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By: Maram4 (30 month(s) ago)


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CHAPTER 17 CLINICAL FEATURES OF GINGIVITIS Inflammation of gingiva is termed as gingivitis. Classification according to COURSE and DISTRIBUTION : Acute gingivitis. Recurrent gingivitis. 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. RECURRENT GINGIVITIS : Reappears after eliminated by treatment or disappearing spontaneously. CHRONIC GINGIVITIS : Slow in onset and of long duration, and is painless, inflammation persists or resolves and normal areas become inflammed.

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Classification According to DISTRIBUTION : 1. LOCALIZED GINGIVITIS : Confined to gingiva of single tooth. Localized Marginal Gingivitis. Localized Diffuse Gingivitis. Localized Papillary Gingivitis. GENERALIZED GINGIVITIS : Involves the entire mouth. a) Generalized Marginal Gingivitis. b) Generalized Diffuse Gingivitis. PAPILLARY GINGIVITIS : Involves interdental papillae, extends into adjacent portion of gingival margin and earliest sign of gingivitis often occur in papillae. DIFFUSE GINGIVITIS: Affects the gingival margin, the attached gingiva, and the interdental papillae.

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LOCALIZED MARGINAL GINGIVITIS : Confined to one or more areas of the marginal gingiva. LOCALIZED DIFFUSE GINGIVITIS : Extends from margin to the mucobuccal fold but is limited in area. LOCALIZED PAPILLARY GINGIVITIS : Confined to one or more interdental spaces in a limited area. GENERALIZED MARGINAL GINGIVITIS : Involves gingival margins in relation to all teeth. The interdental papillae are usually affected in generalized marginal gingivitis. GENERALIZED DIFFUSE GINGIVITIS : Involves the entire gingiva. The alveolar mucosa and attached gingiva are affected. May be caused by systemic conditions.

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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. Bleeding from the gingival sulcus on gentle probing. 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. Appears earlier than a change in color or other visual signs of inflammation.

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GINGIVAL BLEEDING CAUSED BY LOCAL FACTORS : Chronic and recurrent bleeding . Acute bleeding. CHRONIC AND RECURRENT BLEEDING : The most common cause of abnormal gingival bleeding on probing. 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. Sites that bleed on probing have a greater area of inflamed connective tissue than those sites that do not bleed. The cellular infiltrate of sites that bleed on probing is predominantly lymphocytic. The severity of bleeding and the ease with which it is provoked depend on the intensity of the inflammation.

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HISTOPATHOLOGIC CHANGES : Dilation and engorgement of the capillaries. Thinning or ulceration of the sulcular epithelium. ACUTE BLEEDING : CAUSES : Injury or occurs spontaneously in acute gingival disease. Laceration of the gingiva by toothbrush bristles during aggressive tooth brushing. Sharp pieces of hard food. Gingival burns from hot foods or chemicals. GINGIVAL BLEEDING ASSOCIATED WITH SYSTEMIC CHANGES : 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. Hemorrhagic disorders in which abnormal bleeding is encountered are : Vascular abnormalities (vitamin C deficiency, or allergy such as Schonlein-Henoch purpura) . hypoprothrombinemia ( vitamin K deficiency).

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Other coagulation defects (hemophilia, leukemia, christmas disease). Deficient platelet thromboplastic factor (PF3). Drugs such as salicylates and anticoagulants such as dicumoral and heparin. COLOR CHANGES IN THE GINGIVA : COLOR CHANGES IN CHRONIC GINGIVITIS : 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. The gingiva becomes bluish because of venous stasis. The changes start in the interdental papillae and gingival margin and spread to the attached gingiva.

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COLOR CHANGES IN ACUTE GINGIVITIS : The color changes may be marginal, diffuse, or patchlike , depending on the underlying acute condition. In ANUG, the involvement is marginal, in Herpetic Gingivistomatitis, it is diffuse, in acute reactions to chemical irritation, it is patchlike or diffuse. Color changes vary with the intensity of the inflammation. Initially, it is red erythema. In severe acute inflammation, the red color gradually becomes dull, whitish gray. The gray discoloration produced by tissue necrosis is demarcated from the adjacent gingiva by a thin, sharply defined erythematous zone.

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METALLIC PIGMENTATION : Heavy metals (bismuth, arsenic, mercury, lead, silver) may discolor the gingiva and other areas of oral mucosa. They produce a black or bluish line in the gingiva that follows the contour of the margin. The pigmentation may appear as isolated black blotches involving the interdental marginal and attached gingiva. Gingival pigmentation from systemically absorbed metals results from perivascular precipitation of metallic sulfides in the subepithelial connective tissue. Gingival pigmentation is not a result of systemic toxicity and occurs only in areas of inflammation. The increased permeability of irritated blood vessels permits seepage of the metal into surrounding tissue. Gingiva, lips, cheek, and lateral border of tongue are common pigmentation sites.

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COLOR CHANGES ASSOCIATED WITH SYSTEMIC FACTORS : Many systemic diseases may cause color changes in the oral mucosa, including the gingiva. Endogenous oral pigmentation can be due to melanin, bilirubin, or iron. Melanin oral pigmentation can be normal physiologic pigmentations and are commonly found in highly pigmented ethnic groups. Diseases that increase melanin pigmentation are Addison’s disease, Peutz- jeghers syndrome, Albright’s syndrome. In jaundice , the oral mucosa may acquire a yellowish color . The deposition of iron in hemochromatosis may produce a bluish-gray pigmentation of the oral mucosa. Several endocrine and metabolic disturbances, including diabetes and pregnancy, may result in color changes. Tobacco may induce increase in melanin pigmentation of oral mucosa. Localized bluish black areas of pigment are due to amalgam implanted in the mucosa.

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CHANGES IN THE CONSISTENCY OF THE GINGIVA : Both chronic and acute inflammation produce changes in the normal firm, resilient consistency of gingiva. In chronic gingivitis, both destructive (edematous) and reparative (fibrotic) changes coexist. The consistency of gingiva is determined by their relative predominance. CHANGES IN SURFACE TEXTURE OF THE GINGIVA : Loss of surface stippling is an early sign of gingivitis. In chronic inflammation the surface is either smooth and shiny or nodular, depending on whether the dominant changes are exudative or fibrotic. Smooth surface texture is produced by epithelial atrophy in atrophic gingivitis. Peeling of the surface occurs in chronic desquamative gingivitis. Hyperkeratosis results in a leathery texture, and drug-induced gingival overgrowth produces a nodular surface.

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CHANGES IN THE POSITION OF THE GINGIVA : RECESSION : 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. Recession may be localized to one tooth or a group of teeth, or it may be generalized through-out the mouth. A. ACTUAL POSITION OF THE GINGIVA : The level of 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 : VISIBLE : Clinically observable. HIDDEN : Covered by gingiva and can be measured by inserting a probe to the level epithelial attachment.

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ETIOLOGIC FACTORS OF RECESSION : Gingival recession increases with age and varies after age of 50yrs. The following etiologic factors in gingival recession are : Faulty tooth brushing technique (gingival abrasion). Tooth malposition. Friction from soft tissues (gingival ablation). Gingival inflammation. Abnormal frenum attachment. Trauma from occlusion. CLINICAL SIGNIFICANCE : Exposed root surfaces are susceptible to caries. Abrasion or erosion of the cementum exposed by recession cause dentinal sensitivity. Hyperemia of the pulp and associated symptoms results from excessive exposure of root surface. Interproximal recession causes oral hygiene problems and plaque accumulation.

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CHANGES IN GINGIVAL CONTOUR : STILLMAN’S CLEFTS : Apostrophe -shaped indentation of the gingival margin. McCALL FESTOON : Life preserver- shaped enlargement of the margin. ETIOLOGY: Trauma from occlusion. They represent peculiar inflammatory changes of the marginal gingiva.

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