GINGIVAL INFLAMMATION & CLINICAL FEATURES OF

GINGIVITISKIRANPREET KAUR GREWAL

INTERNSHIPGURU NANAK DEV DENTAL COLLEGE

& RESEARCH INSTITUTE, SUNAM, PUNJAB.

Inflammation of gingiva is termed as gingivitis. The main cause of gingivitis is plaque induced

microorganisms. These microorganisms release certain products such

as collagenase, hyaluronidase, protease, chondroitin sulfatase etc. which can cause damage to the epithelial and connective tissue constituents.

The intercellular spaces between the junctional epithelial cells are destroyed and may permit the bacterial products or bacteria themselves to gain access into the connective tissue.

Absence of treatment of gingivitis can lead progress of gingivitis into periodontitis.

INTRODUCTION

STAGE VASCULAR CHANGES

MICROSCOPIC CHANGES

CLINICAL CHANGES

1. Initial lesion (2-4 days)

Classical vaculities subjacent to junctional epithelium

Presence of leukocytes(PMNs),Loss of perivascular collagen, changes in the coronal most portion of junctional epithelium.

Exudation of fluid from the gingival sulcus.Subclinical gingivitis

2. Early lesion (4-7days)

Vascular proliferation Rete peg formation in junctional epithelium, presence of lymphocytes,Loss of collagen, fibroblasts show cytoplasmic alterations

Erythematous, gingival bleeding on probing

3. Established lesion (14-21 days)

Same as early lesion, with blood stasis

Proliferation, apical migration & lateral extension of junctional epithelium, Atrophic areas, plasma cells are predominant, furthur loss of collagen, increased enzyme levels such as acid & alkaline phosphatase, beta glucuronidase etc.

Changes seen in consistency & surface texture.Bluish he around the reddened gingiva.

4. Advanced lesion Same as early & established lesion

Persistence of features seen in established lesion,Ectension of inflammation into deeper structures, presence of all types of inflammatory cells

Formation of periodontal pocket and its aa

STAGES OF GINGIVAL INFLAMMATION:

Depending on course and duration Depending on distribution

Depending on the course and duration:1) Acute gingivitis is of sudden onset and short duration;

and can be painful.2) Subacute gingivitis is a less severe phase of acute

infection.3) Recurrent gingivitis reappears either after treatment or

disappears spontaneously.4) Chronic gingivitis is show in onset, of long duration,

usually painless and the most commonly occuring gingival condition.

TYPES OF GINGIVITIS

Depending on distribution Localized gingivitis: It is the condition is

involving a single tooth or group of tooth. Generalized gingivitis: It is the condition

involving entire mouth. According to distribution: gingivitis could be

marginal, papillary, or diffuse. Marginal gingivitis: In this the inflammation is

limited to the marginal gingiva. Papillary gingivitis: In this the inflammation is

limited to interdental papilla. Diffuse gingivitis: In this the inflammation

involves attached gingiva.

GINGIVA IN HEALTH & DISEASEGINGIVAL FEATURES

IN HEALTH FACTORS RESPINSIBLE

IN DISEASE FACTORS RESPNSIBLE

DISEASE CONDITION

1. Color Coral pink Vascular supply Thickness &

degree of keratinization of epithelium

Presence of pigment containing cells

Color changes may be :

Marginal Diffuse Diffuse or patch

like Varying shades

of reddish blue, deep blue

Color changes Shiny slate gray Dull whitish gray

Chronic Gingivitis

Chronic Gingivitis

Acute gingivitis ANUG/HIV

Gingivitis Herpetic

gingivostomatitis

• Vascular proliferation

• Reduction of keratinization owning to epithelium compression by inflamed tissue.

• Venus stasis• Tissue necrosis.

2. Contour Marginal gingiva: Scalloped & Knife edged

Interdental papilla: Anterior: pyramidal shapedPosterior: Tent shaped

• Shape of the tooth and thus alignment in the arch.

• Location and size of proximal contact.

• Dimensions of facial and lingual gingival embrasures

• Marginal gingiva becomes rolled or rounded, interdental papilla becomes blunt and flat.

• Punched out and crater like depression at the crest of interdental papilla extending to marginal gingiva.

• Exaggerated scalloping apostrophe shaped indentations extending from and into the gingival margins for varying distance on the facial surface.

• Life saver like enlargement of marginal gingiva.

Chronic gingivitis.

ANUG

Stillman’s cleft

McCall’s festoons

Inflammatory changes

• As a result of trauma from occlusion

• Enlargement of interdental papilla with no enlargement of marginal gingiva

GINGIVAL FEATURES IN HEALTH FACTORS RESPINSIBLE

IN DISEASE FACTORS RESPNSIBLE

DISEASE CONDITION

3. Consistency Firm & resilient • Collagenous nature of lamina propria and its contiguity with the mucoperiosteum of alveolar bone

• Cellular and fluid content of the tissue.

• Soggy puffiness that pits on pressure.

• Marked softness and friability.

• Firm leathery.• Defuse puffiness

and softening.• Sloughing.• Vesicle formation.

Chronic gingivitis

Exudative

Fibrotic

Actuate gingivitis

• Infiltration by fluids and cells.

• Degeneration of CT and epi.

• Fibrosis.• Necrosis

4. Size Normal Some total of bulk of cellular and intercellular elements and there vascular supply.

Increased Gingival enlargement Increase in fibers and decrease in cells and vice versa.

5. Surface texture Stippling present • Due to the attachment of gingival fibers to underline bone.

• Microscopically papillary layer of connective tissue projects into the elevations.

Loss of stippling Smooth and shiny

Firm and nodular

Peeling of surface

Leathery texture Minutely nodular

surface

Gingivitis

Exudative chronic gingivitis

Fibrotic chronic gingivitis

Chronic desquamative gingivitis

Hyperkeratosis Non inflammatory

gingival hyperplasia

Due to destruction of gingival fibers as a result of inflammation

6. Position 1mm above the cementoenamel junction

• Position of tooth in arch

• Root bone angle • Mesiodistal

curvature of tooth surface

• Apically placed• Coronally replaced

• Gingival recession• Pseudopockets

• Tooth brush trauma. • Gingival

inflammation• High frenum

attachment• Tooth malposition• Friction from soft

tissue7. Bleeding on probing Intact sulcular

epithelium and normal capillaries

PresentChronic recurrent, spontaneous bleeding or slight bleeding

• Chronic gingivitis • ANUG• Systemic disease

Dilation and engorgement of capillaries and thinning or ulceration of sulcular epithelium.

GINGIVAL BLEEDING ON PROBING: Significance of gingival bleeding on probing:i. It is one of the earliest visual signs of inflammation.ii. It can appear earlier then colour changes or any other

visual signs of inflammation.iii. It also provides an additional advantage, by being a more

objective sign that requires less subjective estimation by the examiner.

iv. Gingival bleeding on probing also helps us to determine whether the lesions is in an active or inactive state. In inactive lesion, there will be little or on bleeding on probing, whereas active lesions bleed more readily on probing.

v. The severity and ease with bleeding can be provoked- indicates the integrity of the inflammation.

CLINICAL FINDINGS

Etiological factors responsible for gingival bleeding on probing:

Etiological factors can be divided into:

Local Factors

•Acute Factors•Chronic Factors

Systemic Factors

•Hematological Disease •Excessive use of drugs

LOCAL FACTORS:

Acute Factors: These factors cause acute bleeding. causes are:

1. Toothbrush trauma.2. Impaction of sharp pieces of hard food.3. Gingival burns from hot foods or chemicals.4. In conditions such as acute necrotizing ulcerative

gingivitis(ANUG). Chronic Factors: These factors cause chronic bleeding. causes are:1. Chronic inflammation due to the presence of plaque

and calculus.2. Mechanical trauma, e.g. from tooth brushing, tooth

picks or food impaction.3. Biting into solids foods such as apple.

SYSTEMIC FACTORS: Hematological disease such as vitamin K

deficiency, platelet disorders such as thrombocytopenia purpura, other coagulation defects such as hemophilia, leukemia and others.

Bleeding could also be as a result of excessive administration of drugs such as salicylates and anticoagulants such as dicumarol and heparin

Microscopic changes associated with gingival bleeding on probing:

1. In the epithelium: Thinning and micro ulcerations of the sulcular epithelium is seen.

2. In the connective tissue: Dilation and engorgement of the capillaries takes place.

COLOR CHANGES IN THE GINGIVA: Color of the gingiva is an important clinical sign of

gingival diseases. Normally, gingiva appears to be coral pink. The factors that are responsible for this are tissue

vascularity, degree of keratinization and thickness of the epithelium.

Generally, color of the gingiva may change to red, to bluish red to pale pink.

Systemically absorbed heavy metals may also cause gingival pigmentation, e.g. bismuth, arsenic, mercury, lead and silver.

Abnormal melanin pigmentation of the gingiva may be observed in conditions like Addison’s disease, peutz-jeghers syndrome.

CHANGES IN CONSISTENCY OF GINGIVA:

Normal gingiva exhibits a firm and resilient consistency.

Factors that are responsible are cellular and fluid content and collagenous nature of lamina propria.

In disease conditions, it can be soggy and edematous or firm; and leathery consistency.

CHANGES IN SIZE OF GINGIVA: Normal size depends on the sum of the bulk

cellular and intercellular elements, and their vascular supply.

In disease, the size is increased, which can be termed as gingival enlargement.

Factors responsible for this are increase in bulk of cellular and intracellular elements.

SURFACE TEXTURE: Under normal conditions, gingiva appears to

be stippled(orange peel appearance) This is due to attachment of gingival fibers

to the underlying bone. Stippling is absent in disease conditions. Hence, the gingiva may appear smooth and shiny.

CHANGES IN POSITION OF GINGIVA: Normally, the gingiva is attached to the

tooth at the cementoenamel junction. In disease, the position can be shifted

either coronally (pseudo-pocket) or apical to the cementoenamel junction (gingival recession).

GINGIVAL RECESSION:Defination:- Gingival recession is defined as the exposure of the root surface by an apical shift in the position of the gingiva.

Types:- In gingival recession, there are two types: Visible, which is clinically observable. Hidden, which is covered by gingiva and

can only be measured with probe.

Gingival recession may also be localized and generalized.

Classification of Gingival Recession:Two classification systems are available:-

1) According to Sullivan & Atkins: Shallow-narrow, shallow-wide and deep-wide.

2) According to PD Miller’s: Class-I ,Class-II, Class III, Class IV.

Etiology of gingival recession:

Plaque-induced gingival inflammation is the primary etiological factor responsible for gingival recession

Other common cause is faulty tooth-brushing.

Other secondary factors on gingival recession are broadly categorized as-

i. Anatomic factorsii. Habitsiii. Iatrogenic factorsiv. Physiologic factors

Clinical significance of gingival recession:

1) The exposed root surface may be extremely sensitive.

2) Hyperemia of the pulp may result due to gingival recession.

3) Interproximal recession creates oral hygiene problems thereby resulting in plaque accumulation.

4) Finally, it is aesthetically unacceptable.

Changes in gingival contour: Normally, marginal gingiva is scalloped and knife

edges, whereas interdental papilla in the anterior region is pyramidal and posteriorly tent-shaped.

The factors that maintain normal contour are, shape of the teeth and its alignment in the arch, location and size of the proximal contact and dimensions of the facial and lingual gingival embrasures.

In diseased conditions, the marginal gingiva may become rounded or rolled, whereas interdental papilla can become blunt and flat.

Stillman’s clefts are apostrophe shaped indentations extending from and into the gingival margin varying distance on the facial surface.

Mccall’s festoon isa life preserver shaped enlargement of gingiva, most commonly seen on the facial surface of canine and premolar area.

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