Bacterial adhesins--their role in tubule invasion and endodontic disease.

Bacterial invasion of dentinal tubules is critical to the progression of dental caries and the development of pulp and periapical disease, and may also influence the progression of periodontal disease. However, little is known about the host or bacterial mechanisms involved in tubule invasion. Recent work has demonstrated that bacterial interactions with dentine, and salivary and tissue molecules influence invasion. Salivary molecules such as mucin and immunoglobulin G (IgG) co-aggregate with bacterial cells, which inhibits dentine invasion, while deposition of dentinal tubule fluid molecules e.g. albumin, IgG, or fibrinogen within dentinal tubules also inhibits invasion. Dentine invasion by streptococci has been shown to be associated with a bacterial growth response and adhesion to unmineralized collagen, which are mediated by streptococcal cell-surface antigen I/II polypeptides. These adhesins possess diverse binding properties including binding to salivary glycoprotein, other bacteria, and to collagen. Additionally, some antigen I/II polypeptides facilitate species-specific co-invasion between streptococci and obligate anaerobes that lack the ability to invade by themselves. An understanding of the mechanisms involved in bacterial invasion of dentine should allow development of new control strategies.