Clonal Diversity of the Taxon Porphyromonas Gingivalis Assessed by Random Amplified Polymorphic DNA Fingerprinting

A total of 97 strains of the periopathogen Porphyromonas gingivalis were collected. This collection included laboratory strains and clinical isolates of human origin with diverse clinical and geographical origins. Biological diversity was further increased by including 32 strains isolated from the oral cavities of nine different animal species. Genomic fingerprints of the 129 strains were generated as random amplified polymorphic DNAs (RAPDs) by the technique of PCR amplification with a single primer of arbitrary sequence. Four nonameric oligonucleotides were used as single primers, and the banding patterns of the DNA products separated on agarose gels were compared after ethidium ethidium bromide staining. Distance coeffients based on the positions of the major DNA fragments were calculated, and dendrograms were generated. We identified 102 clonal types (CTs) that could be assembled into three main groups by cluster analysis by the unweighted pair group method with mathematic averages. Group I (n = 79 CTs) included all 97 human strains and 6 monkey isolates. The strains in group II (n = 22 CTs) and III (n = 1 CT) were strongly differentiated from those in group I and included only strains of animal origin; they likely represent two cryptic species within the present P. gingivalis taxon. We observed that strains from Old World monkeys clustered together with the human genotype, whereas strains from New World monkeys clustered with the animal genotype. Our results with human strains also indicated that (i) the population structure is basically clonal, (ii) no dominant or widespread CT could be observed, and (iii) no relationship could be established between specific clusters of CTs and the periodontal status of the host. Our results corroborate previous findings by B. G. Loos, D. W. Dyer, T. S. Whittam, and R. K. Selander (Infect. Immun. 61:204-212, 1993) and suggest that P. gingivalis should be considered a commensal of the oral cavity acting as an opportunistic pathogen. Our results are not consistent with the hypothesis that only a few virulent clones of P. gingivalis are associated with disease.