RESUMO
CONTEXT: Connective tissue devastation in periodontitis and other chronic inflammatory diseases is a major concern. There are several inflammatory mediators associated with this process among which matrix metalloproteinases (MMPs) play a predominant role. Collagen degradation is primarily mediated by the collagenases. MMP-13 is familiar as collagenase-3, which has the aptitude to humiliate fibrillar collagen. AIMS: This study aims to evaluate MMP-13 promoter polymorphism, 11A/12A, and -77A/G and associated alleles in patients with and without chronic periodontitis (CP). SETTINGS AND DESIGN: This was an observational case-control study. MATERIALS AND METHODS: Of the total 100 patients, 50 with CP (test group) and 50 without CP (Control group), blood was collected for deoxyribonucleic acid isolation. The 11A/12A and -77A/G polymorphisms of the MMP-13 gene were picked out by polymerase chain reaction (PCR)- single-strand conformation polymorphism analysis method and PCR-restriction fragment length polymorphism by BseNI restriction enzyme, respectively. STATISTICAL ANALYSIS USED: Association between MMP-13 genotype (GTs) (11A/12A, 11A/11A, 12A/12A) and (AA, AG, GG) was assessed by Chi-square and Student's t-test for intergroup comparison. RESULTS: 11A/12A GT was seen in 24% and 20%, 11A/11A 64% and 72%, 12A/12A 12% and 8% in test and control groups, respectively. However, the association was not statistically significant. -77A/G polymorphism associated GT s AA was 56% and 62%, AG 24% and 28%, GG 20% and 10% in test and controls, respectively. An association of GG was statistically significant. CONCLUSION: The present study results indicated that MMP-13 -77A/G gene polymorphisms, GG GT may be predicted intensive ability for CP. On the other hand, there was no significant association between MMP-13 11A/12A gene polymorphisms with CP.
RESUMO
AIM: To investigate if cisplatin alters vitamin status and if VR modulates cisplatin induced intestinal apoptosis and oxidative stress in Wistar/NIN (WNIN) male rats. METHODS: Weanling, WNIN male rats (n = 12 per group) received adlibitum for 17 wk: control diet (20% protein) or the same with 50% vitamin restriction. They were then sub-divided into two groups of six rats each and administered cisplatin (2.61 mg/kg bodyweight) once a week for three wk or PBS (vehicle control). Intestinal epithelial cell (IEC) apoptosis was monitored by morphometry, Annexin-V binding, M30 cytodeath assay and DNA fragmentation. Structural and functional integrity of the villus were assessed by villus height/crypt depth ratio and activities of alkaline phosphatase, lys, ala-dipeptidyl amino-peptidase, respectively. To assess the probable mechanism(s) of altered apoptosis, oxidative stress parameters, caspase-3 activity, and expression of Bcl-2 and Bax were determined. RESULTS: Cisplatin per se decreased plasma vitamin levels and they were the lowest in VR animals treated with cisplatin. As expected VR increased only villus apoptosis, whereas cisplatin increased stem cell apoptosis in the crypt. However, cisplatin treatment of VR rats increased apoptosis both in villus and crypt regions and was associated with higher levels of TBARS, protein carbonyls and caspase-3 activity, but lower GSH concentrations. VR induced decrease in Bcl-2 expression was further lowered by cisplatin. Bax expression, unaffected by VR was increased on cisplatin treatment. Mucosal functional integrity was severely compromised in cisplatin treated VR-rats. CONCLUSION: Low intake of vitamins increases the sensitivity of rats to cisplatin and promotes intestinal epithelial cell apoptosis.
