A study on genetic polymorphism in Matrix Metalloproteinases-3 in oral submucous fibrosis patients and in healthy individuals

Abstract

Background: OSF is a potentially malignant condition affecting the oral cavity and oropharynx. MMP-3 also known as Stromelysin -I is a key member of the MMP family which is responsible for degradation of collagen type II,IV,V,IX and X, proteoglycans, gelatins, fibronectin, laminin and elastin. It plays an important role in activation of pro MMP-1 into the active form of MMP-1 in malignant tissues. MMP-3 expression is low in normal tissues but it is altered during tumour formation, where remodeling of ECM is required. Purpose of the study: To assess the association of single-nucleotide polymorphisms, Adenosine (Insertion/ Deletion) in -1171 5A > 6A in the MMP-3 promoter regions of patients with oral submucous fibrosis and in healthy individuals (controls). Methods: Thirty cases of OSF were categorized according to Khanna et al classification into four groups and Twenty age and sex matched controls were included in the study. Blood samples were collected in EDTA coated vacutainers and PCR restriction analysis was done. A statistical analysis was done using Chi-square test and Fisher's exact test to assess the frequency and association of the alleles in the case-control group. Results: The result showed a statistical significance difference between the duration of habit and disease severity with polymorphisms. The result also showed a higher frequency of the 5A allele in the study group as compared to the controls. Conclusion: A long-term follow up of these patients is mandatory to see the prognosis and their susceptibility to malignancy. The positive outcome of an association of the disease with polymorphisms would result in the development of potential diagnostic and therapeutic possibilities in potentially malignant and malignant lesions.

COL1A2 Polymorphism contributes to Oral submucous fibrosis: A possible role in inducing alternative splicing in areca chewers

“…and some other study suggested to be around 30%. 27,28 Previously, polymorphic MnlI restriction endonuclease site of COL1A1 and polymorphic PvuII restriction endonuclease site of COL1A2 are situated in exon 25, reported to be associated with OSMF risk but profound mechanism associated with OSMF pathogenesis is unknown. 9 Moreover, the contribution of collagen polymorphism in association with OSCC is not reported so far despite the elevated level of collagen-type mRNA.…”