Adherence of bacteria to saliva-coated surfaces, saliva-induced aggregation of bacteria and interactions between different genera of oral bacteria (coaggregation, interbacterial adherence) are considered important in the formation and persistence of dental plaque. Changes in parotid saliva proteins after chronic isoproterenol treatment of rats have been associated with substanial decreases in the saliva-induced aggregation and in the adherence to saliva-coated hydroxyapatite of strains of Streptococcus mutans and Streptococcus sanguis. In contrast the aggregation and adherence of Actinomyces viscosus T14V were unaffected. Of the streptococcal strains tested only strains of S. mutans subspecies rattus were aggregated by saliva from isoproterenol- treated rats. Results of experiments that measured salivary protein adsorbed to hydroxyapatite and to bacterial cells suggest a role for an acidic proline-rich protein of Mr 40K in adherence. Lactose-sensitive coaggregation between Propionibacterium acnes PK93 and Streptococcus sanguis DL1 cells bound to saliva-coated hydroxyapatite (SHA) took place at bacterial concentrations between those found in human saliva and 1000-fold higher. Over this range of cell concentrations P. acnes did not adhere to SHA. Adherence to SHA of heat-treated DL1 or S. sanguis 34 (neither of which form coaggregates with PK93) did not increase the binding of P. acnes to the SHA. These results and the inhibition of the SHA-associated coaggregation by lactose or N-acetylgalactosamine support the concept that bacteria unable to attach to saliva-coated surfaces can become established in plaque via lectin-mediated interactions with primary colonizers of the tooth surface.
