Periodontal disease and gingivitis are diseases in which essentially 100% of the population is "at risk." In excess of 80% of tooth loss after the age of 35 has been attributed to this chronic, destructive disease process. With the recognition and general acceptance of a delayed hypersensitivity response as the major factor in the etiology of gingivitis and periodontal disease, the primary thrust of research is shifting toward an identification of the antigens involved. The demonstration of lymphocyte stimulation by sonicated dental plaque samples and disrupted suspensions of Actinomyces viscosis together with the positive correlation with the extent of periodontal involvement implicates indirectly the components of plaque, i.e., bacteria and their products. The recent work of Hammond, et al, has demonstrated the presence of a cell wall polysaccharide antigen in virulent but not in avirulent strain of Actinomyces viscosis. A. viscosis strains will be isolated from dental patients (with periodontal health and pathology) and surveyed for content of virulence antigens. The possible correlation between presence of the virulence antigens and the periodontal health or pathology will be determined. The proposed study will use physical, enzymatic, and chemical methods to extract cell surface antigens from A. viscosis T14V (virulence) and T14AV (avirulent). Extraction will be monitored by analytical serological, ultrastructural, and chemical analysis. Those antigens found to be unique to the virulent strain will be purified and characterized. The blastogenic response of peripheral blood lymphocytes from patients with periodontal disease will be examined to indicate relative biological significance of the antigens.