The prevalence of clinically significant overgrowth related to chronic medication with calcium channel blockers is low, i.e., 6.3% for nifedipine. Males are 3 times as likely as females to develop clinically significant overgrowth. The presence of gingival inflammation is an important cofactor for the expression of this effect.

Eight patients (mean age 15.6 yrs) with severe molar-incisor bone loss and pocket formation characteristic of juvenile periodontitis were entered into a clinical protocol of three sequential stages: scaling and root planing (S/RP); S/RP concurrent with systemic tetracycline therapy (1 gm/day for 28 days); periodontal surgery concurrent with systemic tetracycline therapy. Clinical and microbiological examinations were scheduled at baseline, at 1 to 2 months after Stage I, at 1 to 2 months after completion of tetracycline therapy in Stages II and III, and during recall. A decision to progress to the next stage or to place the patient on a 3-month recall was based solely on clinical findings (suppuration, bleeding upon probing and pocket depth) at the deepest site in each patient. Paperpoint subgingival plaque samples from representative affected sites were analyzed for percentage of total cultivable microflora composed of black-pigmented Bacteroides species (BPB), surface translocating bacteria (STB) and Actinobacillus actinomycetemcomitans (Aa). At baseline, all sites bled to probing, seven of eight sites showed suppuration, and deepest pocket depths averaged 8.0 mm. STB were detected in one and BPB in four sites, respectively, and all sites demonstrated Aa, which constituted approximately 40% of the total cultivable flora. S/RP alone had essentially no effect on either clinical or microbiological findings, and all patients progressed to Stage II. Five went on to Stage III. S/RP with tetracycline was clinically and microbiologically more effective at sites in which Aa was predominant. Surgery was required in all sites containing high levels of both BPB and Aa. These results suggest that microbiological diagnosis may be useful in selecting and monitoring treatment for juvenile periodontitis.

Gingival biopsies from areas characterized as clinically normal, mild gingivitis, or periodontitis were examined. Immunoglobulin (IgG, IgA, IgM, IgE and IgD) bearing cells at the sulcular and oral epithelium -lamina propria junctions as well as the central lamina propria areas were quantitated. Normal gingiva (P. I. = 0-0.2) contained few lymphocytes and plasma cells. Biopsies from areas of mild gingivitis (P.I. = 0.2-1) were infiltrated at the sulcular epithelium -lamina propria junction by lymphocytes lacking membraneassociated immunoglohulins (94 %). Few plasma cells were evident. In contrast, tissue associated with periodontitis (P. I. = 4.0-8.0) contained significant numbers of immunoglobulin hearing lymphocytes (78 %, IgG; 9 %, IgM; and 4 % IgA) and plasma cells (67 %, IgG; 24 %, IgM; and 8 % IgA) distributed throughout all three major tissue areas.These findings indicated that the nature of cellular infiltrates differed in mild gingivitis and periodontitis. The presence of predominantly IgG and IgM containing cells in periodontitis had important implications for the contribution of nonspecific effector mechanisms to the destruction of periodontal tissue. infiltrate has not been resolved. Compara-

The cultivable subgingival microflora in the cynomolgus monkey, Macaca fascicularis, was monitored during the ligature‐induced progression of naturally occurring gingivitis to periodontitis. Clinical and microbiological observations were divided into four stages. Stage I, prior to ligature placement, was characterized clinically by chronic generalized gingivitis and microbiologically by Gram‐positive cocci and rods with B. melaninogenicus ss. intermedius the dominant Gram‐negative organism. Stage II, 1 to 3 weeks following ligature placement, exhibited slightly greater gingival inflammation but no clinical evidence of attachment loss. The subgingival flora showed a significant increase in motile and surface translocating Gram‐negative rods, primarily Capnocytophaga species and Campylobacter sputorum. Stage III, 4 to 7 weeks following ligature placement, revealed increased pocket depth and radiographic evidence of alveolar bone loss. This stage was characterized by a Gram‐negative anaerobic flora with B. asaccharolyticus as the dominant cultivable organism. Stage IV encompassed the remainder of the experimental period, 8 to 17 weeks, during which time no further change in the clinical parameters occurred and levels of B. asaccharolyticus decreased. The subgingival microflora of ligature induced periodontitis in Macaca fascicularis closely resembled that reported for human periodontal disease and the episodic clinical pattern of attachment loss was associated with levels of Gram‐negative anaerobes, primarily B. asaccharolyticus.