When affected these tissues are covered with a dirty yellow to gray smear. The gingiva is extremely red, swollen, inflamed, and excruciatingly painful. On examination, the patients may present the hallmark of the disease, necrosis and crater-like ulceration of the affected interdental papillae. These irritated tissues will induce salivation, and the offensive exudates can be seen and perceived by halitosis. In some cases, spontaneous hemorrhage is also encountered. This discrete clinical picture makes the feasibility of easy diagnosis by clinical examination alone. However, this simplicity is not always the case, where the disease may be generalized within the oral mucosa, rather than being generalized, and sometimes, acute oral pain is also associated with systemic symptoms of fever and malaise. Quite frequently, involvement of the regional lymph nodes is also seen in the form of painful lymphadenopathy. Generalized disease due to contiguity may involve the other areas of buccal mucosa. When involved, most commonly the oral mucosa opposite the third molar is involved. Although rare, sometimes this encompasses tongue, lips, palate. It has been shown that there is an association between plasma ascorbate deficiency and disease risk. When this clinical presentation happens as a part of necrotizing ulcerative stomatitis, it is better to err on the side of HIV infection and rule it out. In this article, the relevance of the condition to dental practice will be explained and explored based on evidence from current literature (Melnick, S. L., Alvarez, J. O., Navia, J. M., Cogen, R. B., and Roseman, J. M., 1988).
Melnick and coworkers investigates the susceptibility of necrotizing ulcerative gingivitis and in doing so they build up their study on the knowledge that impaired immune defense mechanisms and genetic factors play a role in susceptibility of this disease. In the concise literature review, the authors summarize the current literature on this disease. Although oral anaerobic bacteria have been implicated in this disease, the exact role played by them has not been elucidated. The question whether this disease is etiologically related to a genetic basis, is still unanswered, although the authors mention a familial constellation of cases. Many factors such as poverty, stress, and malnutrition have been suggested, but these have not yet been established conclusively. Numerous other associated conditions have been described in the literature, and they are important from the clinical point of view as far as the practice of dentistry is concerned, since they may alert the clinician to take adequate preventive measures when such patients are encountered. Many such conditions pathologically are related to impaired immune defense, and they are chronic cyclic granulocytopenia, agranulocytosis, cyclic neutropenia, and Down's syndrome. In all these conditions, there is either defective polymorphonuclear leukocyte functioning or secondary neutrophils deficiency. It has been suggested that these deficiencies result from presence of abnormal complement components. These complement defects are genetically controlled, and therefore, it can be inferred that these defects in complement synthesis, C3 and C4 may play some role in pathogenesis of necrotizing ul