Degradation of Resin Restorative Materials by Streptococcus Mutans: A Pilot Study.

OBJECTIVE: To evaluate the degradation of three resin based restorative materials by S Mutans. STUDY DESIGN: Class I cavity was prepared in extracted premolars and were randomly divided into 3 groups (Group I - Conventional composite (CC), Group II - Resin Modified GIC and Group III-Giomer). Teeth were then restored by respective restorative material and equally divided in two subgroups (Control and Experimental). Experiment subgroup samples were then incubated in 2 ml of BHI with 1:10 dilution of SM (MTCC-497) grown overnight in BHI whereas control subgroup samples were incubated in BHI without SM. The incubation solution was collected at 2,14 and 30 days interval, and the analysis for identification and quantification of Bis-HPPP was done by High performance Liquid Chromatography. RESULTS: Statistical analysis of the collected data revealed a statistically increased Bis HPPP production in the presence of SM in all the tested materials, with minimum in Resin Modified GIC and a maximum in Conventional Composite (CC). CONCLUSION: SM degrades the resin based restorative materials & among the tested materials Resin Modified GIC appears to be most Biostable.

Griscelli syndrome type 2: a novel mutation in RAB27A gene with different clinical features in 2 siblings: a diagnostic conundrum / 소아과

Griscelli syndrome type 2 (GS2) is a rare autosomal recessive disease caused by mutations in the RAB27A gene. It is characterized by cutaneous hypopigmentation, immunodeficiency, and hemophagocytic lymphohistiocytosis. We describe 2 brothers who had GS2 with clinically diverse manifestations. The elder brother presented with a purely neurological picture, whereas the younger one presented with fever, pancytopenia, hepatosplenomegaly, and erythema nodosum. Considering that cutaneous hypopigmentation was a common feature between the brothers, genetic analysis for Griscelli syndrome was performed. As the elder sibling had died, mutation analysis was only performed on the younger sibling, which revealed a novel homozygous mutation in the RAB27A gene on chromosome 15 showing a single-base substitution (c.136T>A p.F46I). Both parents were heterozygous for the same mutation. This confirmed the diagnosis of GS2 in the accelerated phase in both siblings. The atypical features of GS2 in these cases are a novel mutation, isolated neurological involvement in one sibling, association with erythema nodosum, and 2 distinct clinical presentations in siblings with the same genetic mutation.