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Porphyromonns gingivalis (P. gingivalis) adheres teeth through interaction of its major fimbrial protein with salivary components which have adsorbed onto the teeth. It has been suggested that coadhesion between P. gingivalis and early plaque bacteria like Actinomyces vircosus (A. viscosus) is a major contribution in the colonization of P. gingivalis to teeth and is mediated in part by fimbriae of P. gingivalis. The role and contribution of coadhesion of P. gingivalis with A. viscosus in colonzation of P. gingivalis and the role of P. gingivalis fimbriac in the event were investigated. ^(3)H-labeled P. gingivalis 2561 on fimbria-deficient mutant DPG3 was incubated with 2 ㎎ of HAP beads coated with whole human saliva (sHAP) and then with A. viscosus T14V (T14V-acinobeads) or with WVU627-acinobeads). The mixture was layered on 100% Percoll to separate unbound from beads-bound components. The radioactivity of the washed beads was a raeasure of the bound components. Binding of P. gingivalis 2561 cells to T14V- and WVU627-actinobeads was 1/2 and 1/2.5 of its binding to sHAP beads, respectively. Similary binding of A. viscosus T14V to P. gingivalis 2561-coated sHAP beads (Pg-beads) was reduced by 66% as rompared with its binding to sHAP beads, while binding of WVU627 to Pg-beads was slightly increased (33%). The result suggests that the coadhesion may not play an important role in binding and colonization of P. gingivalis on teeth. Binding of DPG3 to actinobeads was compared with that of P. gingivalis 2561. Although the binding levels of DPG3 to WVU627-actinobeads were almost identical to those of P. gingivalis 2561, its binding levels to T14V-actinobeads were 3 times greater than those of P. gingivalis 2561 in the range of P. gingivalis used. Furthermore, the addition of fimbriae did not significantly inhibit the binding of P. gingivalis 2561 to T14V-actinobeads, indicating that fimbriae may not be important in the coadhesion. Binding inhibition assays were carried out using P. gingivalis 2561 and T14V-actinobeads in the presence of synthetic fimbrillin peptides. The peptides which had appearrd to be inhibitory against the binding of P. gingivalis to sHAP beads, the event in which fimbriae and proline-rich protein-1 (PRP-Ⅰ) were not involved simultaneously, also inhibited P. gingivalis binding to T14V-actinobeads by 53 to 67%. In contrast, the peptide which had been shown to be inhibitory against fimbrial binding to PRP-1 did not block P. gingivalis binding to T14V-actinobeads. Overall these results suggest that coadhesien ofP. gingivalis with A. viscosus is not a major contribution in P. gingivalis binding to teeth and the coadhesion is not mediated by fimbriae, but porsibly by other surface components of P. gingivalis. If there was any invotveinent of fimbriae, this may be due to the binding of the fimbriae to salivary components other than PRP-1, which are not orcupied by A. viscosus.
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