Involvement of Porphyromonas gingivalis fimA genotype in treatment outcome following non-surgical periodontal therapy.
BACKGROUND: Porphyromonas gingivalis is considered a critical pathogen in periodontal diseases. It is classified into six genotypes based on diversity of the fimA gene encoding fimbrillin. The present study evaluated the involvement of the fimA genotype in treatment outcome following non-surgical periodontal therapy. METHODS: Chronic periodontitis patients were enrolled in this study; all received clinical and microbiological examinations at baseline. The detection of subgingival species and identification of P. gingivalis fimA genotypes were performed using polymerase chain reaction based methods. In total, 160 P. gingivalis positive sites with bleeding on probing (BOP) and a probing depth of > or =4 mm were accepted. They were followed up after scaling and root planing. RESULTS: Longitudinal investigation indicated that fimA type I positive sites at baseline were followed by a significantly higher frequency of persistent BOP after treatment than type I negative sites (51.6% versus 27.9%), while types Ib and II were not. Type I positive sites also showed more persistence of Tannerella forsythensis and P. gingivalis after treatment than type I negative sites. In post-treatment investigation, type I positive sites showed higher frequencies of BOP and T. forsythensis detection than type I negative sites (77.8% versus 43.5% and 100% versus 76.1%, respectively). CONCLUSIONS: BOP in initially type I positive sites showed little improvement with treatment, and the combined persistence of fimA type I and T. forsythensis seemed to be involved in this poor treatment outcome. The present study demonstrated the potential of P. gingivalis fimA type I as a predictor of persistent BOP after treatment.[1]References
- Involvement of Porphyromonas gingivalis fimA genotype in treatment outcome following non-surgical periodontal therapy. Fujise, O., Miura, M., Hamachi, T., Maeda, K. J. Periodontol. (2005) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
