Gingival And Periodontal Diseases Question And Answers

Gingival And Periodontal Diseases Question And Answers

Question 1. Write short note on fibromatosis gingivae.
Answer.

• It is also called as elephantiasis gingiva, congenital macrogingivae.
• It appears as diffuse overgrowth of gingival tissues, which is hereditary.

Fibromatosis Gingivae Clinical Features

• It may be present at birth or may become apparent with eruption of deciduous or permanent teeth.
• It is manifested as dense, smooth, diffuse or nodular overgrowth of gingival tissue of one or both arches that usually occurs at time of eruption of teeth.
• Tissue is normal or pale in color.
• Consistency is firm, leathery and dense, so it prevents normal eruption of teeth.
• It is not painful and shows no tendency for hemorrhage
• Extent may be such that crown of fully erupted teeth may be hidden.
• The dense firm gingival swelling results in spacing between the teeth and change in profile and facial appearance.

Read And Learn More:  Oral Medicine Question And Answers

Fibromatosis Gingivae Management

• Surgical removal of excessive tissue with exposure of teeth is necessary.
• Extraction of teeth can also be done.

Question 2. What are the predisposing factors for acute necrotizing ulcerative gingivitis? Describe the clinical features and treatment plan for this condition.
Answer. 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, vitamin B2 leads to the exaggeration of pathologic changes caused by fusospirochetal bacteria.
• Psychosomatic conditions: The disease is associated with the stress and with increment in adrenocortical secretion.
• Debilitating diseases: Diseases such as 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.

Acute Necrotizing Ulcerative Gingivitis Clinical Features 

• It is commonly seen in age group of 16 to 30 years and is commonly seen children of low socioeconomic status.
• Onset of the disease is sudden along with pain, tenderness, profuse salivation and peculiar metallic taste. There is presence of spontaneous bleeding from gingiva.
• Loss of taste sensation is present.
• Patients who used to smoke feel diminished pleasure of the smoking.
• Fetid odor is present which is very unpleasant.
• Teeth get slightly extruded and are sensitive to pressure. Teeth may become mobile.
• Typical lesion in acute necrotizing ulcerative gingivitis is necrotic, punched out crater like ulcer which develops on interdental papillae and the marginal gingiva. As the lesion is manipulated, it leaves raw surface.
• Surface of the gingival crater is covered by grey, pseudomembranous slough which can be demarcated from the remaining gingival mucosa by a linear erythema.
• At times ulcer develop on cheek, lip, tongue and pharynx.
• Regional lymphadenopathy is evident.
• In advanced cases systemic complications such as high fever, malaise, loss of appetite, lassitude, loss of appetite.
• Patient complaints of difficulty in taking food due to salivation and presence of metallic taste in the mouth.

Acute Necrotizing Ulcerative GingivitisTreatment

• The involved areas are isolated with cotton rolls and dried. A topical anesthetic is applied and after 2 to 3 minutes, areas are gently swabbed with a cotton 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 along with metronidazole 400 mg, 8 hourly for a week should be given.
• Scaling is performed, if sensitivity permits. After disease process is diminished, complete gingival curettage and root planning is done.
• Supportive treatment consists of copious fluid consumption and administration of nutritional supplements.

Question 3. Discuss in detail the clinical features, etiology, investigation and management of ANUG in detail.
Answer. For clinical features refer to Ans 2 of same chapter.

ANUG Etiology

It is caused by the two bacteria, i.e. fusiform bacilli and spirochetes.

Systemic predisposing factors

• Malnutrition: This may lead to acute necrotizing ulcerative gingivitis
• Nutritional deficiency: Deficiency of vitamin C, vitamin B1, vitamin B2 leads to the exaggeration of pathologic changes caused by fusospirochetal bacteria.
• Psychosomatic conditions: The disease is associated with the stress and with increment in adrenocortical secretion.
• Debilitating disease: Diseases such as 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.

ANUG Investigations

The investigations are associated with testing of fusiform bacilli and spirochetes.

• Spirochetes and fusiform bacilli are demonstrated in stained smears of exudates from the lesion on microscopic examination. The spirochete T. palladium is visible on dark ground microscopy.
• Direct fluorescent antibody test is done for detection of spirochete T. palladium
• Enzyme immunoassays are also done to detect for spirochetes present in ANUG.
• Antibody tests, i.e. detection of specific IgM antibody is helpful in detection of Treponema.
• Biopsy of the lesion shows destruction of surface epithelium which is replaced by pseudomembranous meshwork of fibrin, necrotic epithelial cells, PMN leukocytes and other microorganism. Underlying connective tissue is hyperemic with multiple engorged capillaries and dense infiltration of PMN leukocytes. At periphery of infiltrate numerous plasma cells are present.

ANUG Management

For details refer to Ans 2 of same chapter.

Question 4. Describe etiopathogenesis, clinical features, differential diagnosis, treatment and complications of acute necrotizing ulcerative gingivitis.
Answer. For clinical features and treatment refer to Ans 2 of same chapter.

Etiopathogenesis

Proliferation of anaerobic fusiform bacteria and spirochetes results in ANUG. The infection mostly occurs in presence of phychological 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.

Etiopathogenesis 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, skin lesions are present.
• Pemphigus: It presents 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.
• Agranulocytosis: On investigation the blood picture demonstrates evidence of systemic disease and because of the diminished immunity, lesion is not marked by severe inflammatory reaction.

Etiopathogenesis Complications

Patient affected by ANUG develop systemic complications such as:

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

Question 5. Enumerate vesiculobullous and ulcerative lesions of oral mucosa. Write in detail etiopathogenesis, clinical features, treatment plan and complications of ANUG.
Answer. For enumeration of vesiculobullous and ulcerative lesions of oral mucosa refer to Ans 1a of chapter VESICuLAR, BuLLOuS AND uLCERATIVE LESIONS.

For etiopathogenesis and complications refer to Ans 4 of same chapter.

For clinical features and treatment refer to Ans 2 of same chapter.

Question 6. Write short note on various causes of generalized gingival enlargement.
Answer. Generalized gingival enlargement is the widespread involvement of gingiva throughout the mouth.

Generalized gingival enlargement may be caused by poor oral hygiene, medications, serious systemic illnesses, hematologic disorders and genetic conditions, or it may be idiopathic.

Inflammatory: Inflammatory gingival enlargements are characterized by swelling or edema, redness and a tendency to bleed on periodontal probing. Long-standing inflammatory enlargements may have a fibrotic component. The primary local factor associated with these enlargements is plaque.

Drug-induced: Fibrotic gingival enlargements resulting from medication are pink, firm and lobulated. This condition frequently presents as a generalized, irregular enlargement of the attached and marginal gingiva on both facial and lingual aspects. Various sorts of drugs (immunosuppressants, anticonvulsants and calciumchannel blockers) may be responsible.

Hereditary: A rare fibrotic gingival enlargement of unknown etiology is hereditary gingival fibromatosis. This condition has been referred to as gingivomatosis, elephantiasis, idiopathic fibromatosis, hereditary gingival hyperplasia and congenital familial fibromatosis. This diagnosis is suggested by a family history of gingival enlargement, which generally begins with the eruption of the primary or permanent dentition.

Conditioned: Hormonal changes occurring during pregnancy and puberty cause generalized gingival hyperplasia, as altered tissue metabolism accentuates the response to local irritants. During pregnancy, the increase in both progesterone and estrogen levels induces changes in vascular permeability leading to gingival edema and an increased inflammatory response to dental plaque. The enlargement is usually generalized and tends to be more prominent interproximally than on the facial and lingual surfaces.

Systemic conditions: Gingival infiltration associated with leukemia produces generalized swelling of gingiva that, clinically, mimics that of inflammatory origin. Typical oral findings with acute leukemias include gingival hyperplasia, oral ulceration, spontaneous gingival bleeding, petechiae, mucosal pallor, herpetic infections and candidiasis. Acute myeloid leukemia (AML) is the most serious condition associated with gingival enlargement. In patients with AML, signs and symptoms of bone marrow failure, such as ecchymoses, night sweats, recent infections and lethargy, can accompany the gingival enlargement.

Question 7. Write short note on conditional gingival enlargements.
Answer. Conditioned gingival enlargement occurs when systemic condition of patient exaggerates or distorts the usual gingival response to dental plaque.

• Bacterial plaque is necessary for the initiation of this type of enlargement.
• The three types of conditioned gingival enlargement are:
  • Hormonal (Pregnancy, puberty).
  • Nutritional (Vitamin C deficiency).
  • Allergic.

Gingival Enlargements Hormonal

Enlargement in Pregnancy or Pregnancy Tumor

• Marginal Enlargement:
  • It results from aggravation of previous inflammation and does not occur without clinical evidence of local irritation.
  • Pregnancy does not cause this condition, the altered tissue metabolism in pregnancy accentuates the response to local irritation.

Marginal Enlargement Clinical features

• Enlargement is generalized and tends to be more prominent interproximally than on facial and lingual surface.
• Enlarged gingiva is bright red or magenta, soft and friable having smooth, shiny surface.
• Bleeding occurs spontaneously.

 Tumor-like Enlargement:

It is not a neoplasm but an inflammatory response to local irritation and is modified by patient condition. It appears after first trimester but may be early also.

 Tumor-like Enlargement Clinical features

• The lesion appears as discrete, mushroom-like flattened spherical mass that protrude from inter-dental papilla or gingival margin and is attached by pedunculated base.
• It tends to expand laterally and pressure from tongue and cheek increases, it flattened appearance.
• The color is dusky red or magenta with smooth glistering surface which exhibits numerous deep red, pinpoint markings.
• Consistency is semifirm, but has varying degrees of softness and friability.
• It is painless, till its size and shape harbors debris in margin or interfere with occlusion where painful ulceration may occur.

 Tumor-like Enlargement Management

• The aim of periodontal therapy for pregnant patient is to minimize potential exaggerated inflammatory response related to hormonal alteration.
• Meticulous plaque control, scaling and root planning, polishing should be nonemergent periodontal procedures performed.
• Second trimester is the safest time in which treatment is performed.
• In conditions like ‘supine hypertensive syndrome’ which occur during third trimester, in this appointment should be short and patient should change her position frequently.
• Fully reclining position should be avoided as far as possible.
• Medication and radiographs are avoided.
• In case of marginal and inter dental enlargement scaling and curettage is done.
• In case of tumor like enlargement, surgical excision is done which is postponed until postpartum. During pregnancy, if it causes problem in mastication, it is removed on patients desire.

 Enlargement in Puberty Clinical Features

• Enlargement is seen in marginal and interdental papilla and is characterized by prominent bulbous interproximal papilla.
• Frequently only the facial gingiva is affected, because mechanical action of tongue prevents accumulation of food on lingual surfaces.
• Patients aged 7 to 11 years show high prevalence of gingival enlargement.

 Enlargement in Puberty Management

• Scaling, curettage and oral hygiene instructions.
• Surgical removal in severe cases.

Nutritional, i.e. Vitamin C Deficiency Enlargement

Acute vitamin C deficiency does not itself cause gingival inflammation but it causes hemorrhage, collagen degeneration and edema of gingival connective tissue. These changes modify response of gingiva to plaque.

Vitamin C Deficiency Enlargement Clinical Features

Gingival enlargement is marginal, bluish red, soft, friable and have smooth, shiny surface.

• Hemorrhage occurring either spontaneously or on provocation.
• The surface necrosis with pseudomembrane formation are common features.

Allergic, i.e. Plasma Cell Gingivitis

It is thought to be allergic in origin, possibly related to the components of chewing gum, dentifrices or various diet components.

Plasma Cell Gingivitis Clinical Features

• It consist of mild marginal gingival enlargement that extends to the attached gingiva.
• Gingiva appears red, friable and bleeds easily. An associated chelitis and glossitis is seen.

Plasma Cell Gingivitis Management

• Scaling, curettage and oral hygiene instructions.
• Surgical removal in severe cases.