PERIODONTOLOGY | PRELIMS

DEA 16-17 | HARA, MARIKO D.

Anatomy and Physiology of the PERIODONTIUM **2 parts of preventive dentistry

- prevention of caries
Introduction - prevention of periodontitis
Attachment apparatus  connective functional unit
 A.K.A Attachment Apparatus/ Supporting tissues of
Periodontium the teeth
(Peri= Around, Odontos= Tooth)  Establishes as a developmental, biologic and
- Consists of structures both as supporting and functional unit which undergoes certain changes
investing tissues of tooth with age
- the statement actually just tells everyone,
when you have something that you want
to equate with age, all of these things can
happen but you just have to categorize if
it’s in a healthy state or pathologic state
- hindiporke aging ka, towards pathology
kalagi, maybe compromised, but not all
individuals may present with that so it’s a
matter of putting the demographics
together
- all of these happen in the young and as
well as in the old
Composed of: - it’s the matter of qualifying the state of
1. Gingiva health; this is normal and this is abnormal,
2. Alveolar bone proper this is still in the state of health and this is
- The alveolar bone proper (or bundle bone) in state of disease
is continuous with the alveolar process,
which is a thin plate that lines the alveolus  Subjected to morphologic and functional alterations
of the tooth
related to changes in oral environment
3. Cementum
- possible factors
4. Periodontal ligaments
 age
st  health
 1 point of connection
 risk factors
- Gingiva via junctional epithelium
 environmental factors
connected to CEJ
- Fators for high caries rate:
 Then cementum
 poor hygiene
- From CEJ to apex
 acidic saliva
- Connects to bone by PDL  deep pits and fissures
 Alveolar bone proper  diet – high refined sugars
- Lining of alveolar socket **Oral cavity
- Connected to PDL - dirtier than the anus because of the hard structures
where bacteria can latch on
** Dental plaque
- inorganic Ca& PO 4
Functions: - organic  peptidoglycans
1. Attachment for teeth to bone tissues of the jaw **Plaque biofilms
- attachment via gingiva, PDL, cementum - well organized community of bacteria that adheres
2. Support of teeth for function to the surface and is embedded in extracellular
- support from alveolar bone not ABP slime layer
- alveolar bone proper is the attachment - community that is interacting and developing
through its signaling processes reactions of the bod
rd
**extraction – done only if there is 3 degree mobility
 PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.

**Flossing
Formative Organs
- Cochrane review
o highest form of review of all evidences; it  Dental Organ: Enamel
said that your evidence is negligible but  Dental Papilla: Dentin and Pulp
not all evidences that is pushed aside  Dental Follicle: Periodontium (Cementum,
becomes insignificant. According to the Periodontal Ligaments, Alveolar bone)
Cochrane review, the use of floss is not including gingiva
really helpful, that’s the evidence. But After crown develops, the roots follows. The
practically, when you apply it on external and internal dental epithelium proliferates
yourselves, you get cleaned. It may not
in apical direction→ Hertwig’s epithelial root
totally eliminate the plaque but you view
sheath, double layer of cells
clinically, you floss and make you feel clean
Ectomesenchymal cells→ Dental Papilla→
** Toothpick
Odontoblasts→ Dentin of root→ Framework of root
- forcing it can create black triangles
(as well as PDL and acellularcementum starts to
**Why don’t we get sick with dirty oral cavity?
develop)
- Due to commensalism
- Equilibrium b/w good and bad bacteria Cementoblasts→ Cementoid→ Formation of the
**Periodontal disease organic matrix, ground tissue and collagen fibers→
- Imbalance of good and bad bacteria coupled with Cellular cementum covers apical third of roots
state of health o Cementoblasts
**so what’s more important, toothbrush or toothpaste? ▪ Enamel related proteins +
- Toothbrush ectomesenchymal cells from
o when you brush, you’re trying to disturb dental follicle
the biofilm, eliminating the bacteria within Ectomesenchymal cells→ Dental Follicle→
Periodontal fibroblast (→ Fibers of PDL) and
the biofilm
Osteoclasts(→ABP)
** so why do you use toothpaste?
- Prolongs smear layer provided by fluoride
Oral Mucosa/ Mucous Membrane
- anti-cavity protection for the tooth.
- Continuous with the skin of the lips and mucosa of
- Secondary minor role is that it makes your tooth the soft palate and pharynx
brushing more pleasant - covers the oral cavity
- Difference between outer skin and oral skin?
Development of the Periodontium
o outer – sebaceous gland
It starts early in the embryonic phase when cells
o oral – salivary gland
from neural crest (w/c comes from neural tube)
migrate into first brachial arch, forms the Three kinds of Oral Mucosa
ectomesenchyme beneath epithelium of the 1. Masticatory Mucosa
stomatodeum (the primitive oral cavity) which - Gingiva and Hard Palate
releases factors that initiate epithelial -mesenchyme - Subjects to wear and tear fxns
interactions  that’s why it’s highly keratinized
Formation of the dental lamina (observe processes;
bud stage, cap stage, bell stage with root 2. Specialized Mucosa
development) → Formation of the tooth and - Dorsum of tongue
periodontal tissues, including the alveolar bone - Gives different taste sensations (receptors)
proper  tastebuds: filiform, foliate,
During cap stage, there will be condensation of fungiform, circumvallate
ectomesenchymal cells in relation to the dental
epithelium 3. Lining Mucosa
- Covers rest of the other areas
Dental Organ→ Dental Papilla (→Dentin and Pulp) and - Highly non-keratinized
Dental Follicle (→Periodontal Tissues) - Thinnest and most fragile

Gingiva
 PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.

- Covers the alveolar process Free Gingiva Attached gingiva

- Surrounds the cervical portion of the teeth Coral pink Coral pink
- Obtains final shape and texture in conjunction with - due to abundance of
tooth eruption keratin and thin CT
Dull surface Firm texture
Two kinds of clinical gingiva
- due to pull of CT fibers
1. Free Gingiva
(collagen)
- Unattached
Firm consistency Consists of stipplings
- Gingival crevice
- Histologically:
- 0-3mm
epithelial ridges /
2. Attached Gingiva
rete pegs / rete ridges
- Attached because of connective tissue
- Outer skin: pores /
fibers
pinpoint depression
- 5mm
- (about 40% of adults)
- for attachment
- if not seen, may have
gingivitis
- more shiny, less
stipplings, epithelium can
easily slough off (eg. HIV,
Mucocutaneous disorders
Boundaries like impetigos,verroca
Coronal: free marginal gingival, scalloped vulgaris ) hinders px from
- as you go from anterior to posterior, the hygiene
scalloping flattens a little bit because of
widening of the anatomy itself Located at the buccal and Firmly attached to the
Apical: continuous with alveolar lining mucosa lingual or palatal aspects underlying alveolar bone
Distinct separation: mucogingival junction of the teeth, including and cementum by
- not actually an anatomic feature but it’s just a
interdental papillae connective tissue fibers
visual delineation between attached gingiva
(immobile)
and alveolar mucosa
**what makes the distinction histologically? The end
point of keratinized layer and the starting point of non-
keratinized layer
**Width of gingiva
= 1 – 9 mm labial / buccal
= 1 – 8 mm lingual

Note: Connective tissue lines the socket, not the epithelium.

**two kinds of fibers
a) gingivalcrestalfibers
b) true PDL fibers
 PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.

Alveolar Mucosa Junctional Epithelium Attachment Loss

- Dark red lining mucosa that is apical to the - Bleeding component due to any movement,
mucogingival junction breaching the epithelial attachment (JE) but has not
- Loosely bounded to the underlying bone open
- Apical boundary  vestibule - Histologically, 0.97 – 1mm is healthy, and as long as
Interdental Papilla there is no loss of bony attachment.
- Influenced by contact relationship between teeth
- Width is determined by approximating tooth surfaces MICROSCOPIC ANATOMY
courses the CEJ Free Gingiva
- Anteriors: Pyramidal, Posteriors: Flattened in BuLI Epithelium
direction Connective Tissue
- One Vestibular portion and one Lingual/Palatal
portion separated by col: Gingival epithelium
Valley-like depression between teeth, a a . Oral Epithelium: Facing the oral cavity
concavity found on posteriors b. Oral Sulcular Epithelium: Faces the tooth without
Thin nonkeratinized epithelium contact with tooth surface
Attached gingiva demarcated by free gingival c. Junctional Epithelium: Provides contact between
groove, more pronounced on vestibular aspect, gingiva and tooth
frequent in the incisor and premolar regions of
mandible, less frequent in the mandibular
molars and maxillary premolar

*absence – means you don’t have teeth; blunting – spaces in

between quite bigger
*presence of disease – recession of papilla
*presence of diastema – lessens the peak
*buccal peak and lingual peak – valleys into non-keratinized
because in between two adjacent teeth
* first time flossing  bleeding; thickens as you floss
because of keratinization Epithelium of the Free Gingiva
a) Oral epithelium
b) Oral sulcular epithelium

Gingival Sulcus
- Invagination by gingiva once it joins the tooth surface
at an infolding formed by the gingival margin sulcus
- Probing artificially opens the sulcus
- Clinically healthy gingiva can present with zero
probing depth but can be up to 3mm

The connective tissue which projects into the
epithelium are called connective tissue papillae,
separated by epithelial ridges or rete pegs, which
are characteristic morphologic features of OE and
OSE.
The subsurface of the oral epithelium (facing the
connective tissue), the depressions corresponding
to connective tissue papillae which projects into the
epithelium
System of epithelial ridges
“Stipplings”
Cell layers of the Oral Epithelium
- Multilayered
a) S.Corneum: Space
b) S.Granulosum: Granules
c) S.Spinosum: Golgi Complex
d) S.Basale: Active mitochondria, Desmosomes
e) Basement Membrane
f) Lamina Propria
- Keratinized, Stratified Squamous Epithelium
- Orthokeratinized has cell nuclei lacking outer cell
layer while Parakeratinized has remnants of nuclei
- At S.Basale, there will be mitosis → S.Spinosum with
spinous polyhedral cells unable to produce cells since
the nucleus is lost→ S.Granulosum with granule-like
cells and has darkest layer with pigments
90% of the cells are keratin-producing cells + melanocytes,
PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.
Langerhans cells, Merkel cells and Inflammatory cells
a) Melanocytes: Pigments
b) Langerhans Cells: Defense of the oral
mucosa, Reacts with antigens, Prevents or
inhibits antigen penetration of tissue
- Prominent in spinosum
- Less in corneum
c) Merkel Cells: Sensory function (tactile)
- At stratum basale
d) Inflammatory Cells
- Basal cells, Basement Membrane and Part of the
adjacent connective tissue
a) Lamina Lucida has desmosomes, involved in
the attachment of epithelium to underlying
basement membrane
2 Hemidesmosomes→ Desmosomes that
are responsible for solid cohesion between
epithelial cells and lamina
- “Clear cells” has no hemidesmosomes,
not keratinocyte
- single cell layer of JE attaches to enamel
by hemidesmosomes (half  easily detach
and easily bleeds)
b) Lamina Densa has anchoring fibers projecting
into the connective tissue
Desmosomes
Composed of:
1. Outer leaflets of cell membrane of 2 adjoining cells
2. Thick inner leaflets of cell membrane
3. Attachment plaques, represents granular clusters
and fibrillary material in cytoplasm
- S. Granulosum has keratohyalin bodies and clusters of
glycogen-containing granules that are related to the
synthesis of keratin.
- The abrupt transition of cells from S.Granulosum to
S.Corneum is the sudden keratinization of cytoplasm
of keratinocyte and its conversion to a horny squame
- S.Corneum is filled with keratin and apparatus for
protein synthesis and energy production (ie nucleus,
mitochondria, endoplasmic reticulum, golgi complex)
- Lining mucosa has no stratum corneum.
*Keratinization is the process of differentiation, not of
degeneration. It’s a process of protein synthesis which
requires energy and dependent on functional cells with
nucleus and normal set of organelles.
 PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.

SUMMARY: The keratinocyte undergoes continuous

differentiation on its way from the basal layer to the
surface of the epithelium. Thus, once the kerati nocyte has
left the basement membrane, it can no longer divide but
maintains a capacity for production of protein. In the
granular layer, the keratinocyte is deprived of its energy
and protein-producing apparatus and is abruptly
converted into a keratin-filled cell, which via the stratum
corneum, is shed from the epithelial surface.
Cel l s of RE replaced by JE, continuous with OE a nd provides
a tta chment between tooth a ndgi ngiva
Dento-Gingival Epithelium
- Achieves final structural characteristics in conjunction
with tooth eruption
a . Enamel is fully formed. The ameloblast is reduced in
height. Together with Outer Enamel Epithelium, the
basal lamina forms the Reduced Dental Epithelium.
The Basal lamina contacts the enamel, contact is
maintained by the hemidesmosomes. RE surrounds
the crown until tooth starts to erupt. Si nce JE developed from OE, we ca n say tha t OE possesses the
ability to differentiate into cells of JE.

Junctional Epithelium
- Provides contact and seal for gingiva and teeth
- REE is transformed and junctional epithelium during
eruption
- Final structural characteristics achieved in conjunction
with tooth eruption
b. Erupting tooth approaches the Oral Epithelium, the - Continually renews through cell division
cells of the RE and basal layer cells of OE shows - Cells continue to migrate until they are shed at the
increased mitotic activity and starts to migrate into gingival sulcus area as dead cells
the connective tissue → Produces epithelial mass
between OE and RE so that tooth will erupt without  Stratum basale
bleeding.  Spinous
 Granular
 Corneum

- lost when you don’t have keratin? Corneum

- does epithelium has blood vessels? None
- Why does gingiva bleed during flossing?
c. Tooth penetrated into the oral cavity, incisal area of o Due to CT – they have inflammatory cells
enamel covered by JE with only few layers of cells but (PMN leukocytes) and formative cells
cervical area covered by a meloblasts a nd outer cells of RE o But active in mitosis so healing is fast (3-5
days)
 PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.

o Immune response (innate)  24hrs

 Why you don’t get sick despite of its
vulnerability for severance? Fast
mitosis. renewal, sloughing off,
turnover of epithelial layers
 PMNs + sloughing off of epithelial
layer = anatomic barrier for immune
responses 24/7 that’s why you don’t
get sick

- oral epithelium – all 4 layers

o sulcular epithelium – no corneum
o junctional epithelium – basal layer retains for
 Between Enamel and JE,
mitosis
>Electron-dense zone = Lamina Densa in Basement
- base of the sulcus is the most vulnerable area
Membrane of CT; Densa-like structures harbors
- underneath the thin layer of junctional epithelium
desmosomes
highly non-keratinized is collagen already, the >Electron-lucent zone = Lamina Lucida in BM of CT;
connective tissue Lucida-like structures has no anchoring fibers

**where does tooth came from?  Thus, interface between JE and enamel is similar to
- Mesoderm  dental organ  dental papilla epithelium-CT interface. JE is not only in contact
(dentin, pulp) and dental follicle (periodontal with enamel but physically attached to the tooth via
tissues including gingiva) hemidesmosomes.
**what stimulates eruption? Masticatory force
**what stops eruption? Antagonistic contact
**remove the contact supraeruption Sulcus = 0.64 = 1mm
**Contact between lamina and epithelial cells is maintained JE = 0.97 = 1mm
by hemidesmosomes CT = 1.07 = 1mm
**cells that line your tooth bud? 2.73mm = 3mm
- Ameloblastsameloblastic layer reduce in size 
REE the outer covering of enamel transformed to JE * End point of attachment (soft tissue) = crest of bone
LOA = Loss of attachment
during eruption in combination with OSE
- Gingival recession
**former ameloblasts are not divided even with increased - From CEJ to the margin of gingiva
mitotic activity at the basal layer of oral epithelium (reason - you have to quality what kind of attachment is lost
why there’s no bleeding during eruption of teeth) a. Epithelial attachment / JE / base of sulcular
* JE has less ridges because there is more CT and PDL that
epithelium  gingivitis
compensate for attachment
b. Connective tissue attachment  periodontitis
*loss of attachment (LOA) –
Probing Depth
- Looking at gingival margin to the base of sulcus
3 Distinct different between OE, OSE and JE
- Healthy sulcus can run the depth from 0-3mm
1. JE cell size, in relation to tissue volume, is larger
- Dynamic
than in OE
2. JE intercellular spaces, in relation to tissue volume,
Attachment Level
is wider than in OE - Starts at CEJ to the base of sulcus
3. The number of desmosomes is smaller in JE than in - With constant reference point
OE
 PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.

Healthy Gingiva *epithelial cells

- No inflammation - Basal layer actively differentiating, until it loses
- Not hyperplastic/hypertrophied nucleus and acquires more cytokeratin filaments
keratinized layer
Probable Attachment Levels
- Repopulate faster – 3-5 days
- Combination of probing depth and attachment loss.

*normal clotting time (fibrin clot)  3-7min

- Inflammation can be a precursor to infection.
- Cause of periodontal disease is the plaque biofilm plus *bleeding time  1-3min
the susceptibility *how long does it have to be in contact?
*READ WHAT HAPPENS AT THE EXTRACTION SITE
Calculus
 denotes the hygiene of the patient but not the Cells
nd
state of the gingiva. 2 etiologic agent of gingivitis  fibrobroblast
o predominant connective tissue cell (65% of
st
1 etiologic agent of gingivitis – plaque biofilm the total cell population).
o production of various types of fibers found
Probe or scale first? in the connective tissue
 Calcular deposits take the place of epithelial o synthesis of the connective tissue matrix
attachments. So check the gingival condition first o active ER &mitochondnria
then probe before scaling. o cytoplasm contains many fine
tonofilaments
WHO probe
 after probing measure the loss of attachment that  mast cell (allergies, IgE)
depends on the gingival recession (probable o produces vasoactive substances
o in vesicles, contain proteolytic enzymes,
attachment level)
histamine and heparin
If there’s visible recession  measure CEJ to gingival
margin  macrophage
o phagocytic and synthetic functions
Gingivitis o from monocytes
 acute / chronic inflammatory disease o microvilli present in large numbers
 reversible by prophylaxis
 manifestation of something that can cause disease  inflammatory cells
(periodontitis) o neutrophilic granulocytes, also called
polymorphonuclear leukocytes
Periodontal disease  with lysosomal enzymes
 check for plaque (material alba)  most motile; soldier cells
o combination of biofilm and patient o lymphocytes
susceptibility. Susceptibility depends on o plasma cells
the pH of saliva.  from b lymphocytes
 Basic - ↑ calculus  for chronic infection
- also seen in px who smoke
 Acid - ↑ caries *WHO probe + Purc 15
*H6/7 – universal scaler
CONNECTIVE TISSUE
Lamina Propria
 predominant tissue component of the gingiva
 major components of the connective tissue are
o collagen fibers (60%)  resilience
o fibroblasts ( 5%)  slow healing
o vessels and nerves within matrix ( 35%)
 matrix  environment for the cell
 PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.

Clinical parameters  oxytalan

Basic Periodontal Exam (BPE) score o numerous in PDL but has unknown
CPITN (Community Periodontal Index of Tx Needs) function
o parallel to long axis of tooth
Code 0 – healthy gingiva; no BOP,
no calculus / defective resto Type of Collagen
Code 1 – (+) BOP, plaque, pockets < / = to 3.5mm, I – oral cavity, bones
(-) calculus / defective resto IV – blood vessel
Code 2 – (-) BOP, calculus / defective resto,
pockets< 3.5mm Supra-alveolar crest fiber group
Code 3–(+) pocket within the color-coded area  circular fibers
> 3.5 – 5.5mm o free gingiva and encircle the tooth in a
Code 4 – (+) pocket color-coded area covered cuff- or ring-like fashion
> 5.5mm
Code * - furcation involvement: > 7mm CAL  dento-gingival fibers
o from cementum of the supra-alveolar
Posterior sextant portion of the root out into the free
4 3 1 /2 gingival tissue
7mm 5mm 3mm
7mm 3mm 4mm  dentoperiostealfibers
4 1 /2 3 o same portion of the cementum as the
dento-gingival fibers, but run their course
Fibers apically over the vestibular and lingual
 collagen fibers bone crest and terminate in the tissue of
o trihelix with covalent bond the attached gingival
o from amino acids via protein synthesis o gingival groove is often present
o amino acids
 glycine (1/3%)  trans-septal fibers
 hydroxyproline o extend between the supra-alveolar
 hydroxylycine cementum of approximating teeth. The
 cystein trans-septal fi ber run straight across the
 proline (1/2%) interdental septum and are embedded in
o amino acids the cementum of adjacent teeth.
procollagentropocollagenprotofibril
s collagen fibrils  collagen fibers Matrix of CT
o all fibers start from tropocollagen differ Ground substance
o
only in other amino acids  1 produced by fibroblasts
o
o glycosylation  binding of glycine to  2 by mast cells
carbohydrate (glucose)  Maintains normal fxn and integrity of CT
o produced by cementoblast and osteoblast  Organic  Protein polysaccharides proteoglycans
(PG) and glycoproteins
 elastic fibers  Proteoglycans
o only present in association with blood o Regulate diffusion and fluid flow
vessels. (ex. Lamina propria, submucosa of o Molecule filter
alveolar (lining) mucosa) o For cell migration
o not present in mucosa coronal to MGJ o Contain glycosaminoglycans
o leucine, isoleucine, analine, valine  Hyaluronansulphate, heparin
sulphate)
 reticular fiber  Glycoprotein
o numerous in tissue adjacent to basement o Predominates
membrane and loose CT surrounding o Fibronectin&osteonectin
blood vessels  Inorganic  Water molecules (hydrogen and
o present in epithelium CT and endothelium oxygen molecules)
CT interfaces

 Structure and hydration maintains gingival
resilience
 For transportation of water, electrolytes, nutrients
and metabolites
 Proteins act as rigid attachments between
basement membrane and connective tissues
 There are also protein molecules on the other side
of the basement membrane (epithelial side), in a
form of fibronectin on your connective tissue side
of the basement membrane. Laminin on epithelial
side of basement membrane.
 Hydroxylation process: synthesis of collagen
*swelling gingival – water with salt; saline / hypertonic
solution
*how long?
*abscess – more concentrated
*chicken soup for the soul
*why are they so about this? Inc resistance penicillin
Epithelial-mesenchymal interaction
 Connective tissue
- Determining factor for normal
development of tooth bud
 Enamel epithelia
- Exert a definite influence on the
development of the mesenchymal
components of the teeth
Experiments on monkeys:
- Tried to implant epithelium and connective tissue and
epithelium.
- They wanted to account for what influences
keratinization
- When you embed just epithelium underneath alveolar
mucosa (highly dense with BV), no keratinization will
happen
- When you embed connective tissue including the
basement membrane with keratinized tissue, it
proliferated with keratinized tissue
- The activity of keratinization is influenced as well by
the basement membrane of connective tissue
- When you transplant something externally internally,
include the connective tissue where you have the blood
vessels to create agenesis.
- Palate: Full bed of keratinized tissue and can transplant
anywhere in the mouth
**elastic fibers lack in gingival CT but numerous in
alveolar mucosa CT
**CT determines the quality of epithelium
PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.
PERIODONTAL LIGAMENTS
- Vascular
- Functions:
 to allow masticatory forces to be distributed to
and resorbed by alveolar process via alveolar
bone proper
 Allows functional/physiologic mobility
depending on width, height and quality of
periodontal ligaments.
 attachment
- cellular CT that surrounds root of teeth & joins root
cementum with the socket wall
- Coronally continuous with lamina propria of gingiva
and is demarcated from the gingiva by alveolar crest
fibers
- PDL space
 hourglass shape bet tooth roots and lamina
dura
 narrowest at midroot
 0.25mm (0.2-0.4mm)
- Alveolar bone  surrounds tooth from apex to a level
approximately 1mm apical to CEJ
Alveolar bones on radiogrpahs
1. Lamina dura – ABP
2. Trabecular bone – meshwork appearance
How does PDL fibers form?
- While the root is developing, PDL is also developing
- Continuation of the lamina propria of the connective
tissue of the gingiva going apically as the root develops
(influenced by Hertwig’s Epithelial Root Sheath)
- Collagen fibers from the cementum and the alveolar
bone will meet at the periodontal space. The fibers in
the cementum and alveolar bone proper are called
sharpey’s fibers. The fibers that extend until periodontal
ligament space that interconnect form the PDL fibers.
- Whatever embedding of fibers in the cementum area
are called Sharpey’s fibers. Same embedding of fibers in
the ABP, what you call cribiform plate of
bone/periosteum/bundle bones, that is what forms the
actual attachment of ATTACHMENT APPARATUS
 Cementum side  smaller in diameter, more
numerous, less elastic
 Alveolar bone side  more vascular, thinner,
more elastic, as it matures, you can get better
quality fibers. (STURDIER)

Cellsof PDL:
 Osteoblast
- Lines the bone surface
 Fibroblast
- Aligned along principal fibers
 Cementoblast
- Lines the surface of cementum
- Middle third to apical third of root
 Osteoclast
 Epithelial cells
- Contain few mitochondria with poorly
developed ER
- Means they are vital but resting
 Nerve fibers
 Cementocytes
- Coronal third of root
*no such thing as cementoclast
- Cementum is mineralized and creates fibers through
cementoblasts and cementocytes.
- Fibroblasts are contained in CT
- Capacity to regenerate contains within the periodontal
ligament space
st nd
- 1 and 2 degree = Horizontal movements
- When you chew = Oblique Fibers
- Vertical movements = Apical and horizontal fibers
- If horizontal attachment is lost = Periodontal disease
- If apical attachment is lost = Endodontics
- Epithelial cell rest of malassez remnants of HERS
CLINICAL
- Horizontal severance -> Scale or root planing
- When you remove attritions, you are cutting fibers,
removing tartar or even the layers of cementum
- When you remove tartar, calcular deposits, there will
always be spaces (sulcus etc)
- If there is bleeding, the calcular deposit took the place
of the C.T.
- When you scale 3-4 mm, you’re already on C.T., you
scale off cementum -> Hypersensitivity
- Thickness in terms of mineralization in cementum:
- Coronal side: Cementocyte -> MATURE
( If you scale this, it’s hard to regenerate)
* When you scale, you are just removing degree of
roughness
- Long term calcular deposit = Darker pigmentation
- Reattachment : Junctional epithelium and C.T.
- It can be attached just because you ha ve PDL space
(fibroblasts abound)
- 1 week after you scale, epithelium will repopulate
PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.
-DO NOT PROBE 1 WEEK AFTER SCALING BECAUSE
YOU’RE DISTURBING THE JUNCTIONAL EPITHELIAL
ATTACHMENT AND KNOWN AS LONG JUNCTIONAL
EPITHELIUM
- When you’re scaling, you’re just reattaching via
EPITHELIUM. Do not destroy!
*dental follicle > attachment apparatus
*HERS lays down cementum and dentin > root
formation
*development of fibers comes from both sides : ABP and
cementum
*upon fxnal occlusion after eruption, PLS form and
strengthen into fiber bundles
*continuous deposition of cementum throughout life
>middle third to apical third of root
*scale it off and its gone forever (coronal thirdof root
bec cells are matured there)
* tissue does not attach to calculus that is why there is
pocket formation > remove all calculus, it is possible to
burnish
*importance of probing > to know until how deep you
will scale (3mm)
*why hourglass shape? PDL space just measures a
quarter of --? so when you have your tooth, then you
have your hourglass shape where PDLs are contained
*when youre scaling, follow root contours (oral ana)
3 FORMS OF CEMENTUM
1. Acellular extrinsic fiber cementum (AEFC)
- Predominantly at coronal
* collagen is derived as sharpey’s fibers
from the PDL
*covers cervical 2/3rds of root
2. Cellular extrinsic mixed stratified (CEMS)
- Middle
* collagen fibers are derived from both
extrinsic from PDL) and intrinsic fibers
(from cemebtoblasts)
3. Cellular intrinsic fiber cementum (CIFC)
- Cementoblasts at apical
* absence of sharpey’s fibers mean
intrinsic fiber cementum has no role in
tooth attachment
*layer ring of collagen fiber bundle is the same pattern with
any CT

 width of keratinized gingiva
o thicker / higher on labial / buccal side (1-9mm)
o thinner on lingual (1-8mm)
 anything with more keratinized tissue > thick biotype
> deeper vestibule or mucobuccal fold
 anything with more alveolar mucosa > thin biotype >
shallower vestibule or mucobuccal fold
 importance: you can imagine the amount of bone
underneath
 mineralized bone is termed lamellar bone
 **read the book**
1. Alveolar bone proper / cribriform plate / bundle bone
- Walls lining alveolus
- Seen when you extract the tooth
2. Spongy bone
- Vascularity
3. Cortical plate
- Highly mineralized
 cribriform plate – higly vasularized; Volkmann’s canal
>> blood vessels
 once you lose bundle bone, that is the stat of losing
vertical dimension of bone
 total breakage of cribriform all the way to cortical >>
big dehiscene (so hard to replace)
 how will you apply compression after extraction?
Never buccolingually >> collapse
 dehiscence – denuded of bone
 fenestration – window of denudation
1. Class 1
- wide or narrow but not has reached MGJ
2. Class 2
- same width and narrowness with Class 1 but has
crossed MGJ
3. Class 3
- raised bone with dehiscence and has crossed MGJ
4. Class 4
- purely horizontal bone loss or even vertical bone loss
and has reached or just above MGJ
Lateral position / Pedicle flap
- 67% mean defect coverage
**it is not always need to be a scalloped incision
**CT influences keratinization
Guided tissue regeneration
- 72% mean defect coverage (bio absorbable)
- 73% (non resorbable)
Connective tissue graft (CTG)
- 84% mean defect coverage; highly predi ctable
PERIODONTOLOGY | PRELIMS
DEA 16-17 | HARA, MARIKO D.
 Crestal height distance is always 1-2mm
1-2 = Biologic Width (JE and CT)
 paralleling technique – 1:1 ratio then you can
measure crestal height distance
Alveolar crest resorption
- In the absence of disease, alveolar bone levels follow
a line parallel to the CEJ 1-2mm apical (Orban 1953)
- Reduction in crestal height with age at 0.017mm/yr –
statistically significant, clinically insignificant (Boyle
1973)
- Greater resorption on bu than li (Massler et al 1967)
- 30% loss in first 4-5 yrs post extraction on disuse and
50% on denture use (Roberts 1970)
- Implant therapy greatly reduces resorption distal to
fixtures compared to complete denture use
Detecting crestal resorption
- Conventional radiographs inaccurate for diagnosing
crestal loss (Hausmann JP 90 3-3)
- Most accurate: subtraction radiography thru digital
radiography reducing 90% radiation exposure
(Jeffcoat JP 92 3-4)
- Problems with conventional radiography: bone loss
undetected until 30-50% of mineral lost,
foreshortening / elongation, processing, exposure
variations, 2 dimensional
**this will come out, read the book**
Healing after extraction
- On the day itself / 24 hrs
- 48 hrs
- 96 hrs
- 7 days
- 21 days after extraction
- 6 weeks after extraction
Blood supply of the periodontium
1. Periodontal
2. Alveolar
3. Supraperiosteal / mucogingival
A. Post-capillary venous plexous
B. Sup-epithelial capillary loops
**osmotic pressure
**innervation
**pressure receptors at apical area
Summary coordinated fxns of the periodontium
Turnover
Adaptation
Defense
Healing
Homeostasis