These results confirm previous studies and indicate that approximately half of the variance in disease in the population is attributed to genetic variance. The basis for the heritability of periodontitis appears to be biological and not behavioral in nature.

Recent theoretical analyses indicate that our findings are most consistent with an interpretation of EOP as a complex, oligogenic disorder, with IL-1 genetic variation contributing an important but not exclusive influence on disease risk.

Recent studies have demonstrated that smoking is associated with periodontal destruction. The majority of these studies have focused on periodontal disease groups with moderate or severe periodontal destruction. Additionally, there have been few reports investigating the relationship between smoking and gingival recession. The goal of this report was to investigate the effect of smoking on periodontal destruction and recession in subjects with minimal or no interproximal attachment loss. This is a cross-sectional study of 142 non-smoking subjects and 51 smoking subjects. Subjects could have no more than one tooth with a site of interproximal attachment loss > or =2 mm. Subjects could, however, have attachment loss associated with recession. For three different methods of summarizing attachment loss measurements at a subject level, including average attachment loss, percentage of teeth with one site of 2 mm of attachment loss, and the percentage of teeth with one site of 5 mm of attachment loss, smoking subjects had approximately twice as much attachment loss than their non-smoking counterparts. Smoking subjects also had significantly greater recession (P < 0.05) [0.056+/-0.017 mm] than non-smoking subjects (0.025+/-0.005 mm). Recession sites occurred primarily on the facial surface of maxillary molars and bicuspids and mandibular central incisors and bicuspids. The results suggest a strong association between smoking and both attachment loss and recession in subjects who have minimal or no periodontal disease.

Interleukin-17 (IL-17), the prototype cytokine produced by the Th17 subset of T-helper cells, plays a role in inflammatory responses, autoimmunity, and antimicrobial responses in a variety of infectious and inflammatory diseases. In view of the inflammatory nature and severity of aggressive periodontitis, we hypothesized that IL-17 might be detected in sera from patients with aggressive periodontitis. We used ELISA to measure IL-17 serum concentrations from 67 periodontally healthy (NP) individuals and from 53 patients with localized (LAgP) and 49 patients with generalized (GAgP) aggressive periodontitis. IL-17 was barely detectable in sera from periodontally healthy individuals (1.9 ± 2.0 pg/mL), but was present at significantly higher concentrations in sera from those with LAgP (7.6 ± 2.2 pg/mL) and GAgP (17.1 ± 2.3 pg/mL). Multivariate analyses demonstrated associations of IL-17 concentrations with periodontal attachment loss, but not with current smoking. Therefore, Th17 responses may be characteristic of AgP, and IL-17 may play a role in the pathogenesis of aggressive periodontitis.

The subgingival microflora of 39 HIV + subjects with gingivitis or adult Periodontitis was cultured quantitatively anaerobically for bacteria, spirochetes, and mycoplasma and aerobically for yeasts. Isolates were characterized by conventional biochemical tests, Polyacrylamide gel electrophoresis of soluble proteins, cellular fatty acid profiles, immunofluorescence, and immunodiffusion. In general, the same types of bacteria were isolated from the subgingival crevice of HIV + subjects as we previously had isolated from the subgingival crevice of non‐HIV subjects. A statistically significant difference was found between the composition of the flora of HIV + subjects with adult Periodontitis (AP) and concurrent studies of a non‐HIV + AP population. Mycoplasma salivarium was significantly elevated in the HIV+ subjects examined. Yeasts were isolated from only 10% of the samples and from 13% of the HIV‐positive subjects at 0.05 to 0.0002% of the total cultivable count when present. J Periodontol 1993; 64:48–56.