Consistent Intrafamilial Transmission of Actinobacillus actinomycetemcomitans Despite Clonal Diversity Bas xak Dog ˘an,* Arzu S xahan Kipalev, Emel O ¨ kte, Nedim Sultan, and Sirkka E. Asikainen § Background: Actinobacillus actinomycetemcomitans is a major pathogen in aggressive periodontitis. Our objectives were to determine the periodontal status and occurrence of A. actinomycetemcomitans in family members of subjects with A. actinomycetemcomitans positive aggressive periodontitis (AgP) and to evaluate the probability of its intrafamilial transmission. Methods: Of the 300 subjects screened, 66 (22%) had AgP and A. actinomycetemcomitans. Eleven (probands) of these 66 sub- jects with AgP met the strict inclusion criteria for the study. The study population consisted of 55 subjects, including probands and their family members (N = 44). Two family groups were formed according to whether the proband was a child (N = 7) or a parent (N = 4). Subgingival samples from all subjects were cultured for A. actinomycetemcomitans, and its clonal types were determined by combining serotype and genotype data for each isolate. Results: Among 42 dentate family members, 16 (38%) exhibited periodontitis and eight (50%) had AgP. Periodontitis was found in nine of 12 (75%) of the dentate parents and six of 17 (35%) siblings of the child probands. A. actinomycetemcomitans was detected in 16 of 31 (52%) family members, i.e., one parent and at least one sibling in six families. The child probands shared A. actinomyce- temcomitans clonal types with their parents in five of six (83%) families and with their siblings in three of six (50%) families. In the four parent–proband families, A. actinomycetemcomitans oc- curred in two spouses and all nine children. The parent probands shared A. actinomycetemcomitans clonal types with their spouses in both families and with their children in three of four families. In all families, the likelihood of intrafamilial transmission of A. actinomy- cetemcomitans was statistically significant. Members of most fam- ilies (eight of 11, 73%) also harbored additional clonal types of A. actinomycetemcomitans. Conclusion: Parents and siblings of an individual with A. actino- mycetemcomitans–positive AgP may have an increased suscepti- bility to periodontitis and shared and/or other clonal types of oral A. actinomycetemcomitans. J Periodontol 2008;79:307-315. KEY WORDS Actinobacillus actinomycetemcomitans; family; genotype; periodontitis; serotype; transmission. T he Gram-negative, faculta- tively anaerobic coccobacillus Actinobacillus actinomyce- temcomitans is one of the major pathogens in aggressive forms of periodontitis. 1-3 It is a member of the indigenous oral flora and can be found in periodontally healthy sub- jects. 4-6 Indigenous oral bacteria can act as pathogens in their own habitat, and there are interspecies differences in their pathogenicity. 7 More recently, in an attempt to explain, at least in part, the dual role of oral bacteria as members of nor- mal flora and as pathogens, research has focused on intraspecies differ- ences of certain oral bacteria. For example, phylogenetic studies 8,9 on A. actinomycetemcomitans have identified separate evolutionary line- ages for serotypes b and c, whereas serotypes a, d, e, and f seem to share an additional lineage. It is tempting to speculate that strains from differ- ent evolutionary lineages of indige- nous oral species may differ in their propensity for oral colonization and infectivity. This notion is supported by the fact that serotype b strains are found more frequently in periodonti- tis than in periodontal health, 10-13 although there may be geographic or ethnic variations, e.g., serotype c seems to predominate in Turkish sub- jects with periodontitis. 6,14 * Department of Basic Health Sciences, Faculty of Health Sciences, Marmara University, Istanbul, Turkey. † Department of Periodontology, Faculty of Dentistry, Gazi University, Ankara, Turkey. ‡ Department of Microbiology, Faculty of Medicine, Gazi University. § Section of Oral Microbiology, Institute of Odontology, Umea ˚ University, Umea ˚ , Sweden. doi: 10.1902/jop.2008.070270 J Periodontol • February 2008 307