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INVASION OF DENTINAL TUBULES BY ORAL BACTERIA

¹ Department of Stomatology, University of Otago School of Dentistry, PO Box 647, Dunedin, New Zealand; ² Department of Oral and Dental Science, University of Bristol Dental School, Bristol BS1 2LY, United Kingdom

View larger version (107K): [in a new window]   Figure 1. Common sites of bacterial invasion of dentin. Bacteria invading from the oral cavity (i, ii, iii, iv, v) extend toward the dental pulp space (A) and may result in inflammatory disease and infection of the pulp and periapical tissues. (B) Periapical radiograph demonstrating chronic periapical periodontitis of an upper left central incisor subsequent to infection of the root canal via an enamel-dentin crack. Bacteria invading radicular dentin (v) from an infected root canal invade outward toward the external root surface (C) and may be responsible for persistent root canal infection and inflammatory disease of the surrounding tissues. (Reprinted and modified with permission from Love, 1997.)

View larger version (74K): [in a new window]   Figure 2. Transmission electron micrographs of sections of dentin colonized by S. gordonii. (A) Individual bacterial cells adhering to the wall of a dentinal tubule, with fibrillar surface material visible at the site of association between bacterial cells and tubule. Bar: 0.5 µm. (B) A group of streptococcal cells in intimate contact with a tubule wall. Bar: 1.0 µm. (Reproduced with permission from Love et al., 1997.)

View larger version (75K): [in a new window]   Figure 3. Transverse sections of human roots showing: (A) invasion of dentinal tubules by S. gordonii wild-type cells; and (B) no dentinal tubule invasion by S. gordonii in the presence of acid-soluble collagen type I. Bar: 50 µm. (Reproduced in modified form with permission from Love et al., 1997.)

View larger version (69K): [in a new window]   Figure 4. Streptococcal invasion of dentinal tubules (upper diagram) and co-invasion with P. gingivalis (lower diagram). Streptococcal cells (•) adhere to unmineralized collagen type I ( ) via antigen I/II polypeptide adhesin (). Growth of streptococci in the presence of collagen peptides leads to up-regulation of antigen I/II production (), long-chaining of cells, and colonization along the length of the tubule. In the lower diagram, P. gingivalis cells (•) and S. gordonii cells both adhere to collagen (1), but P. gingivalis is unable to penetrate the tubules further in monoculture. The presence of S. gordonii (2) provides an additional binding substrate for P. gingivalis and promotes intratubular colonization by P. gingivalis. Up-regulation of streptococcal antigen I/II adhesin production (3) provides additional binding sites for P. gingivalis. These bacteria remain in association with the streptococci (4), and the dentinal tubules become invaded by a mixed bacterial population.