prophylaxis, oral rinses, topical haemostatics

If surgery warranted—platelet count should be minimum should be given
80,000/mm3, international normalised ration (INR) less
Oral candidiasis is very common therefore nystatin
than 2. suspension (100,000 units/mL) should be given
INR 2–3 anticoagulant therapy patients.

In cases of oral ulceration/mucositis, palliative viscous
INR 2.5–3.5 for prosthetic valves patients.

lidocaine should be given.
Infiltration, scaling and root planing INR less than 3.
Question 5

Extraction / minor surgery INR less than 2–2.5.

Complex surgery/multiple extraction INR less than

What is the management of a pregnant female?
1.5–2.
Answer

Severity of expected intra/post-postoperative.

Bleeding to be informed to physician while planning to Management of a pregnant female:
adjust INR. Conservative treatment should be given, i.e. basic oral

Aspirin more than 325 mg demands discontinue drug care protocol, scaling and root planing
7–10 days prior with physician consent. Second trimester is safe time

Avoid aspirin in patients with anticoagulant therapy/ Long stressful appointment should be avoided

bleeding disorder. Supine hypotensive syndrome is very common, which

can be corrected by changing the chair position

Thrombocytopenic Purpura Place patient on her left side with 5–6 degrees of

If platelet less than 100,000/mm —no treatment should be

3
elevation on right side, frequent position change should
done. be done
American dental association (ADA) specification for

Leukaemia drugs—cephalosporins, amoxicillin, clindamycin

Delayed healing, prone to infection, bleeding tendency, ADA guidelines for radiation exposure to be kept

chemotherapy effects minimum, if required proper shielding for mother.
38

Chapter The Treatment Plan
LONG ESSAYS
Question 1 Calculus removal and root planing.

What is treatment plan? What is the goal of treatment plan?
Correction of restorative and prosthetic irritational

What are the phases of periodontal therapy? factors.
Excavation of caries and restoration. It can be temporary

Answer or final, depending on whether definite prognosis for the
Blue print for case management is referred to as treatment tooth has been arrived at and on the location of caries.
plan. Anti-microbial therapy (local or systemic).

Goal of treatment plan is to eliminate gingival Occlusal therapy.

inflammation and correction of the condition that cause or Minor orthodontic movement.

perpetuate it. Provisional splinting and prosthesis.

The patient should be evaluated for the response after
Phases of Periodontal Therapy Are
aetiotropic phase for:
Emergency phase
Packed depth and gingival inflammation

Plaque, calculus and caries.

Etiotropic phase
Surgical Phase
Maintenance phase
This phase is also known as Phase II therapy. It includes
periodontal therapy, including placement of implant and
endodontic therapy.
Surgical phase Restorative phase
Restorative Phase
Emergency Phase/Preliminary Phase
This phase is also known a Phase III therapy. It includes final
Treatment of Emergencies restoration, fixed and removable prosthodontics.

Dental or periapical Evaluation should be done in response to restorative

Periodontal procedures by performing periodontal examination.

Other
Maintenance Phase

Hopeless teeth are extracted and provisional replacement
is given if needed. Maintenance phase (Phase IV therapy), it includes periodic
rechecking of:
Etiotropic Phase (also known as phase I therapy) Plaque and calculus.

Gingival condition (pockets, inflammation).

Plaque Control and Patient Education Occlusion, tooth mobility.

Diet control, especially in patients with rampant caries. Other pathologic changes.

39 Phase I

Chapter
Periodontal Therapy
LONG ESSAYS
Question 1 Treatment Sessions

What are the objectives, rationale and steps in Phase I Upon the analysis and diagnosis of the case, the clinician
periodontal therapy. determines the treatment plan for scaling and root planing
Answer portion of phase I therapy. However, many patients require
several treatment sessions for tooth surface debridement
It is the first step of the periodontal therapy. Phase I along with amount of calculus visualised, following
periodontal therapy is also known as initial therapy, conditions should also be considered in planning of Phase I
nonsurgical periodontal therapy, etiotropic phase of periodontal therapy:
therapy and cause relative therapy. General health and tolerance of patient towards treatment
The objectives of this therapy are to eliminate or alter the

Number of teeth present
microbial etiology and the contributing factors for gingival

Amount of sub-gingival calculus
and periodontal diseases.

Probing pocket depth and attachment loss

Furcation involvement
Rationale

Alignment of teeth

The rationale is complete removal of calculus, correction Margins of restorations

of defective restorations, treatment of carious lesion and Developmental anomalies

restoration and a comprehensive daily plaque control Physical barriers to access like limiting opening or gag

regime for reduction and elimination of etiologic and tendencies.
contributing factors.
The procedures in phase I therapy are required to solve Sequence of Procedures
the patients periodontal problems or may contribute in the
preparatory phase of the surgical therapy.
Step 1: Limited plaque control instructions

Step 2: Supragingival removal of calculus
Long term success of the periodontal treatment depends

Step 3: Recontouring defective restoration and crowns
upon the maintenance of the results achieved by Phase I

Step 4: Obturation of carious lesions
therapy.

Step 5: Comprehensive plaque control instructions
Control or elimination of local contributing factors

Step 6: Sub-gingival root treatment
includes the following therapies:

Step 7: Tissue re-evaluation.
Complete removal of calculus

Correction or replacement of poorly fitting restorations
Results

and prosthetic devices
Restoration of carious lesion It has been seen that comprehensive scaling and root

Treatment of food impaction areas planing causes reduction in bleeding on probing and

Treatment of occlusal trauma probing depth. Also, caries control and correction of poorly

Orthodontic tooth movement fitting restorations, only augment the positive results of

Extraction of hopeless teeth. healing gained by plaque control, scaling and root planing.

154
Healing Transient tooth hypersensitivity and recession of gingival

margins are seen with the process of healing.
About 4 weeks after the completion of phase I therapy, re-

Histologically, there is formation of long junctional
evaluation of the case should be done, as this time period epithelium rather than new connective tissue attachment
permits for epithelial and connective tissue healing and to the root surface. The attachment epithelium reappears
allows the patient to sufficiently practice the oral hygiene within 1–2 weeks.
instructions. With decrease in inflammation there is reduction in
Gingival inflammation is also reduced substantially inflammatory cell population and gingival crevicular fluid
within 3–4 weeks after removal of plaque and calculus. (GCF).
40

Chapter Plaque Control
LONG ESSAYS
Question 1 It delays plaque maturation and inhibits formation of

Define dental plaque and write in detail about antiplaque prostaglandins and leukotrienes
and anticalculus agents.
Metallic Ions
Or
Describe in detail about chemical plaque control. Zinc and copper salts are most commonly use

They act by reducing the glycolytic activity in
Answer

microorganisms and inhibit bacterial growth.
Dental plaque is defined clinically as a structured resilient
yellow greyish substance that adheres tenaciously to the Quaternary Ammonium Compounds
intraoral hard surfaces including removable and fixed These are antiseptics and surface active agents

restorations. They are more effective against Gram positive rather

It is primarily composed of bacteria in a matrix of salivary than Gram negative organisms
glycoproteins and extracellular polysaccharides. They are effective in reducing the development of plaque

as it contains mainly Gram-positive microorganisms
Antiplaque Agents They act by disrupting the cell wall structure of

Idealsrequisites of antiplaque agent are: microorganisms, e.g. benzethonium chloride,
They should be able to reduce plaque and gingivitis to a benzalkonium chloride and cetylpyridinium chloride.

significant leve
Sanguinarine
They should prevent growth of pathogenic bacteria
This is an alkaloid which is derived from a plant,

Should be biocompatible with the oral tissue

Sanguinaria canadensis

Should be inexpensive and easy to use
These inhibit mainly the Gram-negative organisms

Should have good retention

It has good retentive property when used as a mouth

Should not stain teeth or alter taste.
rinse.

Classification Antibiotics
First Generation Vancomycin, erythromycin, neomycin and kanamycin are
the commonly used antibiotics for plaque control.
Triclosan
It is a phenol derivative, non-ionic compound which is Enzymes

used as a topical antimicrobial agent Examples are mucinase, dextranase, lactoperoxidase and

It has a broad spectrum of action against both Gram- thiocyanate synthase enzymes have shown bacterocidal

positive and Gram-negative bacteria activity when applied topically in the mouth.
It acts on the microbial cytoplasmic membrane and uses They are able to break down already formed matrix of

bacteriolysis plaque and calculus.
156
Second Generation Loss of taste sensation specially bitter and salt sensation

Some individuals have reported hypersensitivity to
Bisbiguanides

chlorhexidine
Example: 0.2% chlorhexidine gluconate The dead bacteria due to use of chlorhexidine may act as

It is a cationic bisbiguanide which has a very broad the initiator for supragingival, calculus formation

spectrum of action against a wide area of organisms Can cause oral mucosal erosions when used in high

including gram positive, Gram-negative, fungi, yeast, concentrations.
and viruses
It shows both antiplaque and anti-bacterial action. Third Generation

Delmopinol
Antiplaque Action
It inhibits plaque growth and reduces gingivitis
Chlorhexidine: It shows antiplaque activity, because of

It targets dextran producing streptococci by blocking
the property of sustained availability that is chlorhexidine

synthesis
is slowly released form all oral surfaces resulting in
It reduces bacterial adherence by causing weak binding
bacteriostatic activity in oral cavity.

of the plaque to the tooth surface, thus aiding in easy
Chlorhexidine inhibits plaque by the following mechanisms: removal by mechanical procedures
Prevention of pellicle formation: It blocks acidic groups It is used as a pre-brushing mouth rinse

on salivary glycoprotein thus reducing glycoprotein It can cause transient staining of tongue and teeth

adsorption on tooth surface

Taste alteration and mucosal erosions have also been
It binds to the bacteria thus preventing the adsorption of reported.

bacterial cell wall on tooth surface
Anticalculus Agents
It displaces calcium from the plaque matrix thus

preventing binding of mature plaque Dentifrices containing soluble pyrophosphatase and zinc
Note: Chlorhexidine prevents the formation of new compounds demonstrate anticalculus effect by absorbing

plaque but has little effect on pre-existing plaque. into small hydroxyapatite crystals, thus preventing or
inhibiting growth of larger and organised crystals of
Antibacterial Action calculus.
Exhibits a wide spectrum of activity against gram positive,
Dentifrices

Gram-negative bacteria, fungi, yeast and viruses.
According to American Dental Association (ADA), a
Chlorhexidine is bacteriostatic in low concentrations and
dentifrice is a substance used with a toothbrush for the

bacterocidal in high concentrations
purpose of cleanin, accessible surfaces of the tooth.
After a single mouth rinse with chlorhexidine,

saliva exhibits bacterocidal activity for 5shours and Composition of the Dentifrice
bacteriostatic activity for more than 12 hours. Polishing/abrasive agents: Calcium carbonate, dicalcium
Regular use of chlorhexidine can reduce the aerobic

phosphate dihydrate, alumina, silica—15 to 45%

andcanaerobic bacterial populations in saliva by 80–90%. They clean the teeth mechanically, remove pellicle form

the tooth surface and abrasive action aids in eliminating
Indications
plaque
In moderate to severe inflammation, as an adjunct to Binding/thickening agents (2%): They contain water

mechanical oral hygiene soluble agents (alginates, sodium carboxy methyl
Post-periodontal therapy or oral surgical procedures cellulose) and water insoluble agents (magnesium

Inyphysically, mentally and medically challenged aluminium silicate, colloidal silica, sodium magnesium

individuals silicate)
Patients undergoing fixed or removable orthodontic These agents bind the solids to form homogenous paste

treatment and help in dispersion of dentifrice in mouth.
In patients who have undergone intermaxillary fixation. Detergents/surfactants (1–5%): Sodium lauryl sulphate

and sodium dodecyl sulphate. These agents produce
Adverse Effects of Chlorhexidine foam, which aids in the removal of food debris. These
Reversible brownish staining of teeth or restorations also have antimicrobial property.

157
Chapter 40 Plaque Control

Humectants (25–40%): Sorbitol, glycerine, polyethylene
Medium: 0.010–0.012 inches (no. 10, 11, 12)
glycol. These help in maintaining the consistency of the
Hard: 0.013–0.014 inches (no. 13, 14)

paste and also prevent loss of moisture from paste. Extra hard: 0.015 inches (no. 15).

Flavouring agents (1%): Peppermint oil, spearmint oil,
Handle design
Oil of Wintergreen. Straight

Sweeteners and colouring agents (2%): Saccharin. Angulation in the shank

Water (20–30%): Acts as vehicle and solvent medium. Indentation of handle for a better grip.

Preservatives (0.5%): Benzoic acid.

Therapeutic agents (2%):Tetrasodium, pyrophosphatase, Interdental Cleaning Aids
zinc chloride. These are used for the removal of plaque in interdental
areas. The type of embrasure determines the selection of
Functions of Tooth Pastes interdental aids:

Removal of food debris, stains and plaque Type 1: Interdental papilla fills the embrasure. Dental

Anticaries action floss is advised.

Mouthrfreshener Type 2: Mild-moderate papillary recession is observed.

Some tooth pastes are also used for treating sensitivity. Miniature interdental brush and wooden tips are advised.
Type 3: Complete loss of papilla and interdental gingiva
Question 2

is tightly bound to bone. Untufted brushes are advised.

Describe the various methods of plaque control or describe
oral hygiene aids for plaque control. Dental Floss
Answer It is most common method for interdental plaque control.
Plaque control is the regular removal of dental plaque These are of four types:
and the prevention of its accumulation on the teeth and 1. Twisted or non-twisted
adjacent gingival surfaces. 2. Bonded or non-bonded
Plaque control can be broadly classified into mechanical— 3. Thick or thin
individual and professional, and chemical—individual and 4. Waxed or unwaxed.
professional.
Interdental Brushes
Mechanical Plaque Control Cone shaped or lcylindrical shaped brushes mounted on a
Individual Methods handle.

Toothbrush (manual or powered) Two types:

Interdental aids- Floss, toothpicks, brushes 1. Single tufted brushe

Miscellaneous– Rubber tip stimulator or water irrigator. 2. Small conical brushes.
These are used in furcation areas, isolated gingival
Toothbrushes recession area and on lingual surface of molars and
premolars.
ADA Specifications

Head–11¼ inches long Wooden Tips

24 rows of bristles Two types:
5/16–3/8 inches wide
1. With handle, e.g. perio-aid

5–12 tufts per row

2. Without handle, e.g. Stim U.

80–86 bristles per tuft.
Design–consist of handle, shank and head
Chemical Plaque Control (Refer Answer 1)

Available sizes: Large medium and small.

Bristle Chemicals used of supragingival plaque control (Addy’s
Nylon (synthetic): Preferred

Classification)
Hog (natural): Susceptible to breakage and fraying.

A. Antibiotics:

Hardness Penicillin
Soft: 0.007–0.009 inches (no. 7, 8, 9)

Vancomycin
158
Kanamycin Technique— the brush should be placed with bristles partly

Erythromycin resting on cervical region of teeth and partly on gingiva.

Spiramycin Bristles are pointed in apical direction with an oblique

Metronidazole angle to the tooth long axis.
Brush is moved in short back and forth motions and
B. Enzymes:

Mucinase simultaneously moving into coronal direction
Pressure is applied on the gingival margin to produce
Protease

Lipase mild blanching
The procedure is repeated on all the teeth
Amylase

Brush is held in the vertical direction in order to reach the
Elastase

Lactoperoxidase lingual surfaces of maxillary and mandibular anteriors.
Hypothiocynase
Mutanase
Question 4
Describe modified bass technique.
C. Quaternary ammonium compounds:
Cetylpyridinium chloride Answer
Benzethonium chloride
Benzalkonium chloride Bass Method
Domiphen bromide The head of the brush is placed parallel to occlusal plane
D. Bisbiguanide: covering 34 teeth beginning at the posterior region.
Chlorhexidine Bristles are placed at an angulation of 45 degree to the

Alexidine long axis of the tooth along the gingival margin
Octenidine/bispyridine Gentle short back and forth movements are used without

E. Metallic salts: dislodging the tip of the bristles
The pressure should be firm enough to blanch the
Copper

Tin gingiva
Several strokes should be completed in the same position
Zinc

Move the brush to the adjacent teeth and the process is
F. Herbal extracts:

repeated
Sanguinarine After completing the maxillary arch, move mandibular

G. Fluorides arches
Strontium fluorid In the lingual side of anteriors, the brush is held vertically.

H. Oxygenating agents:
Hydrogen peroxid Modified Bass
I. Phenolic compounds: It combines vibratory and circular motion of bass

Thymol technique and the sweeping motion of roll technique
Menthol Toothbrush is held to 45degrees to the gingival margin

Eucalyptol Brush is moved in back and forth motion while the

J. Othersantiseptics: bristles are gently vibrated
Iodine In a single motion the brush is moved from side of the

Povidone Iodine teeth to occlusal surface
Sodium hypochlorite This method causes excellent sulcus cleaning and good

Hexetidine gingival stimulation.
Triclosan.
Question 5
Question 3 What are disclosing agents?
Describe modified Stillman technique.
Answer
Answer These are commercially available solutions, wafers, tablets,
Modified bass technique is a kind of brushing technique lozenges which are capable of staining only bacterial
which is advocated very frequently. deposits on the surface of teeth, tongue and gingiva.
159
Chapter 40 Plaque Control
Examples
Antibiotics can also be combined through this chip
It is area specific.
Skinners iodine solution


Diluted tincture of iodine Question 7

Mercurochrome solution 5% Describe Proxabrush.

Bismarck brown

Erythrosine Answer

Fast green These are small interdental brushes which are indicated in

Two tone solutions: FD and C Green number 3; FD and type two embrasures.
C Red number 3. These are used as they provide effective cleaning of
This stains mature plaque in blue colour and immature

concave root depressions exposed due to interproximal

plaque in red or pink colour.
gingival recession.

Basic Fuchsine.
Question 8
Question 6
Desensitising agents.
What is PerioChip/chlorhexidine chip?
Answer
Answer
They are used to control tooth/root hypersensitivity.
It is method of local drug delivery. It is a commercially
These act by reducing the diameter of dentinal tubules
available local drug delivery system.
This contains chlorhexidine in a biodegradable device thus, limiting the displacement of fluid in them.
Advantage Examples

High concentrations can be achieved in an area with Cavity varnishes, dentin bonding agents, silver nitrate,
small drug dose restorative resins, zinc chloride, potassium ferrocyanide,

Systemic side effects of chlorhexidine are reduced calcium hydroxide, sodium fluoride, stannous fluoride, etc.
41 Scaling and

Chapter
Root Planing
LONG ESSAYS
Question 1 dental tapes. They can be available in the form of air-

What is the classification of periodontal instruments? powder abrasive system for tooth polishing.
Discuss periodontal probes in detail.
Periodontal Probes
Answer Periodontal probes are used to mark, measure and locate
Classification of periodontal instruments is as follows: pocket and determine their configuration.
Probe is a tapered, rod-like instrument which is calibrated
Diagnostic instruments: Includes mouth mirror, probe,

in millimetres, with a blunt, rounded tip.

explorer and tweezers.
They are generally thin, shank angled to allow easy
Periodontal probes: Used to locate, measure and

insertion into the pocket.

mark pockets.
During measuring the pocket, probe should be held with
Explorers: To locate calculus and caries.

a gentle firm pressure to the bottom of the pocket.

Scaling, root planing and curettage instruments: Used
The shank should be held parallel to the long axis of the

for removal of plaque and calcified deposits from the

tooth.
crown and root of a tooth, removal of altered cementum
from the subgingival root surface and debridement of Characteristics of an Ideal Probe
the soft tissue lining the pocket.
According to National Institute of Dental and Craniofacial
Scaling and curettage instruments can be classified as
Research (NIDCR), an ideal probe should have the following
follows:
criteria:
Sickle scaler: They are heavy instrument which are
Precision of 0.1 mm

used for the removal of supragingival calculus.

Range of 10 mm
Curettes: They are fine instruments used for

Constant and standardised probing force

subgingival scaling, root planing and removal of soft

Non-invasive
tissue lining the pocket.

Light weight and easy to use
Hoe-chisel file scaler: They are the subgingival scalers

Easy to access any location around all teeth

used for removal of tenacious subgingival calculus

Proper angulation through a guidance system
and altered cementum. Curettes are used more

Complete sterilisation of all portions entering the mouth
commonly than these scalers.

Material should not be biohazardous
Ultrasonic and sonic instruments: They are used

No electric shock produced from the material

for scaling and cleaning teeth and curetting the soft

Direct electronic reading and digital output.
tissue wall of the periodontal pocket.

Periodontal endoscope: It is used to visualise deeply Classification of Probes

into the subgingival pockets and furcations, which allow
to detect deposits. Probes can be classified into five generations:
Cleansing and polishing instrument: It is used to clean 1. First generation probes: Conventional manual (hand-

and polish tooth surfaces, e.g. rubber cups, brushes and held probes). For Example- Williams probe.
161
Chapter 41 Scaling and Root Planing
2. Second generation probes: Pressure sensitive probes,

Measures gingival recessions
e.g. true pressure sensitive probes.
Used to measure attached gingiva

30 g of probing pressure is sufficient to determine the

Determines the mucogingival relationship
probing pocket depth.
Used to check bleeding on probing
50 g of probing pressure is required to detect alveolar

Used for bone sounding or transgingival probing
bone defects.
Measures the thickness of gingiva
These probes lack tactile sensitivity
Can identify tooth irregularities, tissue characteristics,
3. Third generation probes: Computerised probes, e.g. calculus, etc.
Florida probe, Foster Miller probe and Toronto automated
probes. Question 2
Drawbacks of automated probes: Describe sickle scaler in detail.
Tactile sensitivity is less
Answer

Patient discomfort is more

Expensive.
They are the supragingival scalers which have a blade,
4. Fourth generation probes: They are still under deve- handle and connecting shank (Fig. 41.1).
lopment. They have a flat surface with two cutting edges which

These probes, attempt to extend linear probing in a

converges of a sharp pointed tip.
serial manner to take account of the continuous and They have two lateral surfaces and one face of the blade.

three dimensional topography of the pocket being Lateral surface and face of the blade join together to

examined. form cutting edge (Fig. 41.2).

5. Fifth generation probe: Without penetrating, they aim It is mainly used to remove the supragingival calculus.

at identification of attachment level. Since its design is large, thus it becomes very difficult to

They are non-invasive

place this instrument subgingivally, without lacerating
E.g. ultrasound probes.

the gingiva.
Small, curved sickle scaler blades such as 204SD can
Various kinds of periodontal probes are as follows:

be inserted under ledges of calculus a few millimetres

1. World Health Organisation (WHO) probe, which has a 0.5 below the gingiva.
mm ball at the tip and millimetres markings at 3.5, 8.5
and 11.5 mm and colour coding from 3.5 mm to 5.5 mm.
2. University of Michigan “O” probe, with William marking at
(1, 2, 3, 5, 7, 8, 9 and 10 mm) and marking absent form 4
and 6.
3. UNC-15 probe: It is a 15 mm long probe with millimetre Fig. 41.1: Parts of a sickle scaler.
marking at each millimetre and colour coding at the fifth,
tenth and fifteenth millimetres.
4. Marquis colour coded probe: In this probe, the
calibrations are in 3 mm section.
5. Nabers probes: They are used to detect furcation areas.
They are colour coded at 3, 6, 9 and 12 mm marking.
6. Florida probes: It is a force sensitive probe.
7. Foster Miller probe: This probe detects CEJ automatically.
It regarded as a highly accurate reading probe. It has a SD
of 0.17 mm and a subject threshold of 0.51 mm.
8. Toronto automated probe: It measures clinical
attachment levels using occluso incisal surface.
9. Interprobe: It has an optical encode transduction
element.
Uses of a probe are as follows:

Most, measure and locate the depth of gingival sulcus
and pockets. Fig. 41.2: Cross section of a blade of a sickle scaler .
162
These scalers are used with a pull stroke. It has sharp cutting edges that converge at a rounded

Sickle scalers come with different blade size and shanks, toe.

but having the same basic pattern. In the cross-section of the blade, it appears semicircular

For example U15/30, Ball, and Indiana University sickle with a convex base.

scalers are large in size, whereas jaquette sickle scalers 1, The lateral border of the convex base forms cutting

2, and 3 have medium blade. edges on both sides of the blades.
Curved 204 sickle scalers are available with large, medium It is both single and double ended

or small blade. Curette can be of two types:

Nevi 2 posterior scaler is thin enough so that it can be 1. Universal cutters

inserted several millimetres subgingivally to remove 2. Gracey curettes
ledges of calculus moderately.
Sickle scalers can have straight shanks used to scale Universal Curettes

anterior teeth and premolars. As the name suggests, these can be used on any area and

Sickle scalers can also have contra angled shank so that it surfaces of the teeth, i.e. one curette for all areas.

can be adapted to posterior teeth. It does have an offset blade that mean that the face of

the blade in at 90° angle to the shank.
Question 3 It is curved in one plane, i.e. curved up and not to the

What are the differences between Gracey curette and side.
universal curette?
It can be double ended or pair of single ended instruments
They are difficult to use in furcation areas.
Answer

Examples of universal curettes are Columbia curette No.

Gracey Curette Universal Curette 13, 14 2R–2L, 4R–4L and Barnhart curette No. 1-2 and 5-6.
• There are area specific curettes • They can be used on all areas
that are used at specific areas. and surface. Gracey Curettes
• Only one cutting edge in used, • Both cutting edges can be They are referred as area-specific curettes since they are

work with outer edge only. used, works with either outer
used on specific areas and surfaces.
or inner edge.
• It is curved in two planes, blade, • Curved in one plane, blade They were designed by Dr Clayton H Gracey in the year

curves up and to the side. curves up and not to the side. 1930 at the University of Michigan.
• They have an offset blade, i.e. • Blade is not offset, i.e. face of They are special types of curettes that are designed to

the face of the blade is bevelled the blade is bevelled at 90° to permit greater accessibility and adaptability.
at 60 degrees to the shank. the shank.
Gracey curettes are as follows:

Gracey No. 1-2 and 3-4 for anterior teeth.
Question 4

Gracey 5-6 for anterior and premolar.

What are the differences between a scaler and a curette? Gracey 7-8 posterior teeth-facial and lingual surface.

Gracey 9-10 posterior teeth facial and lingual surfaces.
Answer

Gracey No. 11-12 posterior teeth mesial surfaces.

Scaler Curette Gracey 13-14 posterior teeth distal surfaces.

• Scalers are used for • Curettes are used for
supragingival scaling. subgingival scaling. Recent Additions
• They have a pointed tip. • They have a curved toe.
• They are heavy instruments. • They are light instruments. Gracey no. 15-16 (modification of Gracey no. 11-12)

• They cannot be used for • They are used for curettage Gracey no. 17-18 (modifications of Gracey no. 13-14)

curettage procedure. procedure. Gracey curettes can be obtained as a single ended, as

a set of 14 instruments.
Question 5 They have an offset blade i.e. the face of blade is at 60–

What is a curette? Explain in detail? 70° to the lower shank.
This angulation allows the blade to be inserted in the

Answer precise areas for subgingival scaling and root planing.
A curette is a periodontal instrument used for curettage, Recent additions of Gracey curette are 15-16 and 17-18

subgingival scaling and root planing and removal of altered 15-16 is a modification of standard 11 and 12 and is

cementum. designated for the mesial surface of the posterior teeth.
163

It has a Gracey number 11-12 combined with shank of
They are made up of aluminium in the shape of a wedge
13-14. New shank of 15-16 allows better adaptation to protruding from a shaft.

posterior mesial surfaces from a front position with intra-
One side of the wedge is diamond coated whereas the
oral rest. other is side is smooth.

17-18 is a modification of 13-14. It has a terminal
There is a special dental handpiece over which files can
elongated shank of 3 mm and an accentuated angled be mounted that generates reciprocating strokes of
shank. variable frequency.

It has better access to all posterior distal surfaces.
The oscillating file swiftly planes the contour of the
restoration and gives a desired shape when the unit is
Modifications of Gracey Curette activated interproximally with the diamond coated side
of the file touching the restoration and the smooth side
Extended shank curettes
adjacent to the papile.

Hu-Friedy after five curettes are modification of

standard Gracey curette design which have an Question 7

extended shank.
What are HOE scalers?
The terminal shank is about 3 mm longer which allows

extension into the deeper periodontal pockets of 5 Answer

mm or above. They are the subgingival scalers which are used for scaling

Miniblade curettes of ledges or rings of calculus.
Hu-Friedy mini five curettes are modifications of after
The blade is bent at an angle of 99°.

five curette The cutting edge is formed by the junction of the

The size of their blades are half the length of the after
flattened terminal surface with the inner aspect of the

five or standard Gracey curette blade.

Mini fives are available in all standard Gracey numbers
The cutting edge is bevelled at 45°.

except for the number 9-10. Back of the blade is rounded.

Larger and mini larger curettes Blade is reduced to minimal thickness to permit access to

It is a set of three curettes.

the root without interference from the adjacent tissues.

It combines the shank design of the standard Gracey

The blade maintains contact at two points on a convex

5-6, 11-12 and 13-14 with a universal blade of 90°. surface.

These curette can be adapted to both the mesial
HOE scalers can be used in the following manner.

and distal sides of the tooth without changing the The blade is inserted to the base of the periodontal

instruments. pocket so that it can make a two point contact with

American Gracey Curvettes the tooth, which stabilizes the instrument.
Set of 4 Mini bladed curettes
A firm pull stroke is used to activate the instrument.

The length of the blade is 50% of that of the

conventional curettes and the blade is slightly curved Question 8

upward. What are general principles of periodontal instruments?
Sub-0 and number 1-2 are for anterior and premolar

Describe in detail.
11-12 for posterior mesial surfaces

13-14 for posterior or distal surfaces.

Answer
Question 6 General principles of instruments are as follows:
What is EVA system?
Accessibility: Proper positioning of patient in the dental
chair.
Answer
Visibility, illumination and retraction.
It is a prophylaxis instrument used for correcting over
Maintaining of clean field.
hanging and over contoured proximal alloy and resin
Sharpening of instrument.
restoration.
Instrument stabilization: grasp and finger rest.
It is the most efficient and least traumatic instrument

Instrument activation.
Diamond files which are motor driven come in symmetric

Controlled strokes for scaling and removal of calculus
pairs. without injury to the tissues.
164
Accessibility (Positioning of Patients and Operator) Properly positioned light and the mirror will result in

shiny surface of the teeth.
Accessibility helps in thoroughness of instrumentation.

The position of the patient and operator should provide Retraction

maximal accessibility to the area of operation. It would provide visibility, accessibility and illumination.
Decreased accessibility impedes thorough

Following method are effective for retraction.

instrumentation, prematurely tires the operator and

Use of mirror to reflect the cheek while the fingers of
lowers their effectiveness.

the non-operating hand retract the lips and protect
Position of Operator the angle of the mouth from irritation by the mirror
handle.
The back should be straight, head should be erect and Use of minor alone to retract the lip and cheek.

shoulders should be relaxed.

Use of fingers of the non-operating hand to retract
Distance from the patients mouth to the eyes of the

the lips.

clinician should be 14–16 inches Use of the mirror to retract the tongue.
Forearm and thighs parallel to the floor and hip angle

Combination of above.

should be 90°

Weight should be evenly balanced.
Maintaining a Clean Field

Height of the seat should be positioned low enough so

that the heels of feet touch the floor A clean field can be maintained by:
When working from 9 to 12 position of the clock, feet Adequate suction

should be spread apart so that the legs and the chair By removing all obstacles in the operating area.

base form tripod which creates a stable position.
Sharpening of Instruments
Patient Position
All instruments should be inspected to make sure that
Patient should be in a supine position and placed in such

they are clean, sterile and in good condition.

a way that the mouth is close to the resting elbow of the The working ends of pointed instruments should be
clinician

sharp enough to be effective.
The back of the chair should be nearby to the floor for

maxillary area and the back of chair should be slightly Advantages of sharp instruments are as follows:
raised for mandible.
Calculus removal is easy
Patients head should be even with the upper edge of the

Patient comfort and improved strokes

head rest.

Clinician’s fatigue reduces because of reduced number of
For mandible the position should be chin down and for

strokes.

maxilla, the position should be chin up
The head rest should be raised or lowered so that the
Instrument Stabilization

patients neck and head are aligned with the torso.
Stability of the instruments and the hand are the primarily

Visibility, Illumination and Retraction
requisites for controlled instrumentation, stability and
Direct vision with direct illumination from the dental control is essential for effective instrumentation and to

light should be present. avoid injury to the patient or clinician.
If this is not possible then indirect vision may be obtained The two factors that provide instrument stability are:

by using a mouth mirror to reflect light where it is needed. 1. Instrumental grasp.
Indirect vision and indirect illumination are often used 2. Finger rest.

simultaneously.
Instrument Grasp
Transillumination A proper grasp is important for precise control of

During transilluminating a tooth, the mirror is used to movements made during periodontal instrumentation:

reflect light through the tooth surface. There are three types of grasps:

The transilluminated tooth almost will appear shiny. 1. Standard pen grasp

It is effective only with anterior teeth as they are thin 2. Modified pen grasp

enough to allow the light to pass through them. 3. Palm and thumb grasp.
165

Standard pen grasp is the grasp in which we hold the
Allows forceful stroke pressure with least amount of
instruments in the same manner as we hold a pen. stress to the hand and finger.

Modified pen grasp is the most effective and stable grasp
Injury to the patient is reduced.
for all periodontal instruments.

This grasp allows precise control of the working end, Extraoral Finger Rests
permits a wide range of movements and facilitates good These are important for effective instrumentation

tactile sensation. specially for maxillary teeth.

Palm and thumb grasp is useful for stabilising instruments 1. Knuckle rest technique or palm up technique.
during sharpening and for manipulating air and water The clinician rests the knuckle against the chin or

syringe. cheek of the patient.

2. Palm down technique.
Finger Rest The clinician rests the palm against the cheek of the

Finger rest helps in stabilising the hand and the patient.
instrument by providing a firm fulcrum, as movements
are made to activate the instruments. Advantage

A good finger rest prevents injury and laceration of the Facilitate instrumentation of the proximal root surfaces of
gingiva and surrounding tissues. maxillary molars

The ring finger is used as finger rest.

Minimal control is achieved when the middle finger Disadvantage
is kept between the instrument shank and the fourth
Least effective of all fulcrum techniques
finger.
Stroke control is more difficult and decreases tactile

The built up fulcrum is an integral part of the wrist information.
forearm action that activates the powerful working Instrument activation

stroke for calculus removal. h Adaptation

h

Finger rest can be classified as intraoral and extraoral h Angulation
h
fulcrum.
Lateral pressure
Strokes
Types of finger rest are as follows:

Intraoral Adaptation
Conventional
It is the manner in which the working end of a periodontal

Cross arch
instrument is placed against the surface of a tooth

Opposite arch
Working end of the instrument should conform to the

Finger on finger

contour of the tooth surface

Extra oral
Precise adaptation must be maintained all instruments

Palm up

to avoid trauma to the soft tissues and root surfaces and

Palm down
to ensure maximum effectiveness of instrumentation.

Intraoral
Instrument which are bladed-like curette and sharp
Conventional finger rest: When finger rest is kept on the

pointed instruments like explorers are more difficult to
tooth next to the tooth being involved. adapt.
Cross arch: When finger rest is kept on the arch next the
Angulation

arch involved.
Opposite arch: Finger rest kept on opposite arch.

It means the angle between the face of a bladed
Finger on finger.

instrument and the tooth surface.
Advantages of intraoral finger rest are as follows:
To insert beneath the gingival margin, the face to tooth
It is very stable and secured support for the hand.

surface angulation should be at an angle between 0° and
It provides leverage and power of instrumentation.
40°.
Excellent tactile sensitivity.

For removal of calculus, angulation should be between
Precise stroke control.

45° and 90°.
166
The exact blade angulation depends on the amount Scaling stroke is a short powerful pull stroke which is

and nature of calculus, the procedure being per- mainly used with bladed instrument for removal of

formed and condition of tissue during scaling or root subgingival and subgingival calculus.
planing. Root planing stroke: It is a moderate to light pull stroke

Angulation should be greater than 90° for curettage. which is used for final smoothening and planing of the

root surface.
Lateral Pressure
It is the pressure created when force is applied against Question 9

the surface of a tooth with the cutting edge of a bladed What are the principles of sharpening?
instrument.
Exact amount of pressure depends upon the procedure
Answer

performed. Following are the principles of sharpening:
It can be firm, moderate or light.
Choose a stone suitable for the instrument to be

If insufficient lateral pressure is applied, rough ledges

sharpened.

or lumps may be shaved to thin, smooth sheets of
burnished calculus.
It the instrument to be sharpened that will be sterilised

Careful application of controlled and varied amounts before it is used on a patient, then use a sterilised

of lateral pressure during instrumentation is an sharpening stone.
important part of effective scaling and root planing

A proper angle between the sharpening stone and the
techniques. surface of the instrument should be established.
A stable, firm grasp of both instrument and the

Strokes sharpening stone should be maintained.
There are mainly three types of strokes, i.e. exploratory Excessive pressure should be avoided.

stroke, scaling stroke and root planing stroke. Avoid the formation of a wire-edge, characterised by

These strokes can be activated either by a pull or a push minute filamentous projections of metal extending as a

motion in a vertical, oblique or horizontal direction. roughened ledge from the sharpened cutting edge.
Exploratory stroke is a light, feeling stroke. During sharpening lubrication of stone in important.

It is mainly used with probe and explorers. If the instruments looks dull, then sharpen the instrument.

42 Chemotherapeutic

Chapter
Agents
LONG ESSAYS
Question 1 It inhibits growth of motile rods and spirochetes and the

What are chemotherapeutic agents? Explain in detail. effect persist up to 3 months after therapy
Minocycline has less phototoxicity and renal toxicity as

Answer compared to tetracycline however may cause vertigo
They can be widely classified into systemic and local drug which is reversible.
delivery system.
Dosage
Systemic Drug Delivery 200 mg per day for 1 week

It can also be given for a period of 2 months for complete

elimination of spirochetes.
Tetracycline
Used in treating refractory periodontitis including Doxycycline

localised aggressive periodontitis Effect is similar to minocycline

Tetracycline’s can concentrate in periodontal tissues and Given only OD therefore has better patient compliance

inhibit growth of Actinobacillus actinomycetemcomitans 100 mg OD. In patients with gastric irritation the doses

These also have anti-collagenase effect that inhibits can be altered to 50 mg BD.

tissue destruction. These also help in bone regeneration
These are derived naturally from certain species of Metronidazole

Streptomyces or manufactured semi-synthetically It has a bactericidal action on anaerobic organisms,

These have bacteriostatic action and inhibit the growth however it is not the drug of choice against aa infection

of rapidly multiplying bacteria It can be used against aa in combination of other

These are more effective against gram-positive bacteria antibiotics

as compared to gram-negative bacteria It is also effective against anaerobic microorganisms such

Studied have shown that long-term regimens as Porphyromonas gingivalis and Prevotella intermedia

of tetracycline are not advisable because of the It is used to treat gingivitis acute necrotising ulcerative

development of resistant bacterial species. In such cases gingivitis, chronic periodontitis and aggressive
amoxicillin with metronidazole have been found to be periodontitis.
more effective.
Doses
Tetracycline 250 mg three times daily for 7 days

It is usually prescribed four times a day (qid) 250 mg. Metronidazole if consumed with alcohol can cause

severe cramps, nausea and vomiting, therefore products
Minocycline containing alcohol should not be consumed till 1 day
Effective against broad spectrum microorganisms after the therapy

168
Patients undergoing anticoagulant therapy should not It contains tetracycline in the concentration of 12.7 mg

be given metronidazole as it prolongs prothrombin time. per nine inches

When applied in periodontal pocket, it gives
Penicillin

concentrations of tetracycline greater than 1300 ug/mL
These act by inhibiting bacterial cell wall formation and for a period of 10 days.

thus bactericidal in nature. Sub-gingival doxycycline, e.g. Atridox®—it is supplied as 10%
Only amoxicillin and Augmentin have been shown to be doxycycline in a gel form in a syringe

effective in periodontal therapy Studies have shown that Atridox® alone was more

Dose of amoxicillin 500 mg for 8 days. effective than other treatment protocols in all time

periods
Azithromycin Sub-gingival minocycline, e.g. Ariston—it is supplied in 2%
Effective against anaerobic and gram negative bacteria concentration encapsulated in biodegradable microspheres

Dose: Initial loading dose of 500 mg followed by 250 mg in a gel carrier

daily for 5 days. These microspheres are placed sub-gingival as an

adjunct to scaling and root planing
Local Drug Delivery Systems Studies have shown that there was an increase in clinical

These are used to treat those periodontal diseases which attachment levels in patients with pockets of 6 mm or
require high concentration of antibiotics in a confined area. greater than 6 mm.
Tetracycline containing fibres, e.g. actisite—it is a non- Sub-gingival metronidazole, e.g.—Elyzol

biodegradable ethylene/vinyl acetate copolymer fibre PerioChip®: Chlorhexidine gluconate—(refer chapter on
(diameter of 0.5 mm) Plaque Control).
43

Chapter
Sonic and Ultrasonic
LONG ESSAYS
Question 1 However in case of deep pockets, ultrasonic micro-inserts

are found to be more effective than manual scaling.
Explain about powered instruments and their efficacy in
Periodontics. Bacterial Reduction and Endotoxin Removal
Answer Both the sonics and ultrasonics along with manual

scaling/root planing (SRP) remove equal amount of
There are two types of powered instruments:
endotoxin from the root surface
1. Sonic scalers Bacterial reduction is also comparable in the same

2. Ultrasonic scalers: amount
Magnetostrictive The ability of ultrasonic to produce cavitation and micro-

Piezoelectric
streaming has shown to reduce the working time to

achieve these common objectives.
Sonic Scalers
Reduction in Bleeding On Probing, Probing Depth, and
They are air-driven. 2000–6500 cps
Clinical Attachment

The scaler tips are large in diameter and universal in design

The strokes are elliptical to orbital in shape, therefore can The results as expected are similar to each other.

be adapted to all tooth surface.
Furcation Access
Ultrasonic Scalers Since the access to furcation is narrower, micro-ultrasonic

inserts work more efficiently in these areas.
Piezoelectric Scalers Sonics and ultrasonic are equivalent to manual

When an electric current is applied to a quartz crystal or instrumentation in class1 furcations but superior than

to a ceramic disc they change in shape due to change in manual in cases of class 2 or 3 furcations.
the polarity of the crystal arrangement
Their tips move in a linear pattern. Question 2

What is frequency, amplitude, and stroke? Discuss about the
Magnetostrictive Scalers water flow in powered scalers.
There are ferromagnetic stacks inside an electromagnetic
Answer

field changes its shape constantly under an alternating
current Frequency: Number of times a tip moves per second in an
Tip movement is elliptical, therefore all the surfaces are elliptical, linear or circular path.

active. Higher frequency, lesser working are:

Stroke: It is the maximum distance travelled by the

Efficacy of Ultrasonic in Periodontics insert tip during one cycle
Amplitude: It is one-half of the stroke. Higher power
Plaque and Calculus

settings produce a longer stroke, with the frequency
Both manual and ultrasonic are equally effective remaining constant.

170
Water Flow Cavitation: When the turbulent water flow reaches

the tip of the scaler it gains the energy of the tip and
Water flow is primarily required for heat dissipation

form a bubble. This bubble is however very unstable

Other beneficial effects of water along with ultrasonics are:
and implodes on the tooth surface.

Acoustic micro-streaming: It is the unidirectional

flow of water powered by ultasonics. This implosion produces shock waves in the liquid which

Acoustic turbulence: It is created when the propagates in the entire area of water flow.

movement of the tip causes the cooling water stream These three phenomenon together causes breakage of

to accelerate and cause an intense swirling effect. This debris, clearance of plaque, and turbulent lavage of the
turbulence continues till cavitation occurs. pocket. It also destroys bacterial colonies.
44 Adjunctive Role of

Chapter
Orthodontic Therapy
LONG ESSAYS
Question 1 Advanced horizontal bone loss: In such cases if the

brackets are placed in order to level the crown, it may alter
Describe the benefits of orthodontic therapy in an adult
the crown root ratio and cause tooth mobility. Thus, the
periodontal patient.
brackets or bands should be placed according to bone
Answer levels. In vital tooth, the equilibration should be performed
gradually to allow the pulp to form secondary dentin and
Orthodontic therapy in an adult periodontal patient can be insulate tooth during the equilibration process.
highly beneficial in the following manner: Root proximity: Closely-placed roots of the posterior

The alignment achieved in crowded or malposed teeth interfere with maintenance of good oral hygiene.

dentition permits easy accessibility, thus allowing the Roots can be moved apart orthodontically as this
patients to clean all surfaces of their teeth. opens up the embrasure spaces, provides additional
Vertical orthodontic tooth repositioning can improve bone support and enhances the patient’s access to

some osseous defect, thus inhibiting the need of osseous interproximal region for hygiene.
surgery. The brackets should be placed obliquely to facilitate this
Orthodontic therapy can aid in alignment of gingival
process. Generally separation of 2–3 mm provides adequate

margins thus avoiding the need of gingival recontouring. bone support. These patients may need occlusal adjustment
Fractured tooth can be forced eruption orthodontically
to recontour the crowns.

allowing enough tooth material for carrying out
restorative procedures. Fractured Tooth
Open gingival embrasure can be corrected especially
Extraction or Forced Eruption

in maxillary anterior region by orthodontics root
movement, tooth reshaping and restoration. The following factors help us in determining the protocol
Orthodontics therapy can be used to correct the supra- to be followed:

erupted teeth, uprighting of drifted molars in extraction Root length: If the fracture extends to the level of bone,

space for the replacement with implants. it may erupt 4 mm.
Question 2 A periapical radiograph is to be taken and 4 mm
subtracted from the apex of fractured tooth root. The
Describe orthodontic treatment of osseous defects.
crown-root ratio should be 1:1 for stability. If it is less than
Answer the tooth, should be extracted.
Root form: The root should be broad and non-tapering
Marginal ridge discrepancies: In such cases, the

rather than triangular and tapering, as they provide a

brackets are placed in a way that the tooth equilibrates
according to flat bone ridge. This in some cases may lead narrow cervical region after 4 mm eruption.
to reduction in crown heights, but is acceptable as the The root canal should be one-third of the total width of
periodontal health is improved because of the favourable root, as more than this will cause the crown preparation to
bone contour. The reduced crown is restored. be thin.
172
Level of the fracture: It is difficult to attach a crown to These gingival marginal discrepancies can be corrected

the root of the tooth which has fractures below 2–3 mm either by orthodontic tooth movement or surgical correction

apical to the bone. of gingival margin discrepancy.
Age: It is preferable to forced erupt a tooth in a younger
Four criteria to make correct decision:

individual as compared to an older individual with
adjacent having prosthetic crown. 1. Patients lip line when the patient smiles (if smile line is
Aesthetics: In patients with high smile line and 2–3 mm below the free margin, then requires no correction)

of gingival display, restorations are very obvious and 2. Labial sulcular depth: If the shorter tooth has a deep
thus it may be preferable to extrude the fractured tooth. sulcus, excisional gingivectomy may be appreciated to
Endodontic/periodontal prognosis: In cases of move the gingival margins of short tooth apically.

compromised periodontal health or vertical fractures, it 3. Evaluate the relationship between shortest central
is more prudent to extract the fractured tooth. incisor and adjacent lateral incisor: If the short central
incisor is longer than laterals then it is possible to
Question 3 extrude the longer tooth and equilibrate the incisal
How can gingival discrepancies are treated with orthodontic edge.
therapy? 4. If the incisal edges are attrited and tooth had supra-
erupted, then the best method to correct the gingival
Answer
discrepancy is to intrude the short central incisor and
Gingival Levels building restoration of incisal edges.
The relationship of the gingival margins of six maxillary
anterior teeth plays an important role in aesthetic
Gingival Form
appearance of the crowns. The presence of papilla between the maxillary central
Four characteristics contribute to ideal gingival form: incisors is a key aesthetic factor in any individual.
1. Free gingival margin of the two central incisors should be Occasionally, adults will have open gingival embrasures
at the same level. or black triangles spaces above contact areas that look
2. Gingival margins of central incisors should be positioned unaesthetic.
more apically then laterals and at the same level as canines. This space is usually due to:
3. The contour of labial gingival margins should mimic the
Tooth shape
cemento-enamel junction CEJ of teeth.

Root angulation
4. There should be a papilla between each tooth and the

Periodontal bone loss.
height of tip of the papilla is usually halfway between

incisal edges and labial gingival height of contour over If triangular tooth shape is the cause, then flatten the
the centre of each anterior tooth. incisal contact and closing the space.
Gingival marginal discrepancies between the adjacent If the roots angulation is divergent causing excessive
teeth could be caused by abrasion of incisal edges or space, they should be corrected to descend the papilla
delayed migration of gingival levels. down and overcome the dark triangular spaces.
45 Occlusal Evaluation

Chapter
and Therapy
LONG ESSAYS
Question 1 Intraoral Evaluation of Occlusion

What are the different occlusal evaluation procedures? Identification of occlusal contacts in maximum

intercuspation.
Answer
Unhindered mandibular guidance should be noted in
There are three types of occlusal evaluation procedures as excursive movements.
follows: Initial contact in centric relation closure arch.

Guidance of patients mandible will allow the first
1. Temporomandibular disorder screening examination.

occlusal contact in centric relation with minimal
2. Intraoral evaluation of occlusion. masticatory muscle recruitment.
3. Role of articulated casts. If tooth to tooth contact occurs, before maximum

intercuspation is acquired, a deflection of mandible is
Temporomandibular Disorder Screening seen.
Examination Tooth mobility: Mobility is recorded as a part of initial

occlusal evaluation and any changes over a period of
Maximum inter incisal opening: The patient is instructed
time are closely monitored.
to open his or her mouth as wide as possible. A mm scale
Attrition: It is defined as wear caused by tooth to tooth
is kept on the incisal edges of the lower incisor and the

contact. A certain amount of physiologic attrition is
interincisal distance between upper and lower incisors are
normal.
measured. Any accelerated attrition should be noted in the form

Opening/closing pathway: The patient is advised to of wear facets
open and close his mouth and the movement is closely Significant attrition of the teeth generally implies

watched to record any deviation or deflection from the chronic occlusal habits, clenching of the teeth and
midline. bruxism.
Temporomandibular joint sounds: Light finger pressure is Question 2
applied bilaterally over the temporomandibular joint (TMJ)
Describe temporomandibular disorder (TMD) screening.
pre-auricularly or post-auricularly and the patient is asked
to open and close the mouth. Joint sounds like clicking or Answer
crepitus are to be recorded. The patients with TMDs can be placed in one of the following
Temporomandibular joint tenderness: Light, bilateral three categories:
palpation over the lateral aspect of condyle is used to elicit Jaw function status is in normal limits:

TMJ tenderness in mild moderate or severe categories. The patient in this category have no complains or jaw

Muscle tenderness: Moderate finger pressure is applied pain or dysfunction.
bilaterally to check for tenderness in masseter, pterygoid They have minimal incisal opening of at least 40 mm,

and temporalis muscle. These are recorded as mild, with no significant joint or muscle tenderness and
moderate or severe. minimal joint sounds.
174
Patients present with a history of jaw problems after long Question 4

appointments which involve wide opening of the mouth. What are the indications and steps of coronoplasty / occlusal

These patients report with several sites of mild to
equilibration?

moderate muscle tenderness.
They may also show TMJ clicking after long Answer

appointment which was previously benign. Coronoplasty is the selective reshaping of occlusal surfaces
These cases show restricted incisal opening, significant with the goal of establishing a stable, non-traumatic

pain in the jaw, severe joint or muscle pain and occlusion.
progressive locking of the jaw episodes.
These patients indicate comprehensive evaluation or Indications

referral before any non-emergency treatment.
It is indicated in patients with evidence of trauma from

Question 3 occlusion.
What are the requirements for oral stability? It is performed after elimination of gingival and infra

bony pockets.
Answer
Maximum intercuspation with: Procedure

Light or absent anterior contacts. Removal of retrusive pre-maturities.

Well-distributed posterior contacts. Adjustment of intercuspal position (ICP).

Coupled contacts between opposing teeth. Test for excessive contact on incisor teeth in ICP.

Cross tooth stabilisation. Remove posterior protrusive supra-contact.

Forces directed along the long axis of each tooth. Correct pre-maturities on balancing sid.

Smooth excursive movements without interferences. Reduce supra-contacts on working sid.

No trauma from occlusion. Eliminate undesirable gross occlusal feature.

Favourable subjective response to occlusal form and Recheck the occlusal contact relationship in all position.

function. Finishing and polishing.

46 Periodontic-Endodontic

Chapter
Continuum
LONG ESSAYS
Question 1 Independent Periodontal and Endodontic Lesions

Classify pulpo-periodontal problems. Describe aetiology, Patients with pulpal disease may have periodontal

diagnosis and treatment. inflammation also.
Pulpal problems are more easily noticeable with
Answer

noticeable signs and symptoms, where the progression
Pulpo-periodontal problems can be classified as: of periodontitis is low, except acute diseases like
Primary endodontic lesions. periodontal abscesses or necrotising ulcerative gingivitis.

Primary periodontal lesions. Thus, prompt management of pulpal lesions become

Independent periodontal and endodontic lesions. important.

Combined periodontal and endodontic lesions.
Pulp extirpation and canal filling usually eliminates the

Primary endodontic, secondary periodontic. patients’ acute symptoms.

Primary periodontic, secondary endodontic.
Treatment for periodontitis or gingivitis can be delayed

until the acute symptoms of pulpal diseases get resolved.
Primary Endodontic Lesions Another situation might arise, if a patient with chronic

periodontitis has loss of pulp vitality.
Patients history, periodontal probing, radiographs and Such patients have both the symptoms of periodontitis

pulpal testing are performed.

and apical periodontitis.
Clinically caries would be present and radiographically Involvement of apical periodontium by a pulpal lesion

periapical radiolucency and dental caries would be

may obscure the symptoms of periodontitis.
present. Therefore sequence of therapy becomes difficult to make
Patients experience active episodes of pain.

as to treat which problem first.

Sign and symptoms are almost similar to initial signs and Patient may also present with both abscesses, i.e. pulpal

symptoms of abscesses.

and periodontal, but the apical lesion tends to be more
Debridement of the pulp chamber and canal and painful.

completion on of appropriate, endodontic therapy, Thus, endodontic therapy would result in resolution of
result in healing of the lesion.

endodontic lesion but a little or no effect on pocket,
and thus periodontal therapy would be required for a
Primary Periodontal Lesions
successful result.
History probing and radiographs are performed.
Combined Periodontal and Endodontic Lesions

Tooth looks clinically healthy, but may be mobility and

pockets are present. When there is an extension of an endodontic lesion

Radiographically there is presence of bone loss. into an existing periodontal lesion, it is referred to as

Patient complains of dull pain which can be intermittent combined periodontal and endodontic lesion.

or continuous in nature. Such lesions have features of both the diseases.

Scaling, root planing followed by flap surgery with or History, clinical radiographic examinations are important

without grafting is the treatment of choice. to formulate a treatment plan.
176
Pain from loss of pulp vitality is the most common feature. typically does not resolve to the same extent as the

Probing confirms presence of periodontal pocket. endodontic lesion.

In such cases, endodontic therapy is most predictable. After a successful endodontic treatment, the residual

Periodontal component is a difficult component of the periodontal pocket can be more predictably treated.

combined lesion. Periodontal treatment includes scaling, root planing and

Even with periodontal treatment, the periodontal defect surgical treatments.

SHORT ESSAYS
Question 1 may be initiated, which is referred to as retrograde

What is retrograde pulpitis and retrograde periodontitis? pulpitis (Fig. 46.1). When a long standing periapical
lesion drains through periodontal ligament, secondarily
Answer complicated, is referred to as retrograde periodontitis
If periodontitis progresses to involve the lateral canal (Fig. 46.2).
or the apex of a tooth then secondary pulpal infection
Figs 46.1: Retrograde pulpitis. Figs 46.2: Retrograde periodontitis.
47 Preparation of the

Chapter
Periodontium for
Restorative Dentistry
LONG ESSAYS
Question 1 Biologic width is defined as the physiologic dimension

of the junctional epithelium and connective tissue
Discuss crown lengthening procedures. What are its attachment.
indications and contraindications. Discuss the importance It measures about 2.04 mm (Fig. 47.1).
of biologic width in crown lengthening.

If the biologic width is violated while performing any
Answer kind of restorative procedure then it may cause following
problems:
Crown lengthening are the procedures that are performed
to increase the clinical height of a crown for restorative or
aesthetic purpose.
Indications are as follows:
Subgingival caries or fracture.

Inadequate clinical crown length for retention.

Unequal or unaesthetic gingival height.

Contraindications are as follows:
Cases where surgery would cause an unaesthetic

outcome.
Deep caries or fracture would require excessive bone

removal on contiguous teeth. Fig. 47.2: More than 3 mm of soft tissue present above the crest
Importance of biologic width: of the alveolar bone, along with adequate attached gingiva,
allows crown lengthening by gingivectomy.
While performing crown lengthening, one should take

care of preserving the biologic width.
Fig. 47.3: Less than 3 mm of soft tissue present above the

crest of the alveolar bone or inadequate gingiva, therefore a
flap procedure with osseous recontouring is done for crown
Fig. 47.1: Diagram depicting biologic width. lengthening.
178
Gingival inflammation. Situation 1: If there is adequate attached gingiva and

Pocket formation. more than 3 mm of tissue coronal to the crest of the

Alveolar bone loss. bone, then external bevel gingivectomy alone can be

performed (Fig. 47.2).
Therefore, biologic width should be preserved while Situation 2: If there is inadequate attached gingiva and
performing any restorative procedure.

less than 3 mm of soft tissue present coronal to the crest
Surgical crown lengthening requires removal of gingiva of the alveolar bone then it requires a flap procedure and
or both gingiva and bone. bone recontouring (Fig. 47.3).
48 Phase II

Chapter
Periodontal Therapy
SHORT ESSAYS
Question 1 Important criteria in selection of the treatment tech-

nique could be of bony craters, horizontal or angular
What are the objectives of surgical phase? What is the
bone loss and other bone deformation.
purpose of surgical pocket therapy and what are the critical
zones in pocket surgery? Zone 4: Attached Gingiva
Answer Presence or absence of an adequate width of attached
Objectives of surgical phase are: gingiva should be considered while selecting a pocket
Improvement of the prognosis of teeth and their treatment method.

replacement. Question 2
Improvement of aesthetic.
What are the indications for periodontal surgery?

Purposes of surgical pocket therapy are:
To eliminate the pathologic change in the pocket walls. Answer

To create a stable, easily maintainable state.
Various indications of periodontal surgery are as follows:

To perpetuate periodontal regeneration.

Pocket and teeth in which a complete removal of root
Critical zones in pocket surgery are as follows:

irritant is not considered clinically possible may call
Zone 1: Soft tissue pocket wall.
for surgery. It is seen mostly in molars and deep molar

Zone 2: Tooth surface.
areas.

Zone 3: Underlying bone.
Areas with irregular bony contours, deep craters and

Zone 4: Attached gingiva.

other defects usually require surgery.

Zone 1: Soft Tissue Packet Wall In cases of intrabony pocket and distal aspect of

One should determine the persistence of inflammatory last molar, frequently complicated by mucogingival
changes in the pocket wall and the clinical features, and problems.
Furcation involvement of Grade II and III.
outcome of therapy of the soft tissue pocket wall.

Persistence of inflammation in areas with moderate to

Zone 2: Tooth surface deep pocket may require surgery.
One should identify the presence of deposits and Question 3

alteration on the cementum surface.
Accessibility of the root surface instrumentation should What are the methods of pocket therapy and what all are

be determined. the criteria for method selection?
Zone 3: Underlying Bone Answer

Thorough careful, clinical and radiographic examinations Methods of pocket therapy are as follows:

should be done. One should establish the height of the New attachment technique: They are the ideal result

alveolar bone to the pocket wall. since they eliminate the pocket depth by reuniting the
180
gingiva to the tooth at a position coronal to the pre- Criteria of Method Selection
existing pocket.
Selection of a technique for treatment of a particular peri-

New attachment basally means filling in new bone
odontal problem depends upon following considerations:

and regeneration of periodontal ligament and cemen-
Characteristics of pocket depth and its relation to bone
tum.

Removal of the pocket wall. and its configurations.

Response to instrumentation, presence of furcation
It is the most common method of pocket therapy.

It can be removed by following methods: involvement.

Shrinkage or retraction: This can be achieved non-surgically Response to phase I therapy.

through scaling, root planing which resolves the inflamed Presence of mucogingival or perioplastic problems.

gingiva. Age and overall health of the patients.

The gingiva shrinks, which further reduces the pocket Patient cooperation which includes ability to perform

depth. effective oral hygiene and for smoker, their willingness to
Surgical removal by means of : quit their habit at least for some time.
Socioeconomic considerations.
Apical displacement of flap.

Removal of the tooth side of the pocket. Overall diagnosis of the case for various types of

This is achieved by tooth extraction or by partial tooth periodontitis like chronic, aggressive or various types of

extraction which is referred to as hemisection or root gingival enlargements.
resection. Previous periodontal treatments.

49 General Principles of

Chapter
Periodontal Surgery
LONG ESSAYS
Question 1 Drug called thrombin can also be used for achieving

What is haemostasis? Describe management of periodontal haemostasis. It can be applied as topically as a liquid
bleeding in detail. or powder.
Answer Question 2
Describe about periodontal dressings.
Controlling of bleeding during surgery is referred to as
haemostasis. Answer
Haemostasis is necessary as it permits an accurate
Periodontal dressings can also be referred as periodontal

visualisation of the extent of disease, pattern of bone packs.
destruction and anatomy and condition of the root They are generally used to cover the surgical areas after

surfaces. the surgery is completed.
It is important for wound debridement and scaling and

root planing. Advantages of Packs
It also prevents excessive loss of blood into mouth,
They assist in healing by protecting the tissue rather than

oropharynx and stomach.

providing healing factors.
Periodontal surgery can lead to profuse bleeding which
They can minimise post-operative infection and

can be managed by following methods:

haemorrhage.
Continuous suctioning of the surgical site.
They can facilitate healing by preventing surface trauma

Application of pressure to the surgical wound with a

during mastication.

moist gauze. Protect against pain induced by contact of the wound
Proper design of the flaps and incisions, can avoid

with food or tongue during mastication.

excessive bleeding.
If a vessel gets lacerated, suturing around the bleeding Disadvantages of Pack

end would control the haemorrhage.
Can be discomforting to patient.
Applying cold pressure to the site with moist gauze

If applied on anterior teeth, can be unaesthetic for the

can be helpful.

patient.
Local anaesthetic with a vasoconstrictor can also be
Can cause allergy to the patient.

used to control bleeding.

Can be a source of plaque accumulation.
Haemostasis can also be achieved by various

haemostatic agents, such as absorbable gelatin Types of Packs
sponge (gelfoam), oxidised cellulose (Oxycel), oxidised
regenerated cellulose (surgical absorbable hemostat) They can be zinc oxide eugenol packs or non-eugenol packs.
and microfibrillar collagen hemostat (CollaCote, Zinc oxide eugenol packs: Example is wonder pack

CollaPlug and CollaTape). developed by Ward in 1923.
182
These packs are based on the reaction of zinc oxide Preparation and Application of Dressings

and eugenol.
A wax paper pad is taken and components from both the

Addition of accelerators like zinc acetate can give the

tubes are dispensed in equal amount.

dressing a better working time.
Eugenol can be allergic which can produce a reddened
Both are mixed with a spatula to form a thick paste of

uniform colour.

area and burning pain in same patients.
The pack is placed in a cup of water at room temperature.
Non-eugenol packs: Example is Coe Pak which is most

In 2–3 minutes, the tackiness of the paste is lost and it

widely used.

These packs work by a reaction between metallic
remains workable for 15–20 minutes.
The pack is then rolled into two strips of approximately

oxide and fatty acids.

It is available in form of two tubes.
equal length.
The end of one strip is fixed around the distal surface of

One tube contains zinc oxide, oil (for plasticity), a gum

last tooth.

(for cohesiveness), and lorothidol (a fungicide).
The second tube consists of liquid coconut fatty acids
The remaining strip brought forward along the facial

surface to the midline and interproximally.

thickened with colophony resin and chlorothymol (a
The second strip is applied on this lingual surface.
bacteriostatic agent).

This pack does not contain eugenol, therefore,
The strips are then joined interproximally by applying

gentle pressure on the pack.

avoiding the side-effects of eugenol.
Examples of other non-eugenol packs are cyano-
Overextension of the pack should be avoided.

Since excess of pack can irritate the mucobuccal

acrylate, methylacrylate gels.

fold and floor of the mouth and interferes with the
Retention of Packs tongue.
Pack should be trimmed, if it interferes with occlusion.
They are retained by mechanically inter-locking in inter-

The patient should be asked to move the tongue
dental spaces and connecting the lingual and facial portion

forcibly out and to each side, and the cheek and lips
of the pack. should be displaced in all directions to mould the pack
while it is still soft.
Anti-Bacterial Properties and Packs Once the pack is set, it should be trimmed to remove

Antibiotics, like bacitracin, oxytetracycline, neomycin the excess.

and nitrofurazone have been tried for improved healing Pack should be kept on for one week after surgery.

and patient comfort with less odour and taste. If a portion of the pack is lost from the operated area and

These drugs have been shown to produce hyper- the patient is uncomfortable, it is usually best to repack

sensitivity reaction. the area.
SHORT ESSAYS
What are the complications which can arise in the first post- What is the treatment for sensitive roots?
operative week?
Answer
Answer It occurs when the root becomes exposed as a result of

gingival recession or pocket formation.
Following complications may arise in the first post-operative
It can also appear after scaling, root planing and surgical
week:

procedures.
Persistent bleeding after surgery. It occurs more commonly in the cervical area of the root,

Sensitivity to percussion. where the cementum is extremely thin.

Swelling. Scaling and root planing procedures remove this

Feeling of weakness. cementum, inducing the hypersensitivity.

183
Chapter 49 General Principles of Periodontal Surgery

A number of agents have been proposed to control root
Iontophoresis.
hypersensitivity.
Strontium chloride.

These desensitising agents can be applied by the patient
Potassium oxalate.
or in office by the dentist.
Restorative resins.

Agents used by patients can be desensitising dentifrices
Dentin binding agents.
which contain strontium chloride, potassium nitrate and
sodium citrate.
Question 3

Fluoride rinsing solutions and gels can also be used after What are the various surgical instruments?
the usual plaque-control procedure.
Answer
Agents used in office are:
Various surgical instruments are as follows:
Cavity varnishes.

Excisional and incisional instruments, such as

Anti-inflammatory agents.

Treatment that partially obturate dentinal tubules.

gingivectomy knives, interdental knives, and surgical
Burnishing of dentin.

blade.
B P Handle.
Silver nitrate.

Surgical curettes.
Zinc chloride and potassium ferrocyanide.

Formalin.

Periosteal elevators.

Calcium compounds:

Surgical chisels.

Calcium hydroxide.

Surgical files.

Dibasic calcium phosphate.

Scissors.

Fluoride compounds:

Haemostat and tissue forceps.

Sodium fluoride.
Needle holder.

Stannous fluoride.
Castroveijo needle holder and scissors.

50 Gingival Surgical

Chapter
Techniques
LONG ESSAYS
Question 1 Bone should not be exposed but the incision should

What is gingivectomy? What are its indications and be close to the bone.
contraindications? Explain surgical gingivectomy with its
healing and various methods of performing gingivectomy.
Answer
Gingivectomy refers to excison of the gingiva.
Indications of gingivectomy are as follows:
To eliminate suprabony pockets.

To eliminate gingival enlargement.

To eliminate suprabony periodontal abscess.

Contraindications of gingivectomy are as follows:
When bone surgery is required or when need to examine

the bone shape and morphology.
In cases when the base of the periodontal pocket lies

apical to the mucogingival junction.
In case of anterior region, where esthetic is a

consideration. Fig. 50.1: Pocket marker making pin-point bleeding
perforations which indicate pocket depth.
Gingivectomy Technique
Following steps are performed for gingivectomy procedure:
Step 1: The pockets are probed with a periodontal probe

and then they are marked with pocket markers to create
bleeding points (Figs 50.1 and 50.2).
Step 2: For incisions on the facial and lingual surfaces,

periodontal knives, such as Kirkland knives are used. For
supplemental interdental incision Orban knives can be
used.
If necessary, BP knives and scissors can also be used as

auxiliary instruments.
The incision is made apical to the bleeding points

created by the pocket marker (Fig. 50.3).
These incisions are directed coronally to a point

between the bottom of the pocket and the crest of
the bone. Fig. 50.2: Pocket marker in position.
185
Chapter 50 Gingival Surgical Techniques

Continuous or discontinuous incisions can be made Healing After Gingivectomy
depending upon the choice of the operator (Figs There is formation of protective surface clot as an initial

50.4A and B).

response after gingivectomy.

The incisions should be bevelled at an angle of 45° to
There is some necrosis and underlying tissue is acutely

the tooth surface.

inflamed.
Normal arcuate pattern of the gingiva should be created.
Clot is replaced by granulation tissue.

If bevelling is not done, it would lead to a broad,

In first 24 hours, there is an increase in new connective

fibrous plateau that takes a lot of time to develop into

tissue, particularly angioblasts just below the layer of

a physiologic contour.
necrosis and inflammation.
Step 3: Excised pocket wall should be removed.
By third day, several fibroblasts are seen.

Area should be cleaned and the root surface should

Granulation tissue grows coronally, creating a new, free

be examined thoroughly.

gingival margins and a sulcus.

Upon examination, some calculus remnant, root
Capillaries from blood vessels of the periodontal

caries or root resorption may be found.

ligament migrate into the granulation tissue and within

Over the excised soft tissue, granulation tissue can be
2 weeks, they connect with gingival vessels.

found. After 12-24 hours, epithelial cells at the margins of the

Step 4: Granulation tissue should be curetted out

wound start to migrate over the granulation tissue,

carefully, and any remaining calculus or necrotic separating it from the contaminated surface layer of the
cementum should be removed to achieve a smooth and clot.
clean surface. Within 24-36 hours, the epithelial activity reaches at a
Step 5: The area should be covered with a periodontal

peak at the margins.

pack.
After 5-14 days, epithelisation of the surface is almost
complete.

Vasodilation and vascularity begin to decrease after the
fourth day of healing, but by the 16th day, it appears
almost normal.

In about 7 weeks, there is a complete repair of the
connective tissue.
Methods of Performing Gingiveletomy

Various methods of performing gingivectomy are as follows:
By scalpels and periodontal knives, such as Kirkland

knives or Orban’s knives.

By electrosurgery.

By lasers: Most commonly used lasers are carbon dioxide

(CO2) or neodymium-doped yttrium aluminium garnet
(Nd:YAG) lasers.
By chemosurgery: Removal of gingiva using chemicals,

Fig. 50.3: Bevelled incision extending apical to the perforation such as 5% paraformaldehyde or potassium hydroxide.
made by pocket marker.
Disadvantages of using chemosurgery are:

h Depth of action cannot be controlled.

h
h Gingival remodelling cannot be accomplished.

h
h Reformation
h
of junction epithelium and
epithelialisation occurs slowly.
Question 2
Define Gingival Curettage . What are the aims of curettage?
A B What are the Indications and contraindications of
Figs 50.4A and B: (A) Discontinuous incision; (B) Continuous curettage? Explain in detail about the basic procedure and
incision. other procedures of curettage.
186
Answer Other Techniques

According to Carranza curettage is used in Periodontics Excisional new attachment procedure.

to mean the scraping of the gingival wall of a periodontal Ultrasonic curettage.

pocket to separate diseased soft tissue. Chemical curettage (caustic drugs).

It is one of the oldest periodontal treatment methods. It

was performed widely and almost routinely in treating Excisional New Attachment Procedure (ENAP)
periodontal pockets.
This procedure has been developed & used by the U.S Naval
dental corps.
Aims of Curettage
It is a definitive subgingival curettage procedure performed
To reduce pocket depth by enhancing gingival shrinkage, with a knife.

new connective tissue attachment.
Combination of the above. Technique

After adequate anaesthesia, an internal bevel incision

Indications is made from the margins of the free gingiva apically to
Curettage can be done as a part of new attachment a point below the bottom of the pocket. The incision is
carried interproximally on both the facial & lingual sides,

attempts in cases of moderately deep intrabony pockets.
Curettage can be done as a non definitive procedure to attempting to retain as much interproximal tissue as
possible.

reduce inflammation prior to pocket elimination.
In patients in whom aggressive surgical techniques (eg. The intention is to cut the inner portion of the soft tissue
wall of the pocket all around the tooth.

flaps) are contraindicated
Remove the excised tissue with a curette & carefully root
Curettage is also frequently performed on recall visits as

plane all exposed cementum, preserve all connective

a method of maintenance.
In supra bony pockets that are relatively shallow (4-6 tissue fibres that remain attached to the root surface.
Approximate the wound edges, place sutures &

mm).

periodontal dressing.
Contraindications
Ultrasonic Curettage
Firm, fibrotic pockets.
Ultrasound is effective for debriding the epithelial lining

Infrabony pockets.

of the pocket.

Acute necrotizing ulcerative gingivitis.
It results in a narrow band of necrotic tissue (micro

Mucogingival involvements.

cauterization) which strips of the inner lining of the

Procedure pocket.
The Morse scaler shaped end ultra sonic instrument is

Basic technique used.
Gingival curettage always requires some of local
It has been reported that ultrasonic instruments to be as

anaesthesia.
effective as manual instruments for curettage.
The curette is selected according to the area involved.

The cutting edge should be against the tissues. Caustic Drugs
The instrument is inserted so as to engage the inner

lining of the pocket wall and carried along the soft tissue, Caustic drugs lead to chemical curettage of the lateral wall
usually in a horizontal stroke. of the pocket or selective elimination of the epithelium.
The curette is then placed under the cut edge of the Drugs such as
junctional epithelium to undermine it. Sodium sulphide.

The area is flushed to remove the debris, the tissue is Alkaline sodium hypochlorite (Antiformin).

partly adapted to the tooth by gentle finger pressure. Phenol.

Suturing of separated papillae & application of The extent of tissue destruction with these drugs cannot

periodontal pack may be needed. be controlled.
187
Chapter 50 Gingival Surgical Techniques
SHORT ESSAYS

Question 1 The intention is to cut the inner portion of the soft tissue
wall of the pocket all around the tooth.
What is gingivoplasty?
Remove the excised tissue with a curette & carefully root

Answer plane all exposed cementum, preserve all connective

tissue fibres that remain attached to the root surface.
It is reshaping of the gingiva to create physiologic gingival
Approximate the wound edges, place sutures &
contours, with the main purpose of recontouring of gingiva

periodontal dressing.
in the absence of pockets.
Gingivoplasty can be performed using a scalpel,

Question 3
periodontal knives, rotary burs, electrodes or lasers.
Discuss the healing after curettage ?
It helps in achieving a tapered gikngival margin, a

scalloped marginal outline, thinned attached gingiva, Answer

vertical interdental grooves, and helps in shaping the Healing after curettage is as follows ?
interdental papillae such that they provide sluiceways Immediately after the procedure (0hrs):- Gingiva is
for the passage of food. hemorrhagic, blue- red & blood clot within the pockets are
Question 2 visible.
1-2 days: Gingiva appears edematous & swollen it still
What is ENAP procedure ?

has bluish red color, clots are seen at the margin .PMNs
Answer are found at the wound surface beneath the blood clot.
A well organised blood clot covers the wound surface,
This procedure has been developed & used by the U.S Naval
which is still devoid of epithelium (after a lag of 12- 24
dental corps.
hrs) epithelial cells from the gingival margin begin
It is a definitive subgingival curettage procedure
to migrate apically between the blood clot and the
performed with a knife.
connective tissue.
Technique 4 days: Edema has diminished , color is normal , clot can

be seen sloughing from the gingival crevice. This area

After adequate anaesthesia, an internal bevel incision
will still bleed on probing.

is made from the margins of the free gingiva apically to

Histologically, the acute inflammatory reaction is
a point below the bottom of the pocket. The incision is

replaced by granulation tissue at the wound surface.

carried interproximally on both the facial & lingual sides,
Connective tissue is disorganized but edematous.
attempting to retain as much interproximal tissue as

Epithelization is progressing but incomplete.

possible (Figs 50.5).

The
epithelium covers the connective tissue
separating it from the clot.
6-7 days: Clinically edema is absent, shrinkage occurs

producing recession of the gingival margin.
Colour is normal.

There is little or no bleeding on probing.

Connective tissue is organized, collagen is being

produced.
10-14 days: Gingiva appears normal, pink in colour, firm.

No evidence of bleeding on probing.

Connective tissue maturation continues for 21-28 days.
Keratinization of the oral aspect of the gingiva increases.
A B
Problems in Healing
Figs 50.5A and B: (A) Internal bevel incision to a point below
the bottom of the pocket; (B) After excision of tissue,
Disturbances in healing may indicate some systemic
scaling and root planing are performed. problem. However in most cases they represent
188
contamination of the curettage wound by plaque/ This should be done 1-2 weeks after curettage has been

calculus left on the tooth surface. completed and healing has occurred.

Evaluating the success of gingival curettage Evaluate the gingiva, measure pocket depth &observe

Re-examination & re-evaluation of the gingiva following bleeding Evaluate plaque control & re-instrument if

curettage is an integral part of the procedure. necessary.
51 Treatment of

Chapter
Gingival Enlargements
SHORT ESSAYS
Question 1
How can a chronic inflammatory enlargement treated?
Answer
They are firstly treated by non-surgical means, such as

scaling and root planing.
The inflammatory component is reduced through scaling

and root planning only.
If the gingiva does not undergo shrinkage after scaling

and root planing, then it is removed surgically either by
gingivectomy or by flap procedure, depending upon the
case.
Question 2
How is a drug-induced enlargement treated?
Answer
Treatment of drug induced enlargement should be based
upon the medication used and the clinical features of the
case.
Firstly the drug should be discontinued or a substitute

for that drug can be given.
For example, patient taking nifedipine can take a

substitute calcium channel blocker, such as diltiazem or
verapamil.
Secondly, the clinician should give importance to plaque

control.
Adequate plaque control would lead to suppression of

inflammatory component, which leads to decrease in
the, size of the enlargement.
Thirdly, in some patients, even after careful consideration,

the gingival enlargement might persist.
So in such patients, surgery is required which could either

be in a form of gingivectomy or in a form of periodontal
flap.
(Fig. 51.1) shows the treatment chart for drug-induced Fig. 51.1: Treatment chart for drug induced gingival

gingival enlargement. enlargement.
52

Chapter The Periodontal Flap
LONG ESSAYS
Question 1
Define periodontal flap? What is the classification of flaps?
Discuss in detail about flap design, incision and elevation of
flap. Draw suitable digrams wherever required?
Answer
According to Carranza a periodontal flap is defined as a
section of gingiva or mucosa surgically separated from
the underlying tissue to provide visibility and access to the
bone and root surface.
A B
Classification of Flaps
Figs. 52.1A and B: (A) Internal bevel Incision to reflect a full
Flaps can be classified as follows: thickness flap. (B) Internal bevel incision to reflect a partial
Bone exposure after flap reflection. thickness flap.

Placement of the flap after surgery.

Management of the papilla. Displaced flaps.

Non-displaced flaps are returned back to then original
Based on Bone Exposure after Reflection

position and sutured.
They can be either full-thickness flap also known as Displaced flaps can be displaced either coronally, apically

mucoperiosteal flap or they could be partial-thickeness

or laterally depending upon the requirement of the case
flap, also known as split thickness flap.
and sutured in the desired position.
In a full-thickness flap, complete reflection of epithelium,
Full thickness or partial thickness—both the flaps can be

and connective tissue along with periosteum is

displaced.
performed so that the bone is exposed.
It is generally indicated in case of resective osseous Based on Management of the Papilla

surgery. It could be either conventional flap or papilla preservation
In a partial thickness flap only epithelium and part of

flap.

connective tissue is reflected, leaving behind some part In a conventional flap the interdental papilla is split
of connective tissue and the periosteum.

beneath the contact point and allows the reflection of
Bone exposure is not there.
flap in both buccal and lingual directions.

It is indicated when the flap is to be positioned apically or
In a papilla preservation flap, the entire papilla is

when the operator wants to expose the bone (Fig. 52.1).

incorporated in one of the flaps by the means of
Based on Placement of Flap after Surgery crevicular interdental incision to sever the connective
It can be either: tissue attachment and a horizontal incision at the base of
Non-displaced flap. the papilla, leaving it connected to one of the flaps.

191
Chapter 52 The Periodontal Flap
Flap Design around the tooth (Fig. 52.2).
Basic requirement of a flap are: Vertical Incision

A good blood supply to the flap is an important Vertical incisions are also known as releasing incisions or
consideration. oblique incisions.

The flap should provide a good acess for instrumentation. They are given on one end or both the ends of the

The flap should provide a good acess to underlying horizontal incision depending upon the purpose of the
structures, i.e. bone and root surface. flap.

Judge the final position. Advantages of vertical incision are:

The two basic flap designs are conventional flap (in They make the flap tension-free.

which the papillae are split) and second one is papilla They make the flap movable because it can be

preservation (in which the papillae are preserved). displaced in the desired position.

Before proceeding with any flap procedure, the operator They aid in better visualization of underlying

must decide the exact location, type of flap, type of structures.

incision, management of the underlying bone and final Disadvantages of vertical incision are:

position of flap and sutures. They compromise the blood supply.

They may lead to delayed healing.

Incisions

Incision should not be made at the centre of an

Incision could be horizontal or vertical. interdental papilla or over the radicular surface of a
tooth, rather they should be made at the line angles of a
Horizontal Incisions tooth either to include the papilla in the flap or to avoid
it completely. (Fig. 52.3).
There are three types of horizontal incision in a periodontal
flap procedure. Elevation of a Flap

The internal bevel incision, which is also known as
A blunt dissection is required when a full-thickness flap
reverse bevel incisions or 1st incision. is raised, whereas a sharp dissection is required when a
It starts from a distance from the gingival margin and

partial thickness flap is to be raised.
is aimed at the crest of the bone.
Elevation of flap is accomplished by a periosteal elevator

Crevicular incision which is the known as 2nd incision or by moving it mesially, distally and apically until the
sulcular incision. desired reflection is accomplished.
It starts from the base of the pocket and is directed

Sometimes, a combination of partial thickness and full
towards the crest of the bone. thickness is done.

Interdental incision which is also known as 3rd incision,
is given to separate the collar of the gingiva that is left
A B C
Figs 52.2A to C: Three different types of horizontal incision
(A) Internal bevel or first incision; (B) Crevicular or second Figs 52.3: (A1 and A2) Incorrect location of a vertical incision;
incision; (C) Interdental or third incision. (B1 and B2) Correct location of a vertical incision.
192
SHORT ESSAYS

Question 1
What are envelope flaps?
Answer
When a flap is raised using only horizontal incision and
no vertical incision are given, then the flap is known as
envelope flap.
If sufficient access is obtained and apical, lateral or
coronal displacement of the flap is not required, then
envelope flaps are ideal choice.
Question 2
Describe the internal bevel incision.
Answer
It is a type of horizontal incision, which starts at a distance

from the gingival margin and is aimed at the crest of the Figs 52.4: Internal bevel incision can be made at different
bone. locations and angles depending upon various anatomic and
pocket situations.
It is also known as the first incision as it is the first incision

given in a modified widman flap procedure.
It is also referred to as reverse bevel incision because Answer

the bevel of the blade, while giving this incision, is in a
reverse direction from that of the gingivectomy incision. Classification of sutures are is as follows:
A #11 or #15 surgical scalpel is used most commonly for Non-absorbable (Non-resorbable)

this incision. Silk-braided

This is the most basic incision for maximum of the flap Nylon-monofilament (Ethilon)

procedures. ePTFE-monofilament (Gore-Tex)

Polyester-braided (Ethibond)
It aims at exposing the underlying bone and root.

Absorbable (resorbable)
There are three main objectives of internal bevel incision.

Surgical: Gut
They are as follows:

Plain gut: Monofilament (30 days)
1. It removes the pocket lining.

Chronic gut: monofilament (45–60 days)
2. It conserves the relatively uninvolved outer surface of

Synthetic
the gingiva.

Polyglycolic-braided (16–20 days)
3. It results in a sharp, thin flap margin for adaptation to

Vicryl
the bone-tooth junction.

Polyglecaprone-monofilament (90–120 days)
The incision starts from a designated area on the gingiva

Monocryl (Ethicon)
and is directed to an area at or near the crest of the bone

Polyglyconate-monofilament (MaxonTM)
depending upon the type and purpose of the flap (Fig.

52.4). Various types of suturing techniques are as follows:
The portion of gingiva, which is left around the tooth Interdental ligation.

after first incision, consists of epithelium of the pocket Sling ligation.

lining and the adjacent granulomatous tissue. Horizontal mattress suture.

It is removed after the crevicular incision and the Vertical mattress suture.

interdental incision are performed. Anchor suture.

Closed anchor suture.
Question 3

Periosteal suture.

Classify suture materials and enumerate various types of Continuous suture.

suturing techniques. Figure of 8 suture.

193
Chapter 52 The Periodontal Flap
Question 4 A week after the flap surgery, an epithelial attachment

to the root is established by the means of a basal lamina
Discuss the healing after flap surgery.

and the hemidesmosomes.
Answer The blood clot gets replaced by granulation tissue which

Upto 24 hours, that is immediately after suturing, a blood is desired from the gingival connective tissue, bone

clot is formed between the flap and the tooth or bone narrow and the periodontal ligament.
surface. 2 weeks after the flap surgery, collagen fibres begin to

This clot consists of a fibrin reticulum with many appear.

polymorphonuclear leucocytes, RBCs, injured cells and There is still a weak union between the flap and tooth
capillaries at the wound edge.

because of presence of immature collagen.
1–3 days after flap surgery, the space between bone and

tooth is thinned and over the border of the flap, epithelial 1 month after the flap surgery, crevice gets fully

cells migrate. epithelised and a well-defined epithelial attachment is
There is only a minimal inflammatory process, when the developed.

flap is closely adapted to the alveolar process. Supracrestal fibres begin to arrange functionally.

ics
53 Flap Technique for

Chapter
Pocket Therapy
LONG ESSAYS
Question 1 Same procedure was described in 1974 by Ramfjord and

What are the aims of a flap procedure for pocket therapy? Nissle and termed it as “Modified Widman flap”.
Enumerate various techniques for access and pocket depth Objectives of this technique are as follows:
reduction or elimination. Describe modified Widman flap It provides accessibility for instrumentation of the root

procedure in detail with diagrams. surfaces and immediate closure of the area.
It provides an intimate postoperative adaptation of
Answer

healthy collagenous connective tissue to the tooth
Aims of a flap procedure for pocket therapy are as follows: surfaces.
To increase accessibility to root deposits.
Steps for this procedure are as follows (Fig. 53.1):

To eliminate or reduce pocket depth by resection of the
Step 1: An internal bevel incision is made which starts

pocket wall.

0.5 to 1 mm away from the gingival margin, hitting the
To expose the area to perform regenerative methods.
alveolar crest.

Various techniques for access and pocket depth elimination Step 2: Gingiva is reflected using a periosteal elevator.

are as follows: Step 3: Then the second incision is made which is referred

Modified Widman flap to as crevicular incision from the base of the pocket of

Undisplaced flap (or unrepositioned flap) the bone.

Apically displaced flap. Step 4: Once the flap is reflected, a third incision

Modified Widman flap: This procedure is aimed at exposing referred to as interdental incision is made in the
the root surfaces for efficient instrumentation and removal
of pocket lining.
Undisplaced flap: It is an excisional procedure of gingiva.
It improves accessibility for instrumentation along with
removal of pocket wall, thereby reducing or eliminating the
pocket.
Apically displaced flap: It improves the accessibility for
instrumentation and also removes the pocket, by apically
positioning of the soft tissue wall of the pocket.
Thus it preserves or increases the width of attached gingiva
by converting the previous unattached keratinized pocket
wall into attached gingiva.
Modifed Widman Flap

Originally, in 1965, Morris described this technique and Fig. 53.1: All the three incisions for Modified Widman flap

named it as “unrepositioned mucoperiosteal flap”. procedure.
195
Chapter 53 Flap Technique for Pocket Therapy
interproximal areas coronal to the bone with a BP

Step 6: Bone contouring is not done except if it prevents
blade or an orbans knife. Thus the gingival collar is good tissue adaptation of the necks of the teeth.

removed.
Step 7: The inside of the flap is trimmed using a

Step 5: A curette is then used to remove the Goldman-Fox scissors or a Castroviejo scissors so that
granulation tissue and tissue tags. Root surfaces are tissue tags are removed from the inner surface of the
checked and scaling and root planing is performed flap and there is a close approximation between the
if required. Residual periodontal ligament fibres flap and the tooth or the bone.
which are attached to the tooth surface should not be
Step 8: Interrupted direct sutures are placed and
disturbed. covered with a periodontal dressing.
SHORT ESSAYS
Question 1
Step 2: Then the second incision, i.e. the crevicular
incision is done, after which the flap is reflected. After
What are the indications of flap surgery?
this the third incision, i.e. the interdental incisions are
Answer given and the wedge of tissue that consists of pocket
wall is removed.
Indications of flap surgery are as follows:

Step 3: After this, two releasing incisions or vertical
To increase the accessibility to root deposits.
incisions are given on both the ends of the flap, which

To eliminate or reduce the pocket depth by resection of

extend beyond the mucogingival junction. If a full

the pocket wall. thickness flap is to be reflected then a blunt dissection is

To expose the area to perform regenerative methods.
done, but if a split thickness flap is to be reflected, then a

To reshape soft and hard tissues to physiologic architecture.

sharp dissection is done.

Question 2
Step 4: After this is done, all the granulation tissue
is removed followed by thorough scaling and root
Explain apically displaced flap procedure.
planing and osseous surgery is performed, if required.
Answer The flap is then displaced apically. Since the vertical
incisions are given beyond the mucogingival junction,
The purpose of apically displaced flap is to:
it becomes very easy to displace the flap as it becomes

Eradicate pocket. freely movable.
Widen the zone of attached gingiva.
Step 5: A sling suture should be given if a full

It can be performed either by a partial thickness or full thickness flap is done, but if a partial thickness flap
thickness depending upon the purpose. is performed, then a periodontal suturing is done
The steps in an apically displaced flap are as follows: using a direct loop suture or a combination of loop
Step 1: About 1 mm away from the crest of the gingival and anchor suture. After suturing, a foil is placed

margin, the internal bevel incision is made which is over the flap and then covered with a periodontal
directed towards the crest of the bone. dressing.
54 Resective

Chapter
Osseous Surgery
LONG ESSAYS
Question 1 Vertical grooving and radicular blending are osteoplastic

techniques whereas last two steps are ostectomy techniques.
Define osseous surgery. What are its types and what are
the rationale of osseous resective surgery? Discuss in detail Vertical Grooving
about the technique for osseous resective surgery. It is the first step of resective osseous surgery.
Answer It is generally performed with rotary instruments, like

round carbide burs or diamond burs.
According to Carranza, osseous surgery it defined as the This step helps to reduce the thickness the alveolar
procedure by which changes in the alveolar bone can be

housing and to provide prominence to the radicular
accomplished to get rid it of deformities induced by the
aspects of the teeth.
periodontal disease process or other related factors, such as It also provides continuity from the interproximal surface
exostosis and tooth supraeruption.

onto the radicular surface.
Types of osseous surgery can be: Verticular grooving provides advantage to bones having

Additive osseous surgery. thick margins, shallow craters or any other area which

Subtractive osseous surgery. require maximal osteoplasty and minimal ostectomy.

This procedure is contraindicated in areas where roots
Additive osseous surgeries are the surgeries which aim at

restoring the alveolar bone to the original level. are closely approximated or having thin alveolar housing.
Subtractive osseous surgeries are the surgeries which Radicular Blending

aim at restoring the form of pre-existing alveolar bone to This is the second step of osseous reshaping technique.

the level present at the time of surgery or slightly more This step is an extension of vertical grooving.

apical to this level. This steps aims at gradualizing the bone over the entire

Rationales of osseous resective surgery are: radicular surface to provide best results from vertical
grooving.
To reshape the marginal bone to resemble that of the
This step provides a smooth, blended surface for good

alveolar process undamaged by periodontal disease.

flap adaptation.
To convert a periodontal pocket to a shallow gingival
This is also an osteoplastic technique which does not

sulcus to enhance the patients ability to remove plaque

remove the supporting bone.
and oral debris from mouth. Shallow crater formations, thick osseous ledges of bone

Technique on the radicular surface and class I and early class II
furcation defects are some of the situations which can
There are four main steps in resective osseous surgery. They be treated mainly with these two steps.
are as follows:
Vertical grooving. Flattening Interproximal Bone

Radicular blending. This is the third step of osseous resective surgery.

Flattening interproximal bone. It involves removal of very small amounts of supporting

Gradualizing marginal bone. bone.

197
Chapter 54 Resective Osseous Surgery

Therefore it is an ostectomy procedure.
Instruments used for this technique should be used very

It is performed when the interproximal bone levels vary carefully as one can tend to over do this step.

horizontally.
Thus instrument used are various hand instruments

One-wall defects or hemiseptal defects are most such as curettes and chisels over rotary instruments for
effectively treated with this step. gradualizing the marginal bone.

It can be helpful in good flap closure and improved
Various instruments used for resective osseous surgery are
healing in the three walled defect.
as follows:
Gradualizing Marginal Bone
Both rotary and hand instrument are used for this procedures.

This is the last step of this technique.
Rotary instruments are mainly used for osteoplastic

It is also an ostectomy procedure. procedures, whereas hand instruments are used where

This step requires minimal bone removal, but it is more precise results are required.
important for a sound, regular base for the gingival
Hand instruments include curettes, rongeurs,
tissue to follow. interproximal files like schluger and sugarman files,

This step also requires gradualization and blending over chisels like back action chisels and oschsenbein chisels.
the radicular surface.
Rotary instruments include carbide and diamond burs.
SHORT ESSAYS
Question 1
What is Widow’s peak?
A
Answer
Widow’s peak refers to the peak of bones which are
typically seen on the facial or lingual/palatal line angles of
the teeth.
Question 2
What is difference between osteoplasty and ostectomy?
B
Answer
Osteoplasty refers to reshaping of the bone without
removing the tooth supporting bone, whereas ostectomy
also known as osteoectomy refers to the removal of tooth
supporting bone.
Question 3
What is meant by positive, negative and flat architecture? C
Answer

Positive architecture means if the radicular bone is apical
to interdental bone.

Negative architecture means if the radicular bone is
coronal to interdental bone.

Flat architecture means when interdental bone and Figs 54.1A to C: (A) Positive architecture; (B) Flat architecture;
radicular bone, both at the same level (Fig. 54.1). (C) Negative architecture
198
Question 4 Answer
What is meant by definitive and compromise osseous Definitive osseous reshaping means that further osseous

reshaping? reshaping would not improvise the overall result, whereas
compromise osseous reshaping means that a bone pattern
which cannot be improved without significant osseous
removal that can be detrimental to the overall result.
55 Reconstructive

Chapter
Periodontal Surgery
LONG ESSAYS
Question 1 Histologic methods: Pre and post-treatment tissue

blocks can be studied and evaluated and it can act as a
What are the possible outcomes of reconstructive periodontal
clear evidence of a new attachment apparatus.
therapy? What are the various methods by which new
attachment and periodontal reconstruction can be evaluated? Various techniques for reconstructive surgery are as follows:
Discuss in detail about reconstructive surgical technique. Non-bone graft-associated procedures

Removal of junctional epithelium.
Answer

Prevention or impeding of epithelial migration.

Bio-modification of root surface.
Possible outcomes of reconstructive periodontal therapy

Biologic Mediators.
are as follows (Fig. 55.1):

Enamel matrix proteins.
Healing with a long junctional epithelium, which can

Graft-associated procedures.

result soon after filling of bone.

Autogenous bone grafts.
Ankylosis of bone and tooth.

Allografts.

Recession.

Recurrence of pocket.

Combination of these results.

Various methods for evaluation of new attachment and
periodontal reconstruction are as follows:
Clinical methods.

Radiographic methods.

Surgical re-entry.

Histologic method.

Clinical method: It includes pre and post-treatment

pocket probing depths.
Probe can be used to determine the pocket depth,

attachment level and bone level.
Radiographic method: It includes pre and post-

treatment radiograph.
Radiographs can depict the entire topography of the

involved area before and after treatment.
Surgical re-entry: Surgical re-entry can provide a good

view of the state of bone crest of a treated defect after a
period a healing.
Models from impressions of the bone taken at the

initial surgery and later at re-entry can be used to Fig. 55.1: Possible outcomes of reconstructive periodontal
assess the outcome of therapy. therapy.
200
Xenografts. This technique consists of placing the barrier membranes

Non-bone graft materials. over the bone and the periodontal ligament, so as to

Combined techniques. separate them from gingival epithelium.

This technique not seperate the gingival epithelium
Non-bone Graft Associated Procedures

from bone and periodontal ligament but also favours
Are intended to achieve periodontal reconstruction without repopulation of the area by the periodontal ligament
the use of bone grafts. and bone cells.
Various techniques used for the above are as follows: Two types of barrier membranes are as follows:

1. Resorbable(e.g. collagenmembrane)andnon-resorbable
1. Removal of Junctional Epithelium membrane (e.g. expanded polytetrafluoroethylene
It is believed that presence of junctional epithelium and (ePTEF) membrane).
pocket epithelium acts as barrier for successful therapy as 2. Those membranes can be obtained in different shapes
its presence interferes with direct communication between and sizes to suit proximal spaces and facial/lingual
the connective tissue and cementum, and various methods surfaces of furcation.
to achieve this are as follows: Technique for placing these barriers membranes are as
Curettage: It has not been a reliable procedure as the
follows:

result of removal of epithelium by means of curettage
Firstly a mucoperiosteal flap is raised along with vertical
vary from complete removal to persistence of as much

incisions.
as 50%.
Other methods have also been used like ultrasonic
Osseous defects are then debrided thoroughly and

granulation tissue is removed.

methods, rotary abrasives stones and lasers, but
because of clinician’s lack of vision and lack of tactile
Through scaling and root planning is done

sense while using these methods, their effects cannot The membrane is then trimmed with a sharp scissors to

be controlled. approximate size of the area being treated. The apical
Chemical agents: Most commonly used chemical border of the material should extend 3–4 mm apical to

agents for the removal of pocket epithelium are sodium the margin of the defect and laterally 2–3 mm beyond
sulphide, phenol, camphor, antiformin, and sodium the defect
hypochlorite. The occlusal border of the membrane should be placed 2

Since their depth of penetration cannot be controlled mm apical to the CEJ.

therefore effect of their agents is not limited to the A sling suture is given so that the membrane is tightly

epithelium. bound around the tooth.
Surgical techniques: Surgical techniques like excisional Flap is then sutured back in its original position or may

new attachment procedure (ENAP) is most oftenly used be slightly coronal to it with the help of independent
method. sutures interdentally and in the vertical incision.
h A gingivectomy procedure can also be performed Care should be taken that the flap covers the membrane
h

h Modified Widman flap procedure can also be done
completely
h
to achieve same result.
Patient should be prescribed antibiotic for 1 week and

placement of periodontal dressing is optional
2. Prevention or Impeding of Epithelial Migration
4–6 weeks after the surgery the margins of the membrane

Since the epithelium from the excised margin may becomes exposed
rapidly proliferate to be interposed between the healing The membrane is then removed with a gentle tug 5
connective tissue and the cementum, thus only elimination

weeks after the procedure.
of junctional and pocket epithelium may not be sufficient.
The most common technique which prevents the
3. Bio-modification of Root Surface

proliferation of epithelium is referred to as guided tissue
regeneration. Interference with new attachment has been seen

The method has been derived from the classic studies because of the presence of degeneration of remnants

of Nyman, Lindhe, Karring, and Gottlow which say that of sharpy’s fibres, accumulation of bacteria and their
only the periodontal ligament cells have the potential for products, disintegration of cementum and dentin, over
regeneration of the attachment apparatus of the tooth. the tooth surface wall of periodontal pockets.
201
Chapter 55 Reconstructive Periodontal Surgery

Although these interference to new attachment can
These biologic mediators are mainly growth factor which
be removed through root planing, but root surface of are mostly secreted by macrophages, endothelial cells,

the pocket can be treated to improve it’s chances of fibroblasts and platelets.
accepting the new attachment of gingival tissues.
These growth factors are platelet derived growth factor
Various substances which are used for this purpose are: (PDGF), insulin like growth factor (IGF), basic fibroblast
growth factor (bFGF), bone morphogenetic protein
Citric acid: The actions of citric acid are as follows:
(BMP) and transforming growth factor (TGF)
1. Citric acid leads to accelerated healing and new
These mediators have shown to stimulate periodontal
cementum formation after detachment of the gingival wound healing or to promote the differentiation of cells
tissues and demineralisation of the root surface. to become osteoblasts, favouring bone formation.
2. On root planed roots, citric acid produces a 4mm deep
For example, promoting migration and proliferation of
demineralized zone with exposed collagen fibres. fibroblast for periodontal ligament formation.
3. On root planed roots, a smear is formed, which can be
Also PDGF has shown to enhance bone formation in
removed using citric acid, exposing the dentinal tubules. periodontal osseous defects.
Not only this, citric acid makes the tubules appear wider
with funnel-shaped orifices. 5. Enamel Matrix Protein
4. Citric acid also removes endotoxins and bacteria from
the diseased tooth surface Amelogenin, is the main enamel matrix protein, which
5. Citric acid also prevents the epithelium from migrating is secreted by Hertwig’s epithelial root sheath during
over the treated roots. tooth development and also induces acellular cementum
formation.
Citric acid should be used in the following ways:
These proteins are believed to cause periodontal

1. A mucoperiosteal flap should be raised and a thorough regeneration

scaling and root planing should be done, removing the Emdogain is an enamel matrix protein derivate which is

calculus the underlying cementum. obtained from developing porcine teeth, approved by
2. Cotton pledgets soaked in saturated solution of citric the US Food and Drug Administration (FDA).
acid whose pH is 1.0 for 2–5 minutes should be applied. Emdogain is viscous gel containing enamel derived
3. Pledgets should be removed and root surface should be

protein from tooth in a polypropylene liquid, 1 mL of a

irrigated profusely with water.
vehicle solution is mixed with a powder and delivered by
4. Flap should be replaced back and sutured.
syringe to the defect site.
Fibronectin: It is a glycoprotein required for fibroblast to

Amelogenin is the main protein in this mixture, about

attach to root surfaces. 90%, with the rest primarily proline rich non-amelogenin,
It is known to promote new attachment. tuft protein, serum proteins, amelin and ameloblastin.
Tetracycline: It is known to stimulate fibroblast

attachment and growth while suppressing epithelial cell The technique of using Emdogain is as follows:
attachment and migration.
A flap for reconstructive purpose is raised.
It also removes the amorphous layer and exposes the All the granulation tissue and tissue tags are removed,

dentinal tubules. exposing the underlying tissues and all the root deposits
are removed.
4. Biologic Mediators
Bleeding is treated completely within the defect.

There are various factors which stimulate a series of events
Citric acid (pH of 1.0) is used for conditioning of 24%
and cascades at some point, which can result in the EDTA (pH of 6.2) for 15 sec. This helps in removal of smear
coordination and completion of integrated tissue formation layer and facilitate adherence of the emdogain.

Many approaches have been used involving polypeptide
Wound should be then rinsed with saline.
growth and differentiation factor, extracellular matrix
Gel should be applied to cover the root surface completely
proteins and attachment factor and proteins involved in
Contamination with blood and saliva should be avoided.
the bone metabolism
Wound should be closed with sutures.

These are physiologic molecules released by cells, or
Patient should be prescribed with medications, i.e.
derivatives of such molecules, that can regulate events system antibiotic coverage for 10–20 days (doxycycline,
in wound healing. 100 mg daily).
202
Graft Materials and Procedure Inability to use aspiration during accumulation of the

coagulum.
The procedure requires placing of graft materials at the

Unknown quantity and quality of the bone fragments in

site of the defect

the collected material.
These graft materials can be evaluated on their

osteoinductive or osteoconductive or osteogenic b. Bone blend: To overcome the disadvantage of osseous
potential. coagulum, the bone bleed technique has been proposed.
Osteogenesis means to the formation or development of Technique: Its technique uses an autoclaved plastic

new bone by cells contained in the graft. capsule and pestle.
Osteoinduction means a chemical process by which Bone is removed from a pre-determined site, triturated in

molecules contained in the graft like BMPs convert their the capsule to a workable, plastic-like mass, and packed
neighbouring cells into osteoblasts, which in turn form into the bony defects.
bone. c.
Cancellous bone marrow transplant: Maxillary
Osteoconduction is referred to a physical effect by which tuberosity, edentulous areas, and healing sockets are the

the matrix of the graft form a scaffold that favours outside sites from where cancellous bone can be obtained.
cells to penetrate the graft and form new bone. Edentulous ridges can be approached will a flap and

Bone graft can be: cancellous bone and marrow can be removed with
curettes and back action chisels or trephines.
1. Autogenous Bone Graft It takes about 8–12 weeks for sockets to heal and apical

Autogenous grafts are the grafts which are obtained portion is used as donor material.
The particles are reduced to small pieces.

from same individual.

Sources of this kind of graft can be bone from healing d. Bone swaging: It is a difficult technique.

extraction wound, bone from edentulous ridges, bone It has a limited use.

trephined from within the jaw without damaging the It requires an edentulous area adjacent to tooth defect,

roots, newly formed bone in wounds especially created from which the bone is pushed into contact with the root
for this purpose, and bone removed during osteoplasty surface without fracturing the bone at its base.
and ostectomy. Bone can be obtained from extra-oral sites also like iliac

Various forms of autogenous grafts are as follows: autografts, tibia autografts. They have been used in
furcations and defects with various numbers of walls.
a. Osseous Coagulum: Mixtures of bone dust and blood is
referred to as osseous coagulum. 2. Allograft
In this technique small particles from cortical bone are
It is the bone obtained from a different individual of

used.

same species.
This particle size provides additional surface area for the
They are commercially available from tissue banks.

interaction of cellular and vascular elements.

They are obtained from cortical bone within 12 hours of
Sources of the graft material can be lingual ridge on

death of the donor.

the mandible, exostoses, edentulous ridges, bone distal
It is then defatted, cut into pieces, washed in absolute
to a terminal tooth, bone removed by osteoplasty or

alcohol and then deep-frozen.
ostectomy and the lingual surface of the mandible or
The material may then be demineralised and
maxilla. Atleast smm from the roots.

subsequently ground and sieved to a plastic size of 250–
Technique 750 µm and freeze-dried.
Bone is removed using a carbide bur #6 and #8 using a Finally, it is vacuum-sealed in glass vials.

speed of 500–30,000 rpm Allografts can be undecalcified or decalcified.

It is placed in a sterile dappen dish or amalgam cloth, and Undecalcified freeze-dried bone allograft (FDBA)

used to fill the defect h It is considered to be a osteo conductive material
h
Advantage of the technique is the ease by which bone h It has less osteogenic potential than DFDBA
h

can be obtained from already exposed surgical site. Decalcified freeze-dried bone allografts (DFDBA)

Disadvantage is its relatively low predictability and the h It is considered to be a osteoinductive graft
h

inability to produce adequate material for large defects. h It has a higher osteogenic potential
h
203
Chapter 55 Reconstructive Periodontal Surgery
h h
Components of the bone matrix are exposed, since 4. Alloplastic Material
the bone is demineralised in cold and diluted in
These are artificial and synthetic materials used for

hydrochloric acid

grafting.
h h
They are associated with collagen fibrils and have
been termed as BMPs They are also referred to as non-bone graft materials:
h h
DFDBA has shown to have positive results in They include:
periodontal defect having significant probing Calcium phosphate biomaterials: There are two types of

depth calcium phosphate ceramics which are being used:

h h
DFDBA has also shown a gain in attachment level Hydroxyapatite (HA) has a calcium to phosphate ratio,

and osseous regeneration similar to that found in bone materials.

h h
Combination of DFDBA and guided tissue Tricalcium phosphate (TLP): It is with a calcium to

regeneration has also been very successful phosphate ratio of 1.5.

specially in treating furcation defect. Bioactive glass: It consists of sodium and calcium salts,

phosphate and silicon dioxide. E.g. perioglass, biogran

3. Xenografts Used in the form of irregular particles measuring 90–170
These are the graft obtained from different species. mm or 300–355 mm.
Earlier calf bone, Kiel bone or ox bone were used, but now

Other alloplastic materials are plastic materials, cartilages,
these materials have been discarded for various reasons sclera and plaster of paris.
Currently, an anorganic bovine derived bone, Bio-Oss has
Combined Techniques

been used in periodontal defects and in implant surgery

It is an osteo-conductive, porous bone mineral matrix

Combination of several technique can also be used
from cancellous or cortical bone
Like bone graft and non-bone grafting materials together
The organic part of the bone is removed but the

can be used for regeneration
trabecular part and the porosity are retained.
For example enamel matrix derivative like emdogain and
It permits clot stabilization and revascularisation to allow

xenografts, i.e. Bio-Oss can be combined together and
migration of osteoblasts, leading to osteogenesis can be used
Bio-Oss is highly compatible with surrounding tissues

Autogenous bone with guided tissue regeneration results
and elicits no systemic immune responses. in new attachment and periodontal reconstruction.
56

Chapter Furcation
LONG ESSAYS
Question 1 4. Grade 4: In this grade the interdental bone is destroyed

and the soft tissue recedes apically, so the furcation can
Define furcation involvement. Classify furcation defects.
be seen clinically. Therefore, a probe is easily passed
Write in detail about diagnosis and treatment of furcation
through and through in the furcation area.
defects.
Answer Diagnosis
It is defined as the invasion of bifurcation or trifurcation of Diagnosis can be made with the help of the “Naber’s probe”.
multi-rooted tooth by periodontitis. The clinician should be able to identify and classify the
extent of furcation involvement and to identify factors
Furcation is an area of complex anatomic morphology
which contribute to the furcation defect development.
which makes it difficult or impossible to clean with regular
periodontal instrumentation. Furcation involvement is These factors may include:
one of the clinical signs for the diagnosis of advanced Morphology of the affected tooth.

periodontitis and potentially less favourable prognosis for Position of the tooth relative to adjacent teeth.

the affected tooth. Anatomy of the alveolar bone.

Configuration of the bony defect.
Classification

Presence and extent of other dental diseases, like caries

Its classification is done in four grades: and pulpal necrosis.
1. Grade 1: It is an early stage of furcation involvement. Treatment
Only soft tissue is involved. Early bone loss may be seen
because of increase in probing depth but there are no There are three objectives of furcation treatment:
radiological signs. 1. To facilitate maintenance.
2. Grade 2: In this the lesion is cul de sac having a definite 2. Prevent further attachment loss.
horizontal component. This implies that the bone loss 3. Obliterate the furcation defects as a periodontal
has occurred at one side of the tooth. If multiple defects maintenance problem.
are present, they do not communicate with each other
as the alveolar bone remains attached to the tooth.
Treatment of Class I Defects
Radiographically it may or may not be depicted. These are early defects which can be treated with
3. Grade 3: In this the bone is not attached to the dome of conservative periodontal approach. Treatment of choice
the furcation, therefore a multiple defects communicate can be scaling, root planning and maintenance of good
with each other. In early grade 3, the opening may be oral hygiene. In the presence of thick overhanging
filled with soft tissue which is generally not visible. A margins of restorations, facial grooves or cervical enamel
periodontal probe also cannot be passed through and projections, the clinicians must opt for odontoplasty,
through completely because of interference with the recontouring or replacement for eradication of such
bifurcational ridges or facial/lingual bony margins. defects.
205
Chapter 56 Furcation
Treatment of Class II Defects

Hemisection: It refers to splitting of a multi-rooted
tooth into two-rooted tooth and converting them into
In the presence of horizontal component, the therapy

separate portions. This process can be referred to as
becomes even more complicated. Odontoplasty and
bicuspidisation or separation since it converts a molar
osteoplasty are the treatment of choice for such defects. In
into two separate teeth. It is generally done in mandibular
cases of isolated deep Class II furcations, flap procedure is
molars with Class II or III furcation. After sectioning both
used in adjunct with above options.
the roots can be retained and can be given separate
Treatment of Class II–IV Defects crowns or one of the roots can be retained removing the
other one on which maximum bone loss has occurred.
These are the advanced defects in which there is
Procedure for root resection or hemisection:
development of significant horizontal components. Vertical

After administration of local anaesthesia a full

components can also be seen which poses additional

thickness flap is reflected. Adequate access for

problems. Non-surgical therapy is generally not useful in
visualisation and instrumentation to minimize the
such defects. Endodontics therapy and periodontal surgery
surgical trauma should be made. After debridement
may be required to treat the defect.
the area of resection or hemisection should be
Surgical therapy can include any of the following: visualised carefully.
Root resection: It refers to resection of one of the roots

This procedure might require removal of small amount

which has the least periodontal and bone support. It is of facial or palatal bone. A cut is made just apical to
generally indicated in multi-rooted teeth with Grade II–IV the contact point of the tooth, through the tooth, and
furcation involvement. It can be performed on both vital to the facial and distal orifices of the furcation with the
and endodontically treated teeth. Teeth planned for root help of a high speed, surgical length fissure or cross
resection includes the following: cut fissure carbide bur.
Teeth that are critically important to the overall dental

In case of hemisection a vertically oriented cut is

treatment plan. made buccolingually through the pulp chamber and

Teeth that have sufficient attachment remaining for

through the furcation.
function. After sectioning the root is elevated from the socket.

Teeth for which more predictable or cost effective

One should not traumatise the bone remaining on the

method is not available. remaining tooth.

Teeth in patients with good oral hygiene and low

Odontoplasty might be required if necessary.

caries activity. Any bony lesion on the adjacent teeth should be

Guidelines to determine which root to be resected are

resected or regenerated.
as follows: The flaps are then approximated and sutured.

Resect the root or roots which eliminate furcation and

Reconstruction: It can be achieved with grafting
allow the production of a maintainable architecture materials. Bone grafts with or without guided tissue
on the remaining side. regeneration (GTR) membrane can be used to reconstruct
Remove the root having the maximum amount of

the furcation defects.
bone and attachment loss. Extraction: Teeth with through and through furcation

Remove the root which will contribute best in the

defects and advanced attachment loss should be
elimination of the periodontal problems. extracted especially for individuals who cannot perform
Remove the root having maximum number of

adequate plaque control, who have high level of caries
anatomic problems. activity, who will not commit to a suitable maintenance
Remove the root which would least complicate the

program, or who have socio-economic factors that may
future periodontal maintenance. preclude more complex therapies.
206
SHORT NOTES

Question 1 Classification of cervical enamel projection:
What are cervical enamel projections (CEPs). Grade I: The enamel projection extends from cemento-

enamel junction (CEJ) of the tooth towards the furcation
Answer entrance.
These are projections of the enamel seen on the cervical
Grade II: The enamel projection approaches the entrance
portion of the tooth.

to the furcation. It does not enter the furcation, and thus
These are found in 8.6%–28.6% molars.
there is no horizontal component.

These projections interfere with plaque removal, plaque

control and therefore, should be removed to facilitate Grade III: The enamel projection extends horizontally

maintenance. into the furcation.
57 Periodontal Plastic and

Chapter
Aesthetic Surgery
LONG ESSAYS
Question 1 Problems associated with shallow vestibules

Problems associated with an aberrant frenum.
Enumerate various mucogingival/perioplastic problems

and surgery procedures. Define periodontal plastic surgery Problem Associated with Attached Gingiva
and what are the objectives of plastic surgery? Enumerate
various techniques to increase the width of attached Creation or widening the zone of attached gingiva

gingiva. Explain in detail about gingival recession along around the teeth and implants is the ultimate goal of
with its treatment. Explain free gingival grafting techniques mucogingival surgical procedures.
the root coverage in detail. The objectives of widening the zone of attached gingiva

are as follows:
Answer To enhance plaque removal around the gingival

Various mucogingival problems are : margin
To improve aesthetics
Shallow vestibule

To reduce inflammation around restored teeth.

Inadequate width of attached gingiva

Aberrant frenal attachment
Problems Associated with Shallow Vestibule

Gingival recession.

Various mucogingival perioplastic surgery procedures are:
Adequate vestibular depth is important for placing the

toothbrush head and maintaining adequate plaque
Crown lengthening
control.

Periodontal prosthetic corrections
In presence of minimal vestibular depth, adequate oral

Ridge augmentation

hygiene is not possible.

Root coverage
Also, adequate vestibular depth is important for proper

Reconstruction papilla

placement of removable and fixed appliances.

Aesthetic surgical correction

Aesthetic surgical correction around implants
Problems Associated with Aberrant Frenum

Surgical exposure of unerrupted teeth for orthodontics.

An aberrant frenum attachment which on the margin of the
Definition of Periodontal Plastic Surgery gingiva may interfere with plaque removal and tension on
According to Carranza, periodontal plastic surgery is defined this frenum may tend to open the sulcus therefore in such
as the surgical procedure performed to correct or eliminate cases surgical removal of frenum becomes important.
anatomic, developmental or traumatic deformities of the Various techniques to increase the width of attached

gingiva or alveolar mucosa. gingiva are as follows:
Techniques can be classified as follows—
Objectives of Periodontal Plastic Surgery

Gingival augmentation apical to the area of recession

Objectives of periodontal plastic surgery are as follows: Gingival augmentation coronal to the area of recession

Problems associated with attached gingiva (root coverage).

208
Gingival augmentation apical to the area of recession 2. Class II: Marginal Tissue recession extends to or beyond

In this case no attempt is made to cover the denuded the mucogingival junction

root surface, where there is gingival and bone There is no loss of bone or soft tissue in interdental area.
recession. 3. Class III: Marginal tissue recession extends to or beyond
A pedicle or a free graft is placed over the recipient the mucogingival junction.

cells apical to the area of recession. There is interdental bone and soft tissue loss along with
Various techniques of augmentation are: malpositioning of the teeth.
Free gingival autografts
4. Class IV: Marginal tissue recession extends to or beyond
the mucogingival junction.

Free connective tissue autografts.
There is severe bone loss and soft tissue loss interdentally

Gingival augmentation coronal to the area of recession
along with severe malpositioning.

(root coverage)
Root coverage options for a gingival recession are as follows:
Gingival recession: Apical shift of the gingival margin is
referred to as gingival recession. Free gingival autograft.

Most accepted classification of gingival recession has Free connective tissue autograft.

been proposed by Miller, it is as follows (Fig. 57.1): Pedicle autograft.

Laterally (horizontally) positional flap.
1. Class I: Marginal tissue recession does not enter to the

Coronally positioned flap.
mucogingival junction

Subepithelial connective tissue graft.
There is no loss of bone or soft tissue in the intradental
Guided tissue regeneration.
area.

Pouch and tunnel technique.

Free Gingival Autograft
Step 1: Prepare the recipient site: The area around the
denuded root surface is de-epithelized.
The root surface is scaled and planed thoroughly.

The purpose of this step is to prepare a firm connective

tissue bed to receive the graft.
Step 2: Obtain the graft from the donor site.
The classic technique consists of transferring a piece of

keratinised gingiva from the donor site to the recipient
site.
The dimension of the root in length and breadth along

with dimension of the de epithelized recipient site are
calculated.
A tin foil template is made by placing the template over

the recipient site and cutting it to the size more than the
dimensions calculated for the root and de-epithelized
area.
Dimension is kept more because the graft would shrink

at the time of healing so to compensate this shrinkage,
size of the graft should be more than the recipient site.
Then place this transplant over the donor, i.e. the palate

between the premolar and molar area, towards the
gingival margin and make a shallow incision around this
template with a #15 blade.
Insert the blade to the desired thickness.

Fig. 57.1: Miller’s classification of gingival recession. Elevate one edge and hold with tissue forceps.

209
Chapter 57 Periodontal Plastic and Aesthetic Surgery

Continue to separate the graft with a blade and lift it
Excess tension should be avoided, which can lead to
gently as the separation progresses. distortion of the graft from the underlying surface.

If sutures are placed at the margins of the graft, it helps
Step 4: Donor site protection.

to control during separation and transfer, and simplifies

The donor site should be covered with a periodontal
placement and suturing the recipient site.

For the survival of the graft, it should have proper dressing for at least a period of one week.
A modified hawley’s retainer is useful to cover the pack
thickness.

It should be thin enough to permit diffusion of nutritive on the palate.
fluid from the recipient site, which is essential in the Step 5: Recipient site protection.
immediate post-transplant period. Once the graft is secured with sutures, the area should

There may be necrosis of the graft due to exposure of the be covered by a tempered tin foil, over which the
recipient site, if the graft is too thin. periodontal dressing should be placed.

If, the graft is too thick, its peripheral layer is jeopardized
because of the excessive tissue that separates, it from Healing of the Graft
new circulation and nutrients. Survival of the connective tissue, leads to the success of

Thick grafts also cause deep wounds at the donor site, grafts.
with the possibility of injuring the major palatal arteries. The graft in the initial stages, is maintained by a diffusion

Ideal thickness of a graft should be between 1 mm of fluid from the host bed, adjacent gingiva and alveolar
to 1.5 mm. mucosa.

Once the graft is separated, loose tissue tags should be The fluid from the host vessels is transudate and provides

cleared from the under surface. nutrition and hydration essential for initial survival of the

Edges should be thinned to avoid bulbous marginal and transplanted tissues.
interdental contours. On first day, the connective tissue becomes oedematous

Precautions should be taken when harvesting a graft and disorganized.
from the palate. Connective tissue undergoes degeneration and lysis of

Since the submucosa is in the posterior region, is thick some of its elements.
and fatty, so therefore it should be trimmed so that it As the healing progresses, the oedema is reduced and

does not interfere with vascularisation. degenerated connective tissue is replaced with new

Graft can be thinned by holding it between two wooden granulation tissue.
tongue depressors and slicing it with a sharp # 15 blade By the second day, revascularisation of the graft takes

longitudinally. place.
Step 3: Transfer and immobilize the graft. Capillaries from this recipient bed proliferates into the

The gauze should be removed from the recipient site.

graft to form a network of new capillaries and anastomose
Excess clot should be removed.
with pre-existing vessels.
The graft should be positioned and adapted firmly over

The central portion of the graft revascularises at the last

the recipient bed so that it covers the root surface and and it is completed by 10th day.
the de-epithelised area completely immobilize. Epithelium undergoes degeneration and sloughing, with

Graft should be then sutured at the lateral borders and a

complete necrosis occurring is some areas.
periosteal suturing can be done if required. It is replaced by new epithelium from the borders of the

The graft should be completely immobilized.

recipient site.
SHORT ESSAYS
Question 1 Step 1: Prepare the recipient site.

De-epithelisation is done around the denuded root
Explain laterally displaced flap.

surface to prepare the recipient site. The root surface

should be thoroughly scaled and root planed.
Answer
Step2: Prepare the flap.
This technique was given by Grupe and Warren in 1956 for The donor sites gingiva should have an adequate width of
root coverage. attached gingiva.
210
Partial thickness or full thickness flap can be raised Answer

depending upon the gingival biotypes.
This procedure is indicated for multiple and larger

Using a #15 blade vertical incisions are made from
defects with adequate vestibular depth and thick

the gingival margin to outline ae flap just next to the
gingival biotype so that a split thickness flap could be
recipient site.
raised.
Periosteum should be incised and the incision should
The technique was given by Langer and Langer in 1985.

extend into the oral mucosa to the level of the base of
the recipient site.
Techniques
The flap should be wide enough so that it coveres the

recipient site completely. A partial thickness flap should be raised with a horizontal

A vertical incision is made along the gingival margin and incision at least 2 mm away from the tip of the papilla.

interdental papilla and separate a flap which consist of Two vertical incisions should also be given 1–2 mm away
from the gingival margin of the adjoining teeth.
epithelium and some part of connective tissue, leaving
These incisions should extend atleast half to one tooth
behind some connective tissue and periosteum.

wider mesiodistally than the area of gingival recession.
A releasing incision also known as cut back incision is Flap should be extended upto the mucobuccal fold.

made to avoid tension at the base of the flap. A short

Root surfaces should be planed through so that if

oblique incision is made into the alveolar mucosa at the convexity is reduced.
distal corner of the flap, facing towards the direction of A connective tissue graft is harvested from the palate. It

the recipient site. should be taken 5–6 mm away from the gingival margins
Step 3: Transfer of flap: of molars and premolars.
Flap should be slided laterally to the adjacent root, so After taking the graft, the palatal wound is sutured in a

that it lies flat and firm on the recipient bed. primary closure
Flaps should be secured by placing sutures specially Connective tissue should be placed over he denuded

sling and interrupted sutures. root surface and sutured using resorbable sutures to the
underlying periosteum.
Step 4: Protection of flap and the donor site The connective tissue graft is then covered with the

The involved area should be covered with a tempered tin outer portion of the partial thickness flap and interdental
foil over which a periodontal dressing should be placed. suturing is done.
Pack and sutures should to be removed after a period of 1 Atleast two-half to two-thirds of the connective tis-

week. sue graft must be covered by the flap for the exposed
portion to survive over the denuded root surface.
Question 2 The area is covered with a tempered tin foil and over

Describe subepithelial connective tissue graft. which periodontal dressing is placed.
58 Recent Advances in

Chapter
Surgical Techniques
SHORT ESSAYS
Question 1 Delayed wound healing.

Define lasers in periodontics.
Plume is generated which has an unpleasant smell.

Answer Precautions
Laser is an acronym for light amplification by stimulated Use glasses for eye protection (patient operator and

emission of radiation. assistants).
Laser can concentrate light energy and can exert strong Prevent inadvertent radiation.

effect targeting tissues at an energy level much higher Protect the patients’ eyes, throat, and oral tissues outside

than the natural light. Once in contact with tissue, laser the target area.
energy is reflected, scattered, absorbed or transmitted to Use wet gauge packs to avoid reflection from shiny metal

the neighbouring tissues (Fig. 58.1). surfaces.
Applications of lasers (Table 58.1).
Potential Risks with Lasers

Advantages Excessive tissue destruction by direct ablation and

Better haemostasis. thermal side effects.

Bactericidal effect. Destruction of the attachment apparatus at the bottom

Wound contraction is less. of the pockets.

Patient and operator comforting. Excessive ablation of root surfaces and gingival tissues

within periodontal pocket.
Disadvantages Thermal injury to the root surface, gingival tissues, pulp

It has strong thermal side effects, leading to melting, and bone tissues.

cracking and carbonisation. Question 2
Define microsurgery in periodontics.
Answer
Periodontal microsurgery introduces the potential for less
invasive surgical approaches in periodontics.
Magnification systems: It includes:
Magnifying loupes.

Microscope.

Magnifying Loupes
They are the most common mode of magnification.

They are dual mononuclear telescopes with side by side

Fig. 58.1: Interaction of human tissue and laser irradiation. lenses convergent to focus on the operative field.
212
Table 58.1: Application of lasers.

Type (wave length) Active medium Dental applications

Excimer laser (193–350) Argon fluoride (ArF) Xenon chloride (XeCl) Hard tissue ablation, dental calculus removal
Gas laser Argon (Ar) (438–515) Curing of composite materials, tooth whitening, intraoral soft tissue
surgery, sulcular debridement (subgingival curettage in periodontitis,
and peri-implantitis)
Helium neon (He Ne) (637) Analgesia, treatment of dentin hypersensitivity, aphthous ulcer treatment
Carbon dioxide (Co2) (10,600) Intraoral soft tissue and soft tissue surgery, aphthous ulcer, gingival
depigmentation , treatment of dentin hypersensitivity, analgesia
Diode lasers (655–980) Indium gallium arsenide phosphorous Caries and calculus detection
(InGaAsP)
Gallium aluminium arsenide (GaAlAs) Intraoral general and implant soft tissue surgery, sulcular debridement
Gallium arsenide (GaAs) (subgingival curettage in periodontitis), analgesia, treatment of dentin
hypersensitivity, pulpotomy, root canal disinfection, removal of enamel
caries, aphthous ulcer treatment, gingival depigmentation
Solid state lasers Frequency doubled alexandrite Selective ablation of dental plaque and calculus
Neodymium: yttrium aluminium garnet Intraoral general and implant soft tissue surgery, sulcular debridement
(Nd:YAG) (1064) (subgingival curettage in periodontitis), analgesia, treatment of dentin
hypersensitivity, pulpotomy, root canal disinfection, removal of enamel
caries, aphthous ulcer treatment, gingival depigmentation
Erbium group Caries removal and cavity preparation, modification of enamel and
Erbium: yttrium aluminium garnet dentin surfaces, intraoral general and implant soft tissue surgery,
(Er:YAG) (2940) sulcular debridement( subgingival curettage in periodontitis and peri-
Erbium: yttrium scandium gallium garnet implantitis), scaling of root surfaces, osseous surgery, treatment of
(Er:YSGG) (2790)w dentin hypersensitivity, analgesia, pulpotomy, root canal treatment and
Erbium, chromium: yttrium scandium disinfection, aphthous ulcer treatment, removal of gingival melanin and
gallium garnet (Er, Cr:YSGG) (2780) metal–tattoo pigmentation
There are three types of loupes: parallel optic axis.

1. Simple loupes: Surgical microscopes allow the dentist to change the

It has a pair of single meniscus lenses. working magnification easily.

They are primitive magnifiers with limited capabilities. For use in periodontics, the surgical microscope should

Weight and size is large because it becomes difficult have both manoeuvrability and stability.

to handle them.
Its magnification is not more than 1.5x.
Periodontal Microsurgery

2. Compound loupes: All the kinds of periodontal procedures can be performed
They are multi-element lenses with intervening air with microsurgical techniques. They require surgical loupes,

spaces to achieve additional refractory surfaces. microscope, or both, microsurgical set of instruments
Its magnification is around 3x. which include special microsurgical blades, needle holders,

3. Prism telescopic loupes: scissors and sutures ranging from 6-0 to 9-0 to approximate
They are the most advanced system of loupes. the wound edges accurately.

They have better magnification, wider depths of fields,
Advantages

longer working distances and larger fields of view.
They have a magnification above 4x. Makes the procedure less invasive

Very precisely and neatly done procedures
Microscope

Better wound healing

As compared to loupes, microscopes provide better Better visualisation of the operating field.

magnification and superior optical performance.
It requires training and practice to gain proficiency.
Disadvantages

Dental microscopes employ Galilean optics with Requires training and practice to gain proficiency

binocular eyepieces joined by offsetting prisms to permit Expensive equipment.

59

Chapter Dental Implants
LONG ESSAYS
Question 1 Endosteal implants.

Sub-periosteal implants.
What is a dental implant? What is osseointegration? Classify

Transosteal implants: A dental implant that penetrates
dental implants.

both cortical plates and passes through the entire
Answer thickness of the alveolar bone.
Sub-periosteal implant: An implant that is placed
Dental implant is a prosthetic device of alloplastic

beneath the periosteum of the bone, it receives its
material(s) implanted into the oral tissues beneath the
primary bone support by resting on it.
mucosal and/or periosteal layer, and on/or within the bone
This implant does not osseointegrate.
to provide retention and support for a fixed or removable

prosthesis.
Endosseous implant: An implant that is present within

the bone, extends into basal bone for support.
Osseointegration Types: Screw form, cylinder form (hollow, solid), blade

form.
This concept proposed by Branemark in 1960.
“The apparent direct attachment or connection of Depending on the Materials Used
osseous tissue to an inert, alloplastic material without Metallic Implants
intervening connective tissue.”
Titanium.

Glossary of Prosthetic Terms Titanium alloy.

Cobalt chromium molybdenum.
Structurally Oriented Definition

“Direct structural and functional connection between the
Depending on their Reaction with Bone (Meffert)
ordered, living bone and the surface of a load carrying Bioactive HA coated, CaP coated.

implants.” Bio-inert implants metals.

Branemarks and Associates (1977) Question 2
What are the various complications of implant surgery?
Histologically
What is peri-implantitis? What is its management?
Direct anchorage of an implant by the formation of bone
directly on the surface of an implant without any intervening Answer
layer of fibrous tissue. Mobility after the healing period.

Mucosal inflammation.
Albrektson and Johnson (2001)

Progressive bone loss.

Dental implants can be classified as: Mechanical problem—component fracture, abutment

Based on Placement within the Tissues screws loosening.

Transosteal implants. Peri-implantitis.

214
Peri-implantitis Contraindications
Peri-implantitits is the inflammation around the Smokers, diabetic patients, hypertensive patients.

peri-implant tissues caused primarily due to plaque Patients undergoing radiation therapy.

accumulation around the implant. Patients on corticosteroid therapy.

This process is similar to the one seen on natural tooth. Patients having psychological problems.

Peri-implant infections can be classified as peri-implant Patients with poor oral hygiene.

mucocitis and peri-implantitis depending on severity. Cost factor.

Peri-implant mucocitis is the reversible inflammatory Non-motivated patients.

process in the mucosa of implant. Whereas, irreversible
Question 4
inflammatory reactions leading to loss of supporting
bone results in peri-implantitis. Discuss the surgical procedures for placement of implants.
What is two-stage and single-stage implants?
Signs and Symptoms of Peri-implatitis
Answer
Bleeding, suppuration, pocket formation, bone loss.
Procedure

Pain is generally absent but when present it is associated

with acute infection. Clinical evaluation.

Radiographic evaluation: Intraoral periapical radiography,
Management
orthopantomography, cone-beam computed tomography.
Non-surgical Therapy Selection of desired implant size depending on clinical

and radiographic evaluation.
Pharmacological therapy: Sub-gingival irrigation for 2–3 Patient preparation.
weeks for 2–3 times daily. Proper recommendation of oral

Local anesthetic administration.
hygiene instructions.

Incision and flap reflection at the desired site.
Chlorhexidine is prescribed as it has an antimicrobial

Preparation of osteotomy site using pilot drills and

effect and substantivity at the affected site.

subsequent drills.
Tetracycline fibres and systemic antibiotics can also be
Upon the preparation of osteotomy site, the implant is

prescribed. placed either mechanically or motor-driven instruments.
Mechanical Debridement Cover screw is placed over the implant and flap is sutured.

Mechanical debridement can be recommended for a failing Two-stage Implant
implant along with coating the implant surface with a
In a two-stage implant, once the implant is placed patient is
super-saturated solution of citric acid for 30–60 seconds,
called after a period of 1 week for suture removal and then
so as to remove endotoxins from the implant surface. Soft after a period of 2–3 months for a second-stage surgery
tissue lasers can also be used for eradication of bacteria. in which the cover screw is exposed by giving an incision
Occlusal Adjustments and the cover screw is replaced by a healing abutment
or a gingival former and then the prosthetic part is done.
Surgical Therapy Therefore, it is termed as two stage implant placement.
If the non-surgical therapy is ineffective, then the surgical Single-stage Implant
techniques are indicated. It includes debriding the implant
surface along with resective and regenerative techniques. In this type of surgery, the implant is loaded with the crown
at the time of implant placement surgery, thus preventing
Question 3 multiple visits.
What are the indications and contraindications of implants?
Question 5
Answer Discuss the maintenance of dental implants.
Indications Answer
Patients with edentulous sites or jaw. The patient should be recalled at regular intervals in

Patients with loss of multiple teeth. order to provide preventive services.

215
Chapter 59 Dental Implants

A plastic probe should be used for checking the probing
A rubber cup should be used to polish the implant
depth around the implants. surface with a non-abrasive polishing paste.

Plastic curettes are available for the removal of any
Proper oral hygiene instructions should be given to the
deposits around the implant surface. patients, which include a soft sulcular tooth brush, anti-
plaque agents and interdental aids.
60 Supportive

Chapter
Periodontal Therapy
LONG ESSAYS
Question 1 Parts of Maintenance Phase

Discuss in detail supportive periodontal treatment. Part 1: Examination:

Changes in medical history if any, post active
Answer

periodontal therapy.
This phase is also known as recall / maintenance / Oral pathological examination.

supervised recall. Status of the present oral hygiene.

It forms an important and integral part of overall Check for any gingival change.

Pocket depth changes.
periodontal treatment and can be considered as an

Development of mobility if any.
extension of periodontal therapy.

This part of periodontal therapy begins post the Changes in the occlusal harmony.

Restorative and prosthetic changes.
completion of active periodontal therapy and is

continued regularly at periodic intervals for the lifetime Part 2: Treatment:

of dentition or implants. Oral hygiene instructions are given and maintenance

Transfer of the treatment from active treatment stage of oral hygiene is reinforced.

to supportive periodontal therapy (SPT) requires careful Oral prophylaxis (scaling and polishing) is performed.

planing on the part of the dental team. Chemical irrigation / site-specific antimicrobial

placement is done.
Rationale Part 3: Report, clean-up and schedule next procedure:

The main rationale of SPT is to prevent recurrence of Write report in the case sheet.

periodontal disease. Discuss the observations with the patient.

Schedule next follow-up visit / periodontal treatment

Aims and Objectives visit / refer to restorative or prosthetic treatment.
The basic aim of SPT is to supervise, control and prevent Part 1: Examination and evaluation:

development of disease by the patient so that he or In this phase, the operator primarily looks for changes

she can maintain a healthy and functional dentition for post the last appointment.
life. Current oral hygiene condition of patient is evaluated.

Any change in the medical or dental history post the
Objectives

last appointment is updated.
Maintenance of a healthy and functional oral environment. Gingival status, periodontal pocket depth and peri-

Preservation and maintenance of alveolar bone support implant probing depth are examined.

and clinical attachment level. Oral mucosa should be thoroughly examined for any

Periodic evaluation of home care. kind of pathological condition.

217
Chapter 60 Supportive Periodontal Therapy
Radiographs are repeated and compared with

Effectiveness of home care: A good home-care regimen
previous radiographs to check bone height, repair of by the patient decreases the frequency of recalls.

osseous defects, periapical changes, signs of TFO and
Degree of control of inflammation achieved: As the
carious lesions. patient regains the total health of oral mucosa or
Patients must be advised to perform their respective
tissue, the frequency of appointments is reduced.
oral hygiene regimen immediately before the
Management of different types of recall patients:
appointment in order to assess the effectiveness of h Patients who are uncooperative in maintaining the
h
plaque control. home-care instructions require frequent office care

Hygiene regimen must be reviewed and corrected till

with thorough root instrumentation.
h In patients who had refused surgical phase in active
the patient shows the necessary proficiency in plaque h
control. periodontal therapy, require regular scheduling of

Instruction sessions should be scheduled till adequate

visits at short-time intervals.
h Patients who have been hospitalised for several
plaque control is achieved. h
Part 2: Treatment:
weeks are treated with periodic scaling and root
planing in the hospital itself if the health condition

Scaling, root planing and polishing are performed.

of the patients permits.

The operator must be careful not to instrument

h Patients who have been fully and successfully

normal sites with shallow sulci (1–3 mm depth). treated yet show distinct breakdown in the
Remaining pockets either irrigated with antimicrobial
localised area in recall visits need to be carefully

agents or site-specific anti-microbial delivery systems inspected.

are placed. h Careful medical history is performed and if
h
Part 3: Determination of recall visit intervals:

favourable, involved areas are retreated.

Following factors are taken in account to determine the h Flap surgery, curettage and antibiotic therapy
h
frequency and time interval between the recall visits: should be administered.
Severity of disease: More severe the disease, more
h Recall visits are scheduled at least once in 2–3
h
frequently the patient is recalled. months.
SHORT ESSAYS
Question 1
Incomplete or inadequate or insufficient treatment
Important factors causing recurrence of periodontal disease. procedure that failed to remove the potential factors
favouring plaque accumulation.
Answer
Persistence of calculus in areas with difficult access.
The following factors are responsible for the recurrence
Improper restorations post the active periodontal
of periodontal disease: therapy.
In most cases, the aetiology of recurrence is associated

Failure of patient to comply with periodic check-ups.
with inadequate maintenance of home care oral
Development or presence of some systemic diseases
hygiene instructions or failure to comply with SPT recall that may affect host resistance to maintain previously
visits. acceptable levels of plaque.
2 SECTION
QUESTIONS
ASKED
RECENTLY

61 Recently Asked

Chapter
Questions
GINGIVA
Long Essays 4. Attached gingiva. [NTR-OR]

5. Sulcular epithelium. [NTR-NR]
1. Describe the normal clinical features of gingiva. [RGUHS] 6. Enzymes in gingival fluid. [NTR-NR]
2. Describe briefly the importance of attached gingiva. 7. Junctional epithelium. [NTR-OR]
[NTR-OR] 8. Dentogingival junction. [NTR-NR]
3. Define gingiva. Describe its macroscopic and microscopic 9. Gingival pigmentation. [NTR-OR]
appearance and functions. Add a note on the importance 10. Histology of gingival surface epithelium. [RGUHS]
of gingival fluid. [NTR-OR] 11. Compare attached gingiva and alveolar mucosa.
4. Write about histological and functional features of [RGUHS]
normal gingiva. Add a note on the role of epithelial 12. Microscopic features of healthy gingiva. [MUHS]
attachment in periodontal disease. [NTR-OR] 13. Gingival fluid. [MUHS]
5. Describe the normal structure of gingiva. Write in detail 14. Difference between attached gingiva and alveolar
about the electron microscopic structure of gingival mucosa.[MUHS]
epithelium.[RGUHS] 15. Describe the various concepts of formation of the
6. Describe the clinical and histological features of normal gingival sulcus and give its significance. [MUHS]
healthy gingiva. [MUHS] 16. Interdental papilla. [RGUHS]
7. Define gingiva. Give different clinical features, between 17. Factors affecting gingival crevicular fluid flow.
normal and diseased gingiva. [MUHS] [NTR-UHS]
8. Define oral mucosa. Describe the clinical and microscopic 18. Inflammatory cell granuloma. [NTR-UHS]
features of normal gingiva. [NTR-UHS] 19. Gingival crevicular fluid. [GOA]
9. Define and classify oral mucosa. Describe the anatomical 20. Clinical features of healthy gingiva. [RGUHS]
and histological features of gingiva. [NTR-UHS]
10. Correlate clinical and microscopic features of healthy Short Notes
gingiva.[GOA]
1. Col.[RGUHS]
11. Define gingiva. Discuss the macroscopic features of
2. Gingiva.[RGUHS]
gingiva.[GOA]
3. Gingival fibres. [RGUHS]
12. Define gingiva. What are the parts of normal gingiva?
4. Gingival sulcus. [RGUHS]
Describe the microscopic picture of normal gingiva.
5. Attached gingiva. [RGUHS; GOA]
[MUHS]
6. Mast cell in gingiva. [RGUHS]
13. Define gingiva. Write in detail the microscopic features
7. Gingival innervations. [RGUHS]
of normal gingiva. [GOA]
8. Blood supply to gingiva. [RGUHS]
9. Long junctional epithelium. [RGUHS]
Short Essays
10. Role of mast cells of gingiva. [RGUHS]
1. Compare attached gingiva and alveolar mucosa.[RGUHS] 11. Classification of gingival fibres. [RGUHS]
2. Histology of gingival surface epithelium. [RGUHS] 12. Functions of gingival fibre system. [RGUHS]
3. Gingival fibres. [NTR-OR; MUHS] 13. Gingival fibres and its importance. [RGUHS]
222
14. Clinical significance of keratinized gingival. [RGUHS] 31. Gingival stippling. [RGUHS]
15. Gingival col. [NTR-NR; RGUHS] 32. Define hypertrophy, hyperplasia and neoplasia.[RGUHS]

16. Free gingiva. [NTR-NR] 33. Biologic width. [RGUHS]
17. Microscopic features of healthy gingiva. [MUHS] 34. Transgingival probing. [RGUHS]
18. Gingival crevicular fluid. [MUHS; RGUHS] 35. Dentogingival unit. [RGUHS; NTR-UHS]
19. Definition and functions of gingival fibres. [MUHS] 36. Functions of periodontal ligament. [RGUHS]
20. Gingival collagen fibres. [MUHS] 37. Stillman’s clefts: [NTR-UHS]
21. Gingival blood supply and innervation. [MUHS] 38. McCall’s festoons. [NTR-UHS]
22. Consistency of gingiva. [MUHS] 39. Orogranulocytes.[NTR-UHS]
23. Defence mechanism of gingiva. [MUHS] 40. Langerhans cells. [NTR-UHS]
24. Mention about macroscopic and microscopic structures 41. Prostaglandins.[NTR-UHS]
of normal gingiva. [MUHS] 42. Palatogingival groove. [NTR-UHS]
25. Define periodontology and periodontics. [MUHS] 43. Importance of attached gingiva. [GOA]
26. Neutrophils. [RGUHS; NTR-UHS] 44. Saliva.[GOA]
27. Define and classify embrasures. [RGUHS] 45. Role of saliva as a defence mechanism of gingiva.[GOA]
28. Cells of gingival epithelium. [RGUHS] 46. Mast cell. [GOA]
29. Lamina dura. [RGUHS; NTR-UHS] 47. Attached gingival. [RGUHS]
30. Mucogingival junction. [RGUHS; NTR-UHS] 48. Fenestration and dehiscence. [RGUHS]
TOOTH SUPPORTING STRUCTURES (PERIODONTAL LIGAMENT, ALVEOLAR BONE, CEMENTUM)
Long Essays 12. Enumerate the principle groups of periodontal ligament

fibres. Add a note on its cellular elements and functions
1. Describe the functions and the structure of periodontal
of periodontal ligament. [NTR-NR]
membrane.[RGUHS]
13. Discuss in detail the functions of the periodontal
2. Discuss in detail about the anatomy, histology and
ligament.[MUHS]
functions of periodontal ligament. [RGUHS]
14. Describe the normal structure and functions of
3. Describe the structure of cementum and add note on
cementum. Discuss the histologic importance of
clinical significance of cementoenamel junction.
cementum in periodontal therapy. [MUHS]
[RGUHS]
15. What is periodontium? Name the different tissues that
4. Describe the histology and functions of the principal
constitute the periodontium. Describe different tissues
fibres of periodontal ligament. What are the periodontal
of the periodontium. [MUHS]
ligament changes in trauma from occlusion? [RGUHS]
16. Define periodontal ligament. Describe in detail the
5. Write in detail the functions of periodontal ligament.
functions of periodontal ligament. [MUHS]
[RGUHS]
17. Enumerate the components of periodontium. Describe
6. Describe the structure and functions of periodontal
the structure of periodontal ligament. [RGUHS]
ligament.[NTR-OR]
18. Define cementum. Write in detail the microscopic
7. Describe briefly the various gingival and periodontal
structure of cementum. [RGUHS]
fibre groups. [NTR-OR]
19. Describe the structure of periodontal ligament. [GOA]
8. Describe in detail the role of alveolar bone in health and
20. Define cementum. Classify and give its microscopic
periodontal disease. [NTR-OR]
structure. Add a note on clinical significance of
9. Define periodontal ligament. Describe the microscopic
cementum.[GOA]
and macroscopic features of periodontal ligament.
[NTR-NR] Short Essays
10. Define cementum. Describe the structure, composition
and clinical significance of cementum. [NTR-OR] 1. Functions of periodontal ligament.
11. Define periodontal ligament. Describe the microscopic [RGUHS; MUHS; NTR-UHS]
features and add a note on its functions. [NTR-OR] 2. Alveolar bone. [RGUHS]
223
Chapter 61 Recently Asked Questions
3. Define periodontal ligament and describe its function. Short Notes

[RGUHS]
1. Physical function of periodontal ligament. [GOA]

4. Enumerate the various groups of principal fibre bundles
with diagrams. [RGUHS] 2. Oxytalan fibres. [RGUHS]
5. Dehiscence.[NTR-OR] 3. Sharpey’s fibres. [RGUHS]
6. Fenestration.[NTR-OR] 4. Functions of cementum. [RGUHS]
7. Lamina dura. [NTR-OR] 5. Cementoenamel junction. [RGUHS; NTR-UHS]
8. Oxytalan fibres. [NTR-OR] 6. Histology of periodontal fibres. [BUHS]
9. Acellular cementum. [NTR-OR] 7. Causes of hypercementosis. [RGUHS]
10. Cellular cementum. [NTR-NR] 8. Blood supply to periodontal ligament. [RGUHS]
11. Intermediate plexus. [NTR-OR] 9. Principal fibres of periodontal ligament. [RGUHS]
12. Mediator of alveolar bone. [NTR-OR] 10. Fenestration and dehiscence. [RGUHS]
13. Composition of cementum. [NTR-NR] 11. Define fenestration and dehiscence. [RGUHS]
14. Cementoenamel junction. [NTR-NR] 12. CEJ.[RGUHS]
15. Fenestration and dehiscence. [NTR-OR; MUHS] 13. Define periodontium. What does it comprise of?[MUHS]
16. Dehiscence and fenestration. [NTR-OR] 14. Hypercementosis. [MUHS; NTR-UHS]
17. Cementoenamel junction relationships. [NTR-OR] 15. Cemental tear. [RGUHS]
18. Physical functions of periodontal ligament. [NTR-OR] 16. Clinical significance of gingival crevicular fluid.[RGUHS]
19. Describe the mechanisms by which periodontal 17. Enamel pearls. [RGUHS]
ligament resists occlusal forces. [MUHS] 18. Functions of periodontal ligament. [GOA]
20. Cementum and its biologic importance. [MUHS] 19. Junctional epithelium. [GOA]
21. Hypercementosis.[MUHS] 20. Periosteum.[NTR-UHS]
22. Oblique fibres. [NTR-UHS] 21. Bundle bone. [NTR-UHS]
23. Functions of periodontal ligament. [NTR-UHS] 22. Functions of periodontal ligament. [GOA]
24. Principal fibres of the periodontal ligament. [NTR-UHS] 23. Periodontal fibres. [GOA]
25. Describe the ultrastructure of junctional epithelium. 24. Cementum.[GOA]
[GOA] 25. Types of cementum. [GOA]
26. Write about supportive periodontal treatment. [GOA] 26. Types CEJ. [RGUHS]
27. Junctional epithelium. [GOA] 27. Schroeder’s classification of cementum. [RGUHS]
AGE-RELATED CHANGES IN PERIODONTIUM

Long Essays Short Notes
1. Describe the effects of ageing upon the periodontal 1. Age changes in gingiva. [RGUHS]
tissues.[RGUHS] 2. Nature of periodontal disease. [RGUHS]
2. Describe the microscopic and macroscopic appearance 3. Age changes in the periodontium. [NTR-NR]
of human keratinized oral mucous membrane. [RGUHS] 4. Enumerate the factors for prognosis of individual tooth
3. Describe the changes in the periodontal tissues due to in periodontal diseases. [MUHS]
ageing.[MUHS]
5. Bruxism.[RGUHS]
4. Age changes in the periodontium. [NTR-NR]
CLASSIFICATION OF DISEASES OF THE PERIODONTIUM

Long Essays 3. Classify periodontitis. Describe the clinical and
radiographic features of chronic periodontitis. [RGUHS]
1. Discuss the role of anatomical factors in aetiology of
periodontal disease. [RGUHS] Short Notes
2. Classify inflammatory diseases of periodontium and
describe in detail anyone of them. [RGUHS] 1. Classify periodontal diseases. [MUHS]
224
EPIDEMIOLOGY OF GINGIVAL AND PERIODONTAL DISEASES

Long Essays 5. Bleeding Point index. [NTR-OR]
6. Oral hygiene simplified. [NTR-OR]
1. Define dental epidemiology and write in detail about
7. Russell’s periodontal index. [NTR-OR]
the indices used in assessing gingival inflammation.
8. Periodontal disease index. [NTR-NR]
[NTR-OR]
9. Ideal requirements of an index. [NTR-NR]
2. “Periodontal health for all by 2000 AD”. What do you
10. Oral halitosis. [RGUHS]
understand by this statement? How are you going to
11. Gingival index. [RGUHS]
implement it by systematic manner? [NTR-OR]
12. Community periodontal index. [RGUHS]
3. Describe the possible causes as to why the incidence
13. Name any two plaque indices. Describe in detail any one
and prevalence of periodontal diseases are very high in
of them. [RGUHS]
India.[GOA]
Short Notes
Short Essays
1. OHIS.[RGUHS]
1. Indices used to measure periodontal destruction.
2. Silness and Leo index. [RGUHS]
[RGUHS]
3. Investigations for gingival bleeding. [RGUHS]
2. CPITN probe. [NTR-OR; RGUHS]
4. Miller’s tooth mobility index. [RGUHS]
3. Russell’s periodontal index. [NTR-OR; RGUHS]
5. Define risk factor and risk determinant. [RGUHS]
4. Silness and Loe index. [NTR-OR]
6. CPITN Index. [NTR-UHS]
PERIODONTAL MICROBIOLOGY
Long Essays 10. Define and give broad classification and composition of
dental plaque. Describe the characteristics of the gel-
1. Discuss supragingival and subgingival plaques.[RGUHS] like matrix of ‘biofilm’. [MUHS]
2. Discuss the role of plaque in aetiology of periodontal 11. What is dental plaque? Give its composition. Describe
disease.[RGUHS] its role in the initiation and progression of gingival and
3. Describe in detail steps in the formation of dental plaque. periodontal diseases. [MUHS]
Add a note on specific plaque hypothesis. [RGUHS] 12. What are the signs and symptoms of periodontal
4. Define dental plaque. Describe its types, composition, diseases? Describe the general aspects of microbiology
bacteriology and role in aetiology of periodontal and immunology of periodontal diseases. [MUHS]
disease.[RGUHS] 13. Define plaque. Describe the classification, composition,
5. Define dental plaque. Write in detail about the formation structure and formation of dental plaque in detail.
of plaque. Add a note on specific plaque hypothesis. [MUHS]
[RGUHS] 14. Define plaque. Describe the composition and formation
of dental plaque. [RGUHS]
6. Write bacterial composition of different types of plaque.
15. Describe in detail the plaque retention factors in the
Describe mechanisms of bacteria-mediated periodontal
aetiology of periodontal disease. [RGUHS]
tissue destruction. [RGUHS] 16. Discuss the role of microorganisms in periodontal
7. Describe the role of microorganisms in the aetiology of disease.[GOA]
periodontal diseases. [NTR-OR; MUHS] 17. Define and classify plaque. Describe the formation
8. Define and classify dental plaque. Write in detail about of plaque and its role in the aetiology of periodontal
its composition and ill effects. [NTR-NR] disease. [NTR- UHS]
9. Define and classify microbial plaque. Discuss the role 18. Define dental ‘biofilm’. Highlight the properties of the
of microbial plaque in the aetiology cff gingival and same and add a note on various plaque hypotheses.
periodontal diseases. [NTR-NR] [RGUHS]
225
Short Essays 16. Socransky’s criteria for identification of periodontal

pathogens.[NTR-UHS]
1. Structure and composition of plaque. [RGUHS]

17. Define plaque. Classify plaque and add a note on its
2. Compare supragingival and subgingival plaque.
mechanism of formation. [GOA]
[RGUHS]
18. Chemical plaque control. [RGUHS]
3. Composition of dental plaque in adult periodontitis.
[RGUHS] Short Notes
4. Materia alba. [NTR-OR]
5. Acquired pellicle. [NTR-NR] 1. Dental pellicle. [RGUHS]
6. Subgingival plaque. [NTR-OR; GOA] 2. Acquired pellicle. [RGUHS]
7. Specific plaque hypothesis. [NTR-NR] 3. Aetiological significance of microbial plaque. [RGUHS]
8. Differences between supra- and subgingival plaque. 4. Specific plaque hypothesis. [NTR-NR; MUHS; GOA]
[NTR- OR] 5. Define and classify dental plaque. [MUHS]
9. Formation of plaque. [RGUHS; GOA] 6. Stages of plaque formation. [MUHS]
10. Oral microorganisms in health and disease. [MUHS] 7. Socransky’s postulates. [RGUHS]
11. Dental plaque. [RGUHS] 8. Giemsa’s stain. [RGUHS]
12. Socransky’s modification of Koch’s postulates. [RGUHS] 9. Co-aggregation.[NTR-UHS]
13. Diagnostic methods used for bacterial identification. 10. Spirochaetes.[NTR-UHS]
[RGUHS] 11. Radius of action. [NTR-UHS]
14. Specific and non-specific plaque hypothesis. 12. Prevotella intermedia. [NTR-UHS]
[NTR-UHS; RGUHS] 13. Subgingival plaque. [GOA]
15. Microbial specificity of periodontal disease. [NTR-UHS] 14. Normal oral bacterial flora. [RGUHS]
DENTAL CALCULUS, IATROGENIC AND OTHER LOCAL PREDISPOSING AETIOLOGICAL FACTORS
Long Essays 3. Calculus.[NTR-OR]

4. Food impaction. [NTR-OR]
1. Define calculus mention its composition. Discuss various
5. Subgingival calculus. [NTR-NR]
theories of calculus formation. [RGUHS]
6. Attachment of calculus. [NTR-OR]
2. Define calculus composition formation and its
7. Theories of calculus formation. [NTR-OR; RGUHS]
aetiological significance in periodontal disease.[RGUHS]
8. Difference between supra- and subgingival calculus.
3. What is calculus, what are the theories of calculus
[NTR-OR; MUHS; RGUHS ]
formation? Write about composition, types of calculus,
9. Dental calculus. [MUHS]
and also anticalculus agents. [RGUHS]
10. Mode of attachment of dental calculus. [MUHS]
4. Define calculus. Give its classification, prevalence,
11. Dental stains. [MUHS]
composition, formation and aetiologic significance in
12. Mechanism of calculus formation. [MUHS]
detail.[MUHS]
13. Mouth breathing habit and the periodontium. [MUHS]
5. Discuss the various local aetiologic factors that are
14. Sequelae of food impaction. [MUHS]
responsible for initiation and progress of periodontal
15. Mechanism of food impaction and its role in periodontal
disease.[MUHS]
diseases.[MUHS]
6. Define and classify gingival recession. Discuss in
16. Composition of dental plaque. [RGUHS]
detail the procedure for free gingival autografts in the
17. Define dental calculus. Discuss theories of mineralization
treatment of gingival recession. [RGUHS]
of dental calculus. [RGUHS]
7. Describe the role of iatrogenic factors in aetiology of
18. Bruxism.[RGUHS]
periodontal disease. [RGUHS]
19. Role of iatrogenic factors in periodontal disease. [GOA]
20. Suprabony and infrabony pockets. [GOA]
Short Essays 21. What is calculus? What is the role of calculus in periodontitis?
1. Plaque retention factors. [RGUHS; NTR-UHS] List the features of subgingival calculus. [GOA]
2. Theories of calculus formation. [RGUHS] 22. Write about composition and formation of calculus.[GOA]
226
Short Notes 10. Iatrogenic factors. [MUHS]

11. Hypersensitivity.[MUHS]
1. Aetiological significance of calculus. [RGUHS]

12. Epitactic concept in calculus formation. [RGUHS]
2. Food impaction. [NTR-NR; MUHS; RGUHS]
13. Any 5 methods to treat dental hypersensitivity and
3. Enumerate various theories of mineralization of calculus.
[MUHS] overhanging restorations. [RGUHS]
4. State the composition of dental calculus. [MUHS] 14. Ill effects of overhanging restorations. [RGUHS]
5. Dental calculus. [MUHS] 15. Supragingival calculus. [GOA]
6. Theories of mineralization of calculus. [MUHS] 16. Composition and attachment of calculus. [GOA]
7. Composition of calculus. [MUHS] 17. Theories regarding mineralization of calculus. [GOA]
8. Theories of calculus formation. [MUHS] 18. Iatrogenic factors in the aetiology of periodontal
9. Sequelae of food impaction. [MUHS] disease.[GOA]
SMOKING AND PERIODONTIUM
Short Essay
1. Smoking and periodontal disease.
HOST RESPONSE—BONE CONCEPTS
Short Essays Short Notes

1. Cytokines.[RGUHS] 1. Type 1 hypersensitivity. [RGUHS]
2. Mast cells. [RGUHS] 2. Cytokines.[RGUHS]
3. Role of macrophages in periodontal disease. [RGUHS] 3. Lymphocytes.[RGUHS]
4. Complement system. [RGUHS] 4. Lymphokines.[RGUHS]
5. IgG.[NTR-OR] 5. Define cytokines. [RGUHS]
6. Mast cell. [NTR-OR] 6. Cytokines.[NTR-NR]
7. Lymphocyte.[NTR-OR] 7. Neutrophils.[NTR-NR]
8. Immunoglobulins.[NTR-NR] 8. Name the functional defects of leukocytes. [NTR-NR]
9. Arthus reaction. [NTR-OR] 9. Antibacterial factors in saliva. [RGUHS]
HOST-MICROBIAL INTERACTIONS IN PERIODONTAL DISEASES
Short Notes
1. Prostadlandins [NTR UHS]
TRAUMA FROM OCCLUSION
Long Essays 2. What is trauma from occlusion? Give the signs,

symptoms and histopathological features of trauma
1. What is trauma from occlusion? Give the signs, symptoms
from occlusion.
and treatment of primary traumatic occlusion. [MUHS] [MUHS]
227
3. Discuss the aetiopathogenesis of pathologic migration 15. Masticatory cycle. [NTR-NR]

and mobility of teeth. [MUHS] 16. Clinical features of bruxism. [RGUHS]

4. What is traumatic occlusion? What is trauma from 17. Injury phase in trauma from occlusion. [RGUHS]
occlusion? Classify and give its signs and symptoms. 18. Management of dentinal hypersensitivity. [RGUHS]
[MUHS] 19. Soft tissue changes to increased occlusal forces.
5. Define trauma from occlusion and discuss its aetiology, [NTR-UHS]
clinical features and management. [NTR-OR] 20. Tooth mobility. [NTR-UHS]
6. Define trauma from occlusion. Discuss the pathology, 21. Trauma from occlusion. [NTR-UHS]
clinical and radiographic features of trauma from
occlusion.[NTR-NR] Short Notes
7. Describe the role of trauma from occlusion in case of 1. Define trauma from occlusion. What are the various stages
periodontal diseases. Describe the physiological and of tissue response in trauma from occlusion? [MUHS]
pathological tooth mobility seen in the teeth involved 2. What is adaptive remodelling of the periodontium
in trauma from occlusion. [NTR-OR] in response to external force? List various changes
8. Discuss the pathology, clinical futures, and diagnosis of produced in the periodontium due to remodelling.
trauma from occlusion. [RGUHS] [MUHS]
9. Define trauma from occlusion and traumatic occlusion. 3. Pathological migration of teeth. [MUHS]
Discuss role of trauma from occlusion. [BUHS] 4. Clinical and radiological changes in trauma from
10. Define trauma from occlusion. Describe in detail clinical occlusion.[MUHS]
manifestations of trauma from occlusion. [BUHS] 5. Traumatic occlusion. [MUHS]
11. Define and classify trauma from occlusion. Write the 6. What is adaptive remodelling of the periodontium
various stages of trauma from occlusion. Add a note on in response to external force? List various changes
the influence of trauma from occlusion on the spread of produced in the periodontium due to remodelling.
inflammation.[RGUHS] [MUHS]
7. Causes of and changes produced by primary trauma
Short Essays from occlusion. [MUHS]
8. Pathologic migration. [MUHS]
1. Primary traumatic occlusion. [MUHS]
9. Primary and secondary trauma. [RGUHS]
2. Pathological migration of teeth. [MUHS]
10. Trauma from occlusion. [RGUHS]
3. Difference between primary traumatic occlusion and
11. Define acute and chronic trauma from occlusion.
secondary traumatic occlusion. [MUHS]
[RGUHS]
4. Secondary trauma from occlusion. [MUHS]
5. Forces of occlusion. [NTR-NR] 12. Facets.[NTR-NR]
6. Pathology migration. [NTR-NR] 13. Parafunctional condition and periodontium. [RGUHS]
7. Pathological tooth migration. [NTR-OR] 14. Define trauma from occlusion. [RGUHS]
8. Define and classify trauma from occlusion. [NTR-NR] 15. Secondary occlusal trauma. [GOA]
9. Classification and diagnosis of trauma from occlusion. 16. Fenestration and dehiscences. [GOA]
[NTR-NR] 17. Therapeutic occlusion. [NTR-UHS]
10. Concepts of trauma from occlusion. [BUHS] 18. Supra contacts. [NTR-UHS]
11. Tissue response to increased occlusal forces. [RGUHS] 19. Acute trauma from occlusion. [GOA]
12. Differentiate between primary and secondary occlusion 20. Primary trauma from occlusion. [GOA]
trauma.[BUHS] 21. Bruxism.[GOA]
13. Bruxism.[NTR-OR] 22. Passive eruption. [GOA]
14. Night guard. [NTR-OR] 23. Fremitus test. [RGUHS]
INFLUENCE OF SYSTEMIC DISEASES ON THE PERIODONTIUM AND PERIODONTAL MEDICINE
Long Essays 2. State the systemic conditions modifying the clinical

appearance of periodontal tissue. Describe in detail the
1. Discuss the causes of gingival bleeding. How will you
clinical features of any three such conditions.
proceed to investigate such case? [MUHS] [MUHS]
228
3. Write in detail about the systemic diseases causing 18. AIDS and periodontal disease. [RGUHS]
periodontal manifestations. [RGUHS] 19. Periodontal management of diabetic patient.[NTR-UHS]

4. Antibiotic prophylaxis for the medically compromised 20. Periodontal manifestations of HIV infection. [NTR-UHS]
patient.[NTR-NR] 21. Kaposi’s sarcoma. [NTR-UHS]
5. Describe pregnancy gingivitis and its management. 22. Risk factors associated with periodontal disease.
[GOA] [NTR-UHS]
6. Relationship between diabetes and periodonotal 23. Antibiotic prophylaxis for infective endocarditis.
disease and management of a diabetic patient with [NTR- UHS]
periodontal disease. 24. Discuss management of a diabetic patient. [GOA]
[GOA] 25. Influence of diabetes on the periodontium. [GOA]
26. Discuss periodontal findings in AIDS. [GOA]
Short Essays 27. Describe the periodontal features in HIV-positive
individuals.[GOA]
1. Describe in short oral manifestations in scurvy. [MUHS]
2. Possible role of ascorbic acid deficiency in aetiology of
Short Notes
periodontal disease. [MUHS]
3. Periodontal manifestations of leukaemia. [MUHS] 1. Scorbutic gingivitis. [RGUHS]
4. Describe the relationship between diabetes and 2. Gingiva in leukaemia. [RGUHS]
periodontitis.[MUHS] 3. Gingival pigmentation. [RGUHS]
5. Vitamin C. [NTR-NR] 4. Vitamin C in gingival disease. [RGUHS]
6. Chediak-Higashi syndrome. [NTR-OR] 5. Periodontal disease in infective endocarditis. [RGUHS]
7. Diabetes and periodontal health. [NTR-NR] 6. Impact of diabetes and periodontium. [RGUHS]
8. Oral lesions in diabetes mellitus. [NTR-OR] 7. Bruxism.[MUHS]
9. Diabetes mellitus and periodontal disease. 8. Stress and periodontal diseases. [MUHS]
[NTR-OR; RGUHS] 9. Treatment for bruxism. [MUHS]
10. Periodontal manifestations of diabetes mellitus. 10. Oral manifestation of diabetes mellitus. [MUHS]
[NTR-NR] 11. Role of systemic conditions on periodontal health.
11. Diabetes as a risk factor in periodontal diseases. [MUHS]
[NTR-UHS] 12. Periodontal medicine. [BUHS]
12. Diabetes and periodontal diseases. [NTR-UHS] 13. Periodontal care of patients on anticoagulant therapy.
13. Periodontal care of patients with cardiac pacemakers. [RGUHS]
[RGUHS] 14. Any five neutrophil disorders causing periodontitis.
14. AIDS and periodontium. [RGUHS] [RGUHS]
15. Effects of smoking on periodontium. [RGUHS] 15. Scurvy.[RGUHS]
16. Periodontitis and metabolic control of diabetes mellitus. 16. Pregnancy gingivitis. [GOA]
[RGUHS] 17. Papillon-Leferve syndrome. [GOA]
17. Periodontal management of a dental transplant patient. 18. Gingival changes in pregnancy. [GOA]
[RGUHS] 19. Impact of diabetes mellitus on periodontium. [RGUHS]
DENTAL IMPLANTS

1. Indications for implant therapy. [RGUHS] 1. Peri-implantitis. [MUHS; NTR-UHS; GOA; RGUHS]
2. Failure of implants. [RGUHS] 2. Maintenance of dental implants. [RGUHS]
3. Osseoinducation, osseoconduction and 3. Peri-implant diseases. [RGUHS ]
osseointegration. 4. Osseointegration.[GOA]
[NTR-UHS] 5. Implant bone interface. [GOA]
4. Osseointegration.[NTR-UHS] 6. Aetiology of peri-implant disease. [GOA]
229
DEFENCE MECHANISMS OF THE GINGIVA

Long Essay 12. Saliva in oral defence. [RGUHS]
1. Describe in detail about the defence mechanism of Short Notes
gingiva. [RGUHS, NTR-OR, NTR-UHS]
1. Gingival fluid. [RGUHS]
Short Essays 2. Functions of GCF. [RGUHS]
3. Intrasulcular drug delivery. [RGUHS]
1. Role of saliva in oral health. [RGUHS]
4. Antibacterial factors of saliva. [RGUHS]
2. Methods of collection of GCF. [RGUHS]
3. Gingival fluid. [NTR-OR] 5. Clinical significance of gingival fluid.
4. Enzymes in gingiva. [NTR-OR] 6. Clinical significance of crevicular fluid. [RGUHS]
5. Gingival crevicular fluid. [NTR-OR] 7. Enumerate the protective component of saliva in
6. Disease activity and inactivity. [NTR-NR] periodontal disease process. [MUHS]
7. Composition of gingival cervical fluid. [NTR-NR] 8. Complement.[RGUHS]
8. Methods of collection of gingival crevicular fluid (GCF). 9. Host modulation therapy (HMT). [NTR-UHS]
[NTR-NR] 10. Active immunity. [NTR-UHS]
9. Role of saliva in oral defence mechanism. [RGUHS] 11. Cytokines.[GOA]
10. Interleukin-I.[NTUHS] 12. Anaphylaxis.[GOA]
11. Immunoglobulins.[GOA] 13. Proinflammatory cytokines. [RGUHS]
GINGIVAL INFLAMMATION AND CLINICAL FEATURES OF GINGIVITIS

Long Essays 5. Pathways of gingival inflammation. [NTR-OR]
6. Established lesion of chronic gingivitis. [NTR-OR]
1. Define gingival recession. Enumerate its causes.[RGUHS] 7. Gingival recession. [NTR-OR]
2. Describe clinical and microscopic features of chronic 8. Gingival pigmentations. [NTROR]
gingivitis.[RGUHS] 9. Management of operative bleeding. [NTR-OR]
3. Define gingival bleeding. Write about causes and 10. Management of localized gingival bleeding. [NTR-OR]
management of gingival bleeding. [RGUHS] 11. Mucogingival problems. [RGUHS]
4. What is gingival recession? How will you treat a case of 12. Enumerate stages of gingivitis. Discuss established
localized gingival recession on mandibular left central lesion. [RGUHS ]
incisor.[MUHS] 13. Gingival bleeding. [NTR-UHS]
5. Discuss the causes of gingival bleeding. How will you 14. Describe the clinical features and management of acute
proceed to investigate such a case. [MUHS] pericoronitis.[GOA]
6. Discuss gingival bleeding. [NTR-OR]
7. Define gingival bleeding. Write about causes and Short Notes
management of gingival bleeding. Define and classify
gingival recession. [NTR-OR] 1. Stillman’s cleft. [RGUHS; NTR-NR]
8. Discuss in detail the aetiology and management of 2. McCall’s festoons. [RGUHS]
gingival recession. [NTR-NR] 3. Gingival recession. [RGUHS]
4. Causes of gingival bleeding. [RGUHS]
5. Causes of gingival recession. [RGUHS]
proceed to investigate such cases. [MUHS]
6. Aetiology of gingival recession. [NTR-NR]
7. Classify the gingival recession. [NTR-NR]
Short Essays
8. Enumerate the stages of gingivitis. [NTR-NR]
1. Gingival recession. [MUHS] 9. Plasma cell gingivitis. [NTR-UHS]
2. Treatment of advanced stage of gingivitis. [MUHS] 10. Gingival abscess. [GOA]
3. Treatment of localized gingival recession. [MUHS] 11. Stages of gingivitis. [RGUHS]
4. Enumerate the stages of gingivitis. [NTR-OR] 12. Transgingival probing. [RGUHS]
230
GINGIVAL ENLARGEMENTS

Long Essays Short Essays
1. Classify gingival enlargements. Write in detail drug- 1. Classify gingival enlargements. Add a note on idiopathic
induced gingival enlargement. [RGUHS; MUHS] enlargement.[RGUHS]
2. Define gingival abscess. Write in detail about aetiology 2. Compare leukaemic gingival enlargement and dilantin
and treatment of the same. [RGUHS] sodium hyperplastic gingival enlargement. [RGUHS]
3. Classify gingival enlargements. Describe clinical features 3. Pregnancy gingival enlargement. [MUHS]
and histopathology of leukaemic enlargement. 4. Give differential diagnosis of epulis. [MUHS]
[RGUHS] 5. Angiogranuloma.[NTR-NR]
4. Describe effects of pregnancy on periodontium. 6. Pregnancy gingivitis. [NTR-NR]
Mention the precautions to be taken during pregnancy 7. Benign tumours of gingiva. [NTR-OR]
in periodontal therapy. [RGUHS] 8. Leukaemic gingival enlargement. [NTR-OR]
5. Classify gingival enlargement. Discuss in detail signs, 9. Conditioned gingival enlargement. [NTR-OR]
symptoms and treatment of dilantin sodium gingival 10. Drug induced gingival enlargements. [NTR-OR]
enlargement.[MUHS] 11. Classification of gingival enlargements. [RGUHS]
6. Define and classify gingival enlargements. Describe 12. Pyogenic granuloma. [NTR-UHS]
aetiology, clinical features and management of any one 13. Drug induced gingival hyperplasia. [NTR-UHS]
type of gingival enlargement. [MUHS] 14. Peripheral giant cell granuloma. [NTR-UHS]
7. Classify gingival enlargement. What is conditioned 15. Idiopathic gingival enlargement. [NTR-UHS]
enlargement in pregnancy?[MUHS] 16. Lymphocytes.[NTR-UHS]
8. Classify gingival enlargement and write in detail about 17. Non-inflammatory gingival enlargement. [RGUHS]
phenytoin enlargement. [NTR-OR]
9. Classify gingival enlargement and describe the drug- Short Notes
induced gingival enlargements. [NTR-NR]
1. Gingival abscess. [RGUHS]
10. Classify gingival enlargement. Discuss the
2. Angiogranuloma.[RGUHS]
histopathology and clinical features of drug-induced
3. Gingival enlargement. [RGUHS]
gingival enlargement (DIGO). [NTR-NR]
11. Define gingival enlargement. Write briefly the differential 4. Drug induced gingival enlargement. [RGUHS]
diagnosis of inflammatory and noninflammatory 5. Pathogenesis of phenytoin sodium gingival
gingival enlargement. [NTR-OR] enlargement.[RGUHS]
12. Classify gingival enlargements. Write about clinical 6. What is the difference between gingival abscess and
features and histopathology of dilantin-induced gingival periodontal abscess? [MUHS]
enlargement.[GOA] 7. Pregnancy tumour. [MUHS; RGUHS; NTR-UHS]
13. Classify gingival enlargements. Describe the 8. Management of periodontal diseases in pregnant
pathogenesis, histopathology, clinical features and patient.[MUHS]
treatment of conditioned gingival enlargement. 9. What is drug-induced gingival hyperplasia? [MUHS]
[NTR-UHS] 10. Gingival enlargement. [BUHS]
14. Classify gingival enlargements. Give indications, 11. Familial gingival enlargement. [RGUHS]
contraindications and method of gingivectomy. 12. Pathogenesis of phenytoin sodium gingival
[GOA] enlargement.[BUHS]
15. Classify gingival enlargement. Describe drug-induced 13. Developmental gingival enlargements. [RGUHS]
gingival enlargement in detail. [GOA] 14. Classification of gingival enlargement. [RGUHS]
16. Classify gingival enlargement. How will you 15. Clinical features of drug-induced gingival hyperplasia.
differentiate between leukaemic and scorbutic gingival [NTR-UHS]
enlargement.[GOA] 16. Conditioned enlargement. [GOA]
17. Classify gingival enlargement. Discuss phenytoin- 17. Rapidly progressive enlargement. [GOA]
induced gingival enlargement in detail. [GOA] 18. Phenytoin-induced gingival enlargement. [GOA]
231
ACUTE GINGIVAL INFECTIONS

1. Describe in detail clinical features of ANUG. [RGUHS] 1. Management of acute pericoronitis. [RGUHS]
2. Describe clinical features and treatment of ANUG. 2. Compare necrotizing ulcerative gingivitis and acute
[RGUHS] herpetic gingivostomatitis. [RGUHS]
3. What are acute infections of gingiva? Describe in detail 3. Enumerate the acute infections of the gingiva. [MUHS]
anyone of them. [RGUHS] 4. Pericoronitis. [NTR-OR; GOA]
4. What is a Vincent’s infection? Write its aetiology, clinical 5. Aphthous ulcer. [NTR-OR]
features and its management. [RGUHS] 6. Gingival abscess. [NTR-OR]
5. Describe aetiology, clinical features, differential 7. Hepatic gingivostomatitis. [NTR-OR]
diagnosis and treatment of ANUG in detail. [RGUHS] 8. Acute herpetic gingivostomatitis. [NTR-NR ]
6. Discuss about clinical features, histopathology and 9. Treatment of ANUG. [NTR-OR]
differential diagnosis of acute herpetic gingivostomatitis. 10. Aetiology of ANUG. [RGUHS]
[RGUHS] 11. Necrotizing ulcerative gingivitis. [NTR-UHS]
7. Classify gingival lesions and discuss in detail about acute
necrotizing ulcerative gingivitis and its management. Short Notes
[RGUHS]
1. Gingivosis.[RGUHS]
8. Give the signs, symptoms, differential diagnosis and
2. Tzanck test. [RGUHS]
treatment of acute herpetic gingivostomatitis. [MUHS]
3. Aphthous ulcer. [RGUHS]
9. Give the signs, symptoms, differential diagnosis and treat-
4. Borrelia vincentii. [RGUHS]
ment of acute necrotizing ulcerative gingivitis. [MUHS]
5. Herpetic gingivostomatitis. [RGUHS]
10. Enumerate acute gingival lesions. Discuss in detail
6. Management of pericoronitis. [RGUHS]
aetiology, clinical features, histopathology and differential
7. EM findings of necrotizing ulcerative gingiva. [RGUHS]
diagnosis of acute herpetic gingivostomatitis. [MUHS]
11. Discuss the clinical features, histopathology and 8. Clinical features of acute herpetic gingiva stomatitis.
management of gingivosis. [NTR-OR] [RGUHS]
12. Describe the aetiology, clinical features and treatment 9. Management of acute herpetic gingivostomatitis.
of acute necrotizing ulcerative gingivitis. [NTR-OR] [MUHS]
13. Describe the aetiology, clinical features and differential 10. Laboratory investigations of acute herpetic
diagnosis of acute herpetic gingivostomatitis. [NTR-OR] gingivostomatitis.[MUHS]
14. Enumerate the acute infections of gingiva. Describe the 11. Treatment of acute pericoronitis. [MUHS]
aetiology, clinical features and histopathology of acute 12. Porphyromonas gingivalis. [NTR-NR]
necrotizing ulcerative gingivitis. [NTR-NR] 13. Differential diagnosis of acute herpetic gingivostomatitis.
15. Enumerate the acute lesions of gingiva and write in detail [RGUHS]
14. Bacterial flora in ANUG. [RGUHS ]
the clinical features, histopathology and management
of acute necrotizing ulcerative gingivitis. [NTR-OR] 15. Gingival abscess. [NTR-NR]
16. Enumerate acute gingival infection. Discuss the aetiopatho- 16. ANUG.[GOA]
genesis, clinical features and treatment of ANUG. [GOA] 17. Acute herpetic gingivostomatitis. [RGUHS]
DESQUAMATIVE GINGIVITIS
Long Essays 2. Describe about aetiology, clinical features, pathogenesis

and management of chronic desquamative gingivitis.
1. What is desquamative gingivitis? Give the clinical
[RGUHS]
features, histopathological and treatment of severe
3. Classify desquamative gingivitis lesions and describe in
form of desquamative gingivitis.
detail the candidiasis lesions.
[MUHS] [NTR-NR]
232
4. Describe the aetiopathogenesis, histopathology, 4. Define and classify chronic desquamative gingivitis
clinical features and treatment of chronic desquamative lesions.[NTR-NR]

gingivitis.[NTR-UHS] 5. Management of chronic desquamative gingivitis.[RGUHS]

1. Treatment of chronic desquamative gingivitis. [MUHS] 1. Acute pericoronitis. [MUHS]
2. Desquamative gingivitis. [NTR-OR] 2. Chronic desquamative gingivitis. [MUHS]
3. Herpetic gingivostomatitis. [NTR-OR] 3. Pericoronitis.[MUHS]
GINGIVAL AND PERIODONTAL DISEASES IN CHILDREN AND YOUNG ADOLESCENTS
Long Essay 4. Aetiology of gingival recession. [RGUHS]

1. Discuss in detail about the gingival diseases in children. Short Notes
[RGUHS]
1. Hypophosphatasia.[BUHS]
2. Papillon-Lefevre syndrome. [RGUHS]
Short Essays
3. Aetiology of gingival recession. [RGUHS]
1. Aetiopathogenesis and clinical features of ANUG.[RGUHS] 4. Linear gingival erythema. [RGUHS]
2. Iatrogenic factors in periodontal disease. [RGUHS] 5. Gingival recession. [NTR-UHS]
3. Endotoxins and periodontal disease. [RGUHS] 6. Periodontal cyst. [NTR-UHS]
PERIODONTAL POCKET
Long Essays 10. Define and classify periodontal pockets. Add a note on
its histopathology and management. [NTR-OR]
1. Discuss the pathogenesis of periodontal pocket. [RGUHS]
11. Define periodontal pocket. Describe its classification,
2. Define and classify periodontal pocket. Describe the
histopathology, pathogenesis and sequale. [NTR-OR]
pathogenesis.[RGUHS]
12. Define periodontal pocket. Classify periodontal
3. Describe the pathogenesis of periodontal pocket. Add a
pocket and discuss the pathogenesis and contents of
note on reattachment concept. [RGUHS]
periodontal pocket. [NTR-OR]
4. Classify periodontal pockets. Describe how would you
treat a suprabony periodontal pocket. [RGUHS] 13. Define periodontal pocket. Describe the nonsurgical
5. Define pocket. Describe the classification, pathogenesis treatment regimen, which may help in pocket
and histopathology in detail with a note on root surface elimination.[NTR-OR]
changes.[RGUHS] 14. Classify periodontal pockets. Describe the clinical and
6. Define periodontal pockets. Classify periodontal microscopic features of the pocket. [NTR-NR]
pockets and methods of eliminating pockets. Write in 15. Define and classify periodontal pocket. Describe the
detail about gingival curettage. [RGUHS] pathogenesis of periodontal pocket and enumerate the
7. Define pocket. Give its classification and describe differences between suprabony and infrabony pockets.
various methods of pocket elimination. [MUHS] [NTR-UHS]
8. Describe the signs, symptoms and treatment of acute 16. Define and classify periodontal pockets. Describe the
periodontal abscess. How would you differentiate histopathology and treatment of periodontal pockets.
between acute periodontal abscess and acute periapical [GOA]
abscess.[MUHS] 17. Define and classify periodontal pocket. Write the various
9. Classify periodontal pockets. Discuss pathogenesis and treatment modalities for pocket elimination procedures.
treatment of pseudopockets. [MUHS] Define and classify periodontal pocket. [NTR-UHS]
233
18. Define and classify pockets. Discuss the 14. Angular defects. [RGUHS]
aetiopathogenesis of a periodontal pocket. [GOA] 15. Aetiopathogenesis of pockets. [RGUHS]

19. Classily periodontal pockets. Describe in detail the 16. Pathogenesis of periodontal pocket. [NTR-UHS]
pathogenesis and histopathology of pocket formation. 17. What are the signs and symptoms of pocket formation?
[GOA] [GOA]
20. Enumerate periodontal pocket management 18. Define and discuss the aetiopathogenesis of periodontal
procedures. Discuss the role of ‘phase I therapy’ in the pocket.[RGUHS]
treatment of periodontal disease. [RGUHS]
21. Define and classify periodontal pocket. Describe in Short Notes
detail about modified Widman’s flap. [RGUHS]
1. Periodontal cyst. [RGUHS]
2. Periodontal pocket. [RGUHS]
Short Essays
3. Supra- and intrabony pocket. [RGUHS]
1. Suprabony and infrabony pocket. [RGUHS; GOA] 4. What is the difference between gingival and periodontal
2. Give the aetiology and line of treatment of a chronic abscess?[MUHS]
periodontal abscess. [MUHS] 5. Classify periodontal pockets. [MUHS]
3. What is the difference between a gingival abscess and 6. Correlation of clinical and histopathological features of
periodontal abscess? [MUHS] periodontal pocket. [MUHS]
4. Infrabony pockets. [MUHS] 7. Root surface changes in presence of periodontal pocket.
5. Micro flora in periodontal pocket. [MUHS] [MUHS]
6. Acute periodontal abscess. [MUHS] 8. Differentiate between suprabony and infrabony pockets.
7. Microtopography of periodontal pocket wall. [MUHS] [MUHS; RGUHS]
8. Periodontal pocket. [MUHS] 9. Changes in root surface wall of periodontal pockets.
9. Suprabony pockets. [NTR-OR] [MUHS]
10. Infrabony pocket. [NTR-OR] 10. Advances in periodontal probing. [MUHS]
11. Classification of periodontal pockets. [NTR-NR] 11. Complex pocket. [NTR-UHS]
12. Root surface changes in periodontal pocket. 12. Cemental changes in periodontal pocket. [GOA]
[NTR-NR; GOA] 13. Infrabony pocket. [GOA]
13. Histopathology of lateral wall of pocket. [RGUHS] 14. Root surface changes in periodontal pocket. [GOA]
BONE LOSS IN PERIODONTAL DISEASES
Long Essays 7. Enumerate the periodontal osseous defects. Describe

the regenerative osseous surgery. [RGUHS]
1. Schematically explain bacterial and host-mediated
8. Describe the features of alveolar bone in health. Discuss
mechanism of bone resorption in periodontitis.[RGUHS]
the various types of osseous defects seen in periodontal
2. Explain the osseous crates. What are the procedures
diseases.[RGUHS]
employed in eliminating osseous craters? [RGUHS]
3. What are different types of osseous defects. Write in Short Essays
detail about the procedure of osseous craters. [RGUHS]
4. Describe the mechanism of bone resorption. Mention 1. Osseous defects. [RGUHS]
the pattern of bone defects in trauma from occlusion. 2. Bone loss in periodontal diseases. [MUHS]
[RGUHS] 3. Osseous defects in periodontal diseases. [MUHS]
5. Classify bony defects in periodontal disease. How would 4. Lipping.[NTR-OR]
you establish the prognosis of such defects? [MUHS] 5. Osseous defects. [NTR-OR]
6. What is meant by bone defect? Describe the various bones 6. Intrabony defects. [NTR-OR]
defects observed in periodontal diseases and discuss 7. Osseous deformity. [NTR-OR]
the various factors that determine the morphology of 8. Angular bone defects. [NTR-OR]
alveolar bone in periodontal diseases. [MUHS] 9. Positive architecture of alveolar bone. [NTR-OR]
234
10. Mediators of alveolar bone destruction. [NTR-OR] 7. Bone destruction patterns in periodontal disease.
11. Tooth mobility. [RGUHS; NTR-UHS] [MUHS]

12. Pathological migration. [NTR-UHS] 8. Tooth mobility. [MUHS; GOA]
13. Bone destruction patterns in periodontal disease.[GOA] 9. Reverse architecture. [NTR-NR; RGUHS]
14. Discuss osseous defects. [GOA] 10. Inconsistent bony margins. [NTR-NR]
15. Patterns of bone destruction in periodontal disease. 11. Enumerate bone destructive patterns in periodontal
[RGUHS] diseases.[NTR-NR]
12. Pathologic migration. [RGUHS]
Short Notes 13. Hemiseptum.[NTR-UHS]
1. Bone factor. [RGUHS] 14. Pathologic tooth migration. [GOA]
2. Osseous defects. [RGUHS; GOA] 15. Mobility.[GOA]
3. Radius of action. [RGUHS] 16. Recession.[GOA]
4. Bone functional unit. [RGUHS] 17. Osseous craters. [GOA]
5. Buttressing bone formation. [MUHS] 18. Bone sounding. [GOA]
6. Describe in short the various osseous defects seen in 19. Buttressing bone formation and its type.
periodontal disease. [MUHS] [RGUHS]
PERIODONTITIS: CHRONIC, REFRACTORY AND NECROTIZING ULCERATIVE
Long Essays 7. Slowly progressive periodontitis. [RGUHS]

8. Refractory periodontitis. [NTR-OR]
1. Discuss the pathology, clinical features, diagnosis of 9. Necrotizing ulcerative periodontitis. [NTR-OR]
trauma from occlusion. [RGUHS] 10. Clinical features of chronic periodontitis. [RGUHS]
2. Define trauma from occlusion and traumatic occlusion. 11. Refractory periodontitis. [GOA]
Discuss role of trauma from occlusion. [RGUHS]
3. Define trauma from occlusion. Describe in detail clinical Short Notes
manifestations of trauma from occlusion. [RGUHS]
4. Classify periodontitis. Compare between rapidly 1. Trauma from occlusion. [RGUHS]
progressive and adult periodontitis. [RGUHS] 2. Define acute and chronic trauma from occlusion.
5. What is ‘juvenile periodontitis’? Describe sign, symptoms [RGUHS]
3. Hypophosphatasia. [RGUHS]
and treatment of the same. [MUHS]
4. Papillon-Lefevre syndrome. [RGUHS]
6. Treatment of acute necrotizing ulcerative gingivitis
5. Refractory periodontitis. [MUHS; NTR-UHS]
(ANUG).[MUHS]
6. Necrotizing ulcerative periodontitis.
7. Classify periodontitis. Describe the clinical features of
[MUHS; NTR-NR; RGUHS]
chronic periodontitis. [RGUHS]
7. Juvenile periodontitis. [MUHS]
8. Treatment of ANUG. [MUHS]
Short Essays
9. Bacteriology of localized aggressive periodontitis.
1. Trauma from occlusion. [RGUHS] [RGUHS]
2. Pathological tooth migration. [RGUHS] 10. Periodontal disease activity. [RGUHS]
3. Primary trauma from occlusion. [RGUHS] 11. Radiographic findings in LJP. [GOA]
4. Concepts of trauma from occlusion. [RGUHS] 12. Rapidly progressive periodontitis. [GOA]
5. Tissue response to increased occlusal forces. [RGUHS] 13. Treatment of localized juvenile periodontitis. [GOA]
6. Differentiate between primary and secondary occlusal 14. Clinical and radiologic features of LJP. [GOA]
trauma.[RGUHS] 15. Prepubertal periodontitis. [GOA]
235
AGGRESSIVE PERIODONTITIS

1. Describe clinical feature, diagnosis and management of 1. Aetiology and clinical features of LJR [RGUHS]
localized juvenile periodontitis. [RGUHS] 2. Localized juvenile periodontitis and its management.
2. Define and classify plaque. Describe the plaque host [RGUHS]
interaction in juvenile periodontitis. [RGUHS] 3. Pre-pubertal periodontitis. [NTR-OR]
3. Classify juvenile periodontitis. Describe in detail clinical 4. Localized juvenile periodontitis. [NTR-OR]
and radiographic features of juvenile periodontitis 5. Localized aggressive periodontitis. [NTR-NR]
[RGUHS] 6. Microorganisms in juvenile periodontitis. [NTR-OR]
4. Describe aetiology, clinical features, radiographic finding 7. Clinical and radiographic features of localized juvenile
and management of localized juvenile periodontitis. periodontitis.[NTR-NR]
[RGUHS] 8. Aetiology, clinical features of localized aggressive
5. What do you mean by prognosis? Discuss the doctors periodontitis.[RGUHS]
you could take into consideration for determining 9. Aggressive periodontitis. [NTR-UHS]
prognosis of juvenile periodontitis. [RGUHS] 10. Aetiology and radiographic features of localized
6. Define juvenile periodontitis. Write in detail about aggressive periodontitis. [RGUHS]
aetiology, clinical features, radiographic findings and
management of such condition. [RGUHS] Short Notes
7. Describe the signs, symptoms, aetiology and treatment
of localized juvenile periodontitis. [NTR-OR] 1. Pre-pubertal periodontitis. [RGUHS]
8. Describe the signs, symptoms, differential diagnosis and 2. Define juvenile periodontitis. [RGUHS]
treatment of localized juvenile periodontitis. [NTR-OR] 3. Plaque in localized juvenile periodontitis. [RGUHS]
9. Describe in detail about the juvenile periodontitis. 4. Role of periodontal disease on systemic health.[RGUHS]
Enumerate the differences between the juvenile 5. Distinguish between localized and generalized
periodontitis and adult periodontitis. [NTR-OR] periodontitis.[RGUHS]
10. Describe the aetiology, clinical radiographic features and 6. Porphyromonas gingivalis. [NTR-NR]
treatment of localized aggressive periodontitis. [RGUHS] 7. Actinobacillus actinomycetemcomitans. [NTR-NR]
PERIODONTAL ABSCESS
Long Essays 4. Periodontal abscess. [NTR-OR]

5. Management of chronic periodontal abscess. [RGUHS]
1. Discuss the diagnosis, management of acute periodontal 6. Difference between gingival, periodontal and periapical
abscess.[RGUHS] abscess.[RGUHS]
2. Describe the aetiology of periodontal abscess. How 7. Periodontal abscess versus periapical abscess. [RGUHS]
would you treat the same? [RGUHS] 8. Periodontal and periapical abscess. [GOA]
3. Give the aetiology, signs, symptoms and treatment of
periodontal abscess. [RGUHS] Short Notes
Short Essays 1. Treatment of periodontal abscess. [MUHS]
2. Give the aetiology, differences and treatment of gingival
1. Compare acute periodontal abscess and acute periapical and periodontal abscess. [MUHS]
abscess.[RGUHS] 3. Periodontal abscess versus periapical abscess. [MUHS]
2. Treatment of periodontal abscess. [MUHS] 4. Periodontal abscess. [NTR-NR]
3. Give the aetiology and line of treatment of a chronic 5. Difference between periodontal and periapical abscess.
periodontal abscess. [MUHS] [NTR-NR]
236
HALITOSIS

1. Halitosis. [NTR-NR; RGUHS] 1. Food impaction. [RGUHS; GOA; NTR-UHS ]
2. Causes and management of halitosis. [RGUHS] 2. Define food impaction, food lodgement and gingival
3. Treatment of oral malodour. [NTR-UHS] ablation.[RGUHS]
4. Food impaction. [NTR-UHS; GOA] 3. Mouth-breathing habit. [GOA]
5. Sequelae of food impaction. 4. Halimeter.[NTR-UHS]
[GOA] 5. Food impaction and its sequelae. [GOA]
CLINICAL DIAGNOSIS AND ADVANCED DIAGNOSTIC METHODS
Long Essays 12. Importance of radiographs in periodontics. [NTR-OR]

13. Microbiological tests used in periodontal diagnosis.
1. What are diagnosis and differential diagnosis? Write the
[RGUHS]
importance of different aids in diagnosis of gingival and
periodontal disease. [MUHS] Short Notes
proceed to investigate such a case? [MUHS] 1. Halitosis. [RGUHS]
3. Discuss the importance of history taking in periodontal 2. Tooth mobility. [RGUHS; NTR-NR]
diagnosis and treatment planning. [MUHS] 3. Wasting disease. [RGUHS]
4. Discuss the causes of gingival bleeding. How will you 4. Causes of tooth mobility. [RGUHS]
proceed to investigate such case? [MUHS] 5. Radiographic features of periodontitis. [RGUHS]
5. Describe the diagnostic aids used in periodontal 6. DNA probes. [RGUHS]
diseases.[NTR-NR] 7. BANA. [MUHS]
6. Define diagnosis. Describe the various microbiological 8. What are the various causes of increased tooth mobility?
investigations used in periodontal diagnosis. Add a note [MUHS]
on the limitations of the radiographs in periodontal 9. Acute episodes of gingival bleeding. [MUHS]
diagnosis.[NTR-NR] 10. Define and give the aetiology of halitosis. [MUHS]
7. Discuss about the diagnosis and diagnostic aids in 11. What is halitosis? [MUHS]
periodontics.[RGUHS] 12. What are the uses of radiography in the periodontal
therapy?[MUHS]
Short Essays 13. Uses and limitations of radiograph in periodontics.
[MUHS]
1. Tooth mobility. [RGUHS; NTR-OR; MUHS]
14. Tension test. [NTR-NR]
2. Diagnostic aids in periodontics. [MUHS]
15. Transgingival probing. [NTR-NR]
3. Root hypersensitivity as a periodontal problem.[MUHS]
16. Causes and measurements of tooth mobility. [NTR-NR]
4. Tooth mobility test. [NTR-OR]
17. Periotemp. [NTR-NR]
5. Halitosis. [MUHS]
18. DNA probe. [NTR-NR]
6. Discuss the causes of gingival bleeding. [MUHS]
19. Fremitus test. [NTRUHS]
7. What are the uses of radiography in the periodontal
20. Perio Aid. [NTR-UHS]
therapy?[MUHS]
21. Limitations of radiographs of radiographs in diagnosis
8. Wasting diseases of teeth. [NTR-OR]
of periodontal disease. [GOA]
9. Physiologic tooth mobility. [NTR-OR]
22. Use of antimicrobials in periodontal therapy. [GOA]
10. Miller’s tooth mobility. [RGUHS]
23. Limitations of radiographs in periodontal diagnosis.
11. Roentgenograms in periodontal diagnosis. [NTR-OR]
[GOA]
237
DETERMINATION OF PROGNOSIS

Long Essays 14. Define prognosis. Discuss in detail factors affecting
prognosis.[NTR-UHS]
1. Define prognosis. Discuss in detail factors taken in to
15. Define prognosis. Discuss the various factors you
consideration in overall prognosis. [RGUHS]
consider to assess the prognosis of periodontally
2. Define prognosis. Describe factors that help in
involved teeth. [NTR-UHS]
determining prognosis of a periodontal patient.
16. Define prognosis. Describe the factors affecting overall
[RGUHS]
prognosis of a case of periodontitis. [GOA]
3. Define prognosis. What factors will you consider while
17. Define prognosis. Discuss the various factors which
evaluating prognosis of periodontally involved teeth?
determine the prognosis of a patient with periodontal
[RGUHS]
disease.[GOA]
4. Define prognosis. What are the points to be considered
in a periodontally affected tooth from the point of Short Essays
prognosis?[RGUHS]
5. Define prognosis. What factors will you take into 1. Tobacco use and its effect on periodontium. [MUHS]
consideration while determining the prognosis of a 2. Overall prognosis. [NTR-OR]
case?[MUHS] 3. Periodontal therapy for pregnant patients. [NTR-NR]
6. Define prognosis. How will you determine the prognosis 4. Assessment of individual tooth prognosis in
of a patient suffering from chronic periodontitis? periodontitis.[RGUHS]
[MUHS] 5. Factors for overall prognosis. [RGUHS]
7. Define prognosis. Describe in detail the various factors 6. Factors affecting overall prognosis. [GOA]
you consider to assess the prognosis. [NTR-OR] 7. Define prognosis. Describe the various factors which
8. Define prognosis. Write in detail the procedures adopted affect individual tooth prognosis. [GOA]
to assess the prognosis for periodontal treatment.
[NTR-OR] Short Notes
9. Define prognosis and discuss the various aspects which 1. Prognosis of teeth with furcation involvement. [RGUHS]
influences the prognosis of periodontal therapy. [NTR- 2. Epithelial attachment. [RGUHS]
OR] 3. Define new attachment and repair. [RGUHS]
10. Define prognosis. What factors would you consider for
4. Phases of periodontal therapy. [MUHS]
determining the prognosis of a tooth with periodontal
5. Mention the importance of cementum in periodontal
disease?[NTR-OR]
therapy.[MUHS]
11. Define prognosis. Write in detail the procedure adopted
6. Give definition and factors influencing ‘individual
to assess the prognosis for periodontal treatment.[NTR-
prognosis’ of periodontal disease. [MUHS]
OR]
12. What do you understand by the term ‘prognosis’? 7. Describe in short the important factors to prevent
recurrence of periodontal disease. [MUHS]
Enumerate the various factors which determine the
prognosis of various factors which determine the 8. Role of tooth morphology in assessing prognosis of
prognosis of periodontal involved teeth. [NTR-OR] individual tooth. [MUHS]
13. Define periodontal prognosis. What are its types? 9. Enumerate the factors for overall prognosis of
Outline the factors influencing individual prognosis. periodontal diseases. [RGUHS]
[RGUHS] 10. Individual prognosis. [NTR-UHS].
PERIODONTAL TREATMENT PLAN
Long Essays 2. What is treatment plan? Describe the various phases of

treatment plan. Discuss in detail about the ‘maintenance
1. Describe the importance of maintenance phase in
phase’.
periodontal therapy. [RGUHS] [MUHS]
238
Short Essays 2. Phase 1 therapy? [NTR-NR Apr 2005]

3. Maintenance phase. [NTR-NR Oct 2002, Apr 2004]
1. Treatment planning in periodontitis. [RGUHS Apr 2001 ]

4. Importance of maintenance phase. [NTR-OR Apr 1996]
PERIODONTAL INSTRUMENTATION
Long Essays 2. Universal curette. [RGUHS]

3. Periodontal probe. [RGUHS; GOA; NTR-UHS]
1. Classify periodontal probes. Add a note on its uses.
4. Gingivectomy knives. [RGUHS]
[RGUHS]
5. Periodontal surgical instruments. [RGUHS]
2. Classify periodontal instruments and describe anyone of
6. CPITN.[GOA]
them in detail. [NTR-OR]
7. Difference between Gracey and universal curettes.
3. Describe the general principles you follow during oral
[RGUHS]
prophylaxis.[NTR-OR]
8. What are the principles of sharpening periodontal
4. Describe the general principles of periodontal
instruments?[MUHS]
instrumentation.[BUHS]
9. Limitations and contraindications of ultrasonic scalers.
Short Essays [MUHS]
10. Classification of periodontal instruments. [MUHS]
1. Periodontal probe. [RGUHS] 11. Periotron.[MUHS]
2. Area specific curette. [RGUHS] 12. Instrument stabilization. [MUHS]
3. Principle of sharpening periodontal instruments. 13. Sharpening of periodontal instruments. [MUHS]
[MUHS] 14. Instrument grasp. [RGUHS]
4. Finger rest. [NTR-NR] 15. Hoe scalers. [RGUHS]
5. Naber’s probe. [NTR-OR] 16. Area-specific curettes. [RGUHS]
6. Kirkland knife. [NTR-OR] 17. DNA probe. [RGUHS]
7. Periodontal probes. [NTR-OR] 18. Features of Florida probe. [RGUHS]
8. Polishing instruments. [NTR-OR] 19. Curettes.[RGUHS]
9. Area-specific curettes. [NTR-NR] 20. William’s periodontal probe. [NTR-UHS]
10. Sharpening of periodontal instruments. [NTR-OR] 21. Langer’s curettes. [NTR-UHS]
11. Differences between scalers and curettes. [NTR-OR] 22. Periodontal knives. [NTR-UHS]
12. CPITN index. [RGUHS ] 23. Naber’s probe. [NTR-UHS]
24. William’s probe. [NTR-UHS]
Short Notes 25. Periotrievers.[NTR-UHS]
1. Gracey curette. [RGUHS; NTR-NR; GOA] 26. Florida probe. [GOA]
PRINCIPLES OF PERIODONTAL INSTRUMENTATION
Long Essays 4. General principles of periodontal instrumentation. [GOA]

1. Describe the general principles of periodontal Short Notes
instrumentation.[RGUHS]
1. Finger rest. [RGUHS]
Short Essays 2. Instrument stabilization. [RGUHS]
3. Finger rest and grasps. [RGUHS]
1. Instrument stabilization. [RGUHS]
4. Principles of instrumentation. [NTR-UHS]
2. Probing techniques in periodontics. [RGUHS]
5. Finger rest in periodontal instrumentation.
3. Finger rest. [NTR-UHS] [RGUHS]
239
SONIC AND ULTRASONIC INSTRUMENTATION

Long Essay 2. Ultrasonic scalers. [GOA]
1. What is ultrasonic scaling? Write about indications, Short Notes

contraindications, unit proper and also recent advances.
[RGUHS] 1. Ultra sonics. [RGUHS; NTR-OR; GOA]
2. Principles of ultrasonic scalers. [RGUHS]
Short Essays 3. Ultrasonic scaling. [NTR-OR]
4. Ultrasonic scaler. [NTR-NR; RGUHS ; GOA]
1. Hazards of ultrasonic scalers. [RGUHS] 5. Ultrasonics in periodontics. [NTR-NR]
GENERAL PRINCIPLES AND CONCEPTS OF GROWTH
Long Essay 2. Root planing. [RGUHS]

1. What is phase 1 therapy? Discuss the importance. Short Notes
[NTR-OR]
1. Importance of phase 1 therapy. [RGUHS]
Short Essays 2. Scaling and root planing. [NTR-UHS]
3. Burn-out phenomenon.
1. Phase 1 therapy. [NTR-NR]
[NTR-UHS]
PLAQUE CONTROL

1. Write in detail about antiplaque and anticalculus agents. 1. Define dental plaque and describe chemical plaque
[RGUHS] control.[RGUHS]
2. Define oral hygiene, oral prophylaxis and oral 2. Chemical inhibition of plaque. [MUHS]
physiotherapy. Describe the various aids available for 3. Merits and limitations of datun and toothbrush.[MUHS]
the plaque control. [MUHS] 4. Dental floss. [MUHS; NTR-UHS]
3. What is preventive periodontics? Describe the different 5. Modified Stillman’s brushing technique. [MUHS]
oral hygiene aids to prevent and control the plaque 6. Factors in selection of a toothbrush. [MUHS]
formation.[MUHS] 7. Bass brushing technique. [MUHS]
4. What is oral physiotherapy? Describe the indications, 8. Interdental cleansing aids. [MUHS]
contraindications, advantages and disadvantages of 9. Disclosing agents. [MUHS; RGUHS]
modified Stillman’s method. [MUHS] 10. Abuses of toothbrush. [MUHS]
5. Describe the various methods of plaque control. 11. Vehicles of local drug delivery in periodontics. [MUHS]
[NTR-OR; GOA] 12. Historical background and current developments in the
6. What is plaque control? Describe the various aids used designs of toothbrushes. [MUHS]
for interdental cleaning. [NTR-OR] 13. Dentifrice. [NTR-OR]
7. What do you understand by plaque control? Discuss the 14. Toothbrush. [NTR-NR]
various interdental clearing aids. [NTR-OR] 15. Dental floss. [NTR-OR]
8. Describe various plaque control methods. [NTR-UHS] 16. Ideal toothbrush. [NTR-OR]
9. Dental plaque control in detail. [GOA] 17. Interdental clearers. [NTR-NR]
240
18. Interdental devices. [NTR-OR] 2. Plaque control. [RGUHS]

19. Interdental cleaning aids. [NTR-OR] 3. Disclosing agent. [RGUHS; GOA]

20. Interdental hygiene aids. [NTR-OR] 4. Interdental brushes. [RGUHS]
21. Disclosing solution. [NTR-NR] 5. Chlorhexidine gluconate. [RGUHS; GOA]
22. Desensitizing agents. [NTR-OR] 6. Interdental cleaning aids. [RGUHS]
23. Chemical plaque control. [NTR-OR] 7. Concepts of brushing teeth. [RGUHS, GOA]
24. Chlorhexidine.[NTR-OR] 8. Adverse effects of chlorhexidine. [RGUHS]
25. Chlorhexidine digluconate. [NTR-NR] 9. Dentifrices. [MUHS]
26. Bass technique of tooth brushing. [NTR-NR] 10. Interdental cleansers in type II embrasures. [MUHS]
27. Uses and abuses of toothbrush. [NTR-OR] 11. Toothbrush. [MUHS; RGUHS; GOA]
28. Chemical antiplaque agents. [NTR-OR] 12. Controlled release local delivery system. [MUHS]
29. Dental floss and technique of flossing. [NTR-NR] 13. Indications and side effects of chlorhexidine. [MUHS]
30. ADA specific confiscations of a toothbrush. [NTR-NR] 14. Enumerate the interdental aids. [MUHS]
31. Oral prophylaxis and physiotherapy. [NTR-OR] 15. Oral physiotherapy. [RGUHS]
32. Adverse effects of chlorhexidine mouthwash. [RGUHS] 16. Chemical plaque control. [RGUHS]
33. Various plaque control methods. [RGUHS] 17. Subgingival irrigation. [RGUHS]
34. Chemical plaque control. [RGUHS; NTR- UHS; GOA] 18. Charters technique of tooth brushing. [RGUHS]
35. Chlorhexidine as a mouth rinse. [RGUHS] 19. Chlorhexidine chip. [RGUHS]
36. Interdental aids. [RGUHS; GOA] 20. Bass technique of brushing. [RGUHS]
37. Toothbrush design. [NTR-UHS] 21. Dentifrices. [RGUHS; NTR-UHS]
38. Powered toothbrushes. [NTR Feb-UHS] 22. Interdental cleaning devices. [NTR-UHS]
39. Modified bass technique. [NTR-UHS] 23. Chlorhexidine. [NTR-UHS; GOA]
40. Bass method of brushing. [NTR-UHS] 24. Proxabrush.[NTR-UHS]
41. Discuss mechanical plaque control. [GOA] 25. Anticalculus agents. [NTR-UHS]
26. Interdental plaque control devices. [GOA]
Short Notes 27. Interdental aids. [GOA]
1. Dental floss. [RGUHS; GOA] 28. Stillman’s method of tooth brushing. [RGUHS]
CHEMOTHERAPEUTIC AGENTS
Long Essay 8. Antibiotic prophylaxis for the medically compromised

patients.[NTR-NR]
1. Enumerate the components of nonsurgical periodontal
9. Metronidazole.[RGUHS]
therapy. Discuss in brief local drug delivery system.
10. Advantages of local drug delivery system. [RGUHS]
[RGUHS]
Short Notes
Short Essays
1. Prophylactic antibiotics. [RGUHS]
1. Metronidazole in periodontal therapy. [MUHS]
2. Tetracycline in periodontitis. [RGUHS]
2. Antibiotics.[NTR-OR]
3. Role of tetracyclines in periodontal diseases. [RGUHS]
3. Periodontal pack. [NTR-OR]
4. Controlled release local delivery system. [MUHS]
4. Periodontal dressing. [NTR-OR]
5. Enumerate various controlled release local drug delivery
5. Desensitizing agents. [NTR-OR]
system.[MUHS]
6. Tetracyclines in periodontics. [NTR-NR]
6. Periodontal dressing. [NTR-NR]
7. Local drug delivery system. [NTR-NR]
7. Desensitizing agents. [NTR-NR ]
241
PERIODONTAL SPLINTS

Long Essays 2. Periodontal splints. [RGUHS; NTR-UHS; GOA]
3. Periodontal dressing. [NTR-UHS]
1. Define periodontal splint. Give classification of
periodontal splints. Discuss their role as adjuncts in Short Notes
periodontal therapy. [RGUHS; GOA]
2. Define periodontal splint. Give the indications and 1. Function of periodontal splint. [RGUHS]
contraindication for splinting of teeth. [RGUHS] 2. Clinical importance of biologic width. [RGUHS]
3. Define periodontal splinting. Mention ideal requisites 3. Treatment of bruxism. [RGUHS ]
of a periodontal splint and write in detail about one 4. Periodontal packs.
periodontal splinting procedure. [RGUHS] [RGUHS; GOA]
5. Permanent splinting. [GOA]
Short Essays 6. Periodontal dressing. [GOA]
1. Classify periodontal splint. [RGUHS] 7. Splinting.[GOA]
GENERAL PRINCIPLES OF PERIODONTAL SURGERY

1. Describe the general principle of periodontal surgery. 1. Periodontal dressing. [RGUHS; MUHS; NTR-OR]
[RGUHS] 2. Objectives of surgical phase in periodontal treatment.
2. Discuss in detail the role and importance of preoperative [MUHS]
management in periodontal surgery. [MUHS] 3. Periodontal pack. [NTR-OR]
3. Discuss the rationale and the procedures employed 4. Suture material used in periodontal surgery. [NTR-OR]
in the ‘etiotropic phase’ and ‘initial phase’ of treatment 5. Difference between frenectomy and frenotomy. [RGUHS]
planning in periodontal therapy. [MUHS] 6. Frenectomy.[RGUHS]
4. Write in detail general principles of periodontal surgery. 7. Factors that affect wound healing. [NTR-UHS]
[MUHS]
5. Discuss in detail the role and importance of adequate Short Notes
preoperative management in periodontal surgery.
1. What are the various indications for hospital periodontal
[MUHS]
surgery?[MUHS]
6. How will you prepare the patient for periodontal surgery?
2. Indications of periodontal surgery and methods of
Discuss in detail the common general consideration to
pocket elimination. [MUHS]
carry out various periodontal surgical procedures.
3. Types of periodontal dressings. [RGUHS]
[MUHS]
4. Factors influencing the successful outcome of surgery.
7. Describe the concept of physiological tissue formation
[NTR-UHS]
as an essential aspect of periodontal surgery. [NTR-OR]
5. Horizontal mattress suture. [NTR-UHS]
GINGIVAL SURGICAL PROCEDURES
Long Essays 3. Mention pocket eradication techniques available. Briefly

describe the procedure for gingival curettage. [RGUHS]
1. How do you manage a case of soft, oedematous 4 mm 4. Give the indications and step-by-step procedure in
deep pocket. [RGUHS] gingivectomy. [RGUHS]
2. Define curettage and write about indications, 5. What are the indications for gingivectomy? Describe the
contraindications and procedure. [RGUHS] healing affect on gingivectomy. [RGUHS]
242
6. Define gingivectomy. Give its indications, Short Essays

contraindications and surgical technique with a note on
1. Define curettage and add a note on ENAR [RGUHS]

healing.[RGUHS]
2. Healing after gingivectomy. [RGUHS]
7. Define gingivectomy. Write indications,
3. Rationale of subgingival curettage. [MUHS]
contraindications, step-by-step procedure. Add a note
4. Merits and demerits of electrosurgery. [MUHS]
on healing after gingivectomy. [RGUHS]
5. Describe the healing process after gingivectomy.
8. What are the indications and contraindications for
[MUHS]
gingivectomy? Describe step-by-step procedures for
6. Gingivoplasty. [MUHS; RGUHS; NTR- UHS]
performing gingivectomy. [RGUHS]
7. Indications and contraindications of gingivectomy.
9. Describe in detail the procedure of subgingival
[MUHS; NTR-UHS; RGUHS]
curettage.[MUHS]
8. High frenal attachment sequelae and” treatment.[MUHS]
10. Describe various aspects of gingivectomy surgery.
9. Definition and indication of mucogingival surgery.
[MUHS]
[MUHS]
11. Mention different surgical procedures for widening the
10. HMT.[NTR-UHS]
zone of attached gingiva. Describe any one technique in
11. Free gingival graft. [GOA]
detail.[MUHS]
12. Define mucogingival surgery. Give the indications for
mucogingival surgery. Describe any one technique to
Short Notes
cover a localized area of gingival recession. [MUHS] 1. ENAP.[RGUHS]
13. Define mucogingival surgery. Give the classification and 2. Gingivoplasty. [RGUHS; NTR-UHS]
indications of it. Describe the free gingival autograft 3. Indications of gingivectomy. [RGUHS]
technique for gingival augmentation apical to recession 4. Differentiate between gingivectomy and gingivoplasty.
in detail. [MUHS] [RGUHS]
14. Define and classify gingival recession. Discuss in 5. What are the indications for gingival curettage?[MUHS]
detail the procedure for free gingival autografts in the 6. Differentiate between area-specific and universal
treatment of gingival recession. [RGUHS] curette.[MUHS]
15. Define gingivectomy. What are the indications and 7. What are the causes of failure of gingivectomy? [MUHS]
contraindications for gingivectomy? Describe the 8. Enumerate the different means of taking a gingivectomy
gingivectomy procedure. [NTR-UHS] incision.[MUHS]
16. Define periodontal plastic surgery. Discuss the 9. Differentiate between gingivectomy and gingivoplasty.
techniques to increase the width of attached gingiva. [MUHS]
[NTR-UHS] 10. Indications of mucogingival surgery. [MUHS]
17. Define mucogingival surgery. Describe the classic 11. Preprosthetic periodontal surgery. [MUHS]
technique of free gingival autograft. [GOA] 12. Operations of removal of frenum. [MUHS]
18. Give indications and contraindications for gingivectomy. 13. Indications of mucogingival surgery. [MUHS]
Describe in detail conventional gingivectomy technique. 14. Frenectomy or frenotomy. [GOA]
Add a note on its healing. [GOA] 15. Electrosurgery.[GOA]
19. Enumerate mucogingival surgeries. Write in detail about 16. Curettage.[GOA]
free gingival autograft procedure. [GOA] 17. Periodontal dressings. [RGUHS]
PERIODONTAL FLAP SURGERY
Long Essays 3. Enumerate various pocket elimination procedures. Give

indications, contraindications and procedures of flap
1. Classify flaps. Write in detail about the laterally
surgery in detail. [RGUHS]
positioned flap. [GOA]
4. Enumerate the various pocket elimination procedures.
2. Describe the various types of healing following What are the indications for flap surgery? Describe the
periodontal surgical procedures. [RGUHS] technique of modified Widman’s flap. [RGUHS]
243
5. Define and give classification of periodontal flaps. modified Widman’s flap. [NTR-UHS]
What are the objectives and essential steps of modified 18. Define and classify periodontal flap. Give indications

Widman’s flap? [MUHS] and techniques of modified Widman’s flap. [GOA]
6. Discuss the different therapeutic procedures available 19. List the causes of recession. Enumerate treatment
for the elimination of periodontal pocket. [MUHS] options for recession. Give indications, contraindications
7. What are the indications of conventional flap operation? and method of laterally positioned flap. [GOA]
Describe its technique in detail. [MUHS] 20. Define periodontal flap. Write indications,
8. Define flap. Classify basic flaps. Give a step-by-step contraindications step-by-step procedure of modified
account of modified Widman’s flap. [MUHS] Widman’s flap. [RGUHS]
9. Give different therapeutic procedures available for 21. Enumerate causes of recession. Describe procedure
evacuation of periodontal pockets. Discuss the healing of the laterally positioned flap, indications and
process following subgingival curettage. [MUHS]
contraindications of the same. [GOA]
10. Define and give classification of periodontal flaps. What
are objectives and essential steps of modified Widman’s Short Essays
flap?[MUHS]
11. Define flap. Classify basic flap. Give a step-by-step 1. Types of periodontal flap surgical procedures. [RGUHS]
account of modified Widman’s flap. [MUHS] 2. Indications for periodontal surgery. [RGUHS]
12. Define and classify periodontal flap. Write the indications 3. Modified Widman’s flap. [RGUHS; GOA]
and technique of modified Widman’s flap. 4. Papilla preservation. [NTR]
[RGUHS] 5. Describe the surgical procedure of modified Widman’s
13. Define and classify gingival recession. Mention the flap.[GOA]
various surgical procedures for root coverage and 6. Modified Widman’s flap technique. [GOA]
describe in detail any one surgical procedure for root 7. Papilla preservation flap. [RGUHS]
coverage.[RGUHS] 8. New attachment procedures. [RGUHS]
14. Enumerate periodontal surgical procedures. Write in
detail indications, contraindications and technique of Short Notes
modified Widman’s flap. [GOA]
15. Define and classify periodontal flap. Discuss the 1. Excisional new attachment procedure (ENAP). [MUEIS]
modified Widman’s flap in detail. [NTR] 2. ENAP.[MUHS]
16. Define periodontal flap. Describe the indications, 3. Methods of pocket elimination. [MUHS]
contraindications and technique of modified Widman’s 4. Horizontal incisions for flap surgery. [RGUHS]
flap procedure. [NTR] 5. New attachment. [RGUHS; NTR-UHS]
17. Define and classify periodontal flap. Describe the 6. Root resection in the management of furcation
indications, advantages and step-by-step procedure of involvement.[GOA]
RESECTIVE OSSEOUS SURGERY

1. Steps in osseous resective surgery. [RGUHS] 1. Resective osseous surgery.
2. Difference between ostectomy and osteoplasty. 2. Osteoplasty.[MUHS]
[RGUHS] 3. Repair, regeneration and new attachment. [NTR-UHS]
3. Define and give classification of periodontal flaps. What 4. Root biomodification. [NTR-UHS]
are objectives and essential steps of modified Widman’s
5. Steps in osseous respective surgery. [GOA]
flap?[MUHS]
6. Bone swaging. [RGUHS]
4. Define osseous surgery. Describe the steps in respective
osseous surgery. [RGUHS; GOA]
5. Describe the various types of osseous defects. Describe
Short Notes
the steps in osseous resective surgery. [GOA] 1. Bone blend. [MUHS]
244
2. Bone swaging. [RGUHS] 6. Steps in osseous respective surgery. [NTR-UHS]

3. Root planing. [RGUHS] 7. Osteoplasty.[GOA]

4. Reversed architecture. [NTR-UHS] 8. Ostectomy.[GOA]
5. New attachment. [NTR-UHS] 9. Osseous coagulum. [RGUHS]
REGENERATIVE OSSEOUS SURGERY
Long Essay 12. Osseous coagulum. [NTR-UHS]

13. Define new attachment. What are GTR membranes and
1. Write in detail about rationale and objectives of bone
rational of use of the same? [GOA]
graft.[RGUHS]
14. Bone grafts. [GOA]
2. Define ‘reattachment’ and ‘new attachment’. Describe
15. Membranes in guided tissue regeneration. [RGUHS]
the various factors that affect the likelihood of new
attachment.[MUHS] Short Notes
3. Describe non-graft associated reconstructive
periodontal surgical techniques. [MUHS] 1. Autogenous bone graft. [RGUHS; GOA]
4. Define periodontal regeneration. Enumerate the 2. Non-bone graft material. [RGUHS]
different methods used to achieve the same. Discuss the 3. Definition of guided tissue regeneration. [RGUHS]
principles of guided tissue regeneration. [RGUHS] 4. Guided tissue regeneration. [MUHS]
5. Define gingival recession. Describe its aetiology and 5. Describe in short the various forms of obtaining bone
classification. Explain any one root coverage procedure. grafts from intraoral sites. [MUHS]
[RGUHS] 6. Commercial allografts. [MUHS]
6. Define osseous surgery. Discuss various osseous grafting 7. Describe in short the various methods of obtaining
procedures.[NTR-UHS] bone grafts from intraoral sites. [MUHS]
7. Classify bone grafts. Discuss rationale and uses of GTR. 8. Bone graft materials. [MUHS]
[GOA] 9. What are the guidelines for preparing splint? [MUHS]
10. Periodontal splints. [MUHS]
Short Essays 11. Rationale of GTR. [GOA]
12. Define regeneration and repair. [RGUHS ]
1. Allograft. [RGUHS; GOA] 13. Pedicle grafts. [RGUHS]
2. Guided tissue regeneration. [RGUHS; NTR-UHS] 14. Osseous coagulum. [RGUHS]
3. Autogenous bone grafts. [MUHS] 15. Tissue bank. [NTR-UHS]
4. Non-bone graft materials. [MUHS] 16. Guided bone regeneration (GBR). [NTR-UHS]
5. Factor affecting healing in periodontal therapy. [MUHS] 17. Platelet-rich plasma (PRP). [NTR-UHS]
6. Bone autografts. [RGUHS] 18. Allografts. [NTR-UHS; GOA; RGUHS]
7. Alloplastic bone graft materials. [RGUHS] 19. Bone fill. [NTR-UHS]
8. Free gingival autograft. [RGUHS] 20. Bone blend. [NTR-UHS]
9. GTR. [RGUHS; GOA] 21. Alloplasts.[GOA]
10. Classification of osseous grafts. [NTR-UHS] 22. GTR.[GOA]
11. Subepithelial connective tissue graft (SCTG). [NTR-UHS] 23. Buttressing bone formation. [GOA]
FURCATION INVOLVEMENT AND ITS MANAGEMENT
Long Essays 2. Classify furcation involvement. Write the treatment of

grade furcation involvement in lower first molar. [RGUHS]
1. Classify furcation involvement. Describe in detail
treatment of class I furcation involvement. 3. Describe furcation involvement, types of furcation and
[RGUHS] various treatment procedures in the management of
245
furcation.[RGUHS] 4. Aetiology and classification of furcation involvement.

4. Define furcation involvement. Describe the classification, [RGUHS]

clinical and radiographic features and treatment of 5. Root biomodification. [RGUHS]
furcation involvement. [MUHS 2005,1993,1995] 6. Root resection in the management of furcation
5. Define furcation involvement. Describe the classification involvement.[GOA]
and give the different modalities of treatment of a grade 7. Discuss furcation involvement. [GOA]
furcation involvement with periapical lesion. [MUHS
2002] Short Notes
6. Define and classify furcation defects. Discuss in detail
1. Hemisepta.[RGUHS]
about the treatment modalities of grade II furcation
2. Root conditioners. [RGUHS; NTR-UHS]
defect. [NTR- UHS Jul 2011]
3. Furcation involvement. [RGUHS]
7. Define and classify furcation involvement. Describe the
4. Classify furcation involvement. [RGUHS; NTR-UHS]
treatment of grade II furcation involvement.[GOA 2000]
5. Name common root conditioners. [RGUHS]
6. Furcation involvement and management. [RGUHS]
Short Essays
7. Management of true pulpo-periodontal problems.
1. Give the management of the furcation involvement. [MUHS]
[MUHS] 8. Indications for root resection. [MUHS]
2. Give the aetiology management of the furcation 9. Furcationoplasty.[NTR-UHS]
involvement.[MUHS] 10. Classification of furcation. [RGUHS]
3. Treatment of grade II furcation involvement. 11. Hemisection. [GOA; NTR-UHS]
[MUHS] 12. Root resection. [NTR-UHS; GOA]
ENDODONTIC PERIODONTAL LESIONS AND THEIR MANAGEMENT
Long Essay Short Notes

1. Classify the pulpo-periodontal problems. Describe its 1. Retrograde periodontitis. [RGUHS; GOA]
aetiology, diagnosis and management. [RGUHS] 2. Pulpo-periodontal lesion. [RGUHS]
3. Pulpal and periodontal lesions. [RGUHS]
Short Essay 4. Retrograde.[RGUHS]
5. Dental endoscope.[NTR-UHS]
2. Retrograde periodontitis.
[NTR-OR; RGUHS] 6. Influence of restorations on gingival health. [GOA]
ORTHODONTIC PERIODONTAL INTERRELATIONSHIP
Short Essays 3. Rationale for orthodontic tooth movement in periodontal

therapy.[GOA]
1. Effects of orthodontics treatment in periodontal tissues.
[RGUHS]
2. Describe features of fixed and removable appliances
which affect periodontal health. [GOA]
246
PERIOPROSTHODONTICS/OCCLUSAL EVALUATION

Long Essay Short Notes
1. Enumerate occlusal prematurities and describe steps of 1. Bruxism. [RGUHS Aug 1995]
occlusal adjustments. [RGUHS Apr 2002] 2. Parafunctional habits and periodontium. [RGUHS]
3. Aetiology, clinical features and management of bruxism.
Short Essays [MUHS 2005]
1. Bruxism. [RGUHS Mar 2004] 4. Define coronoplasty. What are its indications? [MUHS]
2. Enumerate occlusal prematurities and describe the 5. Define occlusal adjustment. Mention the various
steps of occlusal adjustments. procedures by which it is achieved. [MUHS 2004]
3. Detection of premature occlusal contacts. [MUHS 1996] 6. Indications of coronoplasty and enumerate the steps of
4. Coronoplasty. [MUHS 1997] coronoplasty. [MUHS 2006]
5. Coronoplasty and its role in control of periodontal 7. Facets. [NTR-NR Apr 2002, May 2004]
diseases. [MUHS 2003] 8. Supra contacts. [NTR-NR Apr 2006]
6. Coronoplasty. [NTR-OR Nov 1994, Oct 1998, 2005] 9. Occlusal adjustments. [NTR-NR Apr 2000]
7. Occlusal interferences. [NTR-OR Apr 1995] 10. Indications for coronoplasty.
8. Indications for occlusal adjustments.[NTR-OR Nov 1992] [NTR-NR Oct 2002]
SUPPORTIVE PERIODONTAL TREATMENT (MAINTENANCE PHASE)
Long Essay 6. Maintenance phase of periodontal treatment. [NTR-UHS]

7. Supportive periodontal therapy. [GOA]
1. Discuss the rationale and importance of maintenance
phase of treatment planning in periodontics. [MUHS] Short Notes
Short Essays 1. SPT.[RGUHS]
2. Maintenance phase. [RGUHS]
1. Supportive periodontal therapy and its importance.
3. Describe in short the important factors to prevent
[RGUHS]
2. Desensitizing agents. [MUHS] recurrence of periodontal disease. [MUHS]
3. Gingival depigmentation procedures. [RGUHS] 4. Recurrence of periodontal disease. [MUHS]
4. Objectives of supportive periodontal therapy. [RGUHS] 5. Rationale of supportive periodontal therapy. [RGUHS ]
5. Rationale of supportive periodontal therapy. 6. Phases of treatment plan. [NTR-UHS]
[RGUHS] 7. Supportive periodontal treatment. [GOA]

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Priya Verma Gupta

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30. AIDS and Periodontium ..................................................................................................................................................................... 133-135

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Section 2 Recently Asked Questions

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There are Three Zones of Oral Mucosa

and interdental ( Fig. 1.1 ). ‘ \\

side and tooth on the other side.

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Question 1 b. Attached gingiva is separated from the loosely bound

There are Three Zones of Oral Mucosa

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It is found at cemento-enamel junction in healthy  

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consists of internal basal lamina which consists of lamina

Question 1 in this epithelium. There is absence of keratinosomes

found , but its number increases considerably at the

 The length of the junctional epithelium is approxiametely

 Ground substance is mainly composed of proteoglycans

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enamel epithelium combines with the oral epithelium

 GCF samples can be measured on a blotter or a perio

along the crown and ameloblasts gradually transform

 Isotope dilution method.

epithelium continuously renews itself by mitotic activity Dento-gingival Junction

which contains a wide range of biochemical factors which  Dento-gingival group

epithelium, connective tissue, serum, inflammatory cells

 Group of secondary fibres are:

whereas in inflammation, GCF increases and resembles

 It has a cleansing action.

 It provides adhesion of the gingival epithelium to the

tooth as it contains plasma proteins.

teeth in the arch by securing them.

Fig. 1.5: Gingival crevice.  Surface texture

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Question 1 2. Passive eruption is exposure of the crown by the apical

Significance of attached gingiva are as follows:

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 It also enhances the aesthetics.

cementum while other part is on enamel. Whereas,

 Meissner-type tactile corpuscles

 Temperature receptors, i.e. Krause type end bulbs

from adjacent loose alveolar mucosa by mucogingival Question 5

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Question 1 cementum in a coronal direction towards the bone.

Cellular Elements the elastic deformation of the bony socket. Once

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fibres in the periodontal ligament.

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Questiuon 1 Cells and Inter -cellular Matrix

with the alveolar bone. 03

^ The cancellous bone: Cancellous trabeculae act as

It is found at cemento-enamel junction in healthy

The length of the junctional epithelium is approxiametely

Ground substance is mainly composed of proteoglycans

GCF samples can be measured on a blotter or a perio

Isotope dilution method.

which contains a wide range of biochemical factors which Dento-gingival group

Group of secondary fibres are:

It has a cleansing action.

It provides adhesion of the gingival epithelium to the

Fig. 1.5: Gingival crevice. Surface texture

It also enhances the aesthetics.

Meissner-type tactile corpuscles

Temperature receptors, i.e. Krause type end bulbs

Question 1 The cancellous bone: Cancellous trabeculae act as

ions, e.g. sodium, magnesium, and fluorine. These salts

The periodontal ligament width is increased because of

Question 1 Mucocutaneous disorders: Lichen planus, pemphigus,

Associated with a variable microbial pattern.

Gingival/soft tissue recession on facial/lingual/

Generalized form: More than 30 % of sites involved.

gingival display, gingival enlargement, abnormal colour,

Aberrant frenum/muscle position.

Abnormalities in phagocyte function. Periodontitis as a Manifestation of Systemic

Question 1 Aberrant frenum or muscle position

Question 2 2. Early-onset periodontitis Age of onset less than 35 years, rapid

Periodontitis as a manifestation of systemic disease.

Only plaque at the cervical third of the tooth is evaluated

G1 = Mild to moderate inflammatory gingival changes,

Recording of Pocket 2.0–3.0—poor.

0 = No debris or stain present.