STAGES OF GINGIVITIS AND CLINICAL

FEATURES OF GINGIVITIS

Dr. Mazood Ahamad

 GINGIVITIS
 INFLAMMATION OF GINGIVA OR GINGIVAL SOFTTISSUE

 A reversible & mildest form of periodontal disease

 Pathologic changes with gingivitis are associated with the presence of

oral microorganisms in the sulcus.

 These organisms are capable of synthesizing products that cause damage

to the epithelial and connective tissue cells as well as intercellular
components such as collagen, ground substance and glycocalyx (e.g.,
collagenase, hyaluronidase, protease, chondroitin sulfatase, or
endotoxin),
 The resultant widening of the spaces between the junctional epithelial
cells during early gingivitis may permit injurious agents derived from
bacteria or bacteria themselves, to gain access to the connective tissue.
 ETIOLOGY
 Dental plaque
 Systemic factors
 Drug induced
 Malnutrition
 Bacterial origin
 Viral origin
 Fungal origin
 Genetic origin
STAGES OF GINGIVITIS

 The sequence of events cumulating in clinically apparent

gingivitis is categorized into:
I) INITIAL STAGE
II) EARLY STAGE
III) ESTABLISHED STAGE
IV) ADVANCED STAGE
 STAGE I GINGIVITIS: THE INITIAL LESION

 SUBCLINICAL GINGIVITIS

 The first manifestations of gingival inflammation are vascular changes

consisting of dilation of capillaries and increased blood flow.

 These initial inflammatory changes occur in response to microbial

activation of resident leukocytes and the subsequent stimulation of
endothelial cells.

 Microscopically, some classic features of acute inflammation can be seen in the

connective tissue beneath the junctional epithelium.
 Changes in blood vessel morphologic features occur within 1 week and
sometimes as early as 2 days after plaque has been allowed to accumulate .

 Predominant Immune Cells POLYMORPHONUCLEAR

NEUTROPHILS (PMNs)

 Clinically, increase GCF

 Stage II Gingivitis: The Early Lesion
 The early lesion evolves from the initial lesion within about
1 week after the beginning of plaque accumulation.
 clinical signs of erythema may appear, mainly because of the
proliferation of capillaries and increased formation of capillary loops
between rete pegs .
 Bleeding on probing may present
 Predominant Immune Cells (lymphocytes 75%, with the
majority T cells)
 70% of the collagen is destroyed
 The main fiber groups affected appear to be the circular and
dentogingival fiber
 STAGE III GINGIVITIS:THE ESTABLISHED LESION

 In chronic gingivitis (stage III), which occures 2 to 3 weeks after the

beginning of plaque accumulation ,the blood vessels become engorged
and congested, venous return is impaired, and the blood flow
becomes sluggish.
 The result is localized gingival anoxemia, which superimposes a somewhat
bluish hue on the reddened gingiva.
 Clinically estimated as moderate to severely inflamed gingiva
 In histological sections, an intense, chronic inflammatory reaction is
observed.
 A key feature that differentiates the established lesion is the increase in the
number of plasma cells,.
STAGE IV GINGIVITIS: THE ADVANCED LESION

 Extension of the lesion into alveolar bone characterizes a

fourth stage known as the advanced lesion" or phase o f
periodontal breakdown.“
 Microscopically, there is fibrosis of the gingiva andwidespread
manifestations of inflammatory and immunopathologic tissue
damage
 Plasma cell presence dominates connective tissue and
neutrophils continue dominating the junctional epithelium

 Gingivitis will progress to periodontitis only in

individuals who are susceptible
 CLINICAL FEATURES OF GINGIVITIS
 Classification according to COURSE and DISTRIBUTION :
1. ACUTE GINGIVITIS.
2. RECURRENT GINGIVITIS.
3. CHRONIC GINGIVITIS.

1. ACUTE GINGIVITIS :
• It is of sudden onset and short duration and can be painful.
• A less severe form of acute condition is called SUBACUTE.
2. RECURRENT GINGIVITIS :
• Reappears after eliminated by treatment or disappearing
spontaneously.
3. CHRONIC GINGIVITIS :
• Slow in onset and of long duration, and is painless, inflammation
persists or resolves and normal areas become inflammed.
Classification According to DISTRIBUTION :

A) LOCALIZED GINGIVITIS :
 is confined to the gingiva of a single tooth or group of teeth,

1. LOCALIZED MARGINAL GINGIVITIS :

 Confined to one or more areas of the marginal gingiva.
2. LOCALIZED DIFFUSE GINGIVITIS :
 Extends from margin to the mucobuccal fold but is limited in
area
3 LOCALIZED PAPILLARY GINGIVITIS :
 Confined to one or more interdental spaces in a limited area.
GENERALIZED GINGIVITIS :
1. GENERALIZED MARGINAL GINGIVITIS :
 Involves gingival margins in relation to all teeth.
 The interdental papillae are usually affected in generalized
marginal gingivitis.

2. GENERALIZED DIFFUSE GINGIVITIS :

 Involves the entire gingiva.
 The alveolar mucosa and attached gingiva are affected.
 May be caused by systemic conditions.
LOCALIZED PAPILLARY GINGIVITIS GENERALIZED MARGINAL AND PAPILLARY
GINGIVITIS.

GENERALIZED DIFFUSE GINGIVITIS INVOLVES

LOCALIZED, DIFFUSE GINGIVITIS THE MARGINAL, PAPILLARY,AND ATTACHED
GINGIVAE.
CLINICAL FINDINGS :
 A systemic clinical approach requires an orderly examination of
the gingiva for color, contour, consistency, position,
ease and severity of bleeding, and pain.
GINGIVAL BLEEDING ON PROBING :
1. The two earlier symptoms of gingival inflammation preceding
established gingivitis are :
a. Increased gingival crevicular fluid production rate.
b. Bleeding from the gingival sulcus on gentle probing.
2) Gingival bleeding varies in severity, duration and the ease with
which it is provoked. Bleeding on probing is easily detectable
clinically and is of value for the early diagnosis and prevention
of more advanced gingivitis.
3) Appears earlier than a change in color or other visual signs of
inflammation.
Bleeding on probing, a probe has Bleeding appears after a few second
been introduced to the bottom of the
gingival sulcus.

GENERALISED BLEEDING
GINGIVAL BLEEDING CAUSED BY LOCAL FACTORS :
1. Chronic and recurrent bleeding .
2. Acute bleeding.

1. CHRONIC AND RECURRENT BLEEDING :

a) The most common cause of abnormal gingival bleeding on probing is
chronic inflammation.
b) The bleeding is provoked by mechanical trauma ( e.g. from tooth
brushing, tooth pick, or food impaction ) or by biting into solid foods such
as apples.
c) Sites that bleed on probing have a greater area of inflamed connective tissue
than those sites that do not bleed.
d) The severity of bleeding and the ease with which it is provoked depend on
the intensity of the inflammation.
 HISTOPATHOLOGIC CHANGES :
1. Dilation and engorgement of the capillaries.
2. Thinning or ulceration of the sulcular epithelium.
ACUTE BLEEDING :
CAUSES :
 Injury or occurs spontaneously in acute gingival disease.
 Laceration of the gingiva by tooth brush bristles during aggressive tooth
brushing or by sharp pieces of hard food can cause gingival bleeding even
in the absence of gingival disease.
 Gingival burns from hot foods or chemicals increase the ease of gingival
bleeding..
 Spontaneous bleeding or bleeding on slight provocation can occur in acute
necrotizing ulcerative gingivitis.
GINGIVAL BLEEDING ASSOCIATEDWITH SYSTEMIC CHANGES :
 In some systemic disorders, gingival hemorrhage occurs spontaneously or
after irritation is excessive and is difficult to control.
 The hemorrhagic tendency may be due to failure of one or more of the
hemostatic mechanisms and result in abnormal bleeding in the skin,
internal organs,and other tissues, including the oral mucosa..
1. Hemorrhagic disorders in which abnormal bleeding is encountered are :
a) Vascular abnormalities (vitamin C deficiency, or allergy such as Schonlein-
Henoch purpura) .
b) platelet disorders(thrombocytopenic purpura),
c) hypoprothrombinemia ( vitamin K deficiency).
c) Other coagulation defects (hemophilia, leukemia, christmas disease).
d) Deficient platelet thromboplastic factor (PF3).
e) Drugs such as salicylates and anticoagulants such as dicumoral and heparin.
COLOR CHANGES IN THE GINGIVA :

COLOR CHANGES IN CHRONIC GINGIVITIS :

 Changes in color is an important clinical sign o f gingival disease.
 The normal gingival color is "coral pink“
 Change in colour depends upon tissue's vascularity, thickness of the
epithelium , degree of epithelial keratinization
 The gingiva becomes more red when there is an increase in vascularization
or the degree of epithelial keratinization becomes reduced or disappears. The
color becomes pale when vascularization is reduced or epithelial
keratinization increases.
 Thus chronic inflammation intensifies the red or bluish red color because of
vascular proliferation and reduction of keratinization. The gingiva becomes
bluish because of venous stasis.
 The changes start in the interdental papillae and gingival margin and spread
to the attached gingiva.
COLOR CHANGES IN ACUTE GINGIVITIS :

1. The color changes may be marginal, diffuse, or patchlike , depending

on the underlying acute condition.

2. In ANUG, the involvement is marginal, in Herpetic Gingivistomatitis, it is

diffuse, in acute reactions to chemical irritation, it is patchlike or diffuse.

3. Color changes vary with the intensity of the inflammation. Initially, it is red
erythema.

4. In severe acute inflammation, the red color gradually becomes dull, whitish
gray.
NORMAL GINGIVA ANUG
METALLIC PIGMENTATION :

1. Heavy metals (bismuth, arsenic, mercury, lead, silver) may discolor

the gingiva and other areas of oral mucosa.
2. They produce a black or bluish line in the gingiva that follows the
contour of the margin.
3. The pigmentation may appear as isolated black blotches involving the
interdental marginal and attached gingiva.
4. Gingival pigmentation is not a result of systemic toxicity and occurs only in
areas of inflammation.
5. The increased permeability of irritated blood vessels permits seepage of the
metal into surrounding tissue.
6. Gingiva, lips, cheek, and lateral border of tongue are common
pigmentation sites.
Bismuth gingivitis. Note linear black Discoloration of the gingiva caused by
discoloration of the gingiva embedded metal particles (amalgam).
COLOR CHANGES ASSOCIATEDWITH SYSTEMIC FACTORS :

o Many systemic diseases may cause color changes in the oral mucosa,
including the gingiva.

o Endogenous oral pigmentation can be due to melanin, bilirubin, or

iron.
o Melanin oral pigmentation can be normal physiologic pigmentations and
are commonly found in highly pigmented ethnic groups.

o Diseases that increase melanin pigmentation are Addison’s disease,

Peutz- jeghers syndrome, Albright’s syndrome.

o In jaundice, the oral mucosa may acquire a yellowish color.

o The deposition of iron in hemochromatosis may produce a bluish-
gray pigmentation of the oral mucosa.

o Several endocrine and metabolic disturbances, including diabetes

and pregnancy, may result in color changes.
o Blood dyscrasias, such as anemia, polycythemia, and
leukemia, may also induce color changes.

o Exogenous factors capable of producing color changes in the

gingiva include atmospheric irritants, such as coal and metal
dust, and coloring agents in food or lozenges.

o Tobacco causes hyperkeratosis of the gingiva and also may induce a

significant increase in melanin pigmentation of the oral mucosa.
MELANIN PIGMENTATION
 CHANGES IN THE CONSISTENCY OF THE GINGIVA :

1. Both chronic and acute inflammation produce changes in the normal firm,
resilient consistency of gingiva.
2. In chronic gingivitis, both destructive (edematous) and reparative (fibrotic)
changes coexist.
3. The consistency of gingiva is determined by their relative predominance.
CHANGES IN CONSISTENCY OF GINGIVA- CHRONIC
 Soggy puffiness pits on
pressure
 Marked softness and friability
with ready fragmentation on
exploration pin point surface
area of redness and
desquamation
 Firm leathery
 Infiltration of inflammatory
exudates
 Thinning of epithelium
• Edema leucocytic invasion
• Connective tissue degeneration
• Change in connective tissue and
epithelial junction
 Fibrosis and epithelial
proliferation
CHANGES IN CONSISTENCY OF GINGIVA- ACUTE
 Diffused puffiness and  Diffuse edema fatty
softening infiltrarion in
 Sloughing with grayish xanthomatosis
flake like particle  Pseudomembraneous coat
 Vesicle formation  Inter and intra cellular
edema degeneration of
cells
 CHANGES IN SURFACE TEXTURE OF THE GINGIVA :

 LOSS OF SURFACE STIPPLING is an early sign of gingivitis.

 Stippling is restricted to the attached gingiva, but it extends to a
variable degree into the interdental papilla.
 In chronic inflammation the surface is either smooth and shiny
or nodular, depending on whether the dominant changes are
exudative or fibrotic.
 Peeling of the surface occurs in chronic desquamative
gingivitis.
 Senile atropic gingivitis - smooth surface
 Hyperkeratosis results in a leathery texture, and
 drug-induced gingival overgrowth produces a nodular surface.
Normal gingiva desquamative gingivitis.

chronic inflammation
CHANGES IN THE POSITION OF THE GINGIVA :

 RECESSION :
 Gingival recession is a common finding.

 The exposure of the root surface by an apical shift in the

position of the gingiva.

 Recession refers to the location of the gingiva, not its condition.

 localized , or generalized

 The prevalence, extent, and severity of gingival recession increase with age
and are more prevalent in males.
A. ACTUAL POSITION OF THE GINGIVA :
 The level of the coronal end of the epithelial attachment on the tooth,.
B. APPARENT POSITION OF THE GINGIVA :
 The level of crest of the gingival margin.
 The severity of recession is determined y actual position of
gingiva, not its apparent position.

The two types of recession are :

a. VISIBLE :
 Clinically observable.
b. HIDDEN :
 Covered by gingiva and can be measured by inserting a probe to the
level epithelial attachment.
GINGIVAL RESSESION
ETIOLOGIC FACTORS OF RECESSION :

1. Gingival recession increases with age and varies after age of 50yrs.
2. The following etiologic factors in gingival recession are :
a) Faulty tooth brushing technique (gingival abrasion).
b) Tooth malposition.
c) Friction from soft tissues (gingival ablation).
d) Gingival inflammation.
e) Abnormal frenum attachment.
f) Trauma from occlusion.
CLINICAL SIGNIFICANCE :
1. Exposed root surfaces are susceptible to caries.
2. Abrasion or erosion of the cementum exposed by
recession cause dentinal sensitivity.
3. Hyperemia of the pulp and associated symptoms
results from excessive exposure of root surface.
4. Interproximal recession causes oral hygiene problems
and plaque accumulation.
CHANGE IN GINGIVAL CONTOUR
Changes in gingival contour are primarily associated with gingival
gingival enlargement

INFLAMATORY

IDIOPATHIC

DRUG INDUSED
 Stillman’s cleft
 Apostrophe shaped indentation extending from and in
to the gingival margin
 Common in facial surface /gingival margin blunt
 Resuls from occlusal trauma

McCall’s festoons
 Life preserver shaped enlargement of gingiva
 Occur in canine and premolar on the facial surface
 Accumulation of food leads to secondary inflammatory changes
 Patients Education and Motivation

Avoid sticky
Take foods in
more between
fibrous meals
foods

Choose better tooth

Brush regularly paste & Soft brush Meet your dentist
after meals for better cleaning for every 6 months
or 1 year interval
Thank you