Abstract:Objective: This study aims to evaluate the eff ect of soybean milk containing a combination of anti-Streptococcus mutans IgY and chitosan to the colonization of S. mutans in the saliva and to the IgY persistency in the saliva. Materials and Methods: Experimental malnourished Sprague-Dawley rats were fed with soybean milk that is enriched with anti-S. mutans IgY and chitosan. After 15 days of feeding, we evaluated the S. mutans in dental biofi lm, in addition to the persistency level of anti-S. mutans IgY. Results: The rats that received soybean milk supplemented with anti-S. mutans IgY had the lowest number of S. mutans colonies (p < 0.05). Anti-S. mutans IgY was detected in saliva after 15 days of feeding. Conclusions: Soybean milk supplemented with anti-S. mutans IgY and chitosan could signifi cantly reduce S. mutans biofi lm, and the supplemented anti-S. mutans IgY persisted in these rats' saliva following the feeding period.

Saliva and Streptococcus mutans play role in biofilm formation. Saliva and S.mutans virulence are different between subjects with and without caries. objective: The aim of this study was to evaluate the effects of autolog saliva on biofilm formation of S. mutans isolated from caries and caries-free subjects. materials and methods: Saliva and plaque samples are obtained from caries and caries-free subjects. Plaque samples were cultured on TYS20B for 3 days. Selected colonies were picked and cultured on TSB for 3 days. After colony counting, biofilm assay was conducted and inoculated for one day. The biofilm was tested using crystal violet binding assay and quantified by measuring the optical density at 655 nm wavelength. result: The optical density of S. muttans biofilm isolated from subjects with caries were different from taste with no caries. Biofilm formation of S. muttans isolated from caries and caries-free subjects with and without the presence of autolog saliva were different. conclusion: Autolog saliva influences S. mutans biofilm formation and there is a tendency that is higher than those from subjects with no caries.

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Objective: To evaluate the possible association of a polymorphism in the gene encoding methylenetetrahydrofolate dehydrogenase 1 (MTHFD1), 1958G>A, with the susceptibility to orofacial cleft in an Indonesian population. Material and Methods: A total of 200 stored secondary biological samples from 30 cases of orofacial cleft and 170 unaffected controls were analyzed to determine the polymorphism status at base 1958. The analysis was conducted using the PCR-restriction fragment length polymorphism technique after digestion with the Msp1 restriction enzyme. The samples were then subjected to agarose gel electrophoresis to investigate the presence or absence of the following fragments: genotype GG, 196, 86 and 40 base pairs (bp); genotype AA, 282 and 28 bp and genotype AG, 282, 196, 86, 40 and 28 bp. The test groups were compared using the Chi-square test. Results: The wild-type allele containing 1958G, as well as the genotype GG, were significantly more common in the control group than in the orofacial cleft group. Conclusion:The MTHFD1 1958G>A polymorphism was significantly associated with orofacial cleft susceptibility in the tested Indonesian population.

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