Aim: The aim of this systematic review was to produce the best available evidence and pool appropriate data to evaluate the effect of tooth brushing on the initiation and progression of non-inflammatory gingival recession. Material and Methods: A protocol was developed a priori for the question: ''Do factors associated with tooth brushing predict the development and progression of non-inflammatory gingival recession in adults?'' The search covered six electronic databases between January 1966 and July 2005. Hand searching included searches of the Journal of Clinical Periodontology, Journal of Periodontal Research and the Journal of Periodontology. Bibliographies of narrative reviews, conference proceedings and relevant texts known to the authors were also searched. Inclusion of titles, abstracts and ultimately full texts was based on consensus between three reviewers. Results: The full texts of 29 papers were read and 18 texts were eligible for inclusion. One abstract from EuroPerio 5 reported a randomized-controlled clinical trial [Level I evidence] in which the authors concluded that the toothbrushes significantly reduced recessions on buccal tooth surfaces over 18 months. Of the remaining 17 observational studies, two concluded that there appeared to be no relationship between tooth brushing frequency and gingival recession. Eight studies reported a positive association between tooth brushing frequency and recession. Other potential risk factors were duration of tooth brushing, brushing force, frequency of changing the toothbrush, brush (bristle) hardness and tooth brushing technique. None of the observational studies satisfied all the specified criteria for quality appraisal and a valid appraisal of the quality of the randomized-controlled trial was not possible. Conclusion: The data to support or refute the association between tooth brushing and gingival recession are inconclusive.

A major virulence factor of Porphyromonas gingivalis is the extracellular noncovalently associated complexes of Arg-X-and Lys-X-specific cysteine proteinases and adhesins designated the RgpA-Kgp complexes. In this study we investigated the ability of RgpA-Kgp as an immunogen to protect against P. gingivalis-induced periodontal bone loss in the rat. Specific-pathogen-free Sprague-Dawley rats were immunized with either formalin-killed whole P. gingivalis ATCC 33277 cells with incomplete Freund's adjuvant, RgpA-Kgp with incomplete Freund's adjuvant, or incomplete Freund's adjuvant alone. The animals were then challenged by oral inoculation with live P. gingivalis ATCC 33277 cells. Marked periodontal bone loss was observed in animals immunized with incomplete Freund's adjuvant alone; this bone loss was significantly (P < 0.05) greater than that detected in animals immunized with formalin-killed whole cells or RgpA-Kgp or in unchallenged animals. There was no significant difference in periodontal bone loss between animals immunized with formalin-killed whole cells and those immunized with RgpA-Kgp. The bone loss in these animals was also not significantly different from that in unchallenged animals. DNA probe analysis of subgingival plaque samples showed that 100% of the animals immunized with incomplete Freund's adjuvant alone and challenged with P. gingivalis ATCC 33277 were positive for the bacterium. However, P. gingivalis ATCC 33277 could not be detected in subgingival plaque samples from animals immunized with formalin-killed whole cells or with RgpA-Kgp. Immunization with formalin-killed whole cells or RgpA-Kgp induced a high-titer serum immunoglobulin G2a response. Western blot analysis of RgpA-Kgp using pooled protective antisera taken from rats immunized with RgpA-Kgp revealed immunodominant bands at 44, 39, and 27 kDa. In conclusion, immunization with RgpAKgp restricted colonization by P. gingivalis and periodontal bone loss in the rat.

The hypothesis that periodontal disease is associated with pre-term low birthweight was tested in a prospective follow-up study of rural prima-gravida women (N = 227) who were free of tobacco, alcohol, and drug use. Women with 3rd trimester mean probing pocket depths, plaque, and bleeding scores that were greater than the median value in the cohort were defined as "exposed". There were 17 (7.5%) preterm low birthweight singleton deliveries in the cohort (among "exposed" = 12%; among "unexposed" = 5.6%; Odds Ratio = 2.3; 95% CI = 0.9-6.3). After adjustment for the independent variables, the OR for preterm low birthweight in relation to "exposure" was 1.9 (95% CI = 0.7-5.4). Our results are only suggestive of an association between periodontal disease and preterm low birthweight, perhaps indicating that previously reported associations may have been subjected to residual confounding due to tobacco, alcohol, and drug use.