 Redness and sponginess of gingival tissue

 Bleeding on provocation
 Changes in contour
 Presence of calculus or plaque with no
radiographic evidence of crestal bone loss
 Acute

 Recurrent

 Chronic
 Localised gingivitis
 Generalised gingivitis
 Marginal gingivitis
 Papillary gingivitis
 Diffuse gingivitis
 Color
 Contour
 Consistency
 Position
 Ease and severity of bleeding
 Size
 Surface texture
 Two earliest symptoms of gingival inflammation
preceding established gingivitis –

(1) Increased gingival crevicular fluid production rate

(2) Bleeding from the gingival sulcus on gentle probing

Chronic and Recurrent Bleeding
 Most common cause of abnormal gingival bleeding on
probing is chronic inflammation
 Bleeding is chronic or recurrent and is provoked by
mechanical trauma (e.g., from
tooth brushing, toothpicks, or food impaction) or by
biting into solid foods such as apples
 The severity of the bleeding and the ease with
which it is provoked depend on the intensity of
the inflammation
 In cases of moderate or advanced periodontitis,
the presence of bleeding on probing is considered
a sign of active tissue destruction
 Caused by injury (aggressive tooth brushing or
by sharp pieces of hard food) or occur
spontaneously in acute gingival disease

 Gingival burns from hot foods or chemicals

increase the ease of gingival bleeding
 Dilation and engorgement of capillaries

 Thinning or ulceration of sulcular epithelium

Hemorrhagic disorders
 Vascular abnormalities- vitamin C deficiency or allergy such as Schonlein-
Henoch purpura

 Platelet disorders – thrombocytopenic purpura), hypoprothrombinemia

(vitamin K deficiency)

 Coagulation defects (hemophilia, leukemia, Christmas disease)

 Deficient platelet thromboplastic factor (PF3) resulting from uremia, multiple

myeloma, and postrubella purpura

 Drugs such as salicylates and anticoagulants such as dicumarol and heparin

 HRT
 Oral contraceptives
 Pregnancy
 Menstrual cycle
 Fluctuating estrogen/Progesterone levels
 Diabetes
 Drugs- Anticonvulsants, Calcium channel blockers,
Immunosuppressant drugs cause bleeding
secondarily to enlargement
Chronic Gingivitis
 Chronic inflammation intensifies the red or
bluish red color, because of vascular
proliferation and reduction of keratinization due
to epithelial compression by the inflamed tissue

 Venous stasis will contribute a bluish hue

 The color changes may be marginal, diffuse, or
patch like depending on the underlying acute
condition
 It is patch like or diffuse
 Color changes vary with the intensity of the
inflammation

 Initially, there is an increasingly red erythema. If the

condition does not worsen, this is the only color
change until the gingiva reverts to normal

 In severe acute inflammation, the red color gradually

becomes a dull, whitish gray

 The gray discoloration produced by tissue necrosis is

demarcated from the adjacent gingiva by a thin,
sharply defined erythematous zone
 Heavy metals (bismuth, arsenic, mercury, lead,
silver) absorbed systemically from therapeutic
use or occupational or household environments
 Typically, they produce a black or bluish line in the
gingiva that follows the contour of the margin

 The pigmentation may also appear as isolated

 black blotches involving the interdental marginal and

attached gingiva

 This is different from tattooing produced by the

accidental embedding of amalgam or other metal
fragments
 Gingival pigmentation from systemically
absorbed metals results from perivascular
precipitation of metallic sulfides in the
subepithelial connective tissue

 It occurs only in areas of inflammation, where

the increased permeability of irritated blood
vessels permits seepage of the metal into the
surrounding tissue
 In addition to inflamed gingiva, mucosal areas
irritated by biting or abnormal chewing habits
(e.g., the inner surface of the lips, the cheek at the
level of the occlusal line, and the lateral border of
the tongue) are common pigmentation sites
Endogenous oral pigmentations -
melanin, bilirubin, or iron
Diseases that increase melanin pigmentation-
 Addison's disease
 Peutz-jeghers syndrome
 Albright's syndrome (polyostotic fibrous dysplasia)
 Von Recklinghausen's disease
 Skin and mucous membranes can also be stained by bile pigments.
Jaundice is best detected by examination of the sclera, but the oral
mucosa may also acquire a yellowish color

 The deposition of iron in hemochromatosis may produce a blue-

gray pigmentation of the oral mucosa

 Several endocrine and metabolic disturbances, including diabetes

and pregnancy, may result in color changes

 Blood dyscrasias such as anemia, polycythemia, and leukemia may

also induce color changes
 Exogenous factors -atmospheric irritants such as coal
and metal dust and coloring agents in food or lozenges

 Tobacco - hyperkeratosis of the gingiva and increase in

melanin pigmentation of the oral mucosa

 Amalgam implanted in mucosa - Localized bluish

black areas of pigment
 Chronic Gingivitis
Clinical Changes
1. Soggy puffiness that pits on
pressure
2. Marked softness and friability,
with ready fragmentation on
exploration with probe and
pinpoint surface areas redness
and desquamation
3. Firm, leathery consistency
Underlying Microscopic Features
1. Infiltration by fluid and cells of inflammatory
exudate
2. Degeneration of connective tissue and
epithelium associated with injurious substances that
provoke the inflammation and inflammatory
exudate; change in connective tissue-epithelium
relationship, with the inflamed, engorged connective
tissue expanding to within a few epithelial cells of
surface; thinning of epithelium and degeneration
associated with edema and leukocytic invasion,
separated by areas in which rete pegs are elongated
to connective tissue
3. Fibrosis and epithelial proliferation associated with
longstanding chronic inflammation
 Acute Gingivitis
1. Diffuse puffiness and 1. Diffuse edema of acute
inflammatory origin; fatty
softening infiltration in xanthomatosis

2. Necrosis with formation of a

2. Sloughing with grayish,
flake-like particles of
debris adhering to
eroded surface
pseudomembrane composed of
bacteria, PMNs, and
degenerated epithelial cells in a
fibrinous meshwork

3. Vesicle formation 3. Inter- and intracellular edema

with degeneration of nucleus
and cytoplasm and rupture of
cell wall
 Can occur alone or in groups and vary in size, location, shape,
and structure
 May be calcified material removed from the tooth and
traumatically displaced into the gingiva during scaling, root
remnants, cementum fragments, or cementicles
 Chronic inflammation and fibrosis and occasionally foreign
body giant cell activity occur in relation to these masses
 They are sometimes enclosed in an osteoid-like matrix
 Crystalline foreign bodies have also been described in the
gingiva, but their origin has not been determined
 Promotes keratinization of oral epithelium

 Enhances gingival circulation

 Thickens alveolar bone

 Increases proliferative activity of junctional basal

cells- increases turnover rate and desquamation
of JE
 Loss of surface stippling -early sign of gingivitis

 In chronic inflammation the surface is either smooth

and shiny or firm and nodular, depending on whether
the dominant changes are exudative or fibrotic

 Smooth surface texture is also produced by epithelial

atrophy in atrophic gingivitis

 Peeling of the surface occurs in chronic desquamative

gingivitis

 Hyperkeratosis results in a leathery texture

 Drug-induced gingival overgrowth produces a nodular

surface
 Chemical injuries – Aspirin, hydrogen peroxide,
silver nitrate, phenol and endodontic materials
 Physical injuries – Lip, oral and tongue piercing
 Thermal injuries – Hot drinks and foods
 Recession is exposure of
the root surface by an
apical shift in the position
of the gingiva
 Physiologic process related to aging
 Faulty toothbrushing technique (gingival
abrasion)
 Tooth malposition
 Friction from soft tissues (gingival ablation)
 Gingival inflammation
 Abnormal frenum attachment
 Trauma from occlusion
 Orthodontic movement
Susceptibility to recession-

 Position of teeth in the arch

 Root-bone angle
 Mesiodistal curvature of the tooth surface
 Exposed root surface – Caries, hyperemia of pulp
 Abrasion / erosion of cementum – Sensitive
dentine
 Interproximal recession – Oral hygiene problems
plaque accumulation
 Gingival enlargement

 Stillman’s clefts

 McCall festoons