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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