A systematic literature review from 1966 to 2000 revealed 2,730 English-language publications on the role of bacteria in human primary dental caries in vivo. The most pertinent 313 papers were analyzed in evidence tables accessible online (http:// www.nidcr.nih.gov). The search targeted all bacterial types implicated previously in caries and asked two questions. First, what is the association of specific bacteria with tooth decay and can causation be attributed to any of those bacteria? Retrieved studies were categorized as randomized-blinded-interventional, longitudinal, case-control, and cross-sectional and were weighted in descending order in terms of significance. Although many studies, due to ethical requirements, had confounding variables, they still indicate strongly: 1) the central role of the mutans streptococci in initiation of caries of smooth surfaces and fissures of crowns of teeth and suggests their potent role in induction of root surface caries; and 2) that lactobacilli are implicated as important contributory bacteria in tooth decay, but their role in induction of lesions is not well supported. Second, what is the source of infection by cariogenic bacteria? Molecular/genetic studies of implicated bacteria isolated from humans, randomizedblinded-interventional, and longitudinal studies indicate that mutans streptococci are spread vertically among humans, mostly from mothers to their children. Implications of these conclusions are briefly discussed. The most significant problems of literature interpretation include the benefits/shortcomings of salivary and plaque monitoring of the flora, the role of sugar(s) in decay as it influences the flora, and modeling strategies to predict lesion score increments as distinct from determination of the etiological role of specific bacteria. Future directions for microbiological clinical caries research are suggested, and the use of the term "caries" to describe the disease, not its lesions, is urged.

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Background. Oral mucositis is a common complication of bone marrow transplantation (BMT) conditioning therapy. Sequelae consist of increased risk for infection, moderate to severe pain, compromised oral function, and bleeding. This study investigated helium‐neon laser treatment for prevention of conditioning‐induced oral mucositis in BMT patients. Patterns and severity of mucositis for specific conditioning drug regimens also were analyzed. Methods. Twenty patients received laser radiation to their oral mucosa, either left or right of midline. The contralateral side was sham‐treated and served as a control. Mucositis severity was scored independently by two modified versions of the Oral Mucositis Index Scale (OMI‐A and OMI‐B) and the Eastern Cooperative Oncology Group (ECOG) Oral Toxicity Scale; pain severity was scored by subjects on a visual analogue scale (VAS). Cumulative scores were analyzed for differences between the laser‐treated and sham‐treated sides. Results. Oral mucositis and pain scores were significantly lower for the treated versus the untreated side by OMI‐A and B (P < 0.005) and VAS (P = 0.027) criteria, respectively. Ulcerative lesions occurred in all patients bilaterally; severity increased until Day +6, and lesions resolved by Day +21. Mucositis was more severe for patients conditioned with busulfan/carboplatin/thiotepa than for patients conditioned with busulfan/cyclophosphamide/etoposide. Conclusions. Helium‐neon laser treatment was well‐tolerated and reduced the severity of conditioning‐induced oral mucositis in BMT patients.

The virulence of cell surface-associated, glucan synthesis-defective mutants of Streptococcus mutans strain 6715-13 was studied. Representatives from three groups of such mutants were tested for their pathogenicity in conventionalized, specific pathogen-free rats and gnotobiotic rats. The mutants differ from the wild-type strain in that each failed to form plaque on the smooth surfaces of the teeth and to cause smooth surface caries. Although the ability to form cell surface-associated glucans was not a strict requirement for the expression of virulence in the sulci of the teeth, it augmented virulence at such sites. However, the ability to form cell surface-associated glucans and to adhere to the teeth was clearly not the sole determinant of virulence.