Characteristic feature
1976 : Page & Schroeder
Clinical condition Histopathologic condition
Pristine gingiva Histologic perfection
Normal health gingiva Initial lesion of Page & Schroeder
Early gingiva Early lesion of Page & Schroeder
Established gingiva Established lesion with no bone loss
nor apical epithelial migration (plasma
cell density between 10% and 30% of
leukocyte infiltrate.)
Periodontitis Established lesion with bone loss and
apical epithelial migration from the
cementoenamel junction (plasma cell
> 50%)
The character and intensity of the host response will determine whether this lesion
will resolve rapidly or evolve into the chronic inflammatory lesion. If this occurs then
there will be an infiltrate of macrophages and lymphoid cells
Occurs within the first 24 hours.
These changes occur in reponse
to microbial activation to
bacterial plaque
No tissue damage.
Subclinical gingivitis
Light Micrograph of connective tissue in Gingivitis
vasodilatation, edema, and migration of Leukocytes.
Microscopically
Peripheral vessels allow rapid movement of blood
from the arterioles through the capillaries to the
venules.
( blood vessels) Hydrostatic pressure increases. Dilation of capillaries , venules and arteries.
Polymorphonuclear leukocytes (P.M.N.s) are the
characteristic dominant inflammatory cells
Adhesion molecules: ICAM -1 , ELAM-1 inc.
Changes in the cells: Margination , emigration &
Diapedesis.
Changes in GCF
Classic vasculitis of vessels subjacent to the
junctional epithelium.
Exudation of fluid from the gingival sulcus .
Increased migration of the leukocytes into the
junctional epithelium and gingival sulcus .
Presence of serum proteins,, especially fibrin
extravascularly.
Alterations of the most coronal portions of the
junctional epithelium.
Loss of perivascular collagen.
Features of the initial lesion
After approximately after 1 week.
All the changes seen in the initial lesion
continue to intensifywith the early lesion.
There is opening up of previously inactive
capillary beds
Lymphocytes and the neutrophils and also few plasma cells.
Amount of collagen destruction increases.
Leukocytic infilteration.
Inflammatory cell population (15%).
Dentogingival Fibers – most affected .
There is bleeding from the gingival sulcus
with probing, brushing or mastication. This
is a result of epithelial ulceration in the
gingival sulcus and acute inflammation of
the connective tissue.
• Clinical Signs Of Inflammation Appear-
erythema
• Proliferationof Capillaries
• Increased Formation Of Capilloary Loops
B/W Rete Pegs Or Ridges
• Gcf And Transmigratory Leukocytes
Reach Max
.
• Threefold increase in size of fibroblast with cytologic alteration
• T cells are the dominant Lymphocytes, but eventually B cells
dominate. T cells have dense round nuclei with very little
cytoplasm . B cells (plasma cells) are larger than T lymphocytes
and have an eccentric lighter staining nucleus with an almost
equal sized cytoplasm
Accentuation of the features described for the initial lesion.
Accumulation of lymphoid cells immediately subjacent to the J.E. at the site of acute
inflammation.
Cytoplasmic alterations in resident fibroblasts, possibly associated with interactions
with lymphoid cells.
Further loss of the collagen fiber network supporting the marginal gingiva.
Proliferation of the basal cells of the junctional epithelium.
Features of the Early lesion
Cell type
Inverse relation exists between the no. of intact collagen bundles and the number of inflammatory cells
Enzyme histochemistry
With chronic inflammation gingival
blood vessels and inflammatory
cells proliferate into the areas of
destroyed connective tissue.
Established Gingivitis around lower
incisors.
Acute inflammatory changes are superimposed on chronic inflammation charges
Junctional epithelium; Basal lamina, in the CT
Features of the established lesion
Persistence of the manifestations of acute
inflammation.
Predominance of plasma cells but without
appreciable bone loss.
Presence of immunoglobulins
extravascularly in the CT and in the junctional
epithelium.
Continuing loss of CT substance noted in
the early lesion.
Proliferation, apical migration, and lateral
extension of the junctional epithelium: early
pocket formation may or may not be present .
• BLOOD VESSELS BECOME
ENGORGED AND CONGESTED
• VENOUS RETURN IMPAIRED
• BLOOD FLOW BECOMES SLUGGISH
• RESULTING IN TISSUE ANOXEMIA
• -BLUISH HUE ON REDDENED GINGIVA
STAGE IV GINGIVITIS: The advanced lesion
Phase of periodontal breakdown.
Persistence of features for the established lesion.
Extension of the lesion into alveolar bone and PDL with significant
bone loss.
Continued loss of collagen subjacent to the pocket epithelium with
fibrosis at more distant sites.
Formation of periodontal pockets.
Periods of quiescence and excerbation
Conversion of the bone marrow distant from the lesion into fibrous
CT.
Widespread manifestation of inflammatory and immunpathologic
tissue reactions.
STAGE TIME
(Days)
BLOOD VESSELS JUNCTIONAL
&SULCULAR
EPITHELIUM
PREDOMINANT
IMMUNE CELLS
COLLAGEN CLINICAL
FINDINGS
i)Initial lesion 2-4 Vascular dilation,
Vasculitis
Infilteration by
PMN
PMN’s Peri-
vascular loss
Gingival
fluid flow
ii)Early lesion 4-7 Vascular
proliferation
Same as stage
I , rete pegs,
Atrophic areas
Lymphocytes Increased
loss around
infilterate
Erythema,
bleeding on
probing
iii)Established
lesion
14-21 Same as stage II
plus venous stasis
Same as stage
II but more
advanced
Plasma cells Continued
loss
Changes in
the color,
size and
texture.
The initial and the early stages reflect the histopathology of the
Clinically early stages of the gingivitis.
The established lesion reflect the histopathology of
“Chronic” gingivitis.
The advanced lesion reflects the progression of
Gingivitis to periodontitis.
CHARACTERISTICS COMMON TO ALL
GINGIVAL DISEASES
(From Mariotti 1999)
The term “clinically normal” or “clinically healthy” may be used to
designate gingival tissue that is a shade of pale or coral pink varied
by complexion and pigmentation; has a knife edge gingival margin
that adapts closely to the tooth surface, is stippled, firm and has
minimal sulcus depth with no bleeding on probing. Although
“normal” varies with anatomic, physiologic & other general
characteristic form .
Color
Size
Contour &shape
Consistency
Surface texture
Position
Ease of Bleeding
With vasodilatation in Gingivitis
terminal circulation is more convoluted
so gingiva appears red and often has a
purplish color
Vasodilatation results in more complex pathways of
blood flow so that circulation is slowed through
gingival tissues
COLOR
vascularization increases
the degree of epithelial keratinization is reduced or disappears.
the vascularization is reduced
epithelial keratinization increases.
Color changes in chronic inflammation
Color changes in acute inflammation
“Traumatic Crescents”:
Color changes due to metallic pigmentation
Color changes due to systemic factors
It’s the sum total of the bulk of cellular and intercellular elements and their
vascular supply. It’s a common appearance of gingival disease
Depends on
Shape of teeth and
alignment in the arch.
Location and size of the area
of proximal contact
Dimensions of the facial
and Lingual gingival
embrasures
Indentations in the gingival margins are known as:
Stillman’s cleft
McCall Festoons
OF THE INTERDENTAL GINGIVA IS RELATED
WITH THE CONTOUR OF THE PROXIMAL TOOTH
.
THE HEIGHT OF THE PAPILLA VARIES WITH
THE LOCATION OF THE PROXIMAL CONTACT.
IS FIRM AND RESILIENT
Clinical changes Underlying Microscopic changes
Acute form of gingivitis
1) Diffuse puffiness and softening.
2) Sloughing with grayish, flakelike
particles of debris adhering to the
eroded surface.
3) Vesicle formation.
1) Diffuse edema of acute inflammatory
origin, fatty infilteration in
xanthomatosis.
2) Necrosis with formation of
pseudomembrane composed of
bacteria, PMN, and degenerated
epithelial cells in fibrinous meshwork.
3) Intercellular and intracellular edema
with degeneration of nucleus and
cytoplasm and rupture of cell wall.
Clinical changes Underlying Microscopic changes
Chronic gingivitis
1) Soggy, puffiness that pits on pressure.
2) Marked softness and friability, with ready
fragmentation on exploration withprobe and
pinpoint surface areas of redness and
desquamation.
3) Firm, leathery consistency
1) Infiltration by fluid and cells of inflammatory
exudates.
2) Degeneration of connective tissue and
epithelium associated with injurious
substances that provoke the inflammation and
inflammatory exudates; changes in the
connective tissue-epithelium relationship, with
inflamed, engorged connective tissue
expanding to within a few epithelial cells of
surface, thinning of the epithelial and
degeneration associated with edema and
leukocytic invasion, separated by areas in
which the rete pegs are elongated to CT.
3) Fibrosis and epithelial proliferation associated
with long- standing chronic inflammation.
The attached gingiva is stippled
The marginal gingiva is not stippled
Produced by rete pegs
Stippling is a feature of healthy gingiva
The gingival surface may be:
Firm and nodular(depending on whether the
dominant surface is exudative and fibrotic. In
drug induced gingival enlargement a nodular
surface is seen.)
Smooth (produced by epithelial atrophy as in
atrophic gingivitis)
Leathery ( due to hyperkeratosis).
Minutely nodular surface seen in noninflammatory
gingival hyperplasia.
Level of the gingival margin
Actual
Apparent
Faulty toothbrushingOrthodontic tooth
movement Abnormal frenal
attachment .
Iatrogenic dentistry. Deep overbite Root bone angle
position of the teeth in the arch.
Pressure from mastication or
moderate toothbrushing.
Changes in the position of gingiva is also seen in cases of gingival enlargement.
Exposed root surface are susceptible to caries. Underlying dentinal surface – hypersensitive .
IP – plaque accumalation. Hyperemia of the pulp.
GINGIVAL BLEEDING
Plaque and calculus
Anatomic and developmental tooth variations
Frenum pullIatrogenic
factors
Malpositionedteeth
Mouth breathing
Overhangs Partial dentures
Lack of attached ginigiva
Recession
Local Factors
Systemic factors:
• Vascular abnormalities- Vitamin C def., Allergy like Schonlein- Henoch
purpura
• Platelet disorders- Thrombocytopenic purpura
• Hypoprothrombinemia- Vit K deficiency.
• Other coagulation defects- Haemophilia, leukemia, Christmas disease.
• Deficient thromboplastic factor (PF3) resulting from uremia, multiple
myeloma and post rubella purpura.
• Harmonal replacement therapy.
• Oral contraceptives
• Pregnancy & menstrual cycle.
• Endocrine conditions – diabetes.
• Medications – anticonvulsants, antihypersensitive calcium channel blockers
& asprin.
Histopathological alterations
These include dilation and engorgement of capillaries and thinning or ulcerations of the sulcular
epithelium.
The capillaries are engorged and closer to the epithelial surface, and the thinned, degenerated
epithelium is less protective, that are normally innocuous cause rupture of the capillaries and
gingival bleeding.
The intensity of bleeding is dependant on the intensity of inflammation.
After the vessels are damaged and
ruptured, interrelated mechanisms induce
haemostatic.
Blood platelets adhere to the edges of the tissues
and a fibrous clot is formed.
The vessel wall contract and the blood flow is
diminished.
This contracts and results in the
approximation of the edges of the injured area.
Bleeding can recur when the area is irritated
Color
Pale pink (melanin pigmentation
common in certain groups)
Reddish/ bluish red
Size
Papillary gingival fills interdental
spaces; marginal gingiva forms
knife edge with tooth surface ;
sulcus depth < 3mm.
Swelling both coronally and
bucco/lingually; false pocket
formation.
Contour & Shape
Scalloped –troughs in marginal
areas rise to peaks in interdental
areas.
Edema which blunts the marginal
and papillary tissues leads to loss
of knife edge adaptation. Marginal
swelling leads to less accentuated
scalloping.
Consistency
Firm & resilient Soft; pressure induced pitting due
to edema.
Tendency to bleed No bleeding to normal probing Bleeding on probing.
COMMON CLINICAL CHANGES FROM HEALTH TO GINGIVITIS
CHARACTERISTIC CLINICAL FEATURES OF GINGIVA IN CERTAIN
ORAL AND SYSTEMIC CONDITIONS
In certain acute gingival infections:
i) ANUG
•Surface: covered with white pseudomembranous slough demarcated from the remainder of
the gingival mucosa by a pronounced linear gingival erythema
•Color: Red, shiny and haemorrhagic
•Bleeding on probing: Spontaneous bleeding on probing or after slight stimulation.
•Contour: punched out, crater like depressions at the crest of the interdental papillae.
ii) Primary Herpetic gingivostomatitis
•Color: Diffuse erythematous, shiny discoloration
•Consistency: edematous.
•Surface: Has vesicular eruptions
•Bleeding on probing
Menopausal Gingivostomatitis (SENILE ATROPHIC GINGIVITIS):
•The gingival and remaining oral mucosa are dry and shiny.
•Vary in color from abnormal pale to red
•Bleeds easily.
•Extreme sensitivity to thermal changes.
Vit. C deficiency:
•Edematous with a smooth shiny surface and spontaneous haemorrhage.
• Surface may exhibit necrosis and pseudomembrane formation are common features.
Plasma Cell Gingvitis:
•Gingiva appears red, friable
•Bleeds easily.
• May be associated with gingival enlargement.
Leukemia:
•Colour: Bluish red
•Surface texture: Shiny
•Consistency: Moderately firm.
•Bleeding on probing: Either slightly or on slight provocation.
•Position –May be associated with diffuse or marginal enlargement.
Granulomatous Diseases:
•Colour: Reddish purple
•Bleeding on probing: Bleeds easily on stimulation.
•Position: May be enlarged.
IN SOME PATIENTS THE BASAL LAYER OF THE
GINGIVA CONTAINS MELANOCYTES--PIGMENT
CONTAINING CELLS WHICH GIVE A BROWNISH
HUE TO PORTIONS OF THE GINGIVA.
THERE ARE ALSO A FEW CELLS IN THE
CONNECTIVE TISSUE WHICH HAVE TAKEN UP
MELANIN GRANULES -- MELANOPHORES.
Diffuse macular pigmentation of the gingiva in a patient with
Addison’s disease. Pigmented lesions were also present on the
buccal and labial mucosa In contrast to the situation for
physiologic pigmentation the marginal gingiva is involved in
this case.
Heavy pigmentation of the attached gingiva in the region of
the right lower canine in a smoker. The cigarette was
usually held on the right side.
Amalgam tattoo on the right maxillary ridge at an extraction
site. The extracted tooth had a large amalgam filling. The
lesion was asymptomatic. A periapical radiograph failed to
show amalgam particles, and a biopsy was performed
A well-demarcated, smooth, dome-shaped, dark brown
lesion on the right buccal mucosa with an unpigmented halo at the
base. No other pigmented lesions were observed on the oral mucosa.
Biopsy revealed a compound nevus
Photograph taken 1 week after extraction of a loose left
maxillary molar shows an irregular greyish black patch on the
maxillary alveolar ridge, distal and buccal to the extraction socket of
the molar. Smaller satellite lesions were present on the palatal
Mucosa. Showing malignant melanocytes
Which fibers groups are mainly effected in stage II early lesion of
gingivitis?
a) Principle group of fibers
b) Circular group of fibers
c) Dentogingival group of fibers
d) Both b and c
In which stage of gingivitis bleeding on probing is found?
a) Stage I
b) Stage II
c) Both of the above
d) None of the above
In which stage of gingivitis Plasma cells predominate?
a) Stage I
b) Stage II
c) Stage III
d) None of the above
In gingivitis early lesion evolves from the initial lesion with in?
a) 2days
b) 7days
c) 14days
d) 21days
Bluish red gingiva is observed in which stage of gingivitis?
a) Stage I
b) Stage II
c) Stage III
d) Stage IV
Diffuse gingivitis effects the
a) Marginal gingiva
b) Attached gingiva
c) Interdental papilla
d) All of the above
Stillman’s clefts are gingival changes related to?
a) Texture
b) Consistency
c) Contour
d) Position
Smooth surfaced texture is observed in?
a) Desquamative gingivitis
b) Atrophic gingivitis
c) Hyperkeratosis
d) Fibrotic gingiva
`
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