PERIODONTAL DISEASE Gingival inflammation and bleeding, or gingivitis, results from the accumulation of plaque along the gingival margins. Hormonal variations of puberty, adolescence, and pregnancy, as well as many medications such as phenytoin, also may result in gingival inflammation. As the inflammatory process progresses, destruction of the attachment apparatus occurs, and the gingival sulcus deepens, resulting in periodontal pockets and periodontitis. Periodontal pockets create a favorable environment for plaque accumulation, maturation, and mineralization into calculus. Further destruction of the periodontal attachment results. Eventually, sufficient bone loss causes tooth mobility and tooth loss. 110
The pathogenesis of periodontal disease is uncertain, but there is a very strong association between adult periodontitis and Bacteroides gingivalis. Many other specific bacteria have been shown to have a role in periodontitis. Destruction of tissue collagens, proteoglycans, and the connective tissue matrix is a major feature of gingivitis and periodontitis. Three theories for the etiology of this destruction have been proposed. Tissue destruction may occur as a result of the direct effects of bacterial plaque and their metabolic products, an accelerated host immune response, or immune deficiencies involving neutrophil function or the autologous mixed lymphocyte response.1!,0
Four distinctive types of periodontal disease have been identified. These include adult, rapidly progressing, juvenile, and prepubertal periodontitis. 10 Etiology, age and sex predilection, and clinical course of disease vary by type. A definite association between juvenile periodontitis and Actinobacillus actinomycetemcomitans exists. More severe and rapidly progressing periodontitis, especially those types affecting a younger population such as the prepubertal and juvenile periodontitis, appears to be associated with decreased neutrophil chemotaxis or phagocytosis. Systemic illnesses such as human immunodeficiency virus (HIV) infection, diabetes, lazy leukocyte syndrome, Down syndrome, and cyclic neutropenia are associated with severe periodontal disease. 1
Periodontal disease is the most common cause of tooth loss today. It usually progresses painlessly but may present as gingival bleeding or tender, swollen ginigval tissue. Treatment is directed at slowing or arresting the progression of disease primarily by the removal of plaque and its by-products. 1 Antibiotics may play a role in treatment. Referral to a dentist for definitive treatment is indicated because the treatment involves extensive dental cleaning, instruction and improvement in oral hygiene, and periodontal surgery in some cases.
PERIODONTAL ABSCESS When plaque and debris are entrapped in the periodontal pocket, a periodontal abscess may form, resulting in severe pain. Small periodontal abscesses respond to local therapy with warm saline rinses and antibiotics such as penicillin VK 500 mg PO qid or erythromycin 250 mg PO qid. Larger periodontal abscesses require incision and drainage. Saline mouth rinses four times a day are useful. Analgesics are essential.
ACUTE NECROTIZING ULCERATIVE GINGIVITIS Acute necrotizing ulcerative gingivitis (ANUG) is an aggressively destructive process ( Fig,...234-5). Also known as Vincent's disease or trench mouth, it is part of a spectrum of disease ranging from localized ulceration of the gingiva to often fatal noma, in which localized ulceration and necrosis spread to the adjacent tissues of the cheeks, lips, and underlying facial bones. —I2 ANUG is also related to Vincent's angina or tonsilar ulceration and necrosis. The diagnostic triad includes pain, ulcerated or "punched out" interdental papillae, and gingival bleeding. Secondary signs include fetid breath, pseudomembrane formation, "wooden teeth" feeling, foul metallic taste, tooth mobility, lymphadenopathy, fever, and malaise. —I3
The differential diagnosis for ANUG is quite extensive, but herpes gingivostomatitis is most difficult to differentiate. Herpes gingivostomatitis usually has smaller vesicular eruptions, less bleeding, more systemic signs, and lack of interdental papilla involvement. 1213
The etiology of ANUG is still poorly understood, but three patterns of disease have been clearly identified: the malnourished child pattern, the young adult stress pattern, and the HIV-positive adult pattern. It appears to be an opportunistic infection in a host with lowered resistence. It is believed that suppression of the humoral and cell-mediated immune response in HIV infection, severe malnourishment, and perhaps stress are responsible for this lowered host resistence. Anaerobic bacteria such as Treponema, Selenomonas, Fusobacterium, and Prevotella are uniformly identified. These bacteria appear to invade otherwise healthy tissue, resulting in an aggressively destructive disease process.1 I3
The most important predisposing factor is HIV infection. Previous necrotizing gingivitis infection is the second most important predisposer. Other contributing factors include poor oral hygiene, unusual emotional stress, poor diet, inadequate sleep, Caucasian heritage, age less than 21 years, poor socioeconomic status, recent illness, alcohol use, tobacco use, acatalasia, and various infections such as malaria, measles, and intestinal parasites. 1 13
The treatment is threefold. Primarily, identification and resolution of the predisposing factors are essential. Bacterial control using chlorhexidine oral rinses twice daily, professional debridement and scaling by a dentist, and adjunctive antibiotic therapy with metronidazole 250 mg tid are the mainstay of treatment. 12 A significant reduction in pain can be expected within 24 h of institution of this regimen.3 Finally, supportive therapy with a soft diet rich in protein and vitamins and plenty of fluids is important in establishing and maintaining a disease-free state.12
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