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The combined results based on all studies showed that (1) chronic periodontitis cases had a significantly lower frequency of bb genotype of BsmI [OR=0.63, 95% CI=0.42, 0.94; p=0.02] in Asians; (2) chronic periodontitis cases had a significantly higher frequency of AA genotype of ApaI (OR=2.20, 95% CI=1.39, 3.48; p<0.001) in Asians; (3) chronic periodontitis cases had a weak significantly higher frequency of TT genotype of TaqI (OR=1.86, 95% CI=1.002, 3.46; p=0.049) in Asians. After Bonferroni's correction, we found that in Asians chronic periodontitis cases still had a significantly higher frequency of AA genotype of ApaI. No significant difference was found in any genotype of FokI. No association was found for all the VDR gene polymorphisms examined as far as the aggressive form of the disease is concerned. Future studies need to focus on the possible biological consequences and mechanisms of the VDR genetic variants. The current findings confirm that VDR gene is a candidate gene for periodontitis.

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To investigate the effects of ficin on biofilm formation of conditionally cariogenic Streptococcus mutans (S. mutans). Biomass and metabolic activity of biofilm were assessed using crystal violet assay, colony-forming unit (CFU) counting, and MTT assay. Extracellular polysaccharide (EPS) synthesis was displayed by SEM imaging, bacteria/EPS staining, and anthrone method while acid production was revealed by lactic acid assay. Growth curve and live/dead bacterial staining were conducted to monitor bacterial growth state in both planktonic and biofilm form. Total protein and extracellular proteins of S. mutans biofilm were analyzed by protein/bacterial staining and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), severally. qRT-PCR was conducted to detect acid production, acid tolerance, and biofilm formation associated genes. Crystal violet assay, CFU counting, and MTT assay showed that the suppression effect of ficin on S. mutans biofilm formation was concentration dependent. 4 mg/mL ficin had significant inhibitory effect on S. mutans biofilm formation including biomass, metabolic activity, EPS synthesis, and lactic acid production ( p < 0.05 ). The growth curves from 0 mg/mL to 4 mg/mL ficin were aligned with each other. There was no significant difference among different ficin groups in terms of live/dead bacterial staining result ( p > 0.05 ). Protein/bacterial staining outcome indicated that ficin inhibit both total protein and biofilm formation during the biofilm development. There were more relatively small molecular weight protein bands in extracellular proteins of 4 mg/mL ficin group when compared with the control. Generally, ficin could inhibit biofilm formation and reduce cariogenic virulence of S. mutans effectively in vitro; thus, it could be a potential anticaries agent.