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.

Early‐onset periodontitis (EOP) refers to a group of severe periodontal diseases with age of onset near puberty that are characterized by rapid destruction of the tissues supporting the teeth in othewise healthy individuals. Mixed model segregation analyses of 100 families, ascertained through 104 probands with EOP, were carried out to test major locus and multifactorial hypotheses for the etiology of EOP. Heterogeneity tests were used to compare the parameter estimates and conclusions obtained in Black families from those from non‐Black families. The data in these families confirmed that the oftenreported female preponderance of EOP appears to be an ascertainment bias. The segregation analysis results were consistent with an autosomal major locus being sufficient to explain the family patterns of EOP in the entire dataset, and also in both the Black and non‐Black subsets. A dominant mode of transmission was most likely, with penetrance of about 70%. Although the etiologic conclusions were the same for Black and non‐Black families, there was significant heterogeneity in parameter estimates. In particular the Black allele frequency was 0.016 versus the non‐Black frequency of 0.001. J Periodontol 1994;65:623–630.

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The purpose of this study was to determine the clinical course of early onset periodontitis and to investigate factors which may influence its clinical course. For the past 15 years we have been conducting a study of families with early onset periodontitis, and have examined 142 localized juvenile periodontitis and 185 severe generalized early onset periodontitis patients. In order to study the clinical course of early onset periodontitis we recalled our subject population to determine their periodontal status. Forty (40) patients with localized early onset periodontitis (LJP) and 48 with generalized early onset periodontitis (SP) were re‐examined. The time since the most recent visit for LJP patients was approximately 3 years and for SP patients almost 4 years. LJP patients who received periodontal therapy on the average gained periodontal attachment. In contrast, LJP patients who did not receive therapy lost periodontal attachment. SP patients lost periodontal attachment regardless of whether or not they had periodontal therapy. SP patients also lost an average of one tooth during the approximately 4 years of observation. LJP patients lost very few teeth with only 4 teeth being lost in 40 patients. The results of this study suggest that localized juvenile periodontitis is a stable disease in most individuals. In contrast, patients with severe generalized early onset periodontitis continued to lose both periodontal attachment and teeth. J Periodontol 1995; 66:321–328.

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.