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.

A total of 78 bacteriological samples were taken from the supragingival tooth surface after superficial cleaning with toothpicks or from the periodontal sulci of 42 affected sites in 21 adolescents or young adults with severe generalized periodontitis. Of 190 bacterial species, subspecies, or serotypes detected among 2,723 isolates, 11 species exceeded 1% of the subgingival flora and were most closely associated with the diseased sulci. Eleven others were also sufficiently frequent to be suspect agents of tissue destruction. Many of these species are known pathogens of other body sites. In addition, 10 species of Treponema were isolated. One of these and the "large treponeme" were also more closely associated with severe periodontitis than they were with healthy sites or gingivitis. There were highly significant differences between the composition of the flora of the affected sulci and the flora of (i) the adjacent supragingival tooth surface, (ii) the gingival crevice of periodontally healthy people, and (iii) sites with a gingival index score of 0 or 2 in experimental gingivitis studies. The floras of different individuals were also significantly different. There was no statistically detectable effect of sampling per se upon the composition of the flora of subsequent samples from the same sites. The composition of the supragingival flora of the patients with severe generalized periodontitis that had serum antibody to Actinobacillus actinomycetemcomitans was significantly different from the supragingival flora of patients without this serum antibody. However, there was no statistically significant difference in the composition of their subgingival floras.

Statistical comparisons of the floras associated with juvenile periodontitis, severe periodontitis, and moderate periodontitis indicated that differences in the bacterial compositions of affected sites in these populations were not statistically significant. The subgingival flora of affected juvenile periodontitis sites was statistically significantly different from the adjacent supragingival flora and from the subgingival floras of people with healthy gingiva and of children with developing (experimental) gingivitis. However, the subgingival flora of affected juvenile periodontitis sites was not significantly different from the flora of sites with gingival index scores of 1 or 2 in adults with developing (experimental) gingivitis. Of 357 bacterial taxa among over 18,000 isolates, 54 non-treponemal species, 2 treponemal species, and mycoplasma were most associated with diseased periodontal sulci. These species comprised an increasing proportion of the flora during developing gingivitis * Corresponding author.

From replicate trials of experimental gingivitis in four periodontally healthy subjects, 166 bacterial species and subspecies were detected among 3,034 randomly selected isolates from 96 samples. Of these bacteria, Actinomyces naeslundii (serotype III and phenotypically similar strains that were unreactive with available antisera), Actinomyces odontolyticus (serotype I and phenotypically similar strains that were unreactive with available antisera), Fusobacterium nucleatum, Lactobacillus species D-2, Streptococcus anginosus, Veillonella parvula, and Treponema species A appeared to be the most likely etiological agents of gingivitis. Statistical interpretations indicated that the greatest source of microbiological variation of the total flora observed was person-to-person differences in the floras. The next greatest source of variation was the inflammatory status of the sample sites. Person-to-person differences were smallest at experimental day 4. The floras became more diverse with time and as gingivitis developed and progressed. Analyses indicated that sequential colonization by certain species was repeatable and therefore probably predictable. Variation was relatively small between replicate trials, between two sites on the same teeth sampled on the same day, and between the same sites sampled at the same relative time in a replicate trial.

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.