2 5267187706714130398

Short Notes
in
PERIODONTICS
A Handbook
https://t.me/DentalBooksWorld
Short Notes
in
PERIODONTICS
A Handbook
PL Ravishankar MDS
Professor and Head
Department of Periodontics
Sri Sai Dental College
Srikakulam, Andhra Pradesh, India
L Chandrasekhar MDS
Associate Professor
Purvanchal Institute of Dental Sciences
Gorakhpur, Uttar Pradesh, India
Foreword
AR Pradeep
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Short Notes in Periodontics: A Handbook

First Edition: 2013
ISBN 978-93-5090-295-0
Printed at
Dedicated to
Our Teachers
Foreword
There are a lot of books on periodontology.

Why is this one special? We can think of two
reasons.
First, it’s good. The authors have done a
thorough analysis of the most important and
basic topics of periodontology and present a
gist of those in this book.
Second, even though it’s a handbook, it’s
comprehensive enough dealing with
important aspects clearly and efficiently.
This book touches upon all the relevant topics that undergraduate
students and dental hygienist students will find very easy to read and
understand.
I congratulate Dr PL Ravishankar and Dr L Chandrasekhar for being
able to explain important aspects in a very simple yet comprehensive
manner.
AR Pradeep
Professor and Head
Government Dental College and Research Institute, Bengaluru,
Karnataka, India
Preface
The purpose in the making of this book is to provide ease of understanding,

quick reference, and particularly aimed for undergraduates from the
examination point of view.
A great emphasis has been made to include all important short answers
according to question papers of various universities.
As the textbooks are made in huge volumes, it is difficult to refer the
chapters during examination time.
This book is a supportive guide for undergraduates who want to succeed
in their professional course.
PL Ravishankar
L Chandrasekhar
Acknowledgments
First and foremost we are very grateful to our teachers—Dr Mythili

Swaminathan, Professor and Head, Department of Periodontics, Rajah
Muthiah Dental College, Chidambaram, Tamil Nadu, India and Dr Veena A
Patil, Professor and Head, Department of Periodontics, HKE Society’s S
Nijalingappa Institute of Dental Sciences, Gulbarga, Karnataka, India, who
have always helped us and given us immense support and encouragement
in our academic ventures.
We offer our gratitude to all the contributors, who have shared their
valuable knowledge and ideas for the compilation of this book.
We wish to express our sincere gratitude to Dr AR Pradeep, for readily
accepting to write foreword to this book.
We would like to thank our colleagues Dr BVV Srinivas and Dr K Anil
Kumar, Readers, Sri Sai Dental College, Srikakulam, Andhra Pradesh, India,
who have contributed a lot towards the material collected in this book.
Throughout the process of writing this book, many individuals from
the field of periodontics have taken time out to help us. We would like to
give a special thanks to Dr Santosh Sreedhar, Pariyaram Dental College,
Kannur, Kerala; Dr Satyanarayana, Kamineni Dental College, Hyderabad;
Dr Vivek Govila, Babu Banarasi Das Dental College, Lucknow, Uttar
Pradesh; Dr M Narendra, Vishnu Dental College, Bhimavaram, Andhra
Pradesh, and Professor Dr Narendra Dev, Government Dental College,
Vijayawada, Andhra Pradesh, India, for actively participating in the feedback
and contributions for this book.
We would like to appreciate the efforts of Dr S Rajsekhar and Dr Arun
Mozhi, Rajah Muthiah Dental College, Chidambaram, Tamil Nadu and
Professor Dr S Chakrapani, Sibar Dental College, Guntur, Andhra Pradesh,
India, for their fulltime support and encouragement during the editing of
the book.
We would like to thank Shri Jitendar P Vij Sir (Group Chairman),
Mr Ankit Vij (Managing Director) and Mr Tarun Duneja (Director-Publishing)
of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India,
for their constructive suggestions, and unstinted support in publishing
this book. https://t.me/DentalBooksWorld
Contents
1. Normal Periodontium 1
1. Attached Gingiva 1
2. Gingival Fibers 1
3. Functions of Gingival Fibers 4
4. Keratinocytes 4
5. Mast Cells in Gingival Fibers 4
6. Biological Width 5
7. Blood Supply in Gingival Tissues 5
8. Interdental Gingiva or Gingival Col 5
9. Gingival Pigmentation 6
10. Junctional Epithelium/Dentogingival Junction 8
11. Sulcular Epithelium 9
12. Histology of Gingival Surface Epithelium 9
13. Gingival Massage 10
14. Gingival Sulcus 10
15. Active and Passive Eruption 10
16. Long Junctional Epithelium 11
17. Gingival Innervations 11
18. Functions of Periodontal Ligament 11
19. Merkel Cells 12
20. Langerhans Cells 13
21. Cells in Periodontal Ligament (Cellular Component) 13
22. Principal Fibers of Periodontal Ligament 13
23. Lamina Dura 15
24. Oxytalan Fibers and Sharpey’s Fibers 15
25. Acellular and Cellular Cementum 16
26. Functions of Cementum 17
27. Cementoenamel Junction 17
28. Fenestration and Dehiscence 18
29. Effects of Aging on Gingival Epithelium and
Connective Tissue 18
30. Nature of Periodontal Disease 19
xiv Short Notes in Periodontics
2. Classification and Epidemiology of

Periodontal Diseases 20
1.
Classification of Periodontal Diseases 20
2.
Classification of Periodontitis 20
3.
Chronic Periodontitis 21
4.
Aggressive Periodontitis 21
5.
Periodontitis as a Manifestation of Systemic Disease 21
6.
Define Index and its Ideal Requisites 22
7.
Oral Hygiene Index Simplified 22
8.
Community Periodontal Index of
Treatment Needs (CPITN) 24
9. Plaque Index (Silness and Loe Index) 26
10. Periodontal Index (Russel’s) 1956 28
11. Gingival Index (Loe & Silness Index) 30
3. Etiology of Periodontal Diseases 31

1. Dental Plaque 31
2. Steps in the Formation of Dental Plaque 31
3. Specific Plaque Hypothesis 33
4. Nonspecific Plaque Hypothesis 33
5. Materia Alba 34
6. Acquired Pellicle 34
7. Stains 35
8. Actinobacillus Actinomycetem Comitans/
Aggregatibacter Actinomycetem Comitans 35
9. Calculus 36
10. Theories of Calculus Formation 36
11. Differences between Supra and Subgingival Calculus 37
12. Anticalculus Agents 38
13. Food Impaction 38
14. Macrophages 39
15. Neutrophils 40
16. Role of Microorganisms in the Etiology of Periodontal
Diseases 40
17. Arthus Reaction 42
18. Cytotoxicity 42
19. Immunoglobulins (Ig) 43
20. Infective Endocarditis 44
21. Hypophosphatasia 45
Contents xv
22. Widow’s Peak 45

23. Stress-periodontium 46
24. Prostaglandins 46
25. Mast Cells 46
26. Complement 47
27. Smoking and the Periodontium 48
28. Red Complex 49
4. Periodontal Pathology 50
1. GCF—Definition, Function, Clinical Features
and Methods of Collection 50
2. Role of Saliva in Oral Health 51
3. Definition, Causes and Management of
Gingival Bleeding 52
4. Definition, Etiology and Classification of
Gingival Recession 53
5. Stillman’s Cleft 55
6. McCall’s Festoon 55
7. Stages of Gingivitis 55
8. Classification of Gingival Enlargement 56
9. Drug-induced Gingival Enlargement 57
10. Idiopathic Gingival Enlargement 58
11. Gingival Abscess 59
12. Acute Necrotizing Ulcerative Gingivitis (ANUG) 59
13. Primary Herpetic Gingivostomatitis 60
14. Pericoronitis 61
15. Classification and Definition of Periodontal Pocket 62
16. Distinguishing Features of Suprabony and
Intrabony Pocket 64
17. Lipping 64
18. Radius of Action 66
19. Vertical (or) Angular Defects 66
20. Osseous Crater 67
21. Reverse Architecture 68
22. Trauma from Occlusion 68
23. Aphthous Ulcer 71
24. Pulpo-periodontal Lesions 72
25. Periodontal Cyst 73
26. Periodontal Abscess 73
xvi Short Notes in Periodontics
27. Differences between Periodontal Abscess

and Periapical Abscess 74
28. Wasting Diseases of Teeth 74
29. Root Surface Changes in Periodontal Pocket 76
30. Palatogingival Groove 77
31. Atypical Gingivitis 78
32. Pregnancy Gingivitis 78
33. Static Occlusal Prematurities 80
34. Bone Factor Concept 80
35. Focal Infection 81
36. Desquamative Gingivitis 81
37. Pathological Tooth Migration 83
38. Tooth Mobility 84
39. Bruxism 84
40. Necrotizing Ulcerative Periodontitis (NUP) 85
41. Halitosis (Oral Malodor) 86
42. Diabetes Mellitus 88
43. Chediak-Higashi Syndrome 88
44. Papillon-Lefevre Syndrome 89
45. Gingiva in Leukemia 91
5. Diagnosis, Prognosis and Treatment Plan 93

1. Periodontal Disease Activity 93
2. Sounding of Probing/Transgingival Probing 93
3. Bana Test (Benzoyl-DL Arginine-Naphthylamide) 93
4. Treatment Plan in Periodontitis 94
5. Advantages of Radiographs in Periodontitis 95
6. Radiographic Features of Periodontitis 95
7. Night Guard 96
8. Classify Periodontal Probes 96
9. Prognosis of Teeth with Furcation Involvement 97
10. Halimeter 98
11. DNA Probe 98
6. Nonsurgical Therapy 99
1. Management of Bleeding 99
2. Chlorhexidine 100
3. Periochip 100
4. Dentifrice 101
5. Polishing Instruments 102
Contents xvii
6. Gum Stimulator (Stim-U-Dent) 102

7. Coronoplasty 103
8. Methods for Correction of Occlusal Prematurities 103
9. Desensitizing Agents 104
10. Sharpening of Periodontal Instruments 104
11. Naber’s Probe 105
12. Characteristics of an Ideal Tooth Brush 106
13. Root Planing 106
14. Local Drug Delivery System 107
15. Gracey Curettes 108
16. Difference between Scaler and Curette 109
17. Difference between Gracey and Universal Curettes 109
18. Principles of Ultrasonic Scaler 110
19. Plaque Control 111
20. Interdental Cleansing Aids 111
21. Disclosing Agent 112
22. Tetracyclines in Periodontitis 113
23. Probiotics 114
24. Langer Curette and its Uses 115
25. Perioscope 115
26. Periotron 115
27. Periostat 116
28. Periotemp 116
29. Perio-Aid 116
7. Surgical Periodontal Therapy 117

1. Suture Materials used in Periodontal Surgery 117
2. Biopsy 118
3. Curettage 119
4. ENAP 121
5. Periodontal Surgical Instruments 121
6. Surgical Curettes and Sickles 122
7. Osseous Surgery and Osseous Surgical Procedures 122
8. Difference between Ostectomy and Osteoplasty 123
9. Classification of Bony Architecture 123
10. Definitive and Compromised Osseous Reshaping 124
11. Indications for Resective Osseous Surgery 124
12. Steps in Resective Osseous Surgery 124
13. Re-constructive Osseous Surgery 125
14. Enamel Matrix Proteins 126
xviii Short Notes in Periodontics
15. Root Conditioners 126

16. Regeneration, Repair and New Attachment and
Re-attachment 127
17. Hemophilia and Periodontal Surgery 128
18. Pocket Elimination and Pocket Maintenance 128
19. Microbiological Tests used in Periodontal Diseases 129
20. DNA Probe 130
21. Laboratory Aids used in Diagnosis of
Periodontal Diseases 130
22. Finger Rests 131
23. Effects of Faulty Dentistry 132
24. Orthopantomogram 132
25. Cyanoacrylates 133
26. Classification of Bone Graft Materials 133
27. Sources of Autogenous Bone Grafts 134
28. Osseous Coagulum and Bone Blend 134
29. Autogenous Bone Graft 135
30. Non-bone Graft Material/Alloplast 136
31. Bone Swaging 137
32. Bone Allografts 137
33. Xenografts 137
34. Alloplasts 138
35. Bioactive Glass 138
36. Indications for Bone Grafting in Periodontics 138
37. GTR and Classify GTR Membranes 139
38. Classification of Flaps 139
39. Osteoblasts 140
40. Periodontal Dressings (Periodontal Packs) 141
41. Angular Bony Defects 142
42. Hemisection 142
43. Radisection or Root Resection 143
44. Hydroxyapatite 143
45. Grade 2 Furcation (cul-de-sac) 144
46. Vestibuloplasty 144
47. Free Gingival Autografts 145
48. Healing of Free Gingival Graft 145
49. Glickman Classification (Furcation Involvement) 145
50. Retrograde Periodontitis 146
51. Mucogingival Surgery 147
52. Mucogingival Surgical Techniques 147
Contents xix
53. Procedures for Root Coverage 147

54. Periodontal Plastic Surgery and Describe
the Areas of Application in Periodontics 148
55. ‘Rationale’ or Objectives of Periodontal
Plastic Surgery 148
56. Techniques used to Widen the Zone of
Attached Gingiva 149
57. Advantages of Subgingival Connective
Tissue Graft over the Free Gingival Autograft 149
58. Define Frenectomy 149
59. Guided Tissue Regeneration (GTR) 150
8. Oral Implantology 151

1. Implants and Classification 151
2. Implant Complications 151
3. Peri-implantitis 152
4. Osseointegration 153
5. Early Tissue Respone to Osseointegrated Implants 155
6. Osseointegration from a Mechanical and
Biological View Point 156
7. Osseointegration in the Clinical Reality 157
9. Supportive Periodontal Therapy 158

1. Supportive Periodontal Therapy (SPT) 158
2. Importance of Maintenance Phase 158
3. Maintenance Recall Procedures 159
1
CHAPTER
Normal
Periodontium
1. ATTACHED GINGIVA
The attached gingiva or functional mucosa extends from the free gingival
groove to the mucogingival junction where it meets the alveolar mucosa.
The attached gingiva is a mucoperiosteum which is tightly bound to the
underlying alveolar bone.
Appearance : Pale pink
Surface : Stippled-like orange peel.
Stippling varies considerably, most prominent on facial surfaces and often
disappears in old age. Cause of stippling appears to coincide with epithelial
rete pegs.
Width of attached gingiva varies from 0–9 mm.
Widest - Incisor region (3–5 mm)
Narrowest - Mandibular canines and Premolars
In the past, it was assumed that attached gingiva was necessary to maintain
the health of gingival margin by separating the stable margin from mobile
alveolar mucosa, but this does not appear to be the case in clean mouth.
Thus it has given rise to controversy that any width, even a zero width, is
acceptable if the tissue is healthy.
2. GINGIVAL FIBERS (FIG. 1.1)

The gingiva is the part of the oral mucosa that covers the alveolar processes
of the jaws and surrounds the necks of teeth. Beneath the epithelial
integument resides the gingival connective tissue compartment also
referred to as the lamina propria. The lamina propria exhibits an exquisitely
complex architecture which anticipates its functions. Approximately,
60–65% of the connective tissue compartment of healthy gingiva is
occupied by collagen, with the individual fibrils highly organized into
discrete and easily discernible fiber bundles.
2 Short Notes in Periodontics
Fig. 1.1: Parts of the gingiva and epithelium
Normal Periodontium 3
Collectively these fiber bundles have been referred to as the gingival

ligament composed of type I collagen. The gingival fibers have the following
functions:
 To brace the marginal gingiva firmly against the tooth.
 To provide the rigidity necessary to withstand the forces of mastication
without being deflected away from the tooth surface.
 To unite the free marginal gingiva with the cementum of the root and
the adjacent attached gingiva.
The gingival fibers constituting the gingival ligament vary in spatial
orientation and in size there are 5 principal fiber bundle groups as well as
6 minor groups (Fig. 1.2).
Principal Groups Secondary Groups
Dentogingival Periosteogingival
Alveologingival Interpapillary
Dentoperiosteal Transgingival
Circular Inter-circular
Transseptal Inter-gingival
Semi-circular.
Fig. 1.2: Gingival fiber groups
3. FUNCTIONS OF GINGIVAL FIBERS

The connective tissue of the gingiva is organized to keep the gingival
margin tight around the neck of the tooth and to maintain the integrity of
the dentogingival attachment.
- Prevents from occlusal forces.
- Maintains the position of marginal gingiva.
- Prevents entry of bacteria
- Greater resistance to mechanical trauma or muscle pulls than does lining
mucosa.
- Prevents the occurrence of root dehiscence.
4. KERATINOCYTES
The principal cell type of the gingival epithelium, as well as of other stratified
squamous epithelia, is the keratinocyte. The main function of the gingival
epithelium is to protect the deep structures, while allowing a selective
interchange with the oral environment. This is achieved by proliferation
and differentiation of the keratinocytes.
 “Proliferation” of keratinocytes takes place by mitosis in the basal
layer and less frequently in the suprabasal layers, where a small
proportion of cells remains as a proliferative compartment while a large
number begin to migrate to the surface.
 “Differentiation” involves the process of keratinization, which consists
of progressions of biochemical and morphologic events that occur in
the cell as they migrate from the basal layer.
5. MAST CELLS IN GINGIVAL FIBERS

Mast cells, which are distributed throughout the body, are numerous in
the connective tissue of the oral mucosa and the gingiva. It is a large
spherical or elliptical mononuclear cell. Its nucleus is small relative to the
size of the cell and in histologic preparations frequently is obscured by
the large number of intensely staining granules that occupy its cytoplasm.
In human beings the principal contents of the granules are histamine and
heparin. They play a role in maintaining normal tissue stability and vascular
homeostasis. Histamine is known to be important in initiating the vascular
phase of an inflammatory process.
6. BIOLOGICAL WIDTH
Biological width is defined as the physiologic dimension of the junctional
epithelium and connective tissue attachment.
• Approximately 2 mm.
• During crown lengthening procedures there should be at least 3 mm
between the gingival margin and bone crest.
• This allows for adequate biological width when the restoration is placed
0.5 mm within the gingival sulcus.
When the restoration is placed within its zone, it results in–
- Gingival inflammation
- Pocket formation
- Alveolar bone loss
• Biological width=junctional epithelium (0.97 mm) + connective tissue
attachment (1.07 mm)=2.04 mm
7. BLOOD SUPPLY IN GINGIVAL TISSUES

The gingiva has a rich blood supply derived from three sources:
1. Supraperiosteal arterioles: Along the facial and lingual surfaces of the
alveolar bone, from which capillaries extend along the sulcular epithelium
and between the rete pegs of the external gingival surface.
2. Vessels of the periodontal ligament, which extend into the gingiva and
anastomose with capillaries in the sulcus area.
3. Arterioles, which emerge from the crest of the interdental septa and
extend parallel to the crest of the bone to anastomose with vessels of
the periodontal ligament, with capillaries in the gingival crevicular areas
and vessels that run over the alveolar crest.
8. INTERDENTAL GINGIVA OR GINGIVAL COL (FIG. 1.3)

The interdental gingiva occupies the gingival embrasure which is the
interproximal space beneath the area of tooth contact. Interdentally the
gingiva adapts its shape to the form, size and the position of adjacent
teeth. Therefore in the vestibular/oral dimension, the interdental portion
of the gingiva is narrow between the front teeth and broader between
premolars and molars.
Between the vestibular and oral papillae, which reach about halfway to
the incisal edge the interdental gingival portion forms a concave bridge or
col.
Fig. 1.3: Gingival col
The interdental col increases both in buccolingual width from about 2

to 6 mm and in vertical depth from about 0.3 to 1.5 mm anteroposteriorly.
The col is lined by the coronally fused portion of the junctional epithelium
that encircles the adjacent teeth. The intervening portion consists of
attached gingiva.
If diastema is present, the gingiva is firmly bound over the interdental
bone and forms a smooth, rounded surface without interdental papillae.
9. GINGIVAL PIGMENTATION
“Pigmentation” is defined as coloration, either normal or pathologic of the
skin or tissues resulting from a deposit of pigment. Color of attached and
marginal gingiva is coral pink produced by:
- Vascular supply
- Thickness and degree of keratinization
- Presence of pigment containing cells.
Color varies and correlates with cutaneous pigmentation. Lighter in fair
complexions than in swarthy.
Physiologic Pigmentation (Fig. 1.4)

“Melanin”, non-hemoglobin derived brown
pigment responsible for oral tissues pigmentation
and skin. Present in all and absent or diminished
in Albinos. According to ‘Dummett’ distribution
of pigmentation.
Gingiva - 60%
Hard palate - 61% Fig. 1.4: Melanocyte
Mucous membrane - 22%

Tongue - 15%
Gingival pigmentation occurs as diffuse, deep purples/irregularly shaped
brown patches. Appear in gingiva as early as three hours after birth.
Pathologic Pigmentation
A. Ingestion of metals in medicinal compounds and through industrial
contact result in oral manifestations:
• Bismuth intoxication: Narrow, bluish black of gingival margin.
• Lead intoxication: Linear, steel grey (Burtonian line)
• Mercury intoxication: Linear, results from deposition of mercury
sulfide.
B. Diseases that increase melanin pigmentation:
• Addison’s disease
• Albright’s syndrome
• von-Recklinghausen’s disease
• HIV infection and Peutz-Jeghers syndrome.
Gingival pigmentation may be due to exogenous or endogenous factors.
Exogenous Factors
• Atmospheric irritants such as coal and metal dust.
• Coloring agents in food or lozenges.
• Tobacco–Causes increase in melanin pigmentation of oral mucosa.
• Localized bluish black areas of pigment is caused by amalgam implanted
in the mucosa.
Endogenous Factors
• Many systemic diseases may cause color changes in the oral mucosa,
including the gingiva.
Caused by:
- Melanin
- Bilirubin
- Iron
• Melanin pigmentation is seen in:
- Addison’s disease
- Peutz-Jeghers syndrome
- Albright’s syndrome
• Bile pigments–Jaundice
- Oral mucosa acquires yellow color.
• Iron in hemochromatosis produces blue-gray pigmentation of oral mucosa.
• Endocrine disturbances
• Metabolic disturbances
• Blood dyscrasias, e.g. Anemia, polycythemia and leukemia.
10. JUNCTIONAL EPITHELIUM/DENTOGINGIVAL JUNCTION

(FIG. 1.5)
There are three zones of gingival epithelium:
 Oral epithelium
 Sulcular (crevicular) epithelium
 Junctional epithelium
It is a unique anatomic feature concerned with attachment of gingiva to
the tooth. Consists of “epithelial and Connective tissue components”.
Consists of a collar like band of stratified squamous non-keratinizing
Fig. 1.5: Dentogingival unit
epithelium. It is 3–4 layers thick in early life but the number of layers
increases with age to 10–20. It is the only gingival epithelium with two
distinct basal laminas, one on each surface.
- External basal lamina
- Internal basal lamina
In health, the junctional epithelium lies against enamel and extends to
cemento-enamel Junction. Its cells are larger than those of oral epithelium
and loosely connected together. In adults, it is about 40 cells long from
apex to crevicular surface and varies from 0.25–1.35 mm. Listgarten has
calculated the rate of cellular exfoliation from a unit surface of junctional
epithelium is 50–100 times fast as that of oral gingival epithelium (OGE). In
contrast to OGE, junctional epithelium (JE) is relatively permeable and
allows two way movement of a variety of substances: From corium into
the crevice and vice-versa.
Because of the permeability of junctional epithelium it is inevitable that
the tissue defense mechanism should be in a constant state of alertness
and this is manifested by an infiltration of inflammatory cells, lymphocytes
and plasma cells in the corium.
11. SULCULAR EPITHELIUM

• It is a thin, non-keratinized stratified squamous epithelium without rete
pegs; lining the gingival sulcus and it extends from coronal limit of the
junctional epithelium to the crest of the gingival margin.
• It contains cells with hydropic degeneration; K4 and K13 (=esophageal
type of cytokeratins).
• It lacks granulosum and corneum strata and K1, K2 and K10 to K12
cytokeratins, Merkel cells.
Functions
1. It acts as semipermeable membrane.
2. It has potential to keratinize if
• It is reflected and exposed to the oral cavity.
• The bacterial flora of the sulcus is totally eliminated.
12. HISTOLOGY OF GINGIVAL SURFACE EPITHELIUM

Composed of four layers:
• Stratum basale
• Stratum spinosum (prickle cell layer)
• Stratum granulosum (granular layer)

• Stratum corneum (cornified layer)
→ It is keratinized/ parakeratinized
→ Keratinization varies in different areas:
(Palate—most keratinized
Gingiva; ventral aspect of tongue; cheek—least keratinized)
→ K6, K16—Characteristic of highly proliferative epithelia and K5
and K14—stratification—specific cytokeratins are also present
→ K19—Express parakeratinized areas
13. GINGIVAL MASSAGE

Massaging the gingiva with tooth brush/interdental devices produces
epithelial thickening, increases keratinization and increases mitotic activity
in epithelial connective tissue.
The increased keratinization occurs only on the oral gingiva and not on
the areas more vulnerable to microbial attack, the sulcular epithelium and
interdental areas where the gingival col is present.
14. GINGIVAL SULCUS

Gingival sulcus is the shallow crevice or space around the tooth, bounded
by the surface of the tooth on one side and the epithelium lining the free
margin of the gingiva on the other side.
• Shape – v
• At absolute normal condition, depth of gingival sulcus – 0 mm or close
to 0 mm.
• Clinically healthy gingiva, depth of sulcus – 1.8 mm (0–6 mm)
Clinical evaluation: By introducing periodontal probe and estimation of
the distance it penetrates. Probing depth of clinically normal gingival sulcus
– 2 to 3 mm.
15. ACTIVE AND PASSIVE ERUPTION

Active eruption: It is the movement of teeth in the direction of occlusal
plane.
It is coordinated with attrition.
Passive eruption: It is the exposure of teeth by the apical migration of
gingiva.
It is now considered as pathologic process.
16. LONG JUNCTIONAL EPITHELIUM

If the epithelium proliferates along the tooth surface before the cells from
other tissues reach the area, the result will be a long junctional epithelium.
• During periodontitis an anatomic defect occurs, it causes the formation
of long junctional epithelium.
17. GINGIVAL INNERVATIONS

Gingival innervations are derived from fibers arising from nerves in the
periodontal ligament and from the labial, buccal and palatal nerves.
The following nerve structures are present in the connective tissue:
1. A meshwork of terminal argyrophilic fibers, some of which extend into
the epithelium.
2. Meissner – type tactile corpuscles
3. Krause – type end bulbs (temperature receptors)
4. Encapsulated spindles
18. FUNCTIONS OF PERIODONTAL LIGAMENT

The functions of periodontal ligament can be broadly categorized into:
A. Physical functions
B. Formative and remodeling
C. Nutritional and sensory function
Physical Functions
Protection to vessels and nerves: Periodontal ligament provides soft tissue
casing in order to protect the vessels and nerves from injury due to
mechanical forces.
Transmission of occlusal forces to the bone: When axial forces are
applied, oblique fibers of periodontal ligament stretch and transmit the
forces to alveolar bone, that encourages bone formation rather than bone
resorption. But when horizontal/tipping forces are applied, the tooth rotates
around the axis.
Attachment: Periodontal ligament attaches the tooth to the bone with
the help of collagen fibers.
Maintenance of gingival relationship: Periodontal ligament maintains
the gingival tissues in their proper relationship to teeth.
Shock absorption: Periodontal ligament resists the impact of occlusal

forces.
Two theories have been explained for this mechanism:
• Tensional theory
• Viscoelastic theory
According to tensional theory, the principal fibers of periodontal
ligament play a major role in supporting the tooth and transmitting forces
to the bone.
According to viscoelasticity theory tooth displacement is controlled
by fluid movement and fibres play a secondary role.
Formative and Remodeling Functions

• Cells of PDL have the capacity to control the synthesis and resorption
of cementum, periodontal ligament and alveolar bone.
• Old cells and fibers are broken down and replaced by new ones.
• This function helps in physiological tooth movement, in the adoption
of periodontium to occlusal forces and in repair of injuries.
Nutritional and Sensory Functions

It has a rich vascular supply and provides nutrition to the bone, cementum
and gingiva.
It is supplied by nerve fibers that can transmit sensation of touch,
pressure and pain to higher centers.
 Free endings
 Ruffini
 Meissners corpuscles and mechanoreceptors.
19. MERKEL CELLS

These are non-keratinocytes of gingival epithelium. These are present in
low numbers and are found in basal and suprabasal layers in close contact
with adjacent intraepithelial nerve endings. They contain numerous
membrane bands dense granules in cytoplasm nearest the nerve endings
and over all dendritic sheath.These cells occur in clusters and are identified
as tactile receptors.
20. LANGERHANS CELLS (FIG. 1.6)

These cells arise from bone marrow and come to
occupy the gingival epithelium.These cells have
receptors for immunoglobulins and complement.
The presence of surface antigens makes them to
have a defensive role against the microoraganisms.
21. CELLS IN PERIODONTAL LIGAMENT

(CELLULAR COMPONENT)
Periodontal ligament contains four types of cells.
They are:
Fig. 1.6: Langerhans cell
• Connective tissue cells:
- Fibroblasts
- Cementoblasts
- Osteoblasts
- Odontoclasts and osteoclasts
• Epithelial rests of malassez
• Immune system cells:
- Neutrophils
- Lymphocytes
- Macrophages
- Mast cells.
• Cells of neurovascular elements:
- Neuroglial cells
- Endothelial cells.
Fibroblasts are the most common cells. They are ovoid/elongated cells
with pseudopodia like process. Function is to synthesize collagen and
degrade old collagen fibers.
22. PRINCIPAL FIBERS OF PERIODONTAL

LIGAMENT (FIG. 1.7)
The most important elements of the periodontal ligament are the principal
fibers, which are collagenous and arranged in bundles and follow a wavy
course. Terminal portions of principal fibers that insert into cementum and
bone are called Sharpey’s fibers. Sharpey’s fibers have a central uncalcified
core, surrounded by peripheral calcified portion. They contain collagen as
Fig. 1.7: Principal fiber groups of the periodontium
constituent molecule which is arranged in fibrils with striations. Type of

collagen found in principal fibers is type I.
They are arranged in six groups, they are:
1. Transseptal group: Extend inter-proximally over the alveolar bone crest
and embedded in the cementum of adjacent teeth. They can be
reconstructed even after alveolar bone destruction. Do not have any
osseous attachment.
2. Alveolar crest group: They extend obliquely from cementum into alveolar
crest. Prevent the extrusion of the tooth and also prevent the lateral
tooth movement.
3. Horizontal group: They extend horizontally from cementum to alveolar
bone.
4. Oblique group: They extend from cementum to alveolar bone in a coronal
direction. They are largest group of fibers. Bear the vertical forces and
transform them into tension on alveolar bone.
5. Apical group: At the apical region of root, radiate from cementum into
alveolar bone. Not present in incompletely formed roots. Prevents tooth
tipping and luxation.
6. Interradicular group: Fan out from cementum to the bone in furcation
areas of multi-rooted teeth. Not present is anterior teeth.
23. LAMINA DURA

The term lamina dura means interdental septum normally presents a thin,
radio-opaque border that is adjacent to the periodontal ligament and at the
alveolar crest. It is a radiological term used to describe “alveolar bone
proper”. Alveolar bone proper is thin, compact bone present immediately
surrounding the roots. This appears radiographically as a continuous
white line, but in reality it is perforated by numerous small foramina and
traversed by blood vessels lymphatics and nerves, which pass between
the periodontal ligament and the bone. Even though lamina dura appears
radio-opaque, it is not highly calcified as adjacent bone. Increased radio-
opacity is due to geometrical positioning of bone plate.
Clinical Importance of Lamina Dura

1. Fuzziness and break in the continuity of lamina dura at the crest of
interdental septum is considered as initial radiographic change in
periodontitis.
2. Increased thickness of lamina dura along with vertical bone loss could
be seen in trauma from occlusion.
3. Loss of lamina dura along with ground glass appearance can be seen in
hyperparathyroidism.
Double lamina dura: It is a phenomenon seen on the mesial aspect at
mesial root of mandibular molars. This is due to inclination of root.
24. OXYTALAN FIBERS AND SHARPEY’S FIBERS
Sharpey’s Fibers
Terminal portions of principal fibers that insert into cementum and bone
are called Sharpey’s fibers. They have a central uncalcified core, surrounded
by peripheral calcified portion.
Oxytalan Fibers
Periodontal ligament other than collagen fibers contains two immature
forms of elastin fibers. They are:
• Elaunin fibers.
• Oxytalan fibers.
Elastic meshwork composed of elastin lamellae with peripheral oxytalan
fibers and elaunin fibers are present in periodontal ligament. Oxytalan
fibers resemble pre-elastic fibers.
Orientation: Run parallel to the root surface in vertical direction and bend
to attach to cementum, in cervical third of root.
Functions
1. To regulate the vascular flow.
2. They are responsible for elastic properties of periodontal ligament (PL)
along with principal fibers, those fibers develop in regenerated PL.
3. Have a role in tooth support.
25. ACELLULAR AND CELLULAR CEMENTUM (FIG. 1.8)

Dental cementum–The dynamic tissue covering of the root.
Acellular Cementum
It is also called primary cementum which forms during root formation. It is
the first formed cementum present in cervical one-third of root, formed
before tooth reaches the occlusion, hence called acellular, because it doesn’t
contain cementocytes.
Form : Thin surface layer
Contains : Sharpey’s fibers, intrinsic collagen fibers.
Thickness : 30–230 µm
Fig. 1.8: Cementum
It does not contain cementocytes within its substance but as

cementoblasts populate its surface, the term “Acellular” may not be wholly
appropriate. Incremental lines of salter are present, which represent the
rest periods in cementum formation.
Cellular Cementum
It is also called secondary cementum which forms after the eruption of the
tooth and responds to functional demands formed after the tooth reaches
the occlusal plane.
Components: Less number of Sharpey’s fibers, cementocytes in lacunae,
which like osteocytes in bone, communicate with each other through a
network of canaliculi.
26. FUNCTIONS OF CEMENTUM

Primary function of cementum is to furnish a medium for the attachment of
collagen fibers that bind the tooth to alveolar bone.
• Cementum is responsible for connective tissue attachment to the tooth.
• Functional age of the tooth is represented by repeated apposition of
cemental layers.
• Cementum serves as major reparative tissue for root surfaces.
• Damage to roots such as fractures and resorption can be repaired by
deposition of new cementum.
27. CEMENTOENAMEL JUNCTION

Cementum: Calcified avascular mesenchymal tissue that forms the outer
covering of the anatomic root.
Enamel: Calcified avascular mesenchymal tissue that forms the outer
covering of the anatomic crown.
Three types of relationships involving the cementum may exist at the
CEJ:
1. Cementum overlapping the enamel
It is seen in 60–65% of cases.
2. Edge to edge joint of cementum and enamel also called “Butt Joint”.
It is seen in 30% of cases.
3. Cementum doesn’t meet enamel.
It is seen in 5–10%. In this case, dentin will be exposed to oral
environment resulting in hypersensitivity.
28. FENESTRATION AND DEHISCENCE

Fenestrations: Isolated/Circumscribed areas in the alveolar bone in which
the root is denuded of bone and marginal bone is intact.
Dehiscence: Denuded areas of the root which extend through the
marginal bone. In these areas root surface is covered only by periosteum
and overlying gingiva.
Etiology: Due to A. Prominent root contours, B.Tooth malpositions,
C. Thin bony plates.
Frequency
• More common on facial surfaces of the anterior teeth and frequently
bilateral.
• It is seen in 20% of teeth.
Clinical Importance
May complicate periodontal surgery while reflecting the periodontal flaps.
Hence, partial thickness flaps have to be elevated. Progression of
periodontal diseases will be more rapid in these cases.
29. EFFECTS OF AGING ON GINGIVAL EPITHELIUM AND

CONNECTIVE TISSUE (FIG. 1.9)
Epithelium
• Thinning and decreased keratinization of the gingival epithelium occurs.
Fig. 1.9: Fenestration and Dehiscences
• This causes increase in epithelial permeability to bacterial antigens and

decreased resistance to functional trauma.
• This influences long-term periodontal outcomes.
• There will be flattening of rete pegs and altered cell density.
• The junctional epithelium will migrate from its normal position ( i.e. on
enamel) to more apical position on the root surface with gingival
recession.
• The width of attached gingival increases.
Connective Tissue
• The width of attached gingiva increases.
• Gingival connective tissue becomes coarser and denser.
• Collagen synthesis decreases with age but has greater collagen content
and increased collagen stabilization.
• Increased conversion of soluble to insoluble collagen.
• Increased mechanical strength.
• Increased denaturing temperature.
30. NATURE OF PERIODONTAL DISEASE

a. Periods of exacerbation/periods of activity – bone and connective tissue
attachments are lost as pocket deepens. Clinically active periods show
bleeding, either spotaneously or with probing and greater amounts of
attachment loss, presence of exudating or pus.
b. Periods of remission/quiescence/inactivity–reduced inflammatory
response, little or no loss of bone and connective tissue attachment.
Classification and
2
CHAPTER
Epidemiology of
Periodontal Diseases
1. CLASSIFICATION OF PERIODONTAL DISEASES

The ADA/AAP Case Types
I. Gingivitis
II. Early Periodontitis
Progression of gingival inflammation into the marginal bone,
resulting in mild bone loss and mild-to-moderate pocket formation;
usually no increased tooth mobility.
III. Moderate Periodontitis
A more advanced state of the above condition; the increased
destruction of the periodontal attachment apparatus is manifested
by moderate to deep pockets, moderate to severe bone loss and
tooth mobility.
IV. Advanced Periodontitis
Further progression of periodontitis with generalized deep pockets
and/or frank loss of gingival tissue, severe bone loss and marked
tooth mobility patterns.
V. Refractory Periodontitis
Periodontitis which does not respond to conventional therapy or
which recurs soon after treatment. Many cases appear to be
associated with smoking.
2. CLASSIFICATION OF PERIODONTITIS
According to AAP International Workshop for classification of periodontal
diseases, 1999, the periodontitis can be subclassified into the following
three major types based on clinical, radiographical, historical and laboratory
characteristics.
Classification and Epidemiology of Periodontal Diseases 21
3. CHRONIC PERIODONTITIS
Following characteristics are common in patients with chronic periodontitis:
a. Prevalent in adults but can occur in children.
b. Amount of destruction consistent with local factors.
c. Slow to moderate rate of progression with possible periods of rapid
progression.
d. Possible modified by or associated with systemic diseases, local factors
and environmental factors.
It can be further classified as:
• Localized form: <30% of sites involved.
• Generalized form: >30% sites involved.
• Slight: 1 to 2 mm of clinical attachment loss.
• Moderate: 3 to 4 mm of clinical attachment loss.
• Severe: ≥ 5 mm of clinical attachment loss.
4. AGGRESSIVE PERIODONTITIS
Following characteristics are common:
a. Rapid attachment loss and bone destruction.
b. Amount of microbial deposits inconsistent with disease severity.
c. Familial aggregation of diseased individuals.
It can be subclassified as:
• Localized form:
i. Circumpubertal onset of disease
ii. Localized first molar or incisor disease with proximal attachment
loss on at least two permanent teeth, one of which is first molar.
• Generalized form:
i. Usually affecting persons under 30 years of age.
ii. Generalized proximal attachment loss affecting at least three teeth
other than first molars and incisors.
iii. Pronounced episodic nature of periodontal destruction.
5. PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC

DISEASE
Periodontitis may be observed as a manifestation of following systemic
diseases:
• Hematological disorders
i. Acquired neutropenia
ii. Leukemia’s
iii. Others
• Genetic disorders
i. Downs syndrome
ii. Cohen syndrome
iii. Others
• Not otherwise specified.
6. DEFINE INDEX AND ITS IDEAL REQUISITES

Definition: An index has been defined as numerical value describing the
relative status of population on a graduated scale with definite upper and
lower limits, which is designed to permit and facilitate comparison with other
populations classified by the same criteria and methods (Russel AL).
Ideal requisites of an index:
1. Clarity, simplicity and objectivity: The criteria for the index should be
clear and unambiguous, with mutually exclusive categories.
2. Validity: It should measure what is intended to measure, so it corresponds
to the clinical stages of the disease under study at each point.
3. Reliability: The index should measure consistently at different times
and under variety of conditions.
4. Quantifiability: The index should be amenable to statistical analysis,
so that status of a group can be expressed by number that corresponds
to a relative position on a scale from zero to upper limit.
5. Sensitivity: Index should be able to detect small shifts, in either direction
in a group condition.
6. Acceptability: The index should not be painful or demeaning to the subject.
7. ORAL HYGIENE INDEX SIMPLIFIED

It was developed in 1964 by John C Greene and Jack R Vermillion. Tooth
and surfaces to be examined:
Tooth Surface Substitution
16 Buccal 17, 18
11 Labial 21
26 Buccal 27, 28
36 Lingual 37, 38
31 Labial 41
46 Lingual 47, 48
If a designated tooth is
1. Not a fully erupted permanent tooth, or
2. Has a full crown restoration, or
3. Has a surface reduced in height by caries or trauma then substitution is
made as mentioned above.
Debris index-simplified (Fig. 2.1):
Score Criteria
0 No debris or stain present.
1 Soft debris covering not more than one-third of the tooth surface,
or presence of extrinsic stains without other debris regardless of
the surface area covered.
2 Soft debris covering more than one-third, but not more than two-
thirds of the exposed tooth surface.
3 Soft debris covering more than two-thirds of the exposed tooth
surface.
Fig. 2.1: Debris index
Calculus index - simplified (Fig. 2.2):

Score Criteria
0 No calculus present.
1 Supragingival calculus covering not more than one-third of the
exposed tooth surface.
2 Supragingival calculus covering more than one-third but not more
than two-thirds of exposed tooth surface or the presence of
individual flecks of subgingival calculus around the cervical
portion of the tooth or both.
3 Supragingival calculus covering more than two-thirds of exposed
tooth surface or a continuous heavy band of subgingival calculus
around the cervical portion of tooth or both.
Fig. 2.2: Calculus index
Interpretations:
For DI-S or CI-S
Good - 0.0 to 0.6
Fair - 0.7 to 1.8
Poor - 1.9 to 3.0
For OHI -S
Good - 0.0 to 1.2
Fair - 1.3 to 3.0
Poor - 3.1 to 6.0
Total score
Debris index simplified: —————————————————
Total number of examined buccal and
lingual surfaces
Total score
Calculus index simplified: ———————————————
Total number of examined buccal
and lingual surfaces
Oral hygiene index simplified = Debris index + Calculus index

simplified simplified
8. COMMUNITY PERIODONTAL INDEX OF

TREATMENT NEEDS (CPITN)
Teeth to be scored:
Entire mouth is divided into six sextants:
17-14 13-23 24-27

47- 44 43-33 34-37
Third molars are not included except if they are functioning in the place
of second molars.
For epidemiological surveys: For adults of 20 years or more the index
teeth are:
17 16 11 26 27
47 46 31 36 37
Molars are examined in pairs and only one score, the highest is recorded.
For young people of less than 19 years only six index teeth are used.
16 11 26
46 31 36
The second molars are excluded as the index teeth at these ages because
of high frequency of false pockets.
For screening and monitoring purposes in dental practice:
All the teeth in the sextant are examined for adults over age 19 years.
Only one score highest is recorded in each sextant.
Procedure
Score Criteria
X When only one tooth or no teeth are present in a sextant
0 No periodontal disease (Healthy periodontium)
1 Bleeding observed during or after probing
2 Calculus or other plaque retentive factors either seen or felt
during probing
3 Pathological pocket 4–5 mm in depth
4 Pathological pocket 6 mm or more in depth
Classification of Treatment Needs (Fig. 2.3)

TN- 0 : A recording of code 0 or x for all six sextants indicates that
there is no need for treatment
TN- 1 : Indicated for code 1. Need for improving the personal oral
hygiene of that individual
TN- 2 : a. Code 2: Indicates the need for professional cleaning of
teeth and removal of plaque retentive factors
b. Code 3: Oral hygiene and scaling will usually reduce the
inflammation and reduce the depth of the pockets.
Fig. 2.3: Classification of treatment needs
TN- 3: A sextant scoring code 4 may or may not be successfully treated

by means of scaling and efficient personal oral hygiene measures.
Therefore this is assigned as “complex treatment” involving
scaling, root planning and more complex surgical procedures.
CPITN – PROBE (Fig. 2.4)

Force of probing should not be more than 0.75N.
Probe should be moved in a “walking manner” along the gingival margin.
9. PLAQUE INDEX (SILNESS AND LOE INDEX)

Teeth to be scored: Scoring is done on:
Entire dentition (Whole mouth basis)
Or
Selected tooth (selected tooth basis)
Selected teeth include:
16 12 24
44 32 36
If anyone of the above teeth is missing, then scoring is done on all the
teeth.
Only plaque on cervical third is evaluated
Surfaces examined are four gingival areas of the tooth, i.e., Distal-facial,
facial, mesial-facial and lingual surfaces.
Fig. 2.4: CPITN probe
Procedure
Score Criteria
0 No plaque.
1 A film of plaque adhering to free gingival margin and adjacent
area of tooth. Plaque may be recognized only by running a
probe across the tooth surface.
2 Moderate accumulation of soft deposits within the gingival
pocket, on the gingival margin, adjacent tooth surface which
can be seen by the naked eye.
3 Abundance of soft matter within the gingival pocket and/or
on the tooth and gingival margin.
Calculation of Index
Total score of four surfaces
Plaque index of a tooth = ————————————
4
Addition of indices of all teeth
Plaque index of an individual = —————————————
Total no. of teeth examined
16 12 24
44 32 36 score:
Evaluation: Rating Score

Excellent 0
Good 0.1–0.9
Fair 1.0–1.9
Poor 2.0–3.0
10. PERIODONTAL INDEX (RUSSEL’S) 1956

Most widely used periodontal index in epidemiological surveys and records
both reversible and irreversible changes brought by periodontal disease.
Teeth to be scored: All the gingival tissues circumscribing all the teeth are
examined.
Procedure
Score Criteria for field studies Additional radiographic
criteria for clinical studies
0 Negative. There is neither overt Radiographic appearance

inflammation in investing tissues is essentially normal
nor loss of function due to
destruction of supporting tissues
1 Mild gingivitis. An overt area of
inflammation in the free gingiva
does not circumscribe the tooth
2 Gingivitis. Inflammation
circumscribes the tooth, but no
apparent break in epithelial

attachment
4 Used only when radiographs are There is early notch like
available resorption of alveolar crest
6 Gingivitis with pocket formation There is horizontal
Epithelial attachment has been bone loss involving the
broken and there is a pocket. entire alveolar crest up
There is no interference with to half of the length of normal
the masticatory function. The root
root tooth in the socket is firm
in its socket and has not drifted.
8 Advanced destruction with loss There is advanced bone
of masticatory function. The loss involving more than
tooth may be loose, may have half of tooth root, or a
drifted, may sound dull on definite infrabony pocket
percussion with metallic widening of the PDL.
instrument, or may depressible There may be root
in its socket. resorbtion.
Russel’s rule: “ When in doubt assign the lower score”

18 17 16 15 14 13 12 11 21 22 23 24 25 26 27 28
48 47 46 45 44 43 42 41 31 32 33 34 35 36 37 38
Calculation of the index:

Sum of individual scores
PI score per person = ———————————
Number of teeth present
Interpretation:
Clinical condition Individual PI scores
1. Clinically normal supportive tissues 0 to 0.2
2. Simple gingivitis 0.3 to 0.9
3. Beginning of destructive periodontal disease 1.0 to 1.9 (Reversible)
4. Established destructive periodontal disease 2.0 to 4.9 (Irreversible)
5. Terminal disease 5.0 to 8.0 (Irreversible)
11. GINGIVAL INDEX (LOE & SILNESS INDEX)

It is an index used in measuring the severity and quantity of gingival
inflammation.
Teeth to be scored: All the surfaces of all the teeth or selected teeth are
used.
Selected teeth include:
16 12 24
44 32 36
Surfaces to be scored are: Facial, Mesial, Distal, Lingual
Procedure
Score Criteria
0 Absence of inflammation
1 Mild inflammation: Slight change in color and slight edema, no
bleeding on probing
2 Moderate inflammation: Redness, edema, glazing and bleeding
on probing
3 Severe inflammation: Marked redness and edema, ulceration and
tendency to spontaneous bleeding.
Total of all scores of all the teeth

Calculation of the index:
No. of teeth examined
Interpretation:
Gingival scores Condition
0.1–1.0 Mild gingivitis
1.1–2.0 Moderate gingivitis
2.1–3.0 Severe gingivitis
3
CHAPTER
Etiology of Periodontal
Diseases
1. DENTAL PLAQUE
Definition: The soft debris that forms the biofilm adhering to tooth surfaces
or other hard surfaces in the oral cavity including removable and fixed
restorations.
Composition
1gram of plaque contains 2 10 bacteria.
Nonbacterial organisms – Mycoplasma,Yeast, Protozoa, Viruses.
Intercellular matrix (20–30%) consists of organic and inorganic materials
derived from saliva, bacterial products, etc.
Contains host cells–Epithelial cells macrophages leukocytes.
Organic contents
Polysaccharides, protiens, glycoproteins, lipid
(Bacteria derived) Albumin from important commponent debris membranes
Dextran GCF of pellicle disrupted bacteria.
Inorganic content
Primary: Calcium, phosphorus
Traces: Na, K, F derived from saliva
2. STEPS IN THE FORMATION OF DENTAL PLAQUE (FIG. 3.1)

The process of plaque formation at the microscopic level represents a
highly ordered and predictable ecological succession and can be divided
into three phases:
1. Formation of dental pellicle
2. Initial adhesion and attachment of plaque
3. Secondary colonization and plaque maturation.
Formation of Dental Pellicle
It is the initial phase of plaque development.
All the surfaces of oral cavity including all tissue surfaces as well as
surfaces of teeth and removable and fixed restorations are coated with a
Fig. 3.1: Formation of dental plaque
glycoprotein pellicle, derived from components of saliva and crevicular

fluid, as well as from bacterial and host tissue cell products and debris.
Pellicle is formed by selective adsorption of the environmental
macromolecules.
Mechanism involved are electrostatic, van der Waals and hydrophobic
forces.
Initial Adhesion and Attachment of Plaque

Within few hours, bacteria are found on the dental plaque.
Initially, gram positive facultative microorganisms such as Actinomyces
viscosus, Str. sanguis.
Microbial adhesion to surfaces is explanied in four phases.
Phase 1: Transport of bacteria to the tooth surface through Brownian
motion, sedimentation of microorganisms, liquid flow, chemotactic activity.
Phase 2: Initial adhesion
Reversible adhesion of the bacterium initiated by interaction between
bacterium and the surface including van der Waals attractive forces and
electrostatic repulsive forces.
Etiology of Periodontal Diseases 33
Phase 3: A firm anchorage between bacterium and surface will be

established by specific interactions.
Phase 4: Colonization of surface and biofilm formation.
Secondary Colonization of Surface and Biofilm Formation

1. Secondary colonizers are the microorganisms that do not initially
colonize on clean tooth surfaces.
2. They adhere to cells of bacteria already in the plaque mass,
e.g. Prevotella intermedia, Prevotella loescheii, Capnocytophaga
species, Fusobacterium nucleatum, Porphyromonas gingivalis
3. This ability of different species and genera of plaque microorganisms
to adhere to one another is a process called coaggregation.
E.g: F. nucleatum with S. sanguis
P. loescheii with A. viscoses
Capnocytophaga ochrace with A. viscosus
F. nucleatum with P. gingivalis
3. SPECIFIC PLAQUE HYPOTHESIS

The specific plaque hypothesis states that only certain plaque is pathogenic
and its pathogenicity depends on the presence of or increase in specific
microorganisms.
This is based on the fact that the specific microorganisms responsible
for periodontal diseases release certain damaging factors that mediate the
destruction of the host tissue.
Acceptance of the specific plaque hypothesis was spurred by the
recognition of A. adinomycetemcomitans as a pathogen in localized
aggressive periodontitis.
4. NONSPECIFIC PLAQUE HYPOTHESIS (FIG. 3.2)

Walter Loesche from Michigan
The nonspecific plaque hypothesis maintains that periodontal disease
results from the “elaboration of noxious products by the plaque flora.”
According to this theory, when only small amounts of plaque are
present, the noxious products, would essentially ovewhelm the hosts
defences.
Fig. 3.2: Nonspecific plaque hypothesis
Inherent in the nonspecific plaque hypothesis is the concept that the

control of periodontal disease depends on recognition of the differences
in plaque at sites of different clinical status led to a renewed search for
specific pathogens in periodontal diseases and a conceptual transition
from the nonspecific to the specific plaque hypothesis.
5. MATERIA ALBA
Materia alba is creamy white loose and soft accumulations of bacteria, cell
debris and food residues that lack the organized structure of dental plaque
and it is easily displaced with a stream of water.
Contents:
• Microorganisms
• Desquamated epithelial cells
• Leukocytes
• A mixture of salivary proteins
• Lipids
• And a few or no food particles
Yellow or grayish white, soft, sticky deposit less adherent than dental
plaque.
6. ACQUIRED PELLICLE
It is a homogeneous, membranous. Acellular film that covers the tooth
surfaces and frequently forms the interface between the surface of the
dental plaque and calculus.
Contents:
• Glycoproteins (mucins)
• Proline-rich proteins
• Phosphoproteins (Ex:statherin)
• Enzymes (Ex: amylase)
Functions:
• Act as a protective barrier.
• Provide lubrication for the surfaces.
• Prevent tissue dessication.
Also provide a substrate to which bacteria in the environment attach.
7. STAINS
Pellicle and plaque may be stained by food products including tea, coffee,
by tobacco tar, by the products of chromogenic bacteria and by metabolic
particles. These are extrinsic stains may be prevented by good oral hygiene
methods. Brown, black, green and orange stains are seen frequently in
children with poor oral hygiene. Stains on teeth caused by tobacco may
be brown or black. Most of these stains can be removed if not located in
developmental grooves, porous areas and cracks in the enamel. Intrinsic
stains include those due to developmental disturbances such as fluorosis
and tetracycline staining. Extrinsic stains are not significant factors in the
etiology of periodontal disease but it is a significant esthetic concern for
the patient.
8. ACTINOBACILLUS ACTINOMYCETEM COMITANS/

AGGREGATIBACTER ACTINOMYCETEM COMITANS
A. acinomycetem comitans is a small; short (0.4–1 µm) straight or curved
rod with rounded ends.
It is non-motile and gram negative.
Culture conditions and identification:
• It grows as a white; translucent; smooth; non-hemolytic colony on
blood agar; because of its low density.
• It is identified on a specific growth medium (with vancomycin and
bacitracin as antibiotics to suppress other species) under 5 to 10%
carbon dioxide.
• It appears as a, white, translucent colony with a star-shaped internal
structure.
Special pathogenic characteristics:

• It possesses a number of virulence factors, including lipopoly-
saccharides (endotoxin), a leukotoxin (forms pores in neutrophil
granulocytes, monocytes, and some lymphocytes, which die because
of osmotic pressure), collagenase , and a protease (able to cleave IgG).
• The leukotoxin especially plays a significant role in the pathogenicity
of A. actinomycetemcomitans.
• This bacterium is found in high numbers in localized aggressive
periodontal lesions.
9. CALCULUS
Definition: Calculus is a hard deposit formed by mineralization of dental
plaque and is generally covered by a layer of unmineralized plaque.
Composition:
Inorganic content Organic content
70–90% Mixture of protein-polysaccharides
Calcium phosphate–75.9% complexes, desquamated epithelial
Calcium carbonate–3.1% cells, leukocytes, microorganism
Magnesium phosphate 1.9–9.1%
-Traces Others-Ca–39%, P–19%, Carbohydrate: Galactose, glucose,
CO2–1.9%, Mg-0.8% rhamnose, glucoronic acid, galactosamine
Traces-Na, Zn, Sr, Br, Cu, Mn, Salivary protein (5.9–8.2%)
Tn, Au, Al, Si, Fe, F Contain all organic components
Two-thirds of inorganic content except arabinose and
is crystalline in structures rhamnose
Hydroxyapatite–50% Lipids–0.2%
Magnesium white lockite–21% In the form of free fatty acids,
Octocalcium phosphate–12% cholesterol esters and
Brushite–9% phospholipids
10. THEORIES OF CALCULUS FORMATION

It can be explained mainly under two categories:
1. Precipitation of minerals can occur from a local rise in the degree of
saturation of calcium and phosphate ions, this is explained in:
a. Booster mechanism: According to this theory, precipitation of calcium
phosphate salts results from a local rise in the pH of the saliva.
Factors such as loss of carbon dioxide and production of ammonia

could lead to rise in pH.
Other ways by which the precipitation of calcium phosphate salts
can occur are:
b. Colloidal proteins in saliva bind to calcium and phosphate ions thus
producing a super-saturated solution. When saliva stagnates in the
oral cavity, colloids settle and result in the precipitation of calcium
and phosphorus salts.
c. Phosphatase liberated from dental plaque, desquamated epithelial
cells, or bacteria precipitate calcium phosphate by hydrolyzing
organic phosphates in saliva, thus increasing the concentration of
free phosphate ions.
2. Another concept that has been most widely held is “epitactic concept”.
According to this, seeding agents induce small foci of calcification.
These foci enlarge and coalesce to form calculus. Hence more
appropriately called as heterogeneous nucleation. The seeding agents
in calculus is not clearly known, but suspected agents could be
intercellular matrix of plaque, carbohydrate protein complexes and plaque
bacteria.
Inhibition theory: This theory considers the possibility of calcification
occuring only at specific sites because there exists an inhibiting mechanism
at non-calcifying sites. Wherever calcification occurs, the inhibitor is either
altered or removed. One such inhibiting agent could be pyrophosphate
which prevents the initial nucleus from growing, by possibly ‘poisoning’
the growth centers of the crystal.
11. DIFFERENCES BETWEEN SUPRA AND SUBGINGIVAL

CALCULUS
Supragingival Calculus
• Located coronal to the gingival margin.
• White or whitish yellow in color
• Clay in consistency
Common location: Buccal surfaces of maxillary molars
Lingual surfaces of mandibular anterior teeth
Subgingival Calculus
• Located below the crest of the marginal gingiva
• Dark brown or greenish black
• Hard and dense
• Usually extends nearly to the base of periodontal pockets in chronic
periodontitis but does not reach junctional epithelium.
12. ANTICALCULUS AGENTS

Anticalculus agents are mostly designed to inhibit the mineralization of so
called “petrified” plaque. They are known as crystal growth inhibitors.
• Pyrophosphates
• Zinc citrate
• Zinc chloride
• Gantrez acid (a copolymer of methyl vinyl ether and maleic anhydride)
Most dentifrices and some mouthrinses now contain one or more active
anticalculus agents to achieve so-called tartar control.
The anticalculus agent is incorporated in the oral compositions of the
invention in an inhibiting amount, that is, an amount which is sufficient to
prevent or diminish the formation of calculus. Generally, the toothpastes
and prophylactic pastes of this invention contain from about 0.025 to 2.0
percent by weight, preferably about 1.5 to 2.0 percent by weight of the
anticalculus agent. The mouthwashes generally contain about 0.025 to 1.5
percent by weight and preferably about 0.5 to 1.0 percent by weight.
13. FOOD IMPACTION

It is the forceful wedging of food into the periodontium by occlusal forces.
It may occur where mesial and distal cusp ridges make an acute angle so
that food is forced into an embrasure and into interproximal area.
Cusps that tend to forcibly wedge food interproximally are known as
plunger cusps.
Signs and Symptoms

1. Feeling of pressure and urge to dig the material from between the teeth.
2. Vague pain that radiates deep in the jaws.
3. Gingival inflammation with bleeding and a foul taste in the involved area.
4. Gingival recession.
5. Periodontal abscess formation.
6. Varying degress of inflammatory involvement of periodontal ligament,

sensitivity to percussion.
7. Destruction of the alveolar bone.
8. Root caries.
According to Hirschfeld, food impaction can occur in the following
conditions:
a. Uneven occlusion forces: It can lead to food impaction because
deflection of food away from proximal areas does not occur.
b. Loss of proximal contact: Most common
c. Due to periodontal disease, unreplaced missing teeth, proximal caries
and abnormal biting habits.
d. Congenital morphologic abnormalities of teeth.
e. Improperly constructed restorations.
f. Lateral food impaction: In addition to food impaction caused by occlusal
forces. Lateral pressure from the lip, cheeks, tongue may force food
interproximally.
• This usually occurs when the gingival embrasure is enlarged by
periodontitis or by recessions.
14. MACROPHAGES
• Macrophages are chronic inflammatory cells.
• Monocytes in the bone marrow, when they leave the blood are known
as macrophages.
• Monocytes are large mononuclear phagcocytic leukocytes, the
circulating precursors of macrophages.
• They are suited for communicating with lympocytes and other
surrounding cells.
• Half-life is approximately 3 days.
• Macrophages have morphological functional features characteristic of
the tissues, such as alveolar macrophages in the lungs and Kupffer
cells in the liver.
Functions
• Primary function is phagocytosis
• They participate in the induction and execution of the specific immune
response.
• They are activated by lymphokines, complement components or
interference.
15. NEUTROPHILS
These are phagocytic leukocytes which play an important role in chronic
immune response.
Neutrophils or Polymorphonuclear Leukocytes

• Differentiate almost completely within the bone marrow (14 days)
• Contain many lysosomes within their cytoplasm.
• Suited for rapid response.
Neutrophils possess complement receptors-CR1, CR3, CR4, C5, FCrR.
These enable neutrophils to:
1. Be recruited from blood
2. Locate offending agents
3. Ingest phagocytose and kill offending agents.
16. ROLE OF MICROORGANISMS IN THE ETIOLOGY OF

PERIODONTAL DISEASES (FIGS 3.3 AND 3.4)
Periodontal disease is dependent on bacteria and bacteria may directly
interact with the host tissues in mediating tissue destruction.
These include:
• Actinobacillus actinomycetemcomitans
• Porphyromonas gingivalis
• Tannerella forsythia
• Campylobacter rectus
• Eikenella corrodens
• Fusobacterium nucleatum
• Peptostreptococcus micros
• Treponema denticola
The ability of microorganisms to produce disease depends upon their
virulence capacity.
The mere presence of putative periodontal pathogens in the gingival
crevice is not sufficient to initiate or cause periodontal inflammation.
An elevation in the relative proportion or number of these pathogens
to reach a critical mass is more crucial to mount an effective tissue
damaging process.
The role of “beneficial species” of the host is less obvious in the
progression of disease.
Fig. 3.3: Disease progression
Fig. 3.4: Disease progression
They affect disease progression in the following ways:

1. By passively occupying a niche that may otherwise be colonized by
pathogens.
2. By actively limiting a pathogen’s ability to adhere to appropriate tissue

surfaces.
3. By adversely affecting the vitality or growth of a pathogen.
4. By affecting the ability of a pathogen to produce virulence factors, or
5. By degrading virulence factors produced by the pathogen.
Periodontal therapy is necessarily focused on the reduction or
elimination of periodontal pathology for a more beneficial microbiota.
17. ARTHUS REACTION

It is a type 3 hypersensitivity immune complex disease.
When high levels of antigen are present and persist without being
eliminated antigen-antibody (IgG or IgM) complexes precipitate in and
around small blood vessels and with subsequent complement activation
cause tissue damage at the site of the local reaction.
Inflammation, hemorrhage and necrosis may occur.
Tissue damage appears to be due to the release of lysozymal enzymes
from various cells such as neutrophils, mast cells, etc.
This reaction is referred to as immune complex (or) Arthus reaction.
18. CYTOTOXICITY
The quality or state of being cytotoxic. Cytotoxicity is the quality of being
toxic to cells. Antibody-dependent cell-mediated cytotoxicity (ADCC), a
form of lymphocyte-mediated cytotoxicity that functions only if antibodies
are bound to the target cell.
Lymphocyte-mediated cytotoxicity, the toxic or lytic activity of
T-lymphocytes, which may or may not be mediated by antibodies. Cytotoxic
T-lymphocytes may cause lysis of cells by production of cytolytic proteins
such as perforin. B-cells may cause lysis of cells by antibody-complement
binding to a target cell. Natural killer cells are cytotoxic without prior
sensitization.
Antibody-dependent cell-mediated cytotoxicity (ADCC) describes the
cell-killing ability of certain lymphocytes, which requires the target cell
being marked by an antibody. Lymphocyte-mediated cytotoxicity, on the
other hand, does not have to be mediated by antibodies; nor does
complement-dependent cytotoxicity (CDC), which is mediated by the
complement system.
Three groups of cytotoxic lymphocytes are distinguished:

• Cytotoxic T cells
• Natural killer cells
• Natural killer T cells
19. IMMUNOGLOBULINS (Ig)

Glycoprotein molecules that are produced by plasma cells in response to
an immunogen and which function as antibodies. The immunoglobulins
derive their name from the finding that they migrate with globular proteins
when antibody-containing serum is placed in an electrical field.
Any of a group of large glycoproteins that are secreted by plasma cells
and that function as antibodies in the immune response by binding with
specific antigens. There are five classes of immunoglobulins: IgA, IgD,
IgE, IgG, and IgM based on differences in the amino acid sequences in the
constant region of the heavy chains. All immunoglobulins within a given
class will have very similar heavy chain constant regions. These differences
can be detected by sequence studies or more commonly by serological
means (i.e. by the use of antibodies directed to these differences).
1. IgG - γ heavy chains
2. IgM - μ heavy chains
3. IgA – α heavy chains
4. IgD - δ heavy chains
5. IgE - € heavy chains
IgA
 IgA antibodies are found in areas of the body such as the nose, breathing
passages, digestive tract, ears, eyes, and vagina. IgA antibodies protect
body surfaces that are exposed to outside foreign substances. This
type of antibody is also found in saliva, tears, and blood. About 10% to
15% of the antibodies present in the body are IgA antibodies. A small
number of people do not make IgA antibodies.
IgG
 IgG antibodies are found in all body fluids. They are the smallest but
most common antibody (75% to 80%) of all the antibodies in the body.
IgG antibodies are very important in fighting bacterial and viral
infections. IgG antibodies are the only type of antibody that can cross
the placenta in a pregnant woman to help protect her baby (fetus).
IgM
 IgM antibodies are the largest antibody. They are found in blood and
lymph fluid and are the first type of antibody made in response to an
infection. They also cause other immune system cells to destroy foreign
substances. IgM antibodies are about 5 to 10% of all the antibodies in
the body.
IgE
 IgE antibodies are found in the lungs, skin, and mucous membranes.
They cause the body to react against foreign substances such as pollen,
fungus spores, and animal dander. They may occur in allergic reactions
to milk, some medicines, and some poisons. IgE antibody levels are
often high in people with allergies.
IgD
 IgD antibodies are found in small amount in the tissues that line the
belly or chest. How they work is not clear.
20. INFECTIVE ENDOCARDITIS

Infective endocarditis is a disease in which microorganisms colonize the
damaged endocardium or heart valves.
Microorganisms encountered in common-hemolytic streptococci (e.g.
Str.viridans).
Others
• Eikenella corrodens
• Actinobacillus actinomycetemcomitans
• Capnocytophagus
• Lactobacillus
American Heart Association recommends antibiotic prophylaxis before
procedures associated with significant bleeding from hard or soft tissues,
periodontal surgery, scaling and professional teeth cleaning.
Preventive measures to reduce the risk of endocarditis
• Define the susceptible patient
• Provide oral hygiene instruction
• During periodontal treatment, currently recommended antibiotic
prophylactic regimens should be practiced with all susceptible patients.
• Periodontal treatment should be designed for susceptible patients to

accommodate their particular degree of periodontal involvement.
21. HYPOPHOSPHATASIA
Rare familial skeletal disease.
• Characterized by rickets
• Cranial bone formation
• Craneostenosis
• Premature loss of primary teeth particularly the incisors
• Patients have a low level of serum alkaline phosphatase and phospho-
ethanolamine is present in serum and urine.
Clinical Features
• No evidence of gingival inflammation.
• Reduced cementum formation.
• Premature loss of deciduous teeth.
22. WIDOW’S PEAK

In periodontitis two-walled defects (craters) are the most common bony
defects.
These occur at the expense of the interseptal bone.
If resection is confined only to ledges, the interproximal lesion results
in a facial and lingual bone form in which the interproximal bone is located
more apically than the bone on the facial or lingual aspects of the tooth.
This results in reverse architecture.
Peaks of bone typically remain at the facial and lingual/palatal line
angles of the teeth are known as Widow’s Peak.
Treatment
• Ostectomy to a positive architecture requires the removal of the line
angle inconsistencies (Widow’s Peaks) as well as some of the facial,
lingual and palatal and interproximal bone.
• This results in attachment loss at the proximal line angles and the facial
and lingual aspects of the affected teeth without affecting the base of
the pocket.
23. STRESS-PERIODONTIUM
Individuals under stress may have behavioral changes like:
• Poor oral hygiene.
• Habit of clenching and grinding of their teeth.
• May smoke frequently.
• All these increase their susceptibility to periodontal disease destruction.
Psychosocial stress may also impact the disease through alterations in
the immune system.
24. PROSTAGLANDINS
• Prostaglandins are arachidonic acid metabolites generated by
cyclooxygenases (cox-1, cox-2).
• The primary cells reponsible for PGE2 production in the periodontium
are macrophages and fibroblasts.
• PGE2 is elevated gingivitis and periodontitis particularly in active
disease demonstrating inflammation and attachment loss.
• High-risk periodontal patients have a “monocyte hypersecretory trait”
that results in an exaggerated response both locally and systemically to
bacterial LPS.
• Induction of matrix metalloproteinases (MMPs) and osteoclastic bone
resorption is induced by PGE2.
• In advanced periodontitis NSAID’s inhibit prostaglandin synthesis.
25. MAST CELLS

• Mast cells are important in immediate inflammation.
• Mast cells are more concentrated in the connective tissue of oral mucosa
and gingival.
• Stimulation of mast cells results in activation and secretion of vasoactive
substances that cause anaphylaxis.
• Mast cells store inflammatory mediators such as histamine, eosinophil
chemotactic factor, neutrophil chemotactic factor and heparin.
• Mast cells also synthesize other inflammatory mediators such
as releasing substance of anaphylaxis (SRS-A), TNF-, IL-6 and
leukotriene C4.
• Mast cell interleukin enhances collagenase activity.
• Heparin may augment bone resorption.
26. COMPLEMENT
An important consequence of antigen-antibody interaction is the activation
of complement.
Complement consists of at least 11 proteins and glycoproteins that
make up approximately 10% of the proteins in normal sera of humans and
other vertebrates.
They are synthesized in liver, small intestine macrophages other
mononuclear cells. Complement reacts with antibody antigen complexes
when the antibodies are of the IgG and IgM cases and exerts its primary
biologic effects on cell membrane causing lysis and functional alteration
that can promote phagocytosis.
Biologic effects of complement are:
Activity
• Cytolytic and cytotoxic damage to cells
• Chemotactic activity for leukocytes
• Histamine release from mast cells
• Increased vascular permeability
• Kinin activity
• Lysosomal enzyme release from leukocytes
• Promotion of phagocytosis
• Enhancement of blood clottings
• Promotion of clot lysis
• Inactivation of bacterial lipopolysaccharides from endotoxin.
Complement Components
• C1, 9
• C3a, C5a, C567
• C3a, C5a
• C3a, C5a
• C5a
• C3, C5
• C6
• C3, C4, C5, C6
Lymphocytes
Three types based on receptors for antigens:
• T lymphocytes
• B lymphocytes
• Natural killer cells

T Lymphocytes: (Low affinity antigen receptors)
• Based on co-receptors they are of two types: CD4, CD8
• CD4+T cells–Initiate and help with immune responses by providing
proliferation and differentiation signals.
• CD8+T cells–Cytotoxic cells involved in controlling intracellular
antigens (bacteria, virus, fungi).
• T cells are derived from thymus and play a role in cell-mediated
immunity.
B lympocytes (High affinity antigen receptors)
• Derived from liver, spleen and bone marrow
• Precursors for plasma cells and play a role in humoral immunity
• Control extracellular antigens
• Other B cells in the presence of T cells may differentiate forming memory
B cells.
Memory B cells
• Memory B cells give rise to plasma cells on secondary exposure to
antigen and promote antibodies.
Natural killer cells (NK cells)
• NK cells recognize and kill certain tumor and virally infected cells.
• Based on antigen receptors.
• NK cells containing killer inhibiting receptors (KIR).
• NK cells containing killer activating receptors (KAR).
• Cause NK cells to kill the target cells.
27. SMOKING AND THE PERIODONTIUM

• Effects of smoking on prevalance and severity of periodontal
disease:
• Gingivitis—decreased gingival inflammation and bleeding on
probing.
• Periodontitis—increased prevalance and severity of periodontal
destruction.
• Increased pocket depth, attachment loss and bone loss
• Increased rate and periodontal destruction
• Increased tooth loss
Effects of smoking on etiology and pathogenesis of periodontal
disease:
Microbiology
• Smoking results in qualitative rather than quantitative alterations in the
dental plaque.
• Smokers have significantly higher levels of bacteroides forsythus
T. forsythia.
• Increased colonization of shallow periodontal pockets by periodontal
pathogens.
• Increased levels of periodontal pathogens in deep periodontal pockets.
Immunology
• Smoking decreases the immune response to bacterial challenge.
• Altered neutrophil chemotaxis, phagocytosis and oxidative burst.
• Smoking impairs the response of neutrophils to release of tissue
destructive enzymes.
28. RED COMPLEX

The “red complex,” composed of Bacteriodes forsythus, Porphyromonas
gingivalis, and Treponema denticola, is implicate in severe forms of
periodontal diseases.
• Red complex bacteria (RCB) are more prevalent in patients with
periodontal disease.
• A direct association exists between an unhealthy balance in RCB and
increased pocket depth (PD), clinical attachment loss (CAL), and
bleeding on probing (BOP).
4
CHAPTER Periodontal Pathology
1. GCF—DEFINITION, FUNCTION, CLINICAL FEATURES

AND METHODS OF COLLECTION
Definition
Gingival crevicular fluid (GCF) is an inflammatory exudate from leaky
venules adjacent to the sulcus and junctional epithelium.
Functions
1. Flushing action
2. Presence of cellular and humoral immune components,
e.g. Cytokines
3. Presence of diagnostic and prognostic biological markers.
Clinical Significance
Following factors stimulate GCF flow:
1. Gingival inflammation
2. Tooth brushing
3. Gingival massage
4. Smoking
Methods of Collection of GCF

Various methods used are:
1. Absorbing paper strips
2. Twisted threads
3. Micropipettes
4. Intracrevicular washings
Periodontal Pathology 51
1. Absorbing Paper Strips (Figs 4.1A to C)

These strips used in two methods:
a. Intrasulcular method: (Brill method): Paper strip placed in the sulcus.
b. Extrasulcular method: Paper strips placed at the entrance of sulcus.
• Evaluated by periopaper (or) blotter, which uses an electronic
transducer (periotron) to measure the fluid collected.
A B C
Figs 4.1A to C: (A) Intrasulcular method, and (B,C) Extrasulcular method
2. Twisted Threads
• These are placed around and into the sulcus.
• Calculated by weighing the removed thread.
3. Micropipettes
By capillary action, fluid will be collected in the micropipettes.
4. Intracrevicular Washings
A hard acrylic plate covering the maxilla with soft borders and a groove
following the gingival margins. It is connected to four collection tubes.
Washing is obtained by rinsing the crevicular area from side to side.
2. ROLE OF SALIVA IN ORAL HEALTH

Saliva exerts a major influence on plaque by mechanically cleaning the
exposed oral surfaces by buffering acids produced by bacteria and by
controlling bacterial activity.
S.No. Function Salivary components Mechanism

1 Lubrication Glycoproteins, mucoids Coating similar to gastric mucin
2 Physical protection Glycoproteins, mucoids Coating similar to gastric mucin
3 Cleaning Physical flow Clearance of debris and bacteria
4 Buffering Bicarbonate and PhosphateAntacids
5 Tooth integrity Minerals Maturation, remineralization
maintenance Glycoprotein pellicle Mechanical protection
6 Antibacterial action Immunoglobulin A Control of bacterial colonization
Lysozyme Breaks bacterial cell walls
Lactoperoxidase Oxidation of susceptible bacteria
3. DEFINITION, CAUSES AND MANAGEMENT OF GINGIVAL

BLEEDING
Definition: Presence (or) appearance of blood in the gingival sulcus when
irritated by mechanical forces such as probing is called gingival bleeding.
• Bleeding on probing appears earlier than a change in color or other
visual signs of inflammation.
Causes:
Management
a. Chronic bleeding: Removal of plaque and calculus by scaling.
b. Acute bleeding: Removal of irritating factors like tooth brush bristles,
sharp pieces of food.
c. Systemic conditions: Controlled by treating the systemic conditions,
elimination of local factors.
4. DEFINITION, ETIOLOGY AND CLASSIFICATION OF

GINGIVAL RECESSION (FIGS 4.2 AND 4.3)
Definition: Exposure of the tooth by apical migration of gingiva is called
gingival recession.
Causes:
1. Inadequate attached gingiva (High frenum attachment)
2. Malpositioning of teeth
3. Osseous dehiscence
4. Vigorous brushing
Fig. 4.2: Gingival recession

Types:
Two types of recession:
1. Visible–It is clinically observable.
2. Hidden–It is covered by gingiva.
Fig. 4.3: Miller classification

Classification
Proposed by Miller :
Class I: Marginal tissue recession does not extend to the mucogingival
junction. There is no loss of bone or soft tissue in the interdental area.
This type may be narrow or wide.
Class II: Marginal tissue recession extends to or beyond the mucogingival
junction. There is no loss of bone or soft tissue in the interdental area.
Subclassified into narrow and wide.
Class III: Marginal tissue recession extends to or beyond the mucogingival

junction. There is severe bone and soft tissue loss interdentally or severe
malpositioning of the tooth.
Class IV: Marginal tissue recession extends to or beyond the mucogingival
junction. There is severe bone and soft tissue loss interdentally or severe
malpositioning of the tooth.
5. STILLMAN’S CLEFT (FIG. 4.4)

• It is a specific type of gingival recession.
• These are triangular (or) apostrophe shaped indentations seen in gingival
margins.
• They are observed on the facial surface of premolars, canines and incisors.
• Initially, their presence was attributed to trauma from occlusion.
• They represent peculiar inflammatory change of marginal gingiva.
Clinical Significance
• Leads to exposure of root cementum and dentin causing hypersensitivity.
• Unaesthetic.
• Apical border of oral mucosa is inflamed due to inadequate plaque
control as the lesion reaches mucogingival junction.
Fig. 4.4: Stillman’s cleft
6. McCALL’S FESTOON
It is a rolled, thickened band of gingiva usually seen adjacent to the cuspids
when recession approaches mucogingival junction.
• They were attributed to traumatic occlusion.
• It represents peculiar inflammatory changes of the marginal gingiva.
7. STAGES OF GINGIVITIS
Gingivitis is initiated with the presence of microorganisms in the gingival sulcus.
The development of gingivitis can be explained in four stages:

Stage-I : Initial lesion
Stage-II : Early lesion
Stage-III : Established lesion
Stage-IV : Advanced lesion
Stage-I: Initial Stage-II: Early Stage-III: Stage-IV:

lesion lesion Established lesion Advanced lesion
1. Seen after 2-4 1. Seen after 4-7 1. Seen after 14-21 1. Seen after few
days of exposure days of exposure days but may months of
to plaque to plaque extend up to 6 exposure to
2. Histologically, 2. Proliferation of months plaque
dilation of capillaries can 2. Proliferation of 2. Inflammation
capillaries and be seen. capillaries along extends from
increased blood Increased with venous gingiva to
flow is seen. destruction of stasis can be alveolar bone in
3. Predominant collagen is seen. seen as bluish this fourth stage.
inflammatory 3. Predominant hue clinically. 3. Inflammatory
cell is PMNS inflammatory 3. Predominant cell is plasma
4. Increase in cell is inflammatory cell.
gingival lymphocyte cell is plasma 4. Also called as
crevicular fluid 4. Erythema may cell. phase of
is the clinical appear clinically, 4. Clinically, color periodontal
finding seen in and bleeding on change (bluish breakdown. Loss
this stage. probing can be hue (or) reddish of attachment
noticed. pink), size can be seen.
changes, and
loss of stippling
can be observed.
8. CLASSIFICATION OF GINGIVAL ENLARGEMENT

Gingival enlargement (or) gingival overgrowth is an increase in size of the
gingiva.
Classified according to etiologic factors and pathologic changes as
follows:
I. Inflammatory enlargement
a. Chronic
b. Acute
II. Drug-induced enlargement
III. Enlargements associated with systemic diseases or conditions
a. Conditioned Enlargement
i. Pregnancy
ii. Puberty
iii. Vitamin C deficiency
iv. Plasma cell gingivitis
v. Non-specific conditioned enlargement
b. Systemic diseases causing gingival enlargement
i. Leukemia
ii. Granulomatous diseases
E.g: Wegener’s granulomatosis, sarcoidosis
IV. Neoplastic enlargement (gingival tumors)
a. Benign tumors
b. Malignant tumors
V. False enlargement
9. DRUG-INDUCED GINGIVAL ENLARGEMENT

Etiology: Long-term therapy of the respective drug (Phenytoin;
Cyclosporine; Nifedipine).
Phenytoin-induced Gingival Hyperplasia

Phenytoin is an anticonvulsant drug used in the control of epilepsy.
Clinical Features
1. Clinically, it starts as a painless, bead-like enlargement of facial and
lingual gingival margins and interdental papillae.
2. The marginal and papillary enlargement unite and develop into a
massive tissue fold which interferes with occlusion.
3. The lesion is mulberry shaped, firm; pale-pink and resilient with
minutely lobulated surface and no tendency to bleed.
4. The enlargement is generalized throughout the mouth, but more severe
in maxillary and mandibular anterior region.
5. The presence of enlargement will result in a secondary inflammatory
process that complicates gingival hyperplasia caused by the drug.
Pathogenesis
Phenytoin stimulates proliferation of fibroblast with subsequent increase
in collagen production.
Cyclosporine
• It is a potent immunosuppressive agent used to prevent organ transplant
rejection and to treat several diseases of autoimmune origin.
• Mechanism of Action: It inhibits helper T-cells, which play a role in
cellular and humoral immune response.
• Dosage greater than 500 mg/day induce gingival overgrowth.
Nifedipine
It is a calcium channel blocker that induces direct dilatation of coronary
arteries and arterioles, improving oxygen supply to heart muscle.
• It also reduces hypertension by dilating the peripheral vasculature.
10. IDIOPATHIC GINGIVAL ENLARGEMENT

Idiopathic gingival enlargement is a rare condition of undetermined cause
Other terms : Gingivostomatitis
Elephantiasis
Idiopathic fibromatosis
Hereditary gingival hyperplasia
Congenital familial fibromatosis.
Etiology
• It is unknown.
• Some cases have hereditary basis (or) may be due to impairment of
physical development.
• Presence of bacterial plaque may be initiating factors.
Clinical Features
1. Enlargement affects the attached gingiva, gingival margin and interdental
papillae.
2. The enlarged gingiva is pink, firm and leathery in consistency with
minutely pebbled surface.
3. In severe cases, the enlargement projects into oral vestibule.
4. The jaw appears distorted because of the bulbous enlargement of the
gingiva.
11. GINGIVAL ABSCESS

Definition: A localized accumulation of pus in previously disease free
gingiva is called gingival abscess.
It is painful; rapidly expanding lesion and of sudden onset.
Etiology
It may be due to bacteria carried deep into tissue when a foreign substance
(e. g. tooth brush bristle; piece of apple core) are forcefully embedded into
gingiva.
Clinical Features
Site: Limited to marginal gingiva (or) interdental papilla
1. Initially, it is a red swelling with smooth, shiny surface.
2. Within 24 to 48 hours, the lesion becomes fluctuant and points out with
orifice.
3. Purulent exudate is expressed through orifice.
12. ACUTE NECROTIZING ULCERATIVE GINGIVITIS (ANUG)

It is an acute inflammatory infection of gingiva.
Acute necrotizing ulcerative gingivitis (ANUG) is a microbial disease
of the gingiva in the context of an impaired host response.
Synonyms
1. Trench mouth.
2. Vincent infection or stomatitis.
3. Acute ulcerative gingivostomatitis.
4. Fusospirochetal gingivitis.
Etiology
A. It is an multifactorial disease caused by fusospirochetal organisms.
B. Predisposing factors:
i. Local predisposing factors:
a. Pre-existing gingivitis.
b. Injury to the gingiva.
c. Smoking.
d. Periodontal pockets.
e. Pericoronal flaps.
ii. Systemic predisposing factors:

a. Nutritional deficiency.
b. Debilitating diseases.
C. Psychosomatic factor:
a. Stress.
Clinical Features
Oral signs:
1. Punched out, crater like depressions at the crest of the interdental
papillae are the characteristic lesion of ANUG.
2. Gingival craters are covered by gray, pseudomembranous slough.
3. It is demarcated from remainder of gingival mucosa by a linear erythema.
4. Spontaneous gingival hemorrhage on slight provocation.
5. Fetid odor and increased salivation.
Oral symptoms:
1. Extremely sensitive to touch and radiating gnawing pain aggravated
by spicy or hot foods.
2. ‘Metallic’ foul taste and excessive amount of ‘pasty’ saliva.
Extra oral signs and symptoms:
1. Mild to moderate cases—Local lymphadenopathy and slight elevation
in temperature.
2. Severe cases—High fever, increased pulse rate, loss of appetite, general
lassitude, headache can be seen.
13. PRIMARY HERPETIC GINGIVOSTOMATITIS

Primary herpetic gingivostomatitis is an infection of the oral cavity caused
by the herpes simplex virus (HSV-1).
Age: It occurs mostly in infants and children younger than 6 years of age.
Sex: Equal frequency in male and female.
Etiology: Caused by HSV (Herpes simplex virus)
Clinical Features
Oral signs:
1. It appears as a diffuse, erythematous, shiny involvement of the gingiva;
oral mucosa with edema and gingival bleeding.
2. In its initial stage, it appears as discrete spherical gray vesicles dispersed

in different areas.
E.g: Gingiva, labial and buccal mucosa, soft palate and tongue.
3. After 24 hours, the vesicles rupture and form painful small ulcers with
red, elevated halo like margins and a depressed yellow and grayish
white central portion.
Oral symptoms:
1. Generalized “soreness” of oral cavity.
2. Ruptured vesicles are sensitive to touch, thermal changes and foods.
Extraoral and systemic signs and symptoms:
1. Cervical adenitis
2. Fever as high as 101° F to 105° F
3. Generalized malaise.
Histopathology
1. These vesicles show ballooning degeneration of epithelial cells,
consisting of acantholysis and nuclear enlargement.
These cells are called Tzanck cells.
2. Multinucleated giant cells are also seen.
Differential Diagnosis
1. ANUG
2. Erythema multiforme
3. Steven-Johnson syndrome
4. Recurrent aphthous ulcers
14. PERICORONITIS (FIG. 4.5)

Definition: This is an acute infection of gingiva around a partially erupted
tooth. When a tooth begins to erupt breaking through tissue, a small flap
of tissue may remain over the tooth surface.
• Food debris and bacteria accumulates in the space between the
pericoronal flap and tooth leading to inflammation.
Types
1. Acute
2. Subacute
3. Chronic https://t.me/DentalBooksWorld
Clinical Features
1. Site: More common in mandibular third molar area.
2. Pericoronal area is red, swollen, suppurating lesion that is exquisitely
tender with radiating pain to the ear, throat, and floor of the mouth.
3. In acute pericoronitis, size of flap increases and interferes with closure
of jaws.
4. Foul taste may be seen.
5. Lymphadenitis and swelling of the cheek near the angle of the jaw.
6. Difficulty in opening the mouth.
7. Systemic complications like fever, leukocytes and malaise are observed.
8. Pain when chewing.
Complications
1. Pericoronal abscess.
2. Cellulitis.
3. Ludwigs angina.
Treatment Fig. 4.5: Operculum
1. Pericoronal flap excision (Operculectomy).

2. Removal of 3rd molar.
15. CLASSIFICATION AND DEFINITION OF PERIODONTAL

POCKET
Definition: It can be defined as “a pathological deepening of gingival
sulcus”.
Classification
I. Depending upon Morphology:
a. Gingival pocket (or) pseudopocket
b. Periodontal pocket (or) true pocket
Intrabony pocket Suprabony pocket

a. Gingival pocket/pseudopocket:
Coronal migration of the marginal gingiva leads to gingival pocket.
Pocket is formed by gingival enlargement without destruction of the

underlying periodontal tissue. The sulcus is deepened because of increased
bulk of gingiva.
b. Periodontal pocket/True pocket (Figs 4.6A to C):
Apical migration of junctional epithelium causes true pocket.
Pocket is formed due to destruction of the supporting periodontal tissues.
i. Suprabony: (Supracrestal or supra-alveolar)
ii. Intrabony: (Infrabony; subcrestal or intra-alveolar)
a. Gingival pocket
b. Suprabony pocket
c. Intrabony pocket
A B C
Figs 4.6A to C: Periodontal pockets
II. Classification of pocket based on number of tooth surfaces

involved (Figs 4.7A to C):
i. Simple pocket: Only one surface is involved.
ii. Compound pocket: Two (or) more than two surfaces are involved.
iii. Complex pocket: Base of pocket is on one surface and opening of
the pocket will be on another surface. Also called spiral pocket.
III. Based on nature of soft tissue wall:
a. Edematous pocket
b. Fibrous pocket
IV. Based on disease activity:
a. Active pocket
b. Inactive pocket https://t.me/DentalBooksWorld
Figs 4.7A to C: Classification of pockets according to involved tooth surfaces.

(A) Simple pocket, (B) Compound pocket, (C) Complex pocket
Contents of Pocket:
Microorganisms and their products:
• Dental plaque
• Gingival fluid
• Food debris
• Salivary mucin
• Desquamated epithelial cells and leukocytes
• Purulent exudates.
16. DISTINGUISHING FEATURES OF SUPRABONY AND

INTRABONY POCKET
Suprabony pocket Intrabony pocket
1. Base of pocket is coronal to level of 1. Base of pocket is apical to crest of

alveolar bone. alveolar bone so that the bone is
2. Pattern of bone destruction is adjacent to soft tissue wall.
horizontal. 2. Pattern of bone destruction is
3. Interproximally, transseptal fibers vertical (angular)
are arranged horizontally. 3. Interproximally, transseptal fibers
4. Facially and lingually, periodontal are oblique.
fibers are either horizontal (or) 4. Facially and lingually periodontal
obliquely arranged. fibers are oblique in direction.
5. Horizontal bone defects are formed. 5. Vertical defects are formed.
17. LIPPING (FIG. 4.8)

It is defined as shelf-like thickening of alveolar bone margin (Boccal Acular
Exostoses.
• It is a form of peripheral buttressing bone formation.
Fig. 4.8: Lipping
Etiology
1. Heavy occlusion forces
2. Inflammatory bony lesions like periodontitis.
Pathogenesis
When the bone is resorbed by excessive occlusal forces, the body attempts
to reinforce the thinned bony trabeculae with new bone.
• The attempt to compensate the lost bone is called buttressing bone
formation.
• Buttressing bone formation is of two types:
1. Central buttressing bone formation.
2. Peripheral buttressing bone formation.
1. Central buttressing bone formation:
It occurs within the jaw. Endosteal cells deposit new bone, which
restores bony trabeculae and reduce the size of marrow spaces.
2. Peripheral buttressing bone formation:
Occurs on bone surface.
Based on severity, it produces:
a. Shelf-like thickening of alveolar margin referred as lipping.
b. Pronounced bulge in the contour of bone.
Treatment: Osteoplasty.
18. RADIUS OF ACTION

• Garant and Cho suggested that locally produced bone resorption
factors may need to be present in the proximity of the bone surface to
exert their action.
• Page and Schroeder, on the basis of Waerhaug’s measurements, made
on human autopsy specimens, postulated a range of about 1.5 to 2.5
mm within which bacterial plaque can induce loss of bone.
• Beyond 2.5 mm there is no effect; interproximal angular defects appear
only in spaces that are wider than 2.5 mm because narrow spaces would
be destroyed entirely.
• Large defects greatly exceeding a distance of 2.5 mm from the tooth
surface may be caused by the presence of bacteria in the tissues.
19. VERTICAL (OR) ANGULAR DEFECTS

The defects that occur in oblique direction are known as Vertical (or)
Angular defects.
• It leads to hollowed-out trough in the bone along side of the root.
• The base of the defect is located apical to the surrounding bone.
• These are mostly accompanied by intrabony pockets.
Classification (Figs 4.9A to C)

Classified based on number of osseous walls as:
1. One-wall defect/Hemiseptum: One wall is present.
2. Two wall defect: Two walls are present.
3. Three-wall (or) intrabony defect: Three walls are present. Appears mostly
on mesial aspects of second and third maxillary and mandibular molar.
A B C
Figs 4.9A to C: (A) Three long walls: Distal (1), lingual (2) and facial (3), (B)
Two-wall defect: Distal (1) and lingual (2), (C) One-wall defect: Distal wall only (1)
4. Combined osseous defect: The number of walls in the apical portion of

the defect are greater than in occlusal portion (Fig. 4.10).
Fig. 4.10: Combined osseous defect
Vertical defects occurring interdentally can be seen on radiograph and

those which appear on facial and lingual (or) palatal surface are not seen.
20. OSSEOUS CRATER (FIG. 4.11)

Osseous craters are concavities in the crest of the interdental bone confined
within the facial and lingual walls.
• They make one-third of all defects and about two-thirds of all mandibular
defects.
• It can be diagnosed by transgingival probing.
Fig. 4.11: Osseous crater
The reasons for high frequency of interdental craters are:

1. The interdental areas collect plaque and it is difficult to clean.
2. The normal flat (or) concave facio-lingual shape of the interdental
septum in lower molars favor crater formation.
3. Vascular patterns from the gingiva to center of the crest provide a

pathway for inflammation.
21. REVERSE ARCHITECTURE (FIG. 4.12)

Reverse architecture (or) negative architecture refers to the relative
position of interdental bone to radicular bone.
It is produced when the interdental bone is more apical than radicular
bone.
The defects are produced by loss of interdental bone, including the
facial and lingual plates without concomitant loss of radicular bone.
The defects are more common in maxilla.
Fig. 4.12: Reverse architecture
22. TRAUMA FROM OCCLUSION

Trauma from occlusion is defined as, when occlusal forces exceed the
adaptive capacity of the periodontal tissues, the tissue damage results,
i.e, the tissue injury occurs because the periodontium is unable to cope
with the increased stresses it experiences–Orban and Glickman(1968).
Classification
1. Depending on the cause:
a. Primary
b. Secondary
2. Depending on the onset and duration:
a. Acute trauma from occlusion
• Occlusal forces
• Iatrogenic factors (faulty restorations/prosthetic appliances)
b. Chronic trauma from occlusion

• Tooth wear, drifting movement, extrusion of teeth combined with
parafunctional habits such as bruxism and clenching.
a. Acute trauma from occlusion:
Definition: Periodontal injury resulted due to sudden occlusal impact (or)
abrupt change in occlusal forces is called acute trauma from occlusion.
E.g: Biting on a hard object.
Restorations (or) prosthetic appliances that alter the direction of forces.
Clinical features:
1. Tooth pain.
2. Sensitivity to percussion.
3. Increased tooth mobility.
If the offending cause is not removed, it may lead to:
1. Pulp necrosis.
2. Periodontal abscess formation.
3. Cementum tears.
b. Chronic trauma from occlusion:
Definition: Periodontal injury resulted due to gradual change in occlusion
is called chronic trauma from occlusion.
E.g: Tooth wear
Drifting movement.
Extrusion of teeth.
Parafunctional habits – Bruxism and clenching.
Clinical features:
1. Tooth mobility.
2. Facets on occlusal surface.
Trauma from occlusion is classified based on periodontal status as:
a. Primary trauma from occlusion (Figs 4.13A and B):
Trauma from occlusion resulted due to alteration in occlusal forces is
called “primary trauma from occlusion”.
Etiological factor:
Trauma from occlusion is considered as main factor.
Ex: 1. Insertion of high fillings
2. Insertion of prosthetic replacements that create excessive force

on abutment and antagonistic teeth.
3. Drifting or extrusion of teeth.
Primary trauma does not alter the connective tissue attachment (or)
initiate pocket formation.
A B
Figs 4.13A and B: (A) Primary trauma from occlusion;

(B) Secondary trauma from occlusion
b. Secondary trauma from occlusion (Figs 4.13A and B):

It occurs when the adaptive capacity of the tissues to withstand occlusal
forces is impaired by bone loss is called secondary trauma from
occlusion.
• It leads to reduced periodontal attachment area.
Excessive occlusal load can be seen in three cases:
Condition
1. Normal periodontium with normal height of bone—Primary trauma.
2. Normal periodontium with reduced height of bone—Secondary trauma.
3. Marginal periodontium with reduced height of bone—Secondary
trauma.
Signs and symptoms:
1. Presence of gingival recession, Stillman’s cleft and Mccalls Festoons,
traumatic crescent, infrabony pockets
2. Food impaction
3. Excessive wearing of tooth cusps and appearance of wear facets
4. Hypersensitivity of the teeth
5. Increased tooth mobility
6. Tenderness of TMJ and muscles of mastication
7. Widening of periodontal ligament and thickening of lamina dura
8. Vertical bone losshttps://t.me/DentalBooksWorld
9. Condensation of alveolar bone

10. Root resorption
11. Positive fremitus test.
Histological Features
The response of tissues to increased occlusal forces is explained under
three stages:
Stage-1: Injury
• Shows an increase in areas of resorption and a decrease in bone formation.
Stage-2: Repair
• Shows an increase in areas of bone formation and decreased resorption.
Stage-3
• Adaptive remodeling of the periodontium, return of normal resorption
and formation.
23. APHTHOUS ULCER

Other terms:
• Aphthae.
• Canker sores.
• Recurrent aphthous stomatitis.
It is a common disease characterized by the development of painful,
recurring solitary or multiple ulcerations of the oral mucosa.
Etiology
Possible etiological factors are:
1. Bacterial infections: α-hemolytic streptococcus, Streptococcus
sanguis.
2. Immunological abnormalities: It is an autoimmune response of oral
epithelium showing IgG and IgM binding to epithelial cells of spinous
layer.
3. Iron, vitamin B12 (or) folic acid deficiency.
4. Trauma.
5. Endocrine conditions.
6. Psychic factors.
Classification
Based on clinical manifestations:
• Recurrent aphthous minor.
• Recurrent aphthous major.

• Recurrent herpetiform ulcerations.
• Recurrent ulcers associated with Behcet’s syndrome.
Clinical Features
Age: 10 to 30 yrs.
Sex: Female.
• Aphthous ulcer is a single (or) multiple superficial erosion covered by
gray membrane.
• It has well-circumscribed margin.
• It is surrounded by erythematous halo and typically painful.
Recurrent aphthous minor:
1. Number – One to over 100.
2. Size – 2–3 mm to 10 mm in diameter.
3. Persists for 7 to 14 days.
4. Little or no evidence of scarring.
Recurrent aphthous major:
1. Number – 1 to 10.
2. Site – Lips, Cheek, Tongue, and Soft palate.
3. It is a large painful ulcer persists up to 6 weeks.
4. It leaves scar upon healing.
Recurrent herpetiform ulcers:
Characterized by crops of multiple small, shallow ulcers, often upto 100
in number.
24. PULPO-PERIODONTAL LESIONS

Pulpo-periodontal lesion is the simultaneous existence of pulpal problems
and inflammatory periodontal disease.
Classification
Simon’s classification: It is based on etiology, diagnosis, and treatment.
• Type 1: Primary endodontic lesion.
• Type 2: Primary endodontic with secondary periodontal lesion.
• Type 3: Primary periodontal lesion.
• Type 4: Primary periodontal lesion with secondary endodontic involvement.
• Type 5: True combined lesions.
Pathways of communication between pulp and periodontal ligament:

• Pathways of developmental origin:
1. Through apical foramen.
2. Accessory canals.
3. Developmental grooves.
• Pathways of pathological origin:
1. Tooth fractures.
2. Internal resorption.
• Pathways of iatrogenic origin:
1. Accidental lateral perforation during endodontic perforation.
2. Exposure of dentinal tubules during root planning.
25. PERIODONTAL CYST

The periodontal cyst is an uncommon lesion that produces localized
destruction of the periodontal tissues along a lateral root surface.
Etiology
The following possible etiologies suggested are:
1. Odontogenic cyst caused by proliferation of epithelial rests of Malassez.
2. Lateral dentigerous cyst retained in the jaw after tooth eruption.
3. Primordial cyst of supernumerary tooth germ.
Clinical Features
1. Periodontal cyst is usually asymptomatic, without grossly detectable
changes.
2. But it may persist as a localized, tender swelling.
Radiographic Features
Seen as a radiolucent area bordered by a radiopaque line.
26. PERIODONTAL ABSCESS

The periodontal abscess is caused by an infection to the periodontal
pocket and may result in destruction of the periodontal ligament and alveolar
bone. This infection is usually the result of long-continual irritation by
food debris, deep deposits of calculus or a foreign objects.
Clinical Findings
1. Associated with periodontal pocket which may be either suprabony or
infrabony.
2. Tooth elevation and mobility are seen.
3. Tooth is tender on lateral percussion.
4. Pain is localized and patient can identify the offending tooth.

5. Affected tooth may be vital or non-vital.
6. May be associated with a fistula.
Types
1. Acute periodontal abscess: Painful, edematous, red, shiny, ovoid elevation.
2. Chronic periodontal abscess: Abscess becomes chronic after pus gets
exuded. Dull pain may be present.
Radiographic Features
1. Bone loss is seen.
2. Radiolucency along the lateral aspect of the root.
Treatment
• Drainage through pocket retraction (or) incision.
• Scaling and root planning.
• Periodontal surgery.
• Systemic antibiotics.
• Tooth removal.
27. DIFFERENCES BETWEEN PERIODONTAL ABSCESS

AND PERIAPICAL ABSCESS
Periodontal Absces Periapical Abscess

Pulp test vital. Pulp test may be non-vital.
Associated with pre-existing periodontal Associated with deep restoration.
pocket, caries or both.
Swelling is located around involved tooth Swelling located often with fistulae in apical
and gingival margin seldom with fistula area. This may be located away from tooth.
offending.
Pain is dull, constant localized and patient Pain is severe, throbbing and lasts for days.
can usually locate offending tooth. Patients not able to locate offending tooth.
Pain on percussion is not as severe as Pain on percussion is severe.
with periapical abscess.
28. WASTING DISEASES OF TEETH

Definition: Wasting is defined as any gradual loss of tooth substance
characterized by the formation of smooth, polished surfaces, without regard
to the possible mechanism of this loss.
Forms of wasting diseases are:

1. Erosion
2. Abrasion
3. Attrition
4. Abfraction
1. Erosion: Also called corrosion.
It is defined as irreversible loss of dental hard tissue by a chemical
process that does not involve bacteria.
Etiology:
1. Extrinsic causes: • Acidic beverages (or) citrus fruits.
• Medication.
• Environmental acids.
2. Intrinsic causes: • Gastric acids regurgitated into the mouth.
• In conditions such as gastroesophageal reflux
and excessive vomitings.
Clinical appearance:
• Shows wedge shaped depression in the cervical area of the facial tooth
surface.
• The surfaces are smooth, hard and polished.
• Erosions confined to enamel and generally extend to dentin and
cementum.
2. Abrasion:
Abrasion is a pathological wearing of tooth substance through some
abnormal mechanical process other than mastication.
Etiology:
1. Toothbrushing with an abrasive dentifrice.
2. Action of clasps.
3. Habits of holding objects, e.g: Bobby pins, Tacks, Nails.
4. Improper use of dental floss and toothpicks.
Clinical features:
• Saucer shaped or wedge shaped indentations with a smooth, shiny
surface.
• A sharp ‘ditching’ around the cementoenamel junction.
3. Attrition:
Attrition is defined as the physiologic wearing away of a tooth as a result
of tooth-to-tooth, as in mastication.
Clinical features:
• Wear pattern occurs on incisal occlusal and proximal tooth surface.
• Appearance of small polished facets.
• Enamel and dentine wear at same rate.
• Possible fractures of cusps or restorations.
Complications:
• Dentinal hypersensitivity.
• Pulpal exposure.
• Reduced masticatory efficiency.
Contributing factors:
• Dietary habits: Coarse and hard food substances.
• Parafunctional habits, e. g: Bruxism.
Treatment:
• Desensitizing dentrifices like potassium nitrate, strontium chloride and
sodium monofluoride to relieve from hypersensitivity.
• Root canal treatment in severe cases of pulpal involvement.
• Occlusal rehabilitation in severe generalized attrition cases.
4. Abfraction:
Loss of tooth surface at the cervical area of teeth caused by tensile and
compressive forces during tooth flexure.
Clinical features:
• Deep, narrow,V-shaped notch.
• Affects buccal/labial cervical areas of teeth.
29. ROOT SURFACE CHANGES IN PERIODONTAL POCKET

Root surface changes in pocket can be classified as:
• Structural changes.
• Chemical changes.
• Cytotoxic changes.
1. Structural changes:
a. Presence of pathological granules which represents the collagen
fibers which are https://t.me/DentalBooksWorld
not fully mineralized.
b. Areas of increased mineralization: Result of exchange of minerals at

cementum-surface interface.
c. Areas of demineralization: Related to root caries, cementum may
soften and undergo cavitation.
2. Chemical changes:
a. Mineral content of cementum increased.
b. Minerals like calcium, magnesium, phosphorus and fluoride are
increased in diseased root surface.
3. Cytotoxic changes:
a. Bacterial penetration into cementum till CDJ.
b. Lipopolysaccharides or endotoxins a product of G-bacterial cell wall
adhere and penetrate the cementum.
c. Endotoxins prevent the attachment of human gingival fibroblast to
root surface. Endotoxins are potent inflammatory agents.
30. PALATOGINGIVAL GROOVE

A palatogingival groove is a rare developmental anomalous groove usually
found on the palatal aspect of maxillary incisors. This anomaly predisposes
the tooth involved to a severe periodontal defect and further complicates
by pulp necrosis. This groove typically begins in the central fossa area of
incisors and extends over the cingulum and continues apically down the
root surface. As a result they provide a pathway for bacteria to penetrate
into periodontal space.
Classification
1. According to length:
a. 46% of the groove extends till CE junction.
b. 54% extends to varying distances on the root surface.
c. 43% extends less than 5 mm on the root surface.
d. 47% extends less than 10 mm and 10% extends more than 10 mm
apically from CE junction.
2. According to depth —
3. According to location:
a. Distal groove,
b. Mid-palatal groove,
c. Mesial groove.
Treatment: Meticulous scaling, root planning and flap operations with or
without odontoplasty can maintain the periodontal tissues healthy whereas
in severe cases surgical interventions with regenerative approach will be
helpful. https://t.me/DentalBooksWorld
31. ATYPICAL GINGIVITIS

Other terms: Plasma cell gingivitis.
Plasma cell gingivostomatitis.
Etiology
Microbial plaque is the primary etiological factor. Allergic response to
some components in chewing gum, dentifrice or food is responsible for
exaggeration of inflammatory enlargement.
Clinical Features
• Enlargement is usually generalized in nature.
• Enlargement starts at marginal gingiva.
• A localized lesion, referred to as plasma cell granuloma, has also been
described.
• Later stages extend to attached gingiva, to become diffused enlargement.
• Gingiva appears red, friable, and sometimes granular.
• Gingiva bleeds easily upon stimulation.
• Enlargement is located in the oral aspect of attached gingiva and this
feature differentiates from plaque induced enlargement.
• Cheilitis and glossitis have been reported.
Histopathology
Following changes are noticed:
Epithelium:
1. Damaged spinous and basal layer.
2. Spongiosis.
3. Inflammatory infiltrate.
Connective tissue:
Dense infiltrate of plasma cells producing a dissecting type of injury.
Treatment
• Identify the allergin in the food and remove it.
• Removal of local factors by oral prophylaxis.
32. PREGNANCY GINGIVITIS

Pregnancy is one of the systemic conditions that affects the gingival
health. https://t.me/DentalBooksWorld
Hormonal Etiology
1. During pregnancy the levels of progesterone and estrogen increase by
10–30 times the levels during menstrual cycle.
2. These hormonal changes include changes in vascular permeability,
leading to gingival edema and increased inflammatory response to dental
plaque.
Change in Microflora
1. The subgingival microbiota changes to more anaerobic.
2. Elevated counts of Prevotella intermedia are seen.
a. Marginal Enlargement:
Results due to aggravation of previous inflammation.
Clinical features:
i. Enlargement is usually generalized and prominent interproximally
than on facial and lingual surface.
ii. Gingiva appears bright red (or) magenta, soft, friable, smooth
and shiny surface.
iii. Bleeding occurs spontaneously (or) on slight provocation.
b. Tumor like gingival enlargement (or) pregnancy tumor (or)
angiogranuloma (Fig. 4.14):
It is an inflammatory response to bacterial plaque.
Clinical features:
i. Lesion appears as discrete, mushroom like, flattened spherical
mass with dusky red (or) magenta color.
ii. It protrudes from interproximal space and is attached by a sessile
(or) pedunculated base.
iii. Painless in nature.
Fig. 4.14: Pregnancy tumor
Histopathology
1. Angiogranulomas are covered by thickened stratified squamous
epithelium with prominent rete pegs.
2. Connective tissue contains varying degrees of edema; inflammatory
infiltrate and dilated capillaries are seen.
33. STATIC OCCLUSAL PREMATURITIES

Common Interferences
S.No. Position Maxillary cusps Mandibular cusps
1. Retruded contact Mesial inclines of Distal inclines of facial cusps
position (centric lingual cusps (these are and marginal sides of premolars
relation) to be removed first) and molars
2. Protrusive Distolingual inclines Mesiofacial inclines
Prematurities
3. Mediatrusive or Facial inclines of Inner inclines of buccal cusp
balancing non lingual cusp
working (not a
pathological
interference)
4. Laterotrusive Inner inclines of Facial inclines of lingual cusps
or working lingual cusp
Causes: Mostly Iatrogenic

1. Faults in dental restoration
2. Faults in prostheses creating excessive forces on abutment or antagonist
teeth.
3. Extrusion of teeth into space created by replaced missing teeth.
Treatment
Treated by procedure known as occlusal adjustment or coronoplasty.
34. BONE FACTOR CONCEPT

• Local and systemic factors regulate the physiological equilibrium of
bone.
• When there is generalized tendency towards bone resorption, bone
loss is initiated by a local inflammatory process that may be magnified.
• This systemic influence on the response of the alveolar bone has been
termed as the bone factor concept in the periodontal diseases.
• Osteoporosis is a physiological condition of postmenopausal women,
which results in loss of bone mineral content and microstructural bone
changes.
• Periodontal bone loss may also occur in generalized skeletal
disturbances, e. g: hyperparathyroidism, leukemia, etc.
35. FOCAL INFECTION

A focal infection is a localized or general infection caused by the dissemination
of microorganisms (or) toxic products from the focus of infection.
Mechanism of focal infection: Two accepted mechanisms are:
1. Metastasis of microorganisms from an infected focus by either
hematogenesis (or) lymphogenous spread.
2. Secondly, toxins (or) toxic products may be carried through the blood
stream (or) lymphatic channels to a distant site where they may incite a
hypersensitive reaction in the tissue.
Oral foci of infection:
The sources of infection which may set up distant metastases are:
1. Infected periapical lesion such as the periapical granuloma, cysts and
abscesses.
2. Teeth with infected root canals.
3. Periodontal disease with special reference to tooth extraction (or)
manipulation.
36. DESQUAMATIVE GINGIVITIS

Definition: It is a unique nonspecific gingival condition characterized by
intense erythema, desquamation and redness of free and attached gingiva.
Etiology
1. Dermatoses—Lichen planus, Phemphigus
2. Endocrine imbalance
3. Aging
4. Tuberculosis, Candidiasis
5. Idiopathic.
Diagnosis
Clinical Features
Mild form: Diffuse erythema of the marginal, interdental and attached
gingiva, usually painless.
Moderate form: Patchy distribution of bright-red and gray areas involving
marginal and attached gingiva.
Normal resilient gingiva becomes soft, smooth, edematous and massaging
of gingiva results in peeling off the epithelium. Condition is painful.
Severe form: The gingiva appears speckled and the surface epithelium is
shredded, friable and peeled off in small patches. Extremely painful.
There is constant, dry, burning sensation throughout the oral cavity.
Conditions leading to desquamative gingivitis:
1. Lichen planus.
2. Cicatricial pemphigoid.
3. Bullous pemphigoid.
4. Pemphigus vulgaris.
5. Lupus erythematosus.
6. Erythema multiforme.
Therapy: There are two phases:
a. Local treatment.
b. Systemic treatment.
a. Local treatment:
• Scaling and polishing.
• Oral hygiene instructions.
• Oxidizing mouthwashes (H2O2 3% diluted).
• Topical application of corticosteroid ointments (or).
• Cream like triamcinolone 0.1%.

• Fluocinonide 0.05%.
• Protective plastic devices in extremely painful cases.
b. Systemic treatment:
• Systemic corticosteroids in moderate doses.
• Prednisolone 30–40 mg.
37. PATHOLOGICAL TOOTH MIGRATION (FIG. 4.15)

Definition: Pathologic migration refers to tooth displacement that results
when the balance among the factors that maintain physiological tooth
position is disturbed by periodontal disease.
• It is a common sign of moderate to severe chronic periodontitis.
• It is one of the early signs of aggressive periodontitis.
Pathogenesis
Two major factors maintain the normal position of teeth:
1. Normal height of alveolar bone
2. Forces acting on teeth
1. Normal height of alveolar bone: A tooth with weakened periodontal
support is unable to withstand the forces and moves away from opposing
force.
2. Forces acting on teeth: Change in the forces occur as a result of :
a. Unreplaced missing teeth.
b. Failure to replace first molars.
c. Other causes:
i. Pressure from the tongue
ii. Pressure from granulation tissue of periodontal pocket
Fig. 4.15: Pathological migration

Clinical Features
1. Normal position of teeth will be altered.
2. In anteriors, teeth drift labially and extrude (or) flare creating a diastema.
3. In posteriors, teeth may tilt mesially (or) occlusally.
4. Migration may lead to rotation or mobility.
38. TOOTH MOBILITY

Tooth mobility occurs in the following two stages:
1. In the intial or intrasocket stage the tooth moves within the confines of
periodontal ligament. This is associated with viscoelastic distortion
and redistribution of periodontal fluids, inter-bundle content and fibers.
2. The secondary stage occurs gradually and entails elastic deformation
of alveolar bone in response to increase in horizontal forces.
Mobility is graded according to the ease and extent of tooth movement.
• Normal mobility
• Grade 1: Slightly more than normal (0.2–1 mm) in horizontal direction
• Grade 2: Moderately more than normal
• Grade 3: Severe mobility faciolingually and mesiodistally combined
with vertical displacement.
Mobility beyond physiological range is termed abnormal or pathologic.
Increased mobility is caused by the following factors:
Systemic causes Local causes
1. Age 1. Periapical pathology
2. Sex and race 2. Tooth morphology
(Higher in Females)
3. Oral contraceptives 3. Implant mobility
Other causes:
1. Loss of tooth support
2, Trauma from occlusion
3. Extension of inflamation
4. Periodontal surgery
5. Tooth mobility sometimes increased during pregnancy and associated
with use of hormonal contraceptives.
39. BRUXISM
Definition: It is defined as diurnal or nocturnal parafunctional activity that
includes clenching, bracing, gnashing and grinding of the teeth.
Etiology:
1. Emotional or Psychological factor:
Emotional tension, anger, fear
2. Occlusal factors:
Supra contacts, faulty restorations and cuspal interferences
3. Systemic factors:
Nutritional deficiencies, food allergy.
Types:
1. Based on the time:
I. Nocturnal bruxism: Clenching during night time
II. Diurnal bruxism: Clenching during day time
2. Based on the pattern:
III.Central bruxism: Clenching is called centric bruxism
IV. Eccentric bruxism: Grinding is called eccentric bruxism
Effects of Bruxism Clinical Features
1. Dentition Presence of facets, fractured cusps; tooth mobility;
pulpitis and pulpal necrosis
2. Periodontium Tooth mobility, increased bone loss, periodontal
injury
3. Masticatory Tenderness, muscle fatigue upon awakening from
muscles sleep; hypertrophy of masseter muscle, myofascial
pain; headache.
4. TMJ Dull pain, clicking sounds and luxation in severe cases
40. NECROTIZING ULCERATIVE PERIODONTITIS (NUP)

(FIG. 4.16)
NUP is an extension of necrotizing ulcerative gingivitis (NUG) into the
periodontal structures, leading to periodontal attachment and bone loss.
Etiology
1. Microbial flora: Fusiform-spirochete bacterial flora play a key role
In HIV-positive patients there is high prevalence of Candida albicans,
Provotella intermedia, Fusobacterium nucleatum, etc.
2. Immunocompromised status: More prevalent in compromised or
suppressed immune systems.
3. Psychological stress: Stress induced immunosuppression impairs the
host response and leads to necrotizing periodontal disease.
Fig. 4.16: Clinical appearance of NUP
4. Malnutrition: In extreme cases it contributes to diminished host

resistance to infection and necrotizing disease.
Types: There are two Types:
1. Non-AIDS type necrotizing ulcerative periodontitis
2. AIDS-associated necrotizing ulcerative periodontitis
Non-AIDS type necrotizing ulcerative periodontitis
Clinical features:
1. Necrosis and ulceration of the coronal portion of the interdental papillae
and gingival margin.
2. It is painful, bright red marginal gingiva that bleeds easily.
3. Periodontal attachment and bone loss.
4. Deep interdental osseous craters.
5. Advanced lesion.
6. Tooth loss.
7. Oral malodor, fever, malaise (or) lymphadenopathy are observed.
AIDS-associated NUP
1. Large areas of soft tissue necrosis with exposure of bone and
sequestration of bone.
2. Lesions may extend onto the buccal vestibule or palate and become
necrotizing stomatitis.
41. HALITOSIS (ORAL MALODOR)

Halitosis is the term used to describe noticebly unpleasant odor exhaled in
breathing.
Classification of halitosis:
1. Physiological halitosis.
2. Pathological halitosis.
3. Pseudohalitosis.
4. Halitophobia.
Etiology
The resultant substrates with free thiol groups such as cystein and reduced
glutathionine rise to Valentine sulfur compounds (VCS) which are malodor
substances.
Causes of physiological halitosis:
1. Mouth breathing
2. Medication
3. Aging and poor dental hygiene
4. Tongue coating
Causes of pathological halitosis:
1. Periodontal infection
2. Stomatitis
3. Parotitis, cleft palate
4. Aphthous ulcers, dental abscess
Diagnosis of halitosis:
1. Tongue coating
2. Evidence of mouth breathing
3. Xerostomia
Measurement of oral malodor:
1. Subjective organoleptic method
2. Gas chromatography
3. Halimeter
Management of oral malodor:
1. Reduction of anaerobic load by improving oral hygiene and periodontal
health.
2. If oral malodor persists in spite of adequate conventional oral hygiene
tongue brushing should be advised.
3. Halita is a new solution containing 0.05% chlorhexidine 0.05%
Cetylpyridinium Chloride (CPC) and 0.14% zinc lactate.
42. DIABETES MELLITUS

Definition
Diabetes mellitus is a complex metabolic disease characterized by chronic
hyperglycemia, diminished insulin production, impaired insulin action or
combination of both results in the inability of glucose to be transported
from the blood stream into the tissues, which in turn, results in high blood
glucose levels and excretion of sugar in urine.
Oral Manifestations
• Cheilosis
• Mucosal drying and cracking
• Burning mouth (Glossopyrosis)
• Burning tongue (Glossodynia)
• Diminished salivary flow (Xerostomia)
• Alterations in flora of oral cavity (Candida albicans, Hemolytic
streptococci, Staphylococci)
• Increased rate of dental caries
• Increased susceptibility to infections
Periodontal Manifestations
• Tendency towards enlarged gingiva
• Sessile or pedunculated gingival polyps
• Polypoid gingival proliferations
• Destructive periodontitis with severe gingival inflammation
• Deep periodontal pockets, rapid bone loss, frequent periodontal
abscesses
43. CHEDIAK-HIGASHI SYNDROME

Rare disease affecting the production of organelles found in almost every
cell.
It affects mostly
- Melanocytes
- Platelets
- Phagocytes
Pathogenesis
Neutrophils contain abnormal gaint lysosomes that can fuse with
phagosome, but their ability to release their contents is impaired. As a
result killing of ingested microorganisms is impaired.
Clinical Features
• Partial albinism
• Mild bleeding disorders
• Recurrent bacterial infections
• Aggressive periodontitis.
44. PAPILLON-LEFEVRE SYNDROME (FIG. 4.17)

It is a rare genetic disease in which there is a severe and premature
destruction of periodontal supporting structures. It is an inherited disorder
and follows an autosomal recessive pattern.
Males and females are equally affected.
Papillon-Lefevre syndrome is an inherited genetic disorder and follows
an autosomal recessive pattern.
In this syndrome, parents are not affected but carry the autosomal
genes for this disease to appear in their offsprings.
Age: Appear before the age of 4 years.
Sex: Male and females are equally affected.
Fig.https://t.me/DentalBooksWorld
4.17: Papillon lefevre syndrome
Clinical Features
Hyperkeratotic skin lesions on palms, soles, knees, etc.
1. Severe destruction of peridontium
2. Calcification of dura.
Periodontal Findings
1. Bone loss.
2. Exfoliation of teeth
- Primary teeth are lost by 5 to 6 years of age.
- Permanent teeth erupt normally, but are lost within few years.
3. By age 15 of years, patient will be completely edentulous.
Bacterial flora:
i. Spirochete-rich zones appear in the apical portion of the pockets.
ii. Microcolony formation of mycoplasma species are formed.
Management:
i. Medical evaluation.
ii. Root debridement with chlorhexidine application.
iii. Antibiotic therapy based on microbiological testing.
iv. Host modulation therapy.
Ex:Low dose doxycyclines – 20 mg
NSAIDS, e. g. Flurbiprofen
Chemically-modified tetracylines
4. Effects of Vitamin C on periodontium:
Vitamin C deficiency in humans results in:
Scurvy—a disease characterized by:
• Hemorrhagic lesions into muscles of extremities, joints, and sometimes
nail beds.
• Petechial hemorrhages often around hair follicles.
• Increased susceptibility to infections.
• Delayed wound healing.
• Bleeding and swollen gingiva (scorbutic gingivitis).
• Loosened tooth.
In scurvy, there is
• Defective formation and maintenance of collagen.
• Impairment or cessation of osteoid formation.
• Impaired osteoblastic function.
• Increased capillary permeability.

• Susceptibility to traumatic hemorrhages.
• Hyporeactivity of contractile elements of peripheral blood vessels.
• Sluggishness of blood flow.
• Low levels of ascorbic acid influence the metabolism of collagen with-
in the periodontium thereby affecting the ability of tissue to regenerate
and repair itself.
• Ascorbic acid deficiency interferes with bone formation leading to loss
of periodontal bone.
Changes that occur in alveolar bone and other bones as a result of failure
of osteoblasts to form osteoid later place very late in deficiency state.
• Ascorbic acid increases the permeability of the oral mucosa to tritiated
endotoxin and tritiated insulin and of normal human crevicular
epithelium to tritiated dextrin.
• Increasing levels of ascorbic acid enhance both chemotactic and
migratory action of leukocytes without influencing their phagocytic
activity.
• Mega doses of vitamin C seem to impair the bactericidal activity of
leukocytes.
• An optimum level of ascorbic acid is apparently required to maintain
the integrity of periodontal microvasculature as well as vascular
response to bacterial irritation and wound healing.
• Depletion of vitamin C may interfere with the ecologic equilibrium of
bacteria in plaque and thus increases its pathogenicity.
45. GINGIVA IN LEUKEMIA (FIG. 4.18)

Color: It appears bluish red and cyanotic.
Contour: Rounding of gingival margin occurs.
Consistency: Gingiva is soft and friable.
Gingival bleeding:
1. It is caused by thrombocytopenia resulting from replacement of bone
marrow by leukemic cells.
2. It may also occur as a side affect of the chemotherapeutic agents used
to treat leukemia.
3. Gingiva bleeds spontaneously or on slight provocation.
Fig. 4.18: Leukemic enlargement
Size:
1. Leukemic cells infiltrate in the gingiva and less frequently the alveolar
bone. It results in leukemic gingival enlargement.
2. Leukemic gingival enlargement consists of basic infiltration of gingival
corium by leukemic cells that increases the gingival thickness and
creates gingival pockets where plaque accumulates.
3. Increase in size occurs, most often in interdental papilla and partially
covering the crowns of tooth.
4. It usually occurs in patients with acute myelocytic leukemia and absent
in chronic leukemia.
Oral ulcerations and infections:
1. It is caused due to granulocytopenia which results in host susceptibility
to opportunistic infections.
2. Discrete punched out ulcers penetrating deeply into submucosa and
covered by pseudomembrane is present.
5
CHAPTER
Diagnosis, Prognosis
and Treatment Plan
1. PERIODONTAL DISEASE ACTIVITY

Occurs under two stages:
1. Periods of exacerbation/periods of activity bone and connective tissue
attachment are lost as pocket deepens. Clinically active periods show
bleeding either spontaneously or with probing and greater amounts of
attachment loss presence of exudation or pus.
2. Periods of remission/quiescence/inactivity reduced inflammatory
response little or no loss of bone and connective tissue attachment.
2. SOUNDING OF PROBING/TRANSGINGIVAL PROBING

Clinical examination and probing determines the presence and the depth
of periodontal pockets and also gives a general sense of body topography.
Transgingival probing or sounding under local anesthesia confirms
the extent and configuration of the infrabony component or furcation
defects.
There are concavities in the crest of the interdental bone confined within
facial and lingual walls.
It is found to make up two-thirds of all mandibular defects, can be
diagnosed by transgingival probing.
3. BANA TEST (Benzoyl-DL Arginine-Naphthylamide)

It is a simple and quick test for three bacteria (P. gingivalis, T.denticola
and B.forsythus) associated with periodontal disease and bad breath.
The great advantage of identifying the presence of these bacteria is
that the anaerobic periodontal infection can be treated very specifically.
The test kit includes two enzyme coated 5" strips. One strip is used
initially and one after 30–60 days. Each strip accommodates tests for two
areas of the mouth. The interdental cleansers are provided to gather a
plaque sample. Smear it on the strip and wait for 24 hrs. If any of the three
bacteria are present the strip turns blue. The test is very sensitive that can
detect very small number of bacteria.
4. TREATMENT PLAN IN PERIODONTITIS

Preliminary phase or emergency phase
Treatment of Emergencies
• Dental or periapical abscess.
• Periodontal abscess.
Extraction of hopeless teeth and proporcional replacement if needed.
Phase 1 Therapy (Etiotropic Phase)
• Plague control
• Diet control
• Removal of calculus and root planning
• Correction of restoratives and prosthetics irrational factor
• Excavation of caries and restorations (temporary or final)
• Antimicrobial therapy
• Occlusal therapy
• Mind orthodontics treatment
• Provisional splitting.
Evaluation of response to phase 1
Wrecking—pocket depth and gingival and gingival inflammation plaque
and calculus caries.
Phase 2 Therapy (Surgical Phase)
• Periodontal—surgery including placement of implants.
• Root canal treatment.
Phase 3 Therapy (Restorative Phase)
• Final restorations.
• Fixed and removable prosthodontics.
• Evaluation of response to restorative procedures.
• Periodontal examination.
Phase 4 Therapy (Maintenance Phase)

• Periodic recall visit
• Checking for plaquehttps://t.me/DentalBooksWorld
and calculus
Diagnosis, Prognosis and Treatment Plan 95
• Gingival conditions
• Occlusion tooth mobility and other pathologic changes
i. Emergency phase
ii. Etiotrophic phase
iii. Maintenance phase
iv. Surgical phase
v. Restorative phase
5. ADVANTAGES OF RADIOGRAPHS IN PERIODONTITIS

To know
a. Type of bone loss
• Vertical or angular
• Horizontal bone loss
• Crater like loss
• Arc shaped bone loss
b. Contour or architecture of bone
• Positive
• Negative
c. Continuation of lamina dura
d. Trabecular pattern of bone
e. Furcation of bone loss
f. Amount of bone loss
6. RADIOGRAPHIC FEATURES OF PERIODONTITIS

1. Chronic
2. Aggressive
1. Localized Aggressive Periodontitis
Vertical loss of alveolar bone around the first molars and incisors beginning
around puberty in healthy teenagers is diagnostic sign.
Arc shaped loss of alveolar bone extending from distal surface from
second premolar to mesial surface of second molar.
2. Chronic Periodontitis
1. Mild periodontitis:
Early lesions appear as areas of localized erosion of interproximal alveolar
bone crest.
The anterior region shows blunting of alveolar crest and slight loss of
alveolar bone height. https://t.me/DentalBooksWorld
Posterior region may also show a loss of normally sharp angle between
the lamina dura and alveolar crest.
2. Moderate periodontitis:
Patterns of bone loss have been divided into localized buccal or lingual
cortical plate loss, generalized horizontal bone loss in a region or localized
vertical defects (angular) involving just one or two teeth.
3. Severe periodontitis:
In severe adult periodontitis the bone loss is so extensive that the remaining
teeth show excessive mobility.
7. NIGHT GUARD
Night guard is also called stabilization appliance (or) maxillary stabilization
orthosis.
It is used in the treatment of parafunctional habits like Bruxism.
Uses:
1. Protects dentition by redistribution of occlusal forces.
2. Dissipates forces built in the musculoskeletal system.
3. Relaxes strained muscles.
4. It provides stabilization of TMJ.
Shape of Night Guard: Horse Shoe Shaped
Material: Made up of thermosetting acrylic resin.
• Night Guard can be used on both jaws, but maxillary arch is preferable.
• Mandibular night guard appliance is used when there is problem with
aesthetic and phonetics.
• Night Guard appliance is held in place by clasps.
Time of Wearing Night Guard
1. 6–8 hrs per day during night time.
2. In patients with articular disorder of TMJ it can be worn at full time.
8. CLASSIFY PERIODONTAL PROBES

They are classified based on the generation of development
• 1st generation probes; conventional probes
E. g: Williams probe
Uses: Easy to access any location around all the teeth easy to sterilize.
• 2nd generation probes; pressure sensitive probes
Diagnosis, Prognosis and Treatment Plan 97
E.g. Borodontic probes

Uses: These probes have a standardized control on insertion pressure.
Forces up to 30 gms the probe seems to remain within the junctional
epithelium and forces up to 50 gms are necessary to diagnose periodontal
osseous defects.
Standardization of probe tips <1 mm and the addition of registration
stents to maintain reproducible probing angulation have also been
used to overcome errors.
• 3rd generation probes; computer aided probe
E. g: Florida probes Foster-Miller probes
Uses: This automated probe system consists of a probe handpiece
digital read out foot switch computer interface and computer.
The end of probe tip is 0.4 mm in diameter.
This combines the advantage of constant probing force with precise
electronic measurement and computer storage of data.
• 4th generation probes; records sequential probe positions along gingival
sulcus. They are still under research.
• 5th generation probes; ultrasound probes; they are still under research.
9. PROGNOSIS OF TEETH WITH FURCATION

INVOLVEMENT
• Maxillary first premolars and maxillary as well as mandibular molars are
teeth with multiple roots.
• Furcation involvement will be likely to occur in these multi-rooted teeth.
• Maxillary first premolar often shows fusion of roots and furcation area
may be located very much apically and also the roots of maxillary first
premolar are placed buccally and palatally with furcation opening in a
mesiodistal direction.
• For these reasons furcation involvement in maxillary first premolar has
poor prognosis.
• In case of maxillary molars, furcaton may open buccally mesially and
distally because of presence of three roots.
• Since access from proximal area is difficult for plaque control prognosis
of furcation involvement in maxillary molars is not good.
• Mandibular molars have two roots placed mesially and distally and the
furcation opens buccolingually. Roots are divergent especially in
mandibular first molar.
• As a result, prognosis of furcation involvement in mandibular molar
(especially first molar) is considered good.
10. HALIMETER
1. It is laboratory diagnostic aid to detect halitosis.
2. It is a sulphide monitor.
3. A disposable plastic straw is inserted into the air inlet and patients are
instructed to place their slightly opened mouth over the straw.
4. The straw would Extend approximately 4 cm into the mouth during
measuring the halitosis.
5. Three measurements should be taken and the mean value of these
values was determined in parts per billion sulphide.
6. The portable sulphide monitor uses electrochemical voltametric zinc
oxide thin film semiconductor sensors which generate signals on
exposure to sulphide and mercaptan gases.
7. It analyses the concentration of H2S and methyl mercaptan.
Advantages: Portability
• Non-invasisve
• No need skilled personnel
• Inexpensive
• Low likelihood of cross infections
• Less time consumption.
Disadvangages
1. Some of the common sulphides such as mercaptan are not easily
recorded.
2. Very sensitive to alcohol (or using alcohol containing mouth washes
for at least 12 hrs prior to test.
11. DNA PROBE

1. Deoxyribonucleic acid probes. DNA Probes have developed to identify
nucleotide sequences that are specific to bacteria.
2. DNA probes entail segments of single stranded nucleic acids labelled
with an enzyme (or) radioisotope that is able to hybridize the
complementary nucleic acid sequence and that denotes the target
microorganism.
3. It is test for multiple microorganisms like P. gingivalis, A. actinomy-
cetemcomitans, B. itermedius, C. rectus, E. corrodens, Fusobacterium
nucleatum, T. denticola in multiple clinical plaque samples.
6
CHAPTER Nonsurgical Therapy
1. MANAGEMENT OF BLEEDING
In a patient with normal coagulation mechanism the control of haemorrhage
is dependant on veesel contraction retraction and clot formation.
During any surgical procedure complete haemostasis must be achieved.
Local haemostasis
1. Mechanical
2. Thermal
3. Chemical
Mechanical methods
1. Pressure
2. Use of haemostasis
3. Sutures and ligation
4. Embolization of vessels
Thermal agents
1. Cautery
2. Electrosurgery
3. Cryosurgery
4. Argon beam coagulator
5. Lasers
Chemical Agents
Local agents:
Astringent agents and styptics, Bone wax, Thrombin, Gel foam, Oxygel,
Surgical, Fibrin glue, Adrenaline.
Systemic agents:
Whole blood, Platelet rich plasma,Fresh frozen plasma, Cryoprecipitate,
Adrenochrome monosemicarbazon and ehamysalate.
Absorbale haemostatic agents

• Generic.
• Absorbable gelatin sponge.
• Oxidized cellulose.
• Oxidized regenerated cellulose (surgical absorbable haemostat).
• Microfibrillar collagen haemostat (collacote, collatape, collaplug).
• Thrombin (thrombostat).
i. Periodontal dressings (periodontal packs like).
ii. Zinc oxide eugenol packs.
iii. Non eugenol packs- cyanoacrylates.
2. CHLORHEXIDINE
Chlorhexidine is cationic bisguanide that is used as broad spectrum
antiseptic.
• It exhibits gram positive gram negative yeasts, etc.
• It is bacteriostatic and reduces supragingival plaque and gingivitis.
• Plaque reduction up to 45–61% is obtained.
• It is particularly useful in older adults who have difficulty with plaque
removal and those who take phenytoin, calcium channel blockers and
cyclosporine and are at risk of gingival hyperplasia.
• Chlorhexidine oral candidal infections.
• Prescription rinse for short-term use < 6 months.
Long-term use > 6 months.
Peridex Prescription solution of chlorhexidine
Periogard
3. PERIOCHIP
Periochip is a product that contains chlorhexidine for local delivery of

antimicrobials for periodontal therapy. It is biodegradable device
sublingually placed.
After placement of actisite filers rinsing with 0.12% of chlorhexidine
has synergistic effect in reduction of bacterial pathogens.
Adverse Effects:
• Increase in calculus formation.
• Staining of teeth.
• Dysgeusia (altered taste).
• Brown staining of teeth, tongue, silicate resin restoration.
Nonsurgical Therapy 101
4. DENTIFRICE
“A dentifrice is a paste or powder used with a tooth brush or other
mechanical cleansing devices for the purpose of cleaning the accessible
surfaces of the tooth.
—ADA Council on Dental Therapeutics
Composition of Dentifrice
1. Polishing /abrasive agents: Calcium carbonate, dicalcium phosphate
dihydrate, alumina and silicas.
These agents have a mild abrasive action, which aid in eliminating
plaque from the tooth surface. They are useful in restoring natural
luster and enhance enamel whiteness.
2. Binding/thickening agents: Water soluble agents: Carrogenates,
alginates, sodium carboxy methyl cellulose.
Water insoluble agents are: Magnesium aluminum silicate, colloidal
silicate, sodium magnesium silicate.
Uses:
a. Controls stability and consistency of a tooth paste.
b. Effects ease of dispersion of the paste in the mouth.
3. Detergents/surfactants, e.g. Sodium lauryl sulfate.
Uses: Anti-microbial property.
Produces the foam which aids in the removal of food debris and also
dispersion of the product within the mouth.
4. Humectants: Sorbitol, glycerin, polyethylene glycol.
Uses: Aids in reducing the loss of moisture from the tooth paste.
5. Flavoring agents: Peppermint oil, spearmint oil, oil of wintergreen.
Uses: They render the product pleasant to use and leave a fresh
taste in the mouth after use.
6. Sweetness and coloring agent, e.g. saccharine.
7. Antibacterial agent : Triclosan, delmopinol, metallic ions, zinc citrate
trihydrate.
8. Anticaries agent: Sodium monofluorophosphate, sodium fluoride,
stannous fluoride.
9. Active agents: Fluoride.
10. Anticalculus agents: These are mostly designed to inhibit the
mineralization of so called “petrified” plaque. They are also known
as crystal growth inhibitors.
They are—pyrophosphates, zinc citrate, zinc chloride, Gantrez acid.
11. Desensitizing agents: Sodium fluoride, potassium nitrate, strontium

chloride.
Application of Dentifrice
The amount of toothpaste to be taken for effective cleaning is a pea-sized
placed on the top half of the tooth brush.
5. POLISHING INSTRUMENTS
Rubber cups: They consist of a rubber shell with or without webbed
configurations in the hollow interior. They are used in handpiece with
special prophylactic angle. A good cleansing and polishing paste that
contains fluoride should be used and kept moist to minimize frictional heat
as the cup revolves. Polishing pastes are available in fine, medium or
coarse grits.
Agresssive use of rubber cup with any abrasive may remove layer of
cementum.
Bristle brushes: Available in wheel and cup shapes, used in handpiece
with a polishing paste.
As the bristles are stiff; use of the brush should be confined to the
crown to avoid injuring the cementum and gingiva.
Dental tape: Dental tape with polishing paste is used for polishing proximal
surfaces that are inaccessible to other polishing instruments.
Air-powder polishing: The first specially designed handpiece that delivers
air powdered slurry of warm water and sodium bicarbonate: this instrument
is called Prophy Jet.
Effective for the removal of extrinsic stains and soft deposits.
Disadvantages: Tooth substance can be lost.
Damage to gingival tissue is transient and insufficient clinically: But
amalgam restorations and composite resins and cements can be roughened.
Contraindicated in patient with medical histories of respiratory illness,
hypertension and patient on medication affecting electrolyte balance.
6. GUM STIMULATOR (Stim-U-Dent)
Cone shaped rubber tips attached to the handle of regular tooth brushes
are used for stimulating the interdental papilla. It helps in keratinization of
the gingiva and also improves blood circulation because of the massaging
action. Though it is designed for stimulating the gingiva, it can be used for
plaque removal also.
7. CORONOPLASTY
It is the selective reshaping of occlusal surfaces with the goal of
establishing a stable, nontraumatic occlusion.
• It is also called as occlusal equilibrium/occlusal adjustment.
• Many occlusal adjustments exist as altering of contours of single tooth
to major full mouth equilibrium to the degree that maximum intercuspation
is coincident with centric relation.
• It is an irreversible process, so the clinician should evaluatew before
the therapy.
• Occlusal adjustment role in the management of periodontal disease is
more complex because both periodontitis and trauma from occlusion
lead to tooth mobility.
Procedure:
Step 1: Remove retrusive prematurities and eliminate the defective from
retrocuspal position to intercuspal position.
Step 2: Adjust intercuspal position to achieve stable, simultaneous,
multipointed, widely distributed contacts.
Step 3: Test for excessive contacts (fremitus) on the incisor teeth.
Step 4: Remove the posterior protrusive supracontacts and establish
contacts that are bilaterally distributed on the anterior teeth.
Step 5: Remove or lessen mediotrusive (balancing) interferences.
Step 6: Remove excessive cusp steepness on the laterotrusive (working)
contacts.
Step 7: Eliminate gross occlusal disharmonies.
Step 8: Recheck tooth contact relationships.
Step 9: Polish all the rough tooth surface.
8. METHODS FOR CORRECTION OF OCCLUSAL

PREMATURITIES
1. Grooving: Restoring depth of developmental grooves
2. Spheroiding: Reducing supracontact while restoring original tooth
contour
3. Pointing: Restoring cusp point contour

Occlusal adjustment is affected by condylar guidance, incisal
guidance, compensating curves, cusp height, plane of occlusion. In
case of bruxism, interocclusal appliance therapy or occlusal splint is
indicated.
9. DESENSITIZING AGENTS
These are the substances that reduce the root hypersensitivity.
Some of the desensitizing agents are used through our toothpastes.
These are also applied in the dental office.
Agents used by the patient: They are present in dentifrice, strontium
chloride, potassium nitrate and sodium citrate.
Agents used in dental office: Cavity varnishes; anti-inflammatory agents.
Treatments that partially obdurate dentinal tubules—silver nitrate, zinc
chloride, potassium ferrocyanide, formalin.
Calcium compounds like—calcium hydroxide, dibasic calcium phosphate.
Fluoride components like—sodium fluoride, stannous fluoride.
• Iontophores
• Strontium chloride
• Restorative resins
• Dentin bonding agents
Method of action: The most likely mechanism is they reduce the diameter
of the dentinal tubules so as to limit the displacement of the fluid in them
which can be attained by: formation of a smear layer produced by
burnishing the exposed surface.
10. SHARPENING OF PERIODONTAL INSTRUMENTS

It is impossible to carry out periodontal procedures efficiently with dull
instruments. Therefore to avoid wasting time and operating haphazardly,
clinician must be thoroughly familiar with the principles of sharpening and
able to apply them to produce a keen cutting edge on the instruments they
use.
Principles of sharpening:
• Choose a stone with appropriate shape and size for sharpening.
• Use a stabilized sharpening stone as the instrument will be sterilized
before using on patient.
• Establish the proper angle between the stone and the surface of the
instrument.
• Proper angulation is to be maintained during the sharpening strokes.
• Avoid excessive pressure; heavy pressure causes the stone to grind the
surface of the instrument quickly.
• Avoid formation of a “wire-edge”, characterized by minute filamentous
projections of metal extending as a roughened ledge from the sharpened
cutting edge. When the instrument is used on root surfaces, these
projections produce a grooved surface rather than a smooth surface.
Stones used for sharpening:
1. Stones like—India and arkansa oil stones are examples of natural
abrasive stones.
2. Carborundum, ruby, and ceramic stones are synthetically produced.
Another categorization is:
1. Mounted rotary stones.
2. Unmounted stones.
Techniques of Sharpening of Various Instruments

• Universal curettes: Short up and down strokes are given by keeping
the lateral surface of the curette at 100–110° to stone.
• Area specificurettes: Active short, up and down strokes are given and
finish with down strokes with an angle between the blade and stone at
100–110°.
• Sickle scalers: Pull strokes are given with an angle of 100–110° between
the blade and the stone.
• Chisels and Hoes: Push strokes are given.
• Periodontal knives: They are sharpened by drawing the blade across a
stationary stone or by holding the instrument stationary and drawing
the stone across it.
11. NABER’S PROBE

It is a periodontal probe used to measure the depth of furcation areas and
their involvement.
The probe is curved rod-like instrument calibrated in mm with blunt
round tip.
It has colored coated margins at 3, 6, 9 and 12 mm.
It is very much helpful in observing the furcation involvement.
12. CHARACTERISTICS OF AN IDEAL TOOTH BRUSH

The head of the brush should be:
a. 1 inch to 11/4 inches long.
b. 2 to 4 rows of bristles.
c. 5/16 inch to 3/8 inch wide.
d. 5–12 tufts per row.
e. 80–86 bristles per tuft.
Handle design of the tooth brush must be:
a. Straight
b. Angulation in the shank
c. Indentation of handle for a better grip
Frequency of brushing 12 hours.
Frequency of change of brush every 3 months.
Length of brushing time initially 10–20 min is required.
Until the patient becomes more precise, later 3–5 min may suffice.
13. ROOT PLANING

It is the process by which residual embedded calculus and portions of
necrotic cementum are removed from the roots to produce a smooth, hard,
clean surface.
• The primary objects of scaling and root planing is to restore gingival
health by completely removing elements that provoke gingival
inflammation from the tooth surface.
• The nature of tooth surface determines the degree to which the surface
must be scaled or planned.
• Deposits of calculus on root surfaces are frequently embedded in
cemental irregularities.
• When dentin is exposed, plaque bacteria may invade dentinal tubules.
• Therefore scaling alone is insufficient to remove them and a portion of
the root surface.
Technique of Root Planing

Subgingival calculus is usually harder than supragingival calculus and is
often locked into root irregularities, making it more tenacious and therefore
more difficult to remove.
The adjacent pocket wall limits the direction and length of the strokes.
Root planing is accomplished with either universal or area specific curette.
Modified pen grasp is used.
Sickles, hoes, files and ultrasonic instruments also are used for
subgingival scaling of heavy calculus.
Calculus is removed by a series of controlled overlapping, short,
powerful strokes primarily using wristarm motion.
The amount of lateral pressure applied to the tooth surface depends on
the nature of the calculus and whether the strokes are for final root planing.
14. LOCAL DRUG DELIVERY SYSTEM

Criteria for local drug delivery:
1. Inhibit or kill the putative pathogens.
2. Reach the site.
3. Have adequate concentration.
4. Be there long enough.
5. Do no harm. Tetracycline – containing fibers (Actisite).
Actisite: The actisite (tetracycline fiber) delivery system consists of a
polymer, ethylene vinyl acetate, 25% saturated with tetracycline
hydrochloride. It is available in 23 cm length and 0.5 mm in diameter and
contains 12.7 mg of TCL hydrochloride. The fiber is flexible, can be placed
into a periodontal pocket, and can be folded on itself to nearly folded
pocket. The fiber releases the tetracycline at a constant rate of 14 days.
Subgingival doxycycline:
Atridox: 10% doxycycline gel systems using a syringe clinically
attachment level gains and probing depth reduction is seen.
Subgingival minocycline 2% minocycline is encapsulated into
bioresorbable microspheres in a carrier.
Subgingival metronidazole: Oil-based metronidazole 25% dental gel
(glycerol monofoliate and sesame oil).
Periochip: The chlorhexidine chip is a small biodegradable film of
hydrolyzed gelatin into which has been incorporated 2.5 mg of
chlorhexidine gluconate. The chip resembles a baby’s fingernail measuring
4 × 5 mm and 0.35 mm in thickness. It is self-retentive and delivers
chlorhexidine to the site at the concentration of 125 μg/ml for at least
7 days. https://t.me/DentalBooksWorld
Adverse effects: Minimal—slight pain and swelling in first 24 hrs after

chip placement.
15. GRACEY CURETTES

Gracey curettes are a set of area specific instruments that were designed
by Dr Clayton H Gracey of Michigan in mid 1930’s.
Four design feature make the gracey curette unique
1. They are area specific
2. Only one cutting edge on each blade is used
3. The blade is curved in two planes, and
4. Blade is offset.
Area specificity: Seven pairs of curettes #1–2 and 3–4—used on anterior
teeth
#5–6—used on both anterior and premolar teeth
#7–8and 9–10—used on facial and lingual surfaces of posterior teeth
#11–12—mesial surface of posterior teeth
#13–14—adapts to distal surfaces of posterior teeth.
Principles of Use
1. Determine the correct cutting edge.
2. Make sure the lower shank is parallel to the surface to be instrumented.
3. When using intraoral finger rests keep the middle and fourth finger
together with build up fulcrum for maximum control and wrist arm action.
4. Use extraoral fulcrums or mandibular finger rests for optimum angulation
when working on maxillary posterior teeth.
5. Concentrate on using the lower third of cutting edge for calculus removal
especially on line angles or when attempting to remove a calculus
ledge by breaking it away in sections beginning at the lateral edge.
6. Allow the wrist and forearm to carry the burden of the stroke rather
than flexing the fingers.
7. Roll the handle slightly between the thumb and fingers to keep the
blade adapted as the working end is advanced around line angles and
into concavities.
8. Moderate lateral pressure from firm to moderate to light depending on
nature of calculus and reduced pressure as the transition is made from
scaling and root planing strokes.
Extended shank Gracey curette—these are 3 mm longer in terminal

shank than the standard Gracey curette.
Minibladed Gracey curettes such as mini five curettes and Gracey curettes
have terminal shank that is 3 mm longer than the standard Gracey curettes.
16. DIFFERENCE BETWEEN SCALER AND CURETTE
Scaler Curette
Instruments for supragingival Instruments for supra and
scaling subgingival scaling
Two cutting edges with a sharply two cutting edges with a
pointed tip rounded toe
Not adapted well to the root surface Better adapted to the root surface
Removes only supragingival calculus Used to remove subgingival
calculus altered
cementum and remove
soft tissue lining of the
periodontal pocket
Angulation 45–90° <90°
17. DIFFERENCE BETWEEN GRACEY AND UNIVERSAL

CURETTES
Gracey Universal
AREA OF USE Set of many curettes One curette designed
designed for specific areas for all areas and surfaces
and surfaces
CUTTING EDGE One cutting edge used to Both cutting edges used to
work with outer edge only work with either outer or
inner edge
CURVATURE Curved in two planes curves Curved in one plane
up and to the side
BLADE ANGLE Offset blade, face of blade Not offset face of blade beveled
bevel At 60° to the shank at 90° to the shank
FUNCTION Removal of heavy calculs Removal of light and medium
deposits sized deposits
FACE Tilted at 60–70° to the Perpendicular to the lower
shank shank
CROSS-SECTION Semi-circular Semi-circular
EXAMPLES Gracey series Columbia 2R/2L
Kramer-Nevins Columbia 13/14
Turgeon series Baun hart ½
Langer ½
18. PRINCIPLES OF ULTRASONIC SCALER

Ultrasonic scalers are used to remove calculus rapidly from the tooth
surface.
The scaling tip vibrates in the ultrasonic range of 20–45 kHz with an
optimum frequency between 18 kHz and 32 kHz.
There are three basic types:
1. Magnetostrictive–James Prescott Joule
2. Peizoelectric–Pierre Curie
3. Sonic
Principle–How it works?
• The scaling tip vibrates and follows a pattern depending on power rating
and type—elliptical, Curved, Linear or circular.
• The water is energized as it passes over the tip to provide cavitation
which results in a scouring action because of the heat generated at the
tip. It is essential to keep the tip moving over the teeth.
• A good guide is that one should not spend more than 10 sec on any
individual tooth and never to press harder than one ounce of pressure.
• Pressing hard stops the tip from vibrating and reduces the effectiveness.
Of the tip to that of a hand scaler.
• It also concentrates heat in one area with possibly lethal consequences
for the pulp.
• Best practice involves three or four teeth in a sequence to prevent over
heating on any one tooth.
Advantages
• Fast, effective scaling if used properly—light touch and short time on
tooth.
• Subgingival work is possible—Focus spray insert (FSI).
• Slimline or through flow insert (FFI).
Disadvantages
• Iatrogenic heat damage to the tooth.
• Standard bevel tail shape tips cannot be used subgingivally.
Indications
• To remove tenacious calculus.
• Can disrupt calculus from a distance.
• Very effective scaling.
Contraindications
• In cardiac pace makers.
• In respiratory attacks (bronchical asthma).
• In children.
19. PLAQUE CONTROL

Plaque control can be defined as regular removal of dental plaque and the
prevention of its accumulation on the teeth and adjacent gingival surfaces.
It is the primary level of prevention of periodontal diseases and
caries.
Plaque control
Mechanical Chemical
Individual, professional Individual, professional
a. Tooth brushes a. First generation antiplaque agents
• manual reduce plaque score by 20–50%
• electrical • antibiotics
b. Interdental aids • phenols
• dental floss • sanguinarian
• triangular tooth picks b. Second generation antiplaque agent
• hand held reduces plaque score by 70–90%
• proxa pic enzymes-mucinase
• interdental brushes mutase
c. Aids for gingival stimulation dextrase
• rubber tip stimulators antibiotics-penicillin
• balsa wood edge erythromycin cc 10232
d. Others phenols-thymol, triclosan
• gauge strips bisbiguanides-chlorhexidine
• pipe cleaners herbal extracts
e. Aids for edentulous or partially sanguarine
edentulous patients Metallic salts
• denture and partial clasp brushes zinc, tin, copper
• cleansing solutions Other surfactants-sodium lauryl sulfate
c. Third generation antiplaque agents
e.g. delmopinol
20. INTERDENTAL CLEANSING AIDS

Interdental plaque removal is important because most of the pathogenic
organisms originate in the interproximal areas.
Among numerous aids available dental floss and interdental cleaners
such as wooden or plastic tips and interdental brushes are most commonly
recommended.
A. Dental floss—Most commonly recommended method of removing

plaque from interdental areas.
Types of dental floss
1. Twisted or nontwisted
2. Bonded or nonbonded
3. Waxed or unwaxed
4. Thick or thin
B. Interdental brushes—They are cone-shaped or cylindrical brushes made
of bristles mounted on a handle.
a. Single tufted brushes.
b. Small conical brushes—They are mainly useful to clean large irregular
concave tooth surfaces adjacent to wide interdental spaces.
C. Wooden tips—Soft triangular wooden tooth picks such as stim-u-dent
are placed in interdental space in such a way that base of triangle rests
on gingiva and sides are contact with proximal tooth surface,
e.g. perio aid-useful on facial and lingual surfaces throughout mouth.
D. Other aids—gingival massage—can be performed with tooth brushes
rubbertip stimulator or interdental cleaning aids.
Oral irrigation devices—use water faucet to irrigate between and around
teeth.
Intermittent waterjet.
21. DISCLOSING AGENT

Disclosing agents are solutions or wafers capable of staining bacterial
deposits on the surface of the teeth, tongue and gingiva. A disclosing
agent is a preparation in liquid, tablet or lozenge form which contains a
dye or other coloring agent.
Utility of disclosing agents
• Professional and personalized patient instruction and motivation
• Self-evaluation by patient
• Preparation of plaque indices
• To evaluate effectiveness of oral hygiene maintenence
• In research studies with regard to effectiveness of plaque control devices
like tooth brush and dentifrice.
Properties
Intensity of color—contrast color with normal color of oral cavity.
Duration of intensity
• Taste-pleasant as the main reason to motivate the patient.
• Irritation to the mucous membrane—should be non-irritating and non-
toxic.
• Diffusibility—should be thin enough so that it can be applied readily
yet thick enough to impart an intensive color to plaque.
• Astringent and antiseptic properties.
• Agents used for disclosing solutions.
Iodine preparation
• Skinners iodine solution.
• Diluted tincture of iodine.
• Mercurochrome preparation.
• Mercurochrome solution 5%.
• Flavored mercurochrome disclosing solution.
• Bismarck brown (Eastick’s disclosing solution).
Merbromin
• Erythrosine FD and C no.3/ no.28.
• Fast green-FD and C green no.3.
• Fluorescein FD and C yellow no.8.
Two-tone solutions
(It mainly stains thicker plaque blue and thinner plaque red)
• FD and C green no.3.
• FD and C red no.3.
• Basic fuchsin.
22. TETRACYCLINES IN PERIODONTITIS

Pharmacology–tetracyclines are group of antibiotics that are derived
naturally from streptomyces or derived semi-synthetically.
• These antibiotics are bacteriostatic.
• These are very effective against treating periodontal disease mainly
because of their concentration in gingival crevicular fluid which is 2 to
10 times more than in serum.
• They have been frequently used in treating refractory periodontitis
including localized aggressive periodontitis.
• They inhibit the growth of Actinobacillus actinomycetemcomitans.
Clinical use: They have been investigated as adjacent in treatment of

localized aggressive periodontitis.
Systemic tetracyclines can eliminate tissue bacteria and have been
shown to arrest bone loss and suppress.
A. actinomycetemcomitans level in conjuction with scaling and root
planing this combination therapy allows mechanical removal of root surface
deposits and elimination of pathogenic bacteria.
Increased post-treatment bone levels has been noted using this method.
Specific agents
• Tetracyclines.
• Minocyclines.
• Doxycycline.
Tetracycline: 250 mg four times daily.
Minocycline: Effective against broad spectrum of microorganisms used in
patients with adult periodontitis.
• 200 mg day for 1 week
• Doxycycline–loading dose
(i) 2 tab -1st day
(ii) 1 tab- 2nd day
Advantage: Patient compliance.
23. PROBIOTICS
Probiotics are live microorganisms (in most cases, bacteria) that are similar
to beneficial microorganisms found in the human gut. They are also called
“friendly bacteria” or “good bacteria”. Probiotics are available to consumers
mainly in the form of dietary supplements and foods. They can be used as
complementary and alternate medicine (CAM) A group of diverse medical
and health care systems, practices, and products that are not presently
considered to be part of conventional medicine. Probiotics are live
microorganisms thought to be beneficial to the host organism, Probiotics
are: “Live microorganisms which when administered in adequate amounts
confer a health benefit on the host”. Lactic acid bacteria (LAB) and
bifidobacteria are the most common types of microbes used as probiotics;
but certain yeasts and bacilli may also be helpful. Probiotics are commonly
consumed as part of fermented foods with specially added active live
cultures; such as in yogurt, soy yogurt, or as dietary supplements.
24. LANGER CURETTE AND ITS USES

The blade structure of a general purpose curette allows for the treatment
of mesial and distal surfaces with a single instrument by angling the lower
shank of the instrument toward each side of the surface being worked on.
The blade structure of a general purpose curette combined with Gracey
shank angles. Two cutting edges, a round tip and shanks which allow
access to any area. A different but definitely effective solution. We can
use them for both the removal of dental calculus and root planing. Two
different procedures with a single instrument! Three instruments-A red ½
for lower molars, a green ¾ for upper molars and a blue 5/6 for the incisors.
The number of instruments required can be reduced. It’s easier to acquaint
oneself with and properly learn how to use fewer instruments. Clinical
procedures can thus be simpler and more effective due to fewer changes,
among other things.
25. PERIOSCOPE
1. Used to visualize deeply into subgingival pockets and furcation and
for detection of deposits.
2. Perioscope is of 0.99 mm diameter consists of fiberoptic endoscope
over-fitted with a disposable sterile sheat called as (perioscopy system).
3. Perio probes and ultrasonic instruments fitted in the fiberoptic
endoscope.
4. The disposable sheat delivers water for irrigation that flushes the pocket
while endoscopy is being done and will maintain a clean fields.
5. Along with sterile sheat fiberoptic endoscope consists of a medical-
grade “Charged-couple device (CCD)” video camera and light.
6. Perioscope magnification ranges from 24x to 46x thereby can visualize
minute deposition of plaque and calculus.
7. This device system can also be used to evaluate subgingival areas of
caries defective restorations, root fractures and also resorption.
26. PERIOTRON
1. It is a latest method of measuring gingival crevicular fluid collecting
paper strips.
2. It is developed by “Harco Electronics”.
3. This electronic device consists of a functional units is a pair of upper
and lower counterparts which can be opened and closed.
4. Method
a. The sample periopaper strip should insert in between the two
functional jaws of periotron.
b. The paper strip should insert into the sulcus (or) pocket.
c. The wetness of the paper strip affects the flow of electronic current
and gives a digital read out on the screen.
5. Three models of periotron are invented latest they are HAR-600, HAR-
6000 and HAR-8000.
6. Translation of perioton values to gingival clinical condition. The gingival
index is
Periotron reading Level of gingival Gingival index
inflammation
0–20 Healthy 0
21–40 Mild 1
41–80 Moderate 2
81–200 Severe 3
27. PERIOSTAT
It is a sub-antimicrobial dose of doxycycline hyclate capsule of 20 mg for
the patients with chronic periodontitis should take twice a day.
28. PERIOTEMP
It is a probe to detect the temperature differences of period pockets to the
referenced subgingival temperature (difference is of 0.1°C).
Periotemp consists of coper-nickel thermocouple connected with digital
thermometer attached to metal probe.
• The high temperature in pockets signalled with red-emiting diode
normaly.
• Posterior sites are warmer than anteriors, and mandibular sites are
warmer than maxillary sites.
29. PERIO-AID
• It is a tooth-pick holder.
• It is one of the most effective aids available for cleaning exposed
furcation after periodontal therapy.
7
CHAPTER
Surgical Periodontal
Therapy
1. SUTURE MATERIALS USED IN PERIODONTAL SURGERY

Classification
1. Absorbable
• Natural
- Catgut
- Tensor fascia lata, Polyglactin 910
- Collagen tape
2. Synthetic
• Polyglycolic acid
• Polyglactin
• Polydioxanone
3. Nonabsorbable
• Natural
• Cotton silk
4. Synthetic linen
Synthetic
a. Polyglycolic acid – Dixon
b. Polyglactin – Vicryl
c. Polydioxanone – PDS
Non-absorbable
1. Natural
a. Linen
b. Cotton
c. Silk
2. Synthetic
a. Nylon
b. Terylene – Dacron
Advantage of Absorbable
• It gets absorbed due to enzymatic digestion hence sulcus does not
need removal.
• It has good knotting property.
Disadvantage
• It can’t be used in presence of infection.
• Tissue reaction is more with chronic.
• Loose 30% within 28 days.
Other Properties
1. Biological—catgut, silk, cotton.
2. Man made—polyester, polyamide, polyphenylene.
3. Monofilament—polyamide, catgut, PDS.
4. Multifilament—silk, cotton, polyamide.
5. Braide—silk, polyamide.
6. Twisted—cotton.
7. Conated—polyamide, prolene
8. Uncoated—cotton, polyester.
2. BIOPSY
Biopsy is the removal of tissue from the living organism for the purpose of
microscopic examination and diagnosis.
Types of biopsy
1. Excisional
2. Incisional
3. Fine needle aspiration cytology
4. Frozen section biopsy
Methods of obtaining biopsy:
• Surgical excision of tissue by scalps
• Surgical excision by cautery
• Punch biopsy
• Exfoliative cytology
Biopsy Procedure
• The area of wound from where the biopsy will be taken is cleaned first.
• They are anesthetized.
Surgical Periodontal Therapy 119
• The most representative site of wound is identified.

• The tissue is cleaned and put into to present formalin solution for fixation.
• Biopsy site is sutured.
Important points to remember while performing biopsy:
• The wound should not be painted by any coloring agent.
• Anesthetic agent should not be used.
• Sharp instruments are to be used to avoid.
• Biopsy specimen should be used of sufficient thickness and depth.
Labeling of biopsy sample
• Mention name, age, sex of patients.
• Mention date and time.
• Mention type of biopsy.
3. CURETTAGE
Curettage is surgical scraping or removal of soft tissues within the gingival
crevice or periodontal pocket. Curettage is aimed at surgical elimination of
altered periodontal tissues in order to induce connective tissue attachment
to the root suraface, along with the formation of new cementum and bone.
Rationale of Curettage
1. Removal of crevicular debris.
2. Elimination of obstacles to a normal epithelial attachment.
3. Facilitation of connective tissue healing and maturation.
4. Promotion of a normal gingival vascular plexus.
The following instruments or agents are recommended for curettage:
1. Curettes
2. Abrasive stones
3. Ultrasonics
4. Caustics followed by curettage.
Types:
I. Gingival curettage: Consists of removal of inflamed soft tissue
lateral to pocket wall
a. Subgingival curettage: Indicated in edematous gingival
pockets. It is performed apical to junctional epithelial attachment
in which connective tissue attachment is served down to osseous
crest.
b. Inadvertent curettage: Curettage done unintentionally during

scaling and root planing.
II. Surgical curettage: Chemical curettage-ultrasonic curettage.
Indications
• Moderately deep infrabony pocket.
• Nondefinite procedures to reduce inflammation prior to pocket
elimination procedures like flap surgeries.
• In patients where extensive surgical procedures are contraindicated
like aging systemic complications. Curettage causes shrinkage of inter-
dental papilla so not indicated for anterior teeth.
Procedure
1. Basic technique: After adequate local anesthesia correct curette is
selected Instrument is inserted to engage inner wall of pocket wall and
is carried along soft tissue wall usually in horizontal stroke.
After curettage, scaling and root planing are to be done:
Angulations > 90° indicated for the curettage.
2. ENAP: Excisional new attachment procedure
It is definitive subgingival curettage performed with a knife giving
internal bevel incision.
3. Ultrasonic curettage.
4. Caustic curettage: Such as sodium sulfide, antiformin, phenol induces
chemical curettage of lateral pocket wall.
Healing After Curettage
4. ENAP
It stands for Excisional new attachment procedures (ENAP).
• It is developed and used by US Naval Dental Corps.
• It is a definitive subgingival curettage procedure performed with knife.
Technique
• After adequate anesthesia; an internal bevel incision is made which is
carried interproximally on both the facial and lingual sides attempting
to retain as much interproximal tissue as possible and aim is to cut the
inner portion of the soft tissue wall of the pocket; all around the tooth.
• Remove the excised tissue with a curette carefully; perform the root
planing; preserving all the connective tissue fibers that remain attached
to the root surface.
• Approximate the wound edges. Recontour the bone, if required, place
the sutures and give a periodontal dressings.
5. PERIODONTAL SURGICAL INSTRUMENTS

Periodontal surgery is accomplished with numerous instruments and they
were classified as follows:
1. Excisional and incisional instruments
2. Surgical curettes and sickles
3. Periodontal elevators
4. Surgical chisels
5. Surgical files
6. Scissors
7. Hemostats and tissue forceps
Excisional and incisional instruments

1. Periodontal knives (gingivectomy knives): These knives obtained as
either double ended or single ended instruments.
Entire periphery of these kidney shaped knives is cutting edge.
E. g: Kirkland knife
2. Interdental knives: Used interdentally. These are sphere-shaped knives
have cutting edges on both sides of blade and designed with double
ended or single ended.
E. g: Orbans knife #1–2
Merrifield knife #1, 2, 3, 4
3. Surgical blades: Commonly used blades#11, #12D, 15 and 15C.

• 12D- beak shape having cutting edges on both sides.
• 15- tearing flaps.
• 15C- used for making initial scalloping type incision.
6. SURGICAL CURETTES AND SICKLES

These are used during surgery for removal of granulation tissue, fibrous
interdental tissues and tenacious subgingival deposits.
Ex:Prichard curette-heavier surgical curettes.
Ball scaler #B2–B3-heavy sickle.
• Periosteal elevators used to remove flap after incision has been made
for flap surgery.
E. g. Woodson and Prichard elevators, Molt no.9.
• Surgical chisels—back action chisels with pull motion, e.g. Wide Stat
ochsenbein #1-2
• Tissue forceps—used to hold flap during suturing. Used to position
and displace the flap after the flap has been reflected, e.g. Debakey.
• Scissors—Used to remove tabs of tissue during gingivectomy.
• Needle holders: Used to suture the flap at desired position after surgical
procedure has been completed.
E.g. Castroviejo needle holders
7. OSSEOUS SURGERY AND OSSEOUS SURGICAL

PROCEDURES
Osseous surgery may be defined as the procedure by which changes in
the alveolar bone can be accomplished to get rid of deformities induced by
the periodontal disease process or other related factors, such as exostosis
and tooth supereruption.
Osseous surgery can be of two types–Additive or subtractive
a. Additive osseous surgery includes procedures directed at restoring
the alveolar bone to its original level.
b. Subtractive osseous surgery is designed to restore the form of
preexisting alveolar bone to the level existing at the time of surgery or
slightly more apical to its level.
Osteoplasty and Ostectomy

Osteoplasty refers to reshaping the bone without removing tooth
supporting bone.
Ostectomy includes removal of tooth supporting bone.
8. DIFFERENCE BETWEEN OSTECTOMY AND

OSTEOPLASTY
Ostectomy
Definition: It is defined as excision of bone or portion of bone in
periodontitis, ostectomy is done to correct or reduce deformities caused
by periodontitis and includes removal of supporting bone.
E.g: Correction of negative architecture (Interdental bone is apical to
interradicular bone).
• One wall osseous defect.
• Flattening of interproximal bone.
• Gradualizing marginal bone.
Osteoplasty
Definition: It is defined as reshaping of alveolar process to achieve a more
physiologic form without removal of tooth supporting bone.
E.g: Correction of Grade II furcation involvement:
• Shallow craters
• Bone ledges
• Exostoses
• Vertical grooving
• Radicular blending
Osteoplastic procedures are done with rotary instruments whereas
ostectomy procedures are done with hand instruments.
9. CLASSIFICATION OF BONY ARCHITECTURE

The morphologically descriptive terms—negative, positive, flat and ideal
bony architecture have been used to describe the bone form after reshaping.
All these terms relate to a preconceived standard of ideal osseous
form.
• Positive architecture–The architecture is said to be positive if the
radicular bone is apical to the interdental bone.
• Negative architecture–The bony architecture is said to be negative if
the interdental bone is more apical than the radicular bone.
• Flat architecture–The reduction of the interdental bone to the same
height as the radicular bone.
• Ideal architecture–Osseous form is considered to be ideal when the

bone is consistently more coronal on the interproximal surfaces than
on the facial and lingual surfaces.
The ideal form of the marginal bone has similar interdental height, with
gradual, curved slopes between interdental peaks.
10. DEFINITIVE AND COMPROMISED OSSEOUS RESHAPING

Definitive osseous reshaping–Implies that further osseous reshaping
would not improve the overall result.
Compromise osseous reshaping–indicates a bone pattern that cannot
be improved without significant osseous removal that would be detrimental
to the overall result.
11. INDICATIONS FOR RESECTIVE OSSEOUS SURGERY

The technique of ostectomy is best applied to patients with early to
moderate bone loss (2 to 3 mm) with moderate length root trunks that have
bony defects with one or two walls.
Patients with advanced attachment loss and deep intrabony defects
are not candidates for resection since so much of bone has to be removed
to stimulate a normal architecture, that the survial of teeth could be
compromised.
12. STEPS IN RESECTIVE OSSEOUS SURGERY

Only hand instruments or a combination of hand instruments and rotary
instruments are used.
Rotary instruments are useful for the osteoplastic steps whereas hand
instruments provide the most precise and safe results with ostectomy
procedures.
Steps in Resective Osseous Surgery

1. Vertical grooving Osteoplasty
2. Radicular blending
3. Flattening of interproximal bone
4. Gradualizing marginal bone Ostectomy
1. Vertical Grooving
It is indicated to reduce thickness of alveolar housing and it provides
continuity from interproximal surface into radicular surface.
• Indication–Thick bony margins

• Shallow crater formation
• Contraindication: Close root proximity
• Thin alveolar housing
2. Radicular Blending
It attempts to gradualize bone over entire radicular surface and provides
smooth, blended surface for good flap adaptation.
Indications: Thick bone margins
Shallow crater formation
Grade-I: Furcation involvement.
Grade-II: Furcation involvement.
3. Flattening of Interproximal Bone

Requires removal of small amount of supporting bone.
Indications: One wall defects or hemiseptal defects.
Coronally one-walled defects.
Apically three-walled defects.
Contraindication: Advanced defect where much of bone removal is
required.
4. Gradualizing Marginal Bone

Bone removal is minimal but necessary to provide sound regular base for
gingival tissue to follow.
Failure to do so results in Widow’s Peak allows tissue to rise to higher
level than base of bone loss in interdental area.
Results in selective recession and incomplete pocket reduction.
13. RE-CONSTRUCTIVE OSSEOUS SURGERY

Some non bone graft associated new attachment procedures:
The presence of pocket epithelium is perceived as a barrier to surgical
therapy because its presence interferes with the direct apposition of
connective tissue and cementum, thus limiting insertion of PDL fibers.
The recommended pocket eradication procedures are:
a. Curettage
b. Lasers
c. Ultrasonic methodshttps://t.me/DentalBooksWorld
d. Chemical agents, and

e. Surgical techniques.
a. Curettage: At least 50% of pocket epithelium may persist even after
thorough curettage. Hence it is not a reliable method. Ultrasonics and
lasers have also been used but the lack of visibility and tactile sense
are the drawbacks.
b. Chemical agents: The drugs like sodium sulfide, phenol camphor and
sodium hypochlorite were previously used in conjunction with
curettage.This procedure is no longer in use because the depths of
penetration of these drugs are difficult to control.
c. Surgical technique: Gingivectomy and excisional new attachment
procedure (ENAP) give predictable results in suprabony pockets.
Modified Widman flap procedure eliminates pocket epithelium with the
internal bevel incision.
14. ENAMEL MATRIX PROTEINS

Enamel matrix proteins mainly amelogenin are secreted by Hertwig’s
epithelial root sheath during tooth development and include acellular
cementum formation. It is marketed under the trade name Emdogain.
Emdogain is a viscous gel consisting of enamel derived proteins from
tooth buds in a polypropylene liquid; 1 ml of a vehicle solution is mixed
with a powder and delivered by syringe to the defect site. Ninety percent
of protein in this mixture is amelogen and the rest are proline rich non-
amelogenins, tuftelin, tuft protein, serum proteins, etc.
Enamel matrix derivative reults in regeneration of new cementum, bone
and PDL.
15. ROOT CONDITIONERS

Several substances have been used to condition the root surface for
attachment of connective tissue fibers.
These include:
1. Citric acid
2. Fibronectin
3. Tetracycline
4. Doxycycline
1. Citric acid: When used with pH 1 for 2–3 minutes on root surface after
surgical debridement it produces surface demineralization which inturn
induces cementogenesis and attachment of collagen fiber. Reported by
Register and Burdick, 1975.
2. Fibronectin: It is glycoprotein that fibroblasts require to attach to root
surface its addition promotes new attachment.
3. Tetracycline.
4. Polypeptide growth factors: They can be used to control events in
periodontal healing. They are polypeptide.
Molecules released by cells in inflamed area, that regularizes events in
wound healing.
They include:
PDGF Platelet derived growth factor.
IGF Insulin like growth factor.
Basic FGA Basic fibroblast growth factor.
TGF-αβ Transforming growth factors αβ
16. REGENERATION, REPAIR AND NEW ATTACHMENT AND

RE-ATTACHMENT
a. Regeneration is the natural renewal of a structure, produced by growth
and differentiation of new cells and intercellular substances to form
new tissues or parts.
b. Repair is a proces called healing by scar which simply restores the
continuity of the diseased marginal gingiva and re-establishes a normal
gingival sulcus at the same level on the root as the base of the preexisting
periodontal pocket.
c. New attachment is the embedding of new periodontal ligament fibers
into new cementum and the attachment of the gingival epithelium to a
tooth surface previously denuded by disease.
Re-attachment is attachment of gingiva or periodontal ligament to areas
of tooth from which they may be removed in course of treatment or during
preparation of teeth for restorations represent simple healing or
reattachment of periodontium not new attachment. The term new
attachment has been used in the past to refer to restoration of marginal
periodontium but because it is not existing fibers which reattach but new
fibers that form and reattach to new cementum it has been termed new
attachment.
Reattachment is currently used only to refer to repair in areas of root

not previously exposed to pocket such as after surgical detachment of
tissues or following traumatic tears in cementum, tooth fracture or treatment
of periapical lesions.
17. HEMOPHILIA AND PERIODONTAL SURGERY

The clinician should consult the patient’s physician before dental treatment
to determine the risk of bleeding and treatment modifications required.
To prevent hemorrhage, factor 8 levels of at least 30% are needed.
Parenteral 1-deamino 8-D-arginine vasopressin (DDAVP) can be used to
raise factor 8 levels 2–3 fold in patients with mild to moderate hemophilia.
DDAVP has significant advantage of avoiding risk of viral disease
transmission from factor 8 infusion and considered drug of choice in
responsive patients. Most moderate and severe hemophiliacs require
infusion of factor 8 concentrate before surgical procedures.
Hemophilia-B or Christmas disease results in a deficiency of factor 9.
The severity of disorder depends on relative amount of existing factor 9.
Surgical therapy requires a factor 9 level of 30–50% and is usually
achieved by administration of purified prothrombin complex concentrates
or factor 9 concentrates.
18. POCKET ELIMINATION AND POCKET MAINTENANCE

• Treatment of pocket depends on type of pocket.
• Pseudopocket or gingival pocket.
Treatment Options
• Scaling and root planing
• Revaluation and maintenance
• Removal of pocket wall
• Removal of tooth side of pocket
• Treatment of suprabony pocket
• Anterior teeth
• Scaling and root planing
• Maintenance
• If pocket persists, curettage
• For moderate to severe pockets, flap surgery utilizing crevicular
incisions
For posterior teeth,

• Scaling
• Root planing
• Maintenance
• If persistent of pockets and inadequate access, flap surgery
For infrabony pockets
• New attachment procedures
19. MICROBIOLOGICAL TESTS USED IN PERIODONTAL

DISEASES
For identification of bacteria:
1. Direct examination–Microscopy
• Light
• Darkfield
2. Culture and sensitivity assay
a. Culture techniques
• Aerobic
• Anaerobic
b. Specification techniques
• Gas liquid chromatography
• DNA homology
• Light microscopy: Gram’s staining
• Differentiates gram positive from gram negative organisms
• Gram positive appears violet
• Gram negative appears pink
• Dark field or phase contrast microscopy
It uses special condenser in which light rays are either reflected or
refracted off bacterial surface. So, outline of bacterium is dark against light
background and light against dark background.
Culture methods: Used for cultivation and identification of microorganisms
then to determine its susceptibility or resistance to various anti-microbials.
Types of specimens: Blood samples, mucosal surfaces, periodontal pockets.
Subgingival plaque sampling techniques:
• Nickel plated curettes
• Scalers
• Paperpoints
• Irrigation
• Surgical excision.
GLC: In which various metabolic products of anaerobes are studied which
are unique enough to serve as markers for identification.
DNA probes: Based on ability of DNA to hybridize or bind to
complementary strands of DNA having exact base sequence.
20. DNA PROBE

DNA probe entails segments of single stranded nucleic acids labeled
with an enzyme or radioisotope, that can locate and bind to their
complementary nucleic acid sequences with low cross-reactivity to non-
target organisms.
DNA probe may target whole genomic DNA or individual genes. Whole
genomic probes are more likely to cross-react with non-target micro-
organisms due to presence of homologous sequences between different
bacterial species.
However, specific genes such as 16SrRNA genes, contain signature
sequences limited to organisms of same species.To prepare a probe, specific
pathogens used as marker organisms are lysed to remove their DNA.
When a plaque is sent for analysis, it undergoes lysis and degeneration.
This assay can rapidly test for multiple bacteria including:
A. actinomycetemcomitans, P. gingivalis,
B. intermedius,
C. rectus,
E. corrodens,
Fusobacterium nucleatum.
These probes are able to detect as few as 100–10000 bacteria and the
sensitivity and specificity are not affected by the presence of unrelated
bacteria in mixed culture samples.
21. LABORATORY AIDS USED IN DIAGNOSIS OF

PERIODONTAL DISEASES
• Millimeter probe for gingival bleeding
• Measurement of gingival crevicular fluid flow with the help of filter
paper
• Newer method is by use of Periotron 6000
• Measurement of temperatue by pressure sensitive probes

• Mouth odor by olfactometer
• Tooth mobility by mobilometer or periodontometer
• Periodontal screening and recording PSR.
Periodontal Probes
Types of conventional periodontal probes:
• Marquis color coded probe
• UNC15 probe
• University of Michigan ‘O’ probe with Williams markings
• WHO probe
• Furcation areas are best evaluated by curved blunt Naber’s probe.
PSR: Designed for easier and faster screening and recording of periodontal
status of a patient or a group of population. It uses a specially designed
probe that has 0.5 mm ball tip and is color coded from 3.5–5.5 Patient’s
mouth is divided into six sextants and each tooth is examined.
22. FINGER RESTS

Intraoral
1. Conventional finger rest: The finger rest is established on tooth
surfaces immediately adjacent to working area.
2. Cross arch: The finger rest is established on tooth surfaces on other
side of same arch.
3. Opposite arch: The finger rest is established on tooth surfaces of
opposite arch. E. g. Mandibular arch finger rest for instrumentation on
maxillary arch.
4. Finger-on-finger: The fourth finger of operating hand rests on index
finger of non-operating hand while lingual surfaces of maxillary
posterior teeth are instrumented.
Extraoral
1. Palm up fulcrum: The backs of fingers rest on right lateral aspect of
mandible while maxillary right posterior teeth are instrumented.
2. Palm down fulcrum: The front surfaces of fingers rest on left
lateral aspect of mandible while maxillary left posterior teeth are
instrumented.
23. EFFECTS OF FAULTY DENTISTRY

Related to endodontics:
• Iatrogenic root perforations by engine driven burs and reamers occurring
during post preparation or due to curved canals.
• Ledges in canals can result from failure to make access to cavities that
allow direct access to apical parts of canals or from straight or too large
instruments in curved canals.
• Stripping in lateral perforation caused by over instrumentation through
a thin wall in root.
• Zipping is elliptical in shape that may be formed in apical foramen
during preparation of curved canal.
Related to conservative:
• Insertion of high fillings.
• Sub-gingival restorations lead to periodontal disease.
• Overhanging dental restoration contributes to gingivitis and possible
attachment loss.
Related to orthodontics:
• Orthodontic movement of teeth into functionally unacceptable
positions leads to primary trauma from occlusion.
• High orthodontic forces used for tooth movement results in undermined
or rearward resorption.
Related to prosthodontics:
• Insertion of a prosthesis, replacement that creates excessive forces on
abutment or antagonist teeth.
24. ORTHOPANTOMOGRAM
Other name; panoramic radiography
Extraoral radiographs include all views made of orofacial region with
film positioned extraorally. They are useful when large areas of face and
skull are to be visualized.
It enables viewing of both maxillary and mandibular arches with their
supporting structures. Thus the image covers a major portion of facial region.
Uses
• Useful in assessing development by studying deciduous root
resorption and root development of permanent teeth.
• Used to view ankylosed and impacted teeth.

• To study path of eruption of teeth.
• To diagnose presence and extent of pathology and fracture of jaws.
• To diagnose presence or absence of multiple supernumerary teeth.
• Useful aid in serial extraction procedure to study status of erupting teeth.
• Useful in mixed dentition period to study status of unerupted teeth.
Advantages
• Broad anatomic area can be visualized.
• Patient radiation exposure is low.
• Used in patients who are unable to tolerate intraoral filmsor unable to
open mouth.
Disadvantages
• Distortions, magnifications, overlapping of structures.
• Teeth and supporting periodontal structures not clear as in IOPA.
• Inclination of anterior teeth cannot be visualized.
• Requires equipment that is expensive.
25. CYANOACRYLATES
• Cyanoacrylate is a type of tissue adhesive used in mucogingival
surgeries.
• It is a type of noneugenol periodontal pack.
• Retention of pack is obtained by mechanical interlocking in interdental
spaces and by joining facial and lingual portions of pack.
Advantages of periodontal dressings or packs:
• It minimizes likelihood of postoperative infection and hemorrhage.
• Facilitates healing by preventing surface trauma during mastication.
• Protects against pain induced by contact of wound with food or with
tongue during mastication.
• Probing should not be done up to one week of insertion of periodontal
packs.
26. CLASSIFICATION OF BONE GRAFT MATERIALS

A. Based on their osteogenic potential:
• Osteoproliferative(osteogenetic): New bone is formed by bone
forming cells contained in the grafted material.
• Osteoconductive: The grafted material does not contribute to new

bone formation per se but serves as a scaffold for bone formation
originating from adjacent host bone.
• Osteoinductive: The bone formation is induced in the surrounding
soft tissue immediately adjacent to the grafted material.
B. Based on their source:
• Autogenous: Grafts transferred from one position to another within
the same individual.
• Allogenic: Grafts transferred between genetically dissimilar members
of the same species.
• Xenogenic: Grafts taken from a donar of another species.
• Alloplastic: Synthetic or inorganic implant materials which are used
as substitutes for bone grafts.
27. SOURCES OF AUTOGENOUS BONE GRAFTS

A. Intraoral site: Healing extraction wounds, bone from edentulous ridges,
autogenous block grafts from symphysis or ramus and bone removed
during osteoplasty and ostectomy.
B. Extraoral sites: Iliac crest and tibia.
28. OSSEOUS COAGULUM AND BONE BLEND

Osseous coagulum: The mixture of bone dust and blood is termed as
osseous coagulum. This technique is described by Robinson, uses small
cortical bone particles taken from lingual ridge on the mandible, exostoses
or edentulous ridges. The bone particles removed by carbide bur are placed
in a sterile dappen dish and mixed with patient’s own blood and are used
to fill the defect.
The advantage of this technique is the ease of obtaining bone from
already exposed surgical site and the possible disadvantages are low
predictability and inadequacy of material for larger defects.
A. Robinson described a technique using a mixture of bone dust and
blood that he termed osseous coagulum.
Sources of implant material include:
• Lingual ridge on the mandible
• Exostoses
• Edentulous ridges
• Bone distal to terminal tooth
• Bone removed by osteoplasty or osteotomy

• Lingual surface of mandible or maxilla at least 5 mm from the roots.
Advantages
• Provides additional surface area for the interactions of vascular and
cellular elements.
• Ease of obtaining bone from already exposed surgical sites.
• Very quick technique to accomplish.
• Can be performed in areas without great preparations.
Disadvantages
• Relatively low predictability.
• Inability to procure adequate material for larger defects.
29. AUTOGENOUS BONE GRAFT

Autograft: A tissue transfer from one position to new position in same
individual.
1. Intraoral autograft: Sources include healing extraction wound, bone
from edentulous ridges, immature bone removed during osteoplasty
and ostectomy bone removed from tri and symphysis bone removed
from symphysis leads to witch’s chin disfigurement.
2. Osseous coagulum: Sources include lingual ridge of mandible, exostoses
tori, edentulous ridges.
3. Bone blend: Bone is removed from site with chisel placed in capsule
with few drops of saline triturated for 60 sec packed into defect.
4. Intraoral cancellous bone marrow chips: Obtained from maxillary
tuberosity edentulous area adjacent to defect from which bone is pushed
into contact with root surface.
Bone from extraoral sites: Includes iliac autograft extraoral hip marrow graft.
Biologic Properties of Autograft

• Osteoconductive
• Osteoinductive
• Osteogenetic
Size of bone graft ranges from 100–1000 µm which is conductive to
ingrowths of bone. Bone forms in form of cones—Osteons with central
blood supply. https://t.me/DentalBooksWorld
30. NON-BONE GRAFT MATERIAL/ALLOPLAST

• Alloplast is sometimes called implant material.
• It is only osteoconductive in nature.
• Among them are sclera, dura, cartilage, cementum, dentin, plaster of
Paris materials, ceramics, coral derived materials.
Calcium phosphate (ceramics) bio materials are of two types:
a. Hydroxy apatite – Nonrestorable Cal/P ratio 1.67.
b. Tricalcium phosphate – Partially restorable Cal/P ratio 1.5.
Bioactive glass: Consists of sodium and calcium salts, phosphates, silicon
dioxide with particle size ranging from 90–170 μm (Perio Glass) or 300–355 μm
(biogran).
Coral Dervied Materials

They are of two types.
• Natural coral–Biocompatible resorbed slowly.
• Coral derived porous hydroxyapatite biocompatible does not resorb.
Combined techniques: A combination of both graft and nongraft
combination of barrier techniques with bone grafts.
Difference between gingivectomy and gingivoplasty:
Gingivectomy is excision of soft tissue wall of pockets and includes
reshaping as a part of techniques.
Indications:
Eliminations of suprabony pockets, gingival enlargements suprabony
periodontal abscess.
Contraindications:
• Infrabony pockets.
• Esthetic region, e. g. Anterior maxilla.
Disadvantages:
• Long time to heal.
• Loss of attached gingival.
Steps:
• Marking depth of suprabony pockets with pockets maker and producing
bleeding points.
• External beveled incision extends apical to perforation mode by pocket

marker.
• Kirkland knives commonly used kidney shaped.
• Incision should follow tooth contour.
• Excision using BP blade No. 11 and 12 is done.
• Bone blend: This technique uses an autoclaved plastic capsule and
pestle. Bone is removed from a predetermined site, triturated in
the capsule to a workable, plastic like mass and packed into bony
defects.
31. BONE SWAGING

The bone is pushed into the defect from adjacent edentulous area without
fracturing the bone at its base.
The advantage of this tecnique is the blood supply to the bone is
maintained and the disadvantage is the technical difficulty.
32. BONE ALLOGRAFTS

Bone grafts are commercially available from tissue banks. They are obtained
from cortical bone within 12 hours of the death of the donar, deflated, cut
in pieces, washed in absolute alcohol and deep form.
The material then be demineralized and subsequently grined and sieved
to a particle size of 250 to 750 mm and free dried. Finally, it is vacuum sealed
in glass vials.
Allografts may be undecalcified freeze dried bone allograft (FDBA) or
de-calcified freeze dried bone allograft (DFDBA).
Decalcification of freeze dried bone allograft exposes the bone
morphogenetic protein (BMP). The bone is demineralized using diluted
hydrochloric acid.
33. XENOGRAFTS
These are grafts taken from donor of another species.
e. g. calf bone (bovins), kiel bone (calf or ox bone).
The calf or ox bone is denatured with 20% hydrogen peroxide, dried
with acetone and sterilized with ethylene oxide and finally autoclaved.
Recently, a cell binding polypeptide is combined with bovine derived
bone marix to enhance the regenerative effects.
34. ALLOPLASTS
These are synthetic implant materials used as bone grafts. These include:
• Plastic materials
• Calcium phosphate biomaterials
• Bio-active glass
• Coral-derived materials.
Plastic Materials (HTR polymer)

HTR polymer is a nonresorbable, microporous, biocompatible composite
of polymethylmethacrylate and polyhydroxymethylmethacrylate.
Calcium Phosphate Biomaterials

Two types of calcium phosphate biomaterials are used: Hydroxyapatite
and tri-calcium phosphate.
a. Hydroxyapatite has a calcium to phosphate ratio of 1.67, similar to that
found in bone material and is generally nonbioresorbable, e.g. periograft.
However a particular resorbable nonceramic form, e.g. osteograft is
also available.
b. Tri calcium phosphate (TCP) has a calcium to phosphate ratio of 1.5. It
is mineralogically beta-whitlockite and is rapidly resorbed or
encapsulated by connective tissue, with minimal bone formation and
no periodontal regeneration.
35. BIOACTIVE GLASS

Bio active glass consists of sodium and calcium salts, phosphates and
silicon dioxide used in the form of irregular particles-(e. g., perio glass–90-
170 μm particle size or biogran (T)-300–355 μm particle size).
When this material comes into contact with tissue fluids, the surface of
the particles becomes coated with hydroxycarbonate apatite, incorporates
organic ground proteins such as chondroitin sulfate and glycosa–
minoglycans and attracts osteoblasts that rapidly form bone.
36. INDICATIONS FOR BONE GRAFTING IN PERIODONTICS

• Three-walled or two-walled intraosseous defects
• Grade 2 and 3 furcations
• Immediate implant placement
• Ridge augmentation
• Sinus lift.
37. GTR AND CLASSIFY GTR MEMBRANES

Guided tissue regeneration (GTR) is a method used for the prevention of
epithelial migration along the central wall of the pocket.
This tecnique consists of placing different types of barriers to cover
the bone and periodontal ligament, thus temporarily separating them from
the gingival epithelium.
Excluding the epithelium and the gingival connective tissue from the
root surface during the postsurgical healing phase not only prevents
epithelial migration into the wound but also favors repopulation of the
area by cells from the periodontal ligament and the bone.
GTR membranes are of two types: (1) Nonresorbable (2) Resorbable
Non-resorbable, e. g. Millipore filters, expanded polytetraflour-ethylene
(EPTFE).
Their disadvantage is the necessity for second surgery after 5–6 weeks
to remove the membrane.
Resorbable, e.g. polylactic acid, collagen.
38. CLASSIFICATION OF FLAPS

A. Flaps are classified based on:
1. Bone exposure after flap reflection
2. Placement of flap after surgery
3. Management of the papilla
1. Based on bone exposure after flap reflection: There are two types.
They are:
• Full thickness flap (mucoperiosteal flap): In this, all the periosteum
is reflected to expose underlying bone.
• Partial thickness flap (mucosal flap)—It includes only the epithelium
and a layer of the underlying connective tissue.
It is also called as “split-thickness flap”.
2. Based on flap placement after surgery: There are two types:
• Nondisplaced flaps—When the flap is returned and sutured in its
original position.
• Displaced flaps—These are placed apically: Coronally or laterally to
their original position.
3. Based on management of the papilla: There are two types:

• Conventional flaps—In this the interdental papilla is split beneath
the contact point of the two approximating teeth to allow reflection
of the buccal and lingual flaps.
It includes the modified widman, undisplaced flap, the apically
displaced flap and the flap for reconstructive procedures.
• The papilla preservation flap—In this entire papilla is incorporated
into one of the flaps.
39. OSTEOBLASTS
• These occupy a central position in bone metabolism.
• They are well-known for synegizing the organic matrix of bone and
participating in its mineralization.
• In addition respond to circulating hormones, growth factors and
cytokines produced by them play a major role in cell-to-cell communi-
cation and maintenance of bone.
Types
• It is possible to separate mature osteoblasts into several main sub-
populations.
i. Those that synthesize bone matrix.
ii. Those that line trabeculae and endosteal surfaces.
iii. Those that are called osteocytes and are buried in their lacunae.
iv. Those on surface of bone.
Functions
• Found to have gap junctions which provide intercellular communication.
• They have very prominent Golgi apparatus and extensive endoplasmic
reticulum, reflecting its capacity for protein synthesis.
• It produces a bone matrix containing type I collagen as well as non-
collagenous proteins such as osteonectin, osteopontin, osteocalcin,
and various proteoglycans.
• Osteoblasts control the process of bone mineralization at three levels:
i. In its initial phase by production of an extracellular organelle called
the matrix vehicle which has a major role in primary calcification.
ii. At the later stage by controlling the ongoing process of mineralization
by modifying thehttps://t.me/DentalBooksWorld
matrix through the release of different enzymes.
iii. By regulating the number of ions available for mineral deposition in

the matrix.
40. PERIODONTAL DRESSINGS (PERIODONTAL PACKS)

These are used to protect the wounds created by the periodontal surgery
and to maintain the close flap adaptation to the bone and the teeth during
the initial stage of healing. The periodontal dressing material should be
mixed so that it is firmly hard and rolled into a long thin roll like a thin
pencil.
Advantages
1. If minimizes likelihood of postoperative infection and hemorrhage.
2. Facilitates healing by preventing surface trauma during mastication.
3. Protect against pain induced by contact of wound with food or with
tongue during mastication.
Types of Packs
A. Zinc oxide eugenol packs
B. Noneugenol packs
a. Zinc Oxide Eugenol Packs:
• Based on reaction of zinc oxide and eugenol
• Example Wonder—Pak developed by Ward in 1923
• Composition: Zinc oxide
• Eugenol—causes allergic reaction
• Zinc acetate—acceleration
• Asbestos—Binder fillers
• Causes lung disease
• Should be eliminated
• Tannic acid—causes live disease should be eliminated
b. Non-Eugenol Packs:
Based on reaction between metallic oxide and fatty acids.
Example is Coe–Pak.
Composition: One tube contains:
• Zinc oxide
• Oil for plasticity https://t.me/DentalBooksWorld
• Gum for cohesiveness

• Lorothiodol–fungicide
• Other tube contains liquid coconut fatty acids colophony rosin
• Chlorothymol–bacteriostatic
Coe-Pak is contraindicated where strength is not primary consideration.
Other noneugenol packs include cyanoacrylates and methacrylic gels.
Retention of packs is obtained by mechanical interlocking in interdentally
spaces and by joining lingual and facial portions of pack placed for one
week, after surgery.
After one week, it is removed. Probing should not be done at this stage.
41. ANGULAR BONY DEFECTS

Also called as vertical bony defects.
They occur in oblique direction, leaving a hollowed out trough in
the bone along side the root; the base of the defect is located apical to
the surrounding bone. Radiograph helps to some extent to locate vertical
defects; but surgical exposure is best . These are accompanied by infrabony
pockets.
Angular defects are classified on the basis of number of walls:
• One-walled or hemiseptal defects—One wall is present.
• Two-walled defects—Two walls are present.
• Three-walled or intrabony defects—Three walls are present. The walls
are more common on mesial surfaces of upper and lower molars.
• Combined or osseous defect—The number of walls in the apical portion
of the defect are greater than that in the occlusal portion.
42. HEMISECTION
Definition: Procedure in which one root and its corresponding crown
portion is cut and removed.
Indications:
• When the periodontal involvement of one root is severe.
• When loss of bone is extensive in the furcation area.
• When caries involves much of the roots.
Contraindications:
• When loss of bone involves more than one root and the remaining root
would have inadequate support.
• When the roots are https://t.me/DentalBooksWorld
fused.
43. RADISECTION OR ROOT RESECTION

Definition: It is the removal of one or more roots of a molar.
Indications:
• When endodontic treatment of one root is technically impossible.
• When untreatable furcation involvement is present and removal of the
root will facilitate oral hygiene in that area.
• When extensive loss of bone has occurred around one root of an upper
molar.
• When a furcation root of an upper molar is present.
• When a root has been destroyed by extensive decay.
• When a root has been perforated and cannot be treated endodontically.
Contraindications:
• When loss of bone involves more than one root and the remaining root
would have inadequate support.
• When the bridge span is long and the abutment tooth would tend
inadequate support.
• When the roots are fused.
44. HYDROXYAPATITE
• These are the crystals formed by matrix vesicles of oseoblasts which
contain alkaline phosphatase an enzyme that helps in nucleation of
these crystals.
• They play a major role in the formation of enamel and alveolus.
• Their width ranges from 90 nm and length from 0.05–1 micron.
• Each crystal is composed of thousand of unit cells that have highly
ordered arrangement of atoms each crystal is enveloped in an organic
matrix.
• The basic formula of hydroxyapatite 3Ca3(PO4)2Ca(OH)2.
• In supra-and subgingival calculus hydroxyapatite is seen as much as
58% in 97–100% of cases.
• It is the popular coating material for implants surfaces as it resembles
bone tissue.
Gingivoplasty
Reshaping of gingival to create physiologic gingival contours with sole

purpose of recontouring gingival in absences of pockets.
Indications:
• Gingival clefts
• Crates
Shelf like interdental papilla caused by ANUG deformities in gingival
that interfere with food excursion, collect plaque and aggravate disease
process.
Steps in gingivoplasty:
• Tapering gingival margins
• Scalloped marginal outline
• Thinning of attached gingival and creating vertical interdental
grooves
• Shaping interdental papilla to provide sluiceways for passage of
food.
45. GRADE 2 FURCATION (cul-de-sac)

In this, the furcation has a cul-de-sac appearance with a definite horizontal
component.
Radiographs may or may not depict the furcation involvement. Vertical
bone loss is present. The extent of horizontal probing of the furcation
determines whether the defect is early or advanced.
Treatment
• For shallow grade 2 invasions: Usually respond to localized flap
procedures like osteoplasty with limited osteoctomy and odontoplasty
can be performed.
• In severe grade 2 invasions elimination of furcation by:
1. Root resection or amputation
2. Bone grafting guided tissue regeneration
3. Hemisection or root separation
4. Bicuspidization : Splitting of a 2 rooted tooth into 2 separate portions;
frequently performed in mandibular molars.
5. Tunnel preparation: It is the transformation of grade 2 furcation into
grade 3 and 4 for better access. But this procedure is not performed
because of root caries.
46. VESTIBULOPLASTY
In this procedure we provide relative ridge extension by deepening the
sulcus without any addition of bone so that the denture bearing area is
increased. https://t.me/DentalBooksWorld
• The procedure is more commonly in mandible than maxilla.

• The incision is placed on lip mucosa, buccal mucosa, alveolar crest and
in the vestibule either supra or subperiosteally.
It is of two types:
1. Labial vestibuloplasty
2. Lingual vestibuloplasty
47. FREE GINGIVAL AUTOGRAFTS

This system was introduced by Bjorn in 1963.
Advantages
1. High degree of predictability
2. Simplicity
3. Ability to treat multiple teeth at the same time.
Disadvantages
1. Two operative sites
2. Compromised blood supply
3. Creates discomfort
4. Lack of predictability in attempting root coverage
5. Post-operative color match.
Indications
1. Inadequate zone of attached gingiva
2. Gingival recession
3. Shallow vestibular depth.
48. HEALING OF FREE GINGIVAL GRAFT

The success of the graft depends on the healing of connective tissue.
The graft is initially maintained by diffusion of fluid from the host bed,
adjacent gingival and alveolar mucosa.
The fluid is a transudate from host vessels and provides nutrition and
hydration essential for the initial survival of the transplanted tissues.
49. GLICKMAN CLASSIFICATION (FURCATION

INVOLVEMENT)
Grade-I: • It is incipient or early lesion.
• Pocket is suprabony involving soft tissue.
• Slight bone loss in function.

• No radiographic changes.
Grade-II: • Bone is destroyed on one or more aspects of furcation, but
portion of alveolar bone and periodontal ligament remains intact.
• Partial penetration of probe into furcation.
• Lesion is essentially cul–de–sac.
• Radiograph may or may not reveal grade-II involvement.
Grade-III: • Interdental bone is completely lost but facial or lingual surfaces
are occluded by gingival tissues.
• Furcation opening not seen clinically but is essentially through
tunnel.
• If radiographs are taken with proper angulation, roots are
divergent. Lesion is radiolucent between roots.
Grade-IV: • Interadicular bone is completely lost, gingival tissues reeceds
apically so that furcation opening is seen clinically.
• Radiographic changes are same as grade-III.
50. RETROGRADE PERIODONTITIS

Definition: Periodontitis caused by pulpal infections that have entered
periodontal ligament either through apical foramen or through lateral canals.
Etiology: Caused by Bacteroides forsythus.
Pathways of Communication between Pulp and Periodontium

Three categories:
I. Pathways of developmental origin:
• Apical foramen
• Accessory canals
• Developmental grooves
II. Pathways of pathologic origin:
• Tooth fracture
• Idiopathic resorption
• Loss of cementum due to external irritants
III. Pathways of iatrogenic origin:
• Lateral perforation during endodontic procedure.
• Root fracture due to endodontic procedure .
51. MUCOGINGIVAL SURGERY

Definition
The term mucogingival surgery was introduced by Friedman in 1957 and
was defined as surgical procedures for the correction of relationships
between the gingiva and the oral mucous membrane with reference to three
specific problem areas attached gingiva, shallow vestibules and aberrant
frenum.
It is Defined as periodontal surgical procedures designed to correct
defects in morphology position and/or amount of gingiva—problems
associated with three specific entities are considered those associated
with attached gingival shallow vestibule and frenum interfering with
marginal gingiva.
Indications
• Augmentation of edentulous ridge
• Prevention of ridge collapse associated with tooth extraction
• Crown lengthening
• Loss of interdental papilla
• Contraindication
• Same as in any other periodontal surgery.
52. MUCOGINGIVAL SURGICAL TECHNIQUES

Gingival Extension Operation
Free soft tissue autograft
Step 1 Eliminate pocket.
Step 2 Preparation of recipient site.
Step 3 Obtaining graft from donor site.
Step 4 Transfer and immobilizations of graft.
Step 5 Protection of donor site.
• Apically displaced flap
• Fenestration operation/periosteal separation.
53. PROCEDURES FOR ROOT COVERAGE

Conventional procedures Regenerative procedures
Laterally displaced flap Guided tissue regeneration
Double papilla flap
Coronally positioned flap Tarnow’s technique
Gingival autograft Miller’s technique
List out Various Root Coverage Procedures

• Free gingival autograft
• Free connective tissue graft
• Subepithelial connective tissue graft
• Lateral pedicle flap
• Pouch and tunnel technique
• Coronally advanced flap technique
• GTR.
54. PERIODONTAL PLASTIC SURGERY AND DESCRIBE THE

AREAS OF APPLICATION IN PERIODONTICS
The 1996 World Workshop in Clinical Periodontics renamed mucogingival
surgery as “periodontal plastic surgery”—a term originally proposed by
Miller in 1993.
Periodontal plastic surgery is designed as the surgical procedures
performed to correct or eliminate anatomic, developmental or traumatic
deformities of the gingiva or alveolar mucosa.
Various plastic surgical procedures are aimed at:
a. Gingival augmentation.
b. Root coverage.
c. Correction of mucosa defects at implants.
d. Crown lengthening.
e. Removal of aberrant frenum.
f. Ridge augmentation.
g. Reconstruction of papillae.
Since the procedures have moved beyond the traditional treatment of
problems associated with the amount of gingival and recession, to include
correction of ridge form and soft tissue esthetics, the term ‘periodontal
plastic surgery’ is considered as more appropriate than “mucogingival
surgery”.
55. ‘RATIONALE’ OR OBJECTIVES OF PERIODONTAL

PLASTIC SURGERY
The three main objectives of periodontal plastic surgery are:
1. Correction of problem associated with attached gingival.
2. Correction of problems associated with shallow vestibule.
3. Correction of problems associated with an aberrant frenum.
a. Problems associated with attached gingiva:

The original rationale for mucogingival surgery was based on thought
that minimal width of attached gingival was required to maintain optimal
gingival health. However the concept was challenged by many studies
stating that minimum width of attached gingiva has been established as a
standard necessary for gingival health. There were opinions that narrow
gingival in combination with a shallow vestibule might favor the
accumulation of food particles during mastication and impede proper oral
hygiene measure.
b. Problems associated with shallow vestibule:
Recession of gingiva will displace the gingival margin apically, thus
reducing the vestibular depth. When the vestibular depth is inadequate it
is difficult to maintain proper oral hygiene. Hence vestibular extension is
another important objective of periodontal plastic surgery.
c. Problems associated with aberrant frenum:
Tension on the frenum may pull the gingival margin apically and also tend
to open the sulcus. Also encroachment of frenum on the gingival margin
may cause difficulties in oral hygiene maintenance. Hence it is an important
objective to correct frenal or muscle attachments.
56. TECHNIQUES USED TO WIDEN THE ZONE OF

ATTACHED GINGIVA
a. Gingival augmentation apical to the area of recession, such as–
• Free gingival autograft
• Free connective tissue graft, and
• Lateral pedicle graft.
b. Flap technique like apically repositional flap
57. ADVANTAGES OF SUBGINGIVAL CONNECTIVE TISSUE

GRAFT OVER THE FREE GINGIVAL AUTOGRAFT
• The color matching is superior in subgingival connective tissue graft
(SCTG).
• The donor site heals by primary intention in SCTG.
• The percentage of root coverage is much higher in SCTG.
58. DEFINE FRENECTOMY

A frenum is a fold of mucous membrane that attaches the lips and cheeks
to the alveolar mucosa or gingival and underlying periosteum. If the frenum
attachment is too close to the marginal gingival it may pull the gingival
margin away from the tooth and cause plaque accumulation, such scenario
requires frenectomy or frenotomy.
Frenectomy is complete removal of frenum, including its attachment to
the underlying bone. This may be required in the correction of abnormal
diastema between maxillary central incisors.
Frenotomy is incision of the frenum to relocate the frenal attachment.
This is generally sufficient for most of the periodontal purposes.
59. GUIDED TISSUE REGENERATION (GTR)

Based on assumption that periodontal ligament cells have potential for
regeneration of attachment apparatus (new attachment) of tooth techniques
consists of placing barriers of different types to cover the bone and
periodontal ligament to prevent migration of epithelium.
Used mostly in Grade–II furcation involvement.
Barrier membranes used in GTR should be biocompatible and have cell
occlusivity and space making.
Nondegradable, e.g. Polytetrafluoroethylene (GORETEX)
Membranes Biodegradable, e.g. Poly lactic acid vicryl synthetic
(Biobrane) resorbed after a few weeks.
8
CHAPTER Oral Implantology
1. IMPLANTS AND CLASSIFICATION

An alloplastic material or device that is surgically placed into the oral
tissue beneath the mucosal or periosteal layer or within bone for functional,
therapeutic and esthetic purposes.
Classification of Implants
1. Depending on the placement within the tissues:
• Sub-periosteal
• Transosteal
• Endosteal
i. Blade like
ii. Pins
iii. Cylindrical (hollow and full)
iv. Disc-like
v. Screw-shaped
vi. Tapered and screw shaped
2. Depending on the materials used:
• Metallic (Ex: titanium, titanium alloy, cobalt-chromium, molybdenum
alloy).
• Non-metallic (Ex: ceramics, carbon).
3. Depending on the reaction with bone
• Bio-active (Ex: hydroxyapatite).
• Bio-inert (Ex: metals).
2. IMPLANT COMPLICATIONS
• Peri-implant mucositis.
• Peri-implantitis.
• Infection. https://t.me/DentalBooksWorld
• Incision opening.
• Inflammation.
• Bone loss.
• Implant overload.
• Failure/breakage.
• Rejection.
3. PERI-IMPLANTITIS (FIG. 8.1)

It is defined as an inflammatory process affecting the tissues around an
osseo-integrated implant in function, resulting in loss of supporting bone.
Etiology
Bacteria play a major role in etiology of peri-implantitis and peri-mucositis.
• Anaerobic bacteria.
• Porphyromonas gingivalis.
• Prevotella intermedia.
• Prevotella nigrescens.
• Tannerella forsythensis.
• Actinobacillus actinomycetemcomitans.
• Treponema denticola.
Clinical Features
• Color changes, bleeding upon gentle probing.
• Pocket formation and radiographic bone destruction.
Fig. 8.1: Peri-implantitis
Oral Implantology 153
• Suppuration, calculus build-up and swelling.

• Mobility.
Treatment
1. Mechanical
• Supra- and subgingival calculus and plaque removal from implant
surfaces using scalers specially designed for implants.
2. Chemical
• Arestin.
• Atridox.
• 1 ml of 1% chlorhexidine gel inserted submucosally.
3. Surgical
• Re-osseointegration.
Maintenance
• Oral hygiene instructions.
• Not to brush for 12 hrs.
• Do not use inter-proximal cleaning devices for 10 days.
• Recall after every 3 months.
4. OSSEOINTEGRATION (FIGS 8.2 AND 8.3)

It is defined as a direct structural and functional connection between
collagen of bone and hydroxyapatite crystals of the implants.
Fig. 8.2: Osseointegration

Fig. 8.3: Osseointegration
Factors Affecting Osseointegration

• Occlusal load
• Biocompatibility of the material
• Implant design
• Implant surface
• Implant bed (surgical site)
• Surgical technique
• Infection.
Theories
• Branemark.
• Weiss theory.
• Implant insertion.
• Slight tissue necrosis due to surgical trauma.
• It is replaced by multinucleated osteoclasts.
• Later replaced by osteoid.
• Woven bone formation.
• Replaced by lamellar bone.
Steady bone-implant interface formation (Osseointegration).

Branemark’s team was the first to suggest a direct bone anchorage and the
potential clinical advantages of osseointegration.
Definition of osseointegration, based on stability, “A process where
by clinically asymptomatic rigid fixation of alloplastic materials is achieved
and maintained in bone during functional loading (Zarb & Albrektsson
1991).
Osseointegration represents a direct connection between bone and
implant without interposed soft tissue layers. However, 100% bone
connection to the implant does not occur.
Albrektsson presented information on series of background factors that
needed to controlled in order for a reliable osseointegration of an implant:
1. Biocompatibility
2. Design
3. Surface conditions of the implant
4. The status of the host bed
5. The surgical technique at insertion
6. The loading conditions applied afterwards.
5. EARLY TISSUE RESPONE TO OSSEOINTEGRATED

IMPLANTS
To aquire proper conditions for healing the implant following installation
must exhibit good mechanical stability. The damage of the soft and hard
tissue initiates the process of wound healing which ultimately allows the
implant to become “ankylotic” with the bone that is osseointegrated
establishment of a delicate mucosal attachment or barrier to the titanium
device which serves as a seal that prevents products from the oral cavity
reaching the anchoring bone tissue.
Healing in the cortical bone region resorption of mineralized avascular
necrotic tissue must occur before new bone can form on the implant surface.
Healing on the spongeous region, on the other hand woven bone
formation and osseous integration occur early in the process of healing.
Proper stability can be achieved when the marginal apical portion of
the site harbors sufficient amounts of trabeculae. Implant with proper
mechanical stability can be achieved by press-fit that is the minute lateral
displacement of bone tissue and tight contact that was established between
the metal screw and the avascular cortical bone in the marginal two-thirds
of the site this zone of press-fit is about 1 mm wide.
During site preparation and fitting of the implant, bone trabeculae were
in the apical portion of the site dislocated into marrow space, blood vessels
were severe and bleeding occurred.
Blood clot formation can be observed between the implant body and
host bone. The blood clot matures and is replaced by granulation tissue
which is rich in neutrophils and macrophages.
Leukocytes start decontaminate the wound. Vascular structures from
the marrow spaces of peripheral vital bone proliferate into the granulation
tissue.
About one week of implant insertion reparative macrophages and
undifferentiated mesenchymal cells start to produce and release growth
factors which stimulate fibroblasts through which stimulate fibroplasis
through which an undifferentiated provisional connective tissue forms in
the apical trabeculae regions of the implant site and furcation sites of a
screw shaped implant.
At this stage, osteoclasts appear in the bone marrow spaces and the
necrotic bone will gradually be resorbed.
The provisional connective tissue is rich in newly formed vessels,
fibroblasts and undifferentiated mesenchymal cells which gradually mature
into an osteoid from which owen bone will form to fill the void with bone
tissue, this phase of wound healing and early bone formation is called
modeling.
After two weeks of installation, woven bone formation with primary
osteons has formed at the base of the surgical site and that newly formed
bone has been laid down in the apical part of implant and in the furcation
sites of the implant surface. The phase of modeling is followed by a phase
of remodeling during which the woven bone is substituted with the lamellar
bone with good potential to take up and distribute load.
The titanium surface is lined with a thin rim of lamellar bone lateral of
which a bone marrow rich in adiopose sites can be seen. Typical secondary
osteoids with concentric lamellae and a central Haversian canal can be seen
in lamellar bone within the zone of press-fit and in the adjacent bone tissue.
6. OSSEOINTEGRATION FROM A MECHANICAL AND

BIOLOGICAL VIEW POINT
Osseointegration is a time related phenomenon with increasing time of
loading there is a clear tendency for there to be more bone in contact with
mandibular implants than the maxillary ones.
• The nature of osseointegration bond is predominantly biomechanical.

• Complete bone in-growth does not occur in spaces much smaller than
100 microns. However, bone ground substance will adapt to surface
irregularities in the 1 to 100 microns range explaining the change in
surface topography at this level will result in a profound impact on the
holding power of the implant.
• Surface irregularities in the 2 microns range or greater will show a
diminished bone response possibly because of increasing ionic leakage.
• Perio test measurements and RFA (reasonance frequency analysis)
technique are used to measure implant stability and thereby assess its
degree of osseointegration.
• Continuous dynamic overloading of osseointegrated implants lead to
micromovements and subsequent bone resorption leading to implant
failure.
• Peri implantitis also causes failure of implants.
7. OSSEOINTEGRATION IN THE CLINICAL REALITY

Astra tech implant has been documented with positive results for 5 yrs
whereas the newer osteoblast design has been reported for long-term
only in clinical materials most limited in size.
The original ITI solid screw implant has been positively documented
for survival for more than 5 yrs.
Newer ITI designs such as osseotite implant lack proper long-term
documentation.
Endo pore is positively documented for a full 5 yrs at least in the
mandible.

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Short Notes

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

Jaypee Brothers Medical Publishers (P) Ltd

Jaypee Brothers Medical Publishers (P) Ltd

Short Notes in Periodontics: A Handbook

There are a lot of books on periodontology.

The purpose in the making of this book is to provide ease of understanding,

First and foremost we are very grateful to our teachers—Dr Mythili

2. Classification and Epidemiology of

3. Etiology of Periodontal Diseases 31

22. Widow’s Peak 45

27. Differences between Periodontal Abscess

5. Diagnosis, Prognosis and Treatment Plan 93

6. Gum Stimulator (Stim-U-Dent) 102

7. Surgical Periodontal Therapy 117

15. Root Conditioners 126

53. Procedures for Root Coverage 147

8. Oral Implantology 151

9. Supportive Periodontal Therapy 158

2. GINGIVAL FIBERS (FIG. 1.1)

Fig. 1.1: Parts of the gingiva and epithelium

Collectively these fiber bundles have been referred to as the gingival

Fig. 1.2: Gingival fiber groups

3. FUNCTIONS OF GINGIVAL FIBERS

5. MAST CELLS IN GINGIVAL FIBERS

7. BLOOD SUPPLY IN GINGIVAL TISSUES

8. INTERDENTAL GINGIVA OR GINGIVAL COL (FIG. 1.3)

Fig. 1.3: Gingival col

The interdental col increases both in buccolingual width from about 2

Physiologic Pigmentation (Fig. 1.4)

Mucous membrane - 22%

10. JUNCTIONAL EPITHELIUM/DENTOGINGIVAL JUNCTION

Fig. 1.5: Dentogingival unit

11. SULCULAR EPITHELIUM

12. HISTOLOGY OF GINGIVAL SURFACE EPITHELIUM

• Stratum granulosum (granular layer)

13. GINGIVAL MASSAGE

14. GINGIVAL SULCUS

15. ACTIVE AND PASSIVE ERUPTION

16. LONG JUNCTIONAL EPITHELIUM

17. GINGIVAL INNERVATIONS

18. FUNCTIONS OF PERIODONTAL LIGAMENT

Shock absorption: Periodontal ligament resists the impact of occlusal

Formative and Remodeling Functions

Nutritional and Sensory Functions

19. MERKEL CELLS

20. LANGERHANS CELLS (FIG. 1.6)

21. CELLS IN PERIODONTAL LIGAMENT

22. PRINCIPAL FIBERS OF PERIODONTAL

Fig. 1.7: Principal fiber groups of the periodontium

constituent molecule which is arranged in fibrils with striations. Type of

23. LAMINA DURA

Clinical Importance of Lamina Dura

24. OXYTALAN FIBERS AND SHARPEY’S FIBERS

25. ACELLULAR AND CELLULAR CEMENTUM (FIG. 1.8)

Fig. 1.8: Cementum

It does not contain cementocytes within its substance but as

26. FUNCTIONS OF CEMENTUM

27. CEMENTOENAMEL JUNCTION

28. FENESTRATION AND DEHISCENCE

29. EFFECTS OF AGING ON GINGIVAL EPITHELIUM AND

Fig. 1.9: Fenestration and Dehiscences

• This causes increase in epithelial permeability to bacterial antigens and