Diseases Of Periodontium Important Question And Answers

Diseases Of Periodontium

Question.1. Write note on acute necrotizing ulcerative gingivitis.
Or
Write short note on acute necrotizing ulcerative gingivitis.
Or
Write short note on ANUG.

Answer. It is an endogenous oral infection which is characterized by the necrosis of gingiva.

It is also called as Trench mouth, Vincent’s infection, acute ulcers membranous gingivitis, and acute ulcerative gingivitis.

Etiology

It is caused by the fusiform bacilli and spirochete.

Predisposing Factors

Systemic Predisposing Factors

• Malnutrition: This may lead to acute necrotizing ulcerative gingivitis
• Nutritional deficiency: Defiiency of Vitamin C, Vitamin B1, and Vitamin B2 leads to the exaggeration of pathologic changes caused by fusospirochetal bacteria.
• Psychosomatic conditions: Disease is associated with the stress and with increment in adrenocortical secretion.
• Diseases like leukemia, syphilis, AIDS and gastrointestinal disturbances also leads to ANUG.

Read And Learn More: Oral Pathology Question And Answers

Localized Predisposing Factors

• Marginal gingivitis
• Poor oral hygiene
• Faulty dental restorations
• Deep periodontal pockets
• Tobacco smoke

Clinical Features

• Acute necrotizing ulcerative gingivitis usually occurs among young and middle-aged adults, between the ages of 16 and 30 years and males suffer more often than females.
• Stressed professionals like army recruits tend to suffr more from the disease.
• Moreover, young children suffring from malnutrition are also prone to the disease.
• Initially, the gingiva becomes red, edematous, hemorrhagic and painful.
• Later, on, a sharply demarcated “punched- out” crater-like erosion of the inter­dental papillae occurs.
• Gingiva is often covered by a gray “pseudomembrane”with accumulation of necrotic tissue debris.
• Patient have pronounced spontaneous bleeding tendency,exquisite pain and an extremely unpleasant fetid odor in the mouth.
• Patients often develop headache, fever, malaise and lymphadenopathy of the affected area.
• Often there is difficulty in taking food due to increased salivation and a metallic taste in the mouth.
• When the necrotizing process leads to the development of periodontitis with loss of epithelial attachment the condition is called necrotizing ulcerative periodontitis.
• When the necrotizing process of ANUG extends further through the oral mucosa and reaches to the extraoral skin surface, the condition is called ‘noma’ or cancrum oris.

Histopathology

• It involves both stratified squamous epithelium and underlying connective tissue.
• Surface epithelium is destroyed and is replaced by pseudomembranous meshwork of firin, necrotic epithelial cells, polymorphonuclear neutrophils and various microorganisms.
• Underlying connective tissue is hyperemic with numerous engorged capillaries and dense infiltration of polymorphonuclear neutrophils.
• Numerous plasma cells may appear in periphery of infitrate.

Treatment

• Conservative treatment is employed, i.e. superficial cleaning of oral cavity by chlorhexidine, diluted hydrogen peroxide or warm salt water. This is followed by scaling and polishing. Topical anesthetics are used to produce pain during procedure.
• Use of antibiotics is coupled with local treatment.

 

Question.2. Write short note on etiology of gingivitis.

Answer. Gingivitis is the inflammation of gingiva and occurs in acute, sub-acute and chronic form.

Etiology

• Local Factors
  • Microorganisms: Plaque associated with gingivitis is complex and heterogeneous.
  • Actinomyces group of organisms are dominant in supragingival plaque.
  • Calculus: Supragingival or subgingival or both causes irritation of contacting gingival tissue. Irritation is produced by the mechanical friction resulting form hard, rough surface of calculus.
  • Food impaction: Impaction of food and accumulation of debris on teeth due to oral negligence results in gingivitis.
  • Faulty and irritating restorations or appliance may act as irritant to gingival tissue and induce gingivitis.
  • Mouth breathing: It leads to drying of oral mucus membrane which results in gingival irritation with accompanying irritation.
• Systemic factors
  • Nutritional disturbances: The nutritional imbalance if frequently manifested leads to changes in gingiva.
  • Pregnancy: During pregnancy gingiva undergoes changes causing pregnancy gingivitis.
  • Diabetes mellitus
  • Hormonal changes: Puberty and menstruation may result in gingival inflmmation.

 

Question.3. Describe in detail necrotizing ulcerative gingivitis.

Answer. It is an endogenous oral infection characterized by necrosis of gingiva. It is also called as trench mouth.

Etiopathogenesis

Proliferation of anaerobic fusiform bacteria and spirochaetes results in ANUG. Infection mostly occurs in presence of pschycological stress. Stress related corticosteroid hormones are thought to alter T4/T8 lymphocyte ratios and may cause the decreased neutrophilic chemotaxis and phagocytic response seen in patients with ANUG. Stress related epinephrine may result in localized ischemia which predisposes gingiva to ANUG.

Following are the predisposing factors for acute necrotizing Ulcerative Gingivitis:

• Systemic predisposing factors
• Local predisposing factors

Systemic predisposing Factors

• Malnutrition: This may lead to acute necrotizing ulcerative gingivitis
• Nutritional deficiency: Deficiency of Vitamin C, Vitamin B1, and Vitamin B2 leads to the exaggeration of pathologic changes caused by fusospirochetal bacteria.
• Psychosomatic conditions: Disease is associated with the stress and with increment in adrenocortical secretion.
• Diseases like leukemia, syphilis, AIDS and gastrointestinal disturbances also leads to ANUG.

Localized Predisposing Factors

• Marginal gingivitis
• Poor oral hygiene
• Faulty dental restorations
• Deep periodontal pockets
• Tobacco smoke

Clinical Features

• Acute necrotizing ulcerative gingivitis usually occurs among young and middle aged adults, between the ages of 16 and 30 years and males suffr more often than females.
• Stressed professionals like army recruits tend to suffr more from the disease.
• Moreover, young children suffring from malnutrition are also prone to the disease.
• Initially, the gingiva becomes red, edematous, hemorrhagic and painful.
• Later, on, a sharply demarcated “punched-out” crater-like erosion of the inter­dental papillae occurs.
• Gingiva is often covered by a gray “pseudomembrane”with accumulation of necrotic tissue debris.
• Patient have pronounced spontaneous bleeding tendency, exquisite pain and an extremely unpleasant fetid odor in the mouth.
• Patients often develop headache, fever, malaise and lymphadenopathy of the affected area.
• Often there is difficulty in taking food due to increased salivation and a metallic taste in the mouth.
• When the necrotizing process leads to the development of periodontitis with loss of epithelial attachment the condition is called necrotizing ulcerative periodontitis.
• When the necrotizing process of ANUG extends further through the oral mucosa and reaches to the extraoral skin surface, the condition is called ‘noma’ or cancrum oris.

Investigations

Investigations are associated with testing of fusiform bacilli and spirochaetes:

• Spirochetes and fusiform bacilli are demonstrated in stained smears of exudates from the lesion on microscopic examination. The spirochete T.pallidum is visible on dark ground microscopy.
• Direct fluorescent antibody test is done for detection of spirochete T. pallidum
• Enzyme immunoassays are also done to detect for spirochetes present in ANUG.
• Antibody tests, i.e. detection of specifi IgM antibody is helpful in detection of Treponema.

Differential Diagnosis

• Benign mucous pemphigoid: In this as compared to ANUG,it is seen in elderly people and no necrosis is evident.
• Pemphigoid lichen planus: It does not show any acute course,no foul breadth is observed.
• Pemphigus: It present a very regular histology. Seen in older people.
• Syphilitic gingivitis: Lesion is seen on gingiva and it does not get spread to adjacent gingiva.
• Streptococcal gingivostomatitis: Diffuse erythema is seen on posterior parts of oral mucosal lining and no necrosis is evident.
• Gingivostomatitis by candida: Covering of white membrane is seen which can be removed by scrapping. On laboratory investigation, the membrane reveals of candida.

Complications

Patients affected by ANUG develop systemic complications such as:

• Pulse rate get increased
• High fever
• Loss of appetite
• Generalized lassitude.

Treatment

• The involved areas are isolated with cottn rolls and dried.
  A topical anesthetic is applied and after 2 to 3 minutes, areas are gently swabbed with a cottn pellet to remove pseudomembrane. After the area is cleaned with warm water, superficial calculus is removed.
• Patient is told to rinse the mouth every 2 hours with glassful of an equal mixture of warm water and 3% hydrogen peroxide. Twice daily rinsing with 0.12% chlorhexidine are effective.
• Penicillin V 250 or 500 mg, 6 hourly or erythromycin 250 or 500 mg, 6 hourly are given.
• Scaling is performed, if sensitivity permits. After disease process is diminished, complete gingival curettage and root planing is done.
• Supportive treatment consists of copious fluid consumption and administration of nutritional supplements.

 

Question.4. Describe in detail the clinical features, etiology and histopathology of necrotizing ulcerative gingivitis.

Answer.

Etiology

• It is caused by fusiform bacilli and by a spirochete known as borrelia vincentii.
• Mainly precipitating factors are there which lead to necrotizing ulcerative gingivitis.
• For precipitating factors in detail refer to Ans 3 of same chapter.

Histopathology

• Affected gingiva show inflammation, ulceration and necrosis.
• Gingival stratifid squamous epithelium is replaced by thick firinopurulent pseudomembrane.
• Pseudomembrane shows PMNs and necrotic debris.
• In unaffected areas of gingiva, keratinization is absent.
• Underlying connective tissue show hyperemia and acute inflammatory cells i.e. PMNs.

 

Question.5.Classify gingival hyperplasia. Describe clinical features and histopathology of idiopathic gingival hyperplasia.

Answer.

Classifiation of Gingival Hyperplasia

On basis of etiological factors and pathologic changes

• Inflammatory enlargement
  • Chronic
  • Acute
• Drug induced enlargement
• Enlargement associated with systemic disease
  • Conditional enlargement
    • Pregnancy
    • Puberty
    • Vitamin C deficiency
    • Plasma cell gingivitis
    • Non-specific conditioned enlargement (Pyogenic granuloma)
• Systemic diseases causing gingival enlargement
  • • Leukemia
    • Granulomatous disease (E.g. Wegener’s Granulomatosis, sarcoidosis)
• Neoplastic enlargement
  • • Benign tumors
    • Malignant tumors
• False enlargement

Using the criteria of location and distribution gingival enlargement is designated as follows:

• Localized: Gingival enlargement limited to one or more teeth.
• Generalized: Involving the gingiva throughout the mouth.
• Marginal: Confied to marginal gingiva.
• Papillary: Confied to interdental papilla.
• Diffuse: Involving the marginal and attached papillae.
• Discrete: Isolated sessile or pedunculated tumor like enlargement.

On basis of degree of gingival enlargement

Grade 0: No sign of gingival enlargement.

Grade I: Enlargement confimed to interdental papilla

Grade II: Enlargement involves papilla and marginal gingiva.

Grade III: Enlargement covers three-quarters or more of the crown.

Idiopathic Gingival Hyperplasia

• Idiopathic gingival enlargement is a rare condition of undetermined cause.
• It is also known as angiomatosis or elephantiasis gingivae or idiopathic fibromatosis or hereditary gingival hyperplasia or congenital fibromatosis.

Clinical Features

• Enlargement affcts attched gingiva, gingival margin and interdental gingiva.
• Facial and lingual surfaces of mandible and maxilla are affcted.
• Involvement may be limited to one jaw.
• Enlarged gingiva is pink, fim and leathery in consistency and has minutely pebbled surface.
• In severe cases teeth are completely covered by enlarged gingiva.

Histopathology

• Epithelium is hyperplastic with elongation of rete ridges.
• Mild hyperkeratosis is also seen.
• Underlying connective tissue stroma consists of dense bundles of collagen and numerous firoblasts.
• At times presence of chronic inflammatory infiltrate is seen.

 

Question.6.Write short note on gingival firomatosis.

Answer. It is also known as hereditary gingival firomatosis or elephantiasis gingivae.

Gingival fibromatosis is the condition characterized by the diffuse gingival enlargement and it also covers major parts of total tooth surfaces.

It is the slowly progressive gingival enlargement caused by collagenous overgrowth of gingival firous connective tissue.

It may be familial or idiopathic.

Clinical Features

• Gingival enlargement starts before age of 20 years and it is correlated with eruption of deciduous and permanent teeth.
• It occurs as diffuse or nodular growth of gingiva over maxillary or mandibular arch.
• Maxilla is affcted more frequently.
• Surface of gingiva is pebbled.
• Gingiva is pink or pale in color.
• Consistency of gingiva is fim and leathery.
• Gingiva is non­tender and does not bleed.
• Gingival swelling leads to spacing between the teeth.
• Extension of gingiva is so severe that it can cover the crown of the erupted tooth.

Histology

• Surface epithelium exhibits long, thin rete ridges that extend deep into underlying firous connective tissue.
• Connective tissue is dense hypocellular and hypovascular.
• Collagen fiers are present in form of bundles which are interspersed with firoblasts.
• Inflammation is mild to absent.
• At times scattered islands of odontogenic epithelium, foci of dystrophic calcification or areas of osseous metaplasia may be seen.

Treatment

Gingivectomy should be done.

 

Question.7. Write short note on gingival enlargement.
Or
Write short note on gingival hyperplasia.

Answer. Gingival enlargement is the increase in size of gingiva.

Gingival Hyperplasia Associated with Vitamin C Deficiency

Vitamin C deficiency leads to scurvy and the disease has following manifestations:

• Gingiva becomes tender, edematous and swollen.
• Frequent bleeding is present from gingiva.
• Crest of the inter­dental papillae appear reddish or purple in color.
• Ulceration and necrosis of gingiva occur.
• Foul smell is present from the mouth.

Gingival Hyperplasia Associated With Leukemia

• Gingiva becomes soft, edematous and swollen.
• Gingiva is painful and has purplish and has glossy appearance.
• Surrounding mucosa is pale and petechiae is seen.
• Ulceration and severe hemorrhage occur on gingiva.

Gingival Hyperplasia Associated With Endocrine Imbalance

Hormonal imbalance mostly increases the proliferative potential of gingival tissue in response to irritation caused by plaque,bacteria and local irritants. Following manifestations develop clinically:

• Gingiva becomes red, edematous and swollen.
• Frequent bleeding is present.
• At times localized tumor growth develops on gingiva during pregnancy.
• Gingiva becomes soft, edematous and swollen.
• Gingiva becomes soft, edematous and swollen.

Gingival Hyperplasia Associated With Dilantin Sodium Therapy

It causes gingival hyperplasia as its side effct. Manifestations associated are:

• Presence of painless enlargement of interdental papilla.
• Swelling is rough, lobulated and has a pebbled surface.
• Gingiva is normal in color and increased stippling is present.
• Gingiva is fim and tender and there is no tendency to bleed.
• As drug therapy is stopped gingival growth ceases.

Question.8.Classify gingival enlargement. Give a detailed account of enlargement caused by drugs.

Answer.

Gingival Enlargement Caused By Drugs

• Drug-related gingival enlargement is an abnormal growth of gingival tissue which is secondary to the use of systemic medication.
• Drug-related gingival enlargement is a misnomer because neither the epithelium and nor the cells inside the connective tissue undergo hyperplasia or hypertrophy.
• Increase in the size of gingiva is because of increased amount of extracellular matrix mainly collagen.
• Strong association of drug induced gingival enlargement is related to three drugs, i.e. cyclosporine, phenytoin and nifedipine.
  All the drugs causing gingival enlargement lead to calcium dysregulation which disrupt normal collagen phagocytosis and remodeling process.
• Prevalence related to use of phenytoin is 50% while cyclosporine and nifedipine produce changes in 25%.
• Degree of drug-induced gingival enlargement is related significantly to patient’s susceptibility and level of oral hygiene.
• Degree of drug-induced gingival hyperplasia is higher in smokers.
• Dilantin sodium was the fist drug reported to cause gingival enlargement.

Clinical Features

• Phenytoin is commonly given in young patients so it induces a problem in people younger than 25 years of age.
• Patients taking calcium channel blockers are of middle age and cyclosporine has a broad age range.
• As any of the drug is used for 1 to 3 months enlargement occur in interdental papillae and spread to the tooth surface. Anterior and facial segments are more frequently involved areas. Enlargement is painless.
• In extensive cases of hyperplasia, gingiva cover almost complete crown surface.
• If there is extension of gingiva lingually and occlusally this can interfere with speech and mastication.
• Edentulous areas are usually not affcted but hyperplasia is seen under poorly maintained dentures as well as around the implants.
• Non­gingival soft tissue growths which look like pyogenic granulomas are seen in allogenic bone marrow transplant recipients who are taking cyclosporine for graft versus host disease.
• Enlarged gingiva is normal in color and is fim, it has smooth, stippled or granular surface.
• If inflammation occurs affected gingiva is dark red and edematous, surface become friable, bleeds easily and occasionally ulcerated.

Histopathology

• Gingival overgrowth caused by phenytoin shows redundant tissue of normal composition.
• Gingival overgrowth caused by cyclosporine shows increase amount of collagen per unit volume with normal density of fibroblast.
• Overlying surface epithelium show elongation of rete ridges with long extension in underlying lamina propria.
• Patients with secondary inflammation show increased vascularity and increased chronic inflammatory cell infiltrate composed of lymphocytes and plasma cells.

Treatment

• Discontinue the offending medication which leads to regression in size of gingiva.
• If drug substitution can be done than cyclosporine is replaced with tacrolimus; phenytoin with carbamazepine, lamotrigine, gabapentin etc and nifedipine with atenolol.
• Professional cleaning, frequent re­evaluation and home plaque control is done.
• Systemic or topical folic acid is beneficial in some cases.
• Cyclosporine-induced gingival hyperplasia resolve after short course of metronidazole or azithromycin.
• When objectionable alterations are present and all other interventions fail, gingivectomy is the treatment of choice.