Studies are continuing to define the fimbriae of Actinomyces viscosus and A. naeslundii that mediate the adherence of these oral bacteria to various cells and oral tissue surfaces and thereby contribute to microbial colonization, dental plaque formation and the initiation of gingivitis and periodontal disease. The type 1 fimbriae of A. viscosus are involved in bacterial attachment to the acquired salivary pellicle to teeth. The amino acid sequence of the type 1 fimbrial subunit has now been deduced from the nucleotide sequence of the cloned gene. Certain anti-type 1 fimbrial antibodies were previously shown to block bacterial adsorption to saliva-treated hydroxyapatite; however, antibodies directed against the 59 Kd fimbrial subunit appear to be poor inhibitors of adsorption even though they reacted with the type 1 fimbriae on actinomyces. Thus, the fimbrial subunit may not be directly involved in the adhesive interaction. Type 2 fimbriae of A. Viscosus and A. naeslundii have been associated with a Gal/GalNAc specific lectin activity. The type 2 fimbrial subunit of A. naeslundii was identified as a 60 kD protein by cloning and expression of the corresponding gene in Escherichia coli. DNA- DNA hybridization was observed between the genes for A. naeslundii and A. viscosus type 2 fimbrial subunits as well as those for A. naeslundii type 2 and A. viscosus type 1 subunits. Thus, the different fimbriae of Actinomyces sp. may be composed of subunits encoded by genes derived from a common ancestor. The receptor for type 2 Actinomyces fimbriae on S. sanguis 34 has been identified as a linear polysaccharide formed by identical hexasaccharide units linked through phosphodiester bridges. Different structural features of the hexasaccharide appear to be involved in lectin and antibody recognition since the specificity of bacterial coaggregation is strikingly different from that of antibody against the polysaccharide. These studies have begun to provide a structural basis for understanding the specificity of oral microbial adherence and mechanisms by which oral bacteria resist the immune system.
