BACKGROUND: Oral lichen planus (OLP) is a chronic inflammatory disorder defined as a precancerous condition. Special attention has been paid to the expression of cyclooxygenase-2 (COX-2) and its potential role in development of oral squamous cell carcinoma. The identification of single nucleotide polymorphisms that affect gene function or expression and contribute to disease predisposition has become a major area of investigation toward understanding the mechanisms for cancer. OBJECTIVE: The objective of this study is to investigate the association between the COX-2 765G>C gene polymorphism, tissue COX-2 expression and the development of OLP as a chronic inflammatory condition. METHODS: This study was done on 50 patients with OLP and 50 healthy controls. COX-2 activity was assessed by measuring tissue prostaglandin E (PGE)2 levels by enzyme immunometric assay kit. COX-2 765G>C gene polymorphism was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR) followed by restricted fragment length polymorphism (RFLP). RESULTS: OLP patients showed statistically significant higher mean PGE2 than the control group. We did not observe any statistically significant differences in genotype distribution or allele frequency between the patients and the control group (P > 0.05). Odds ratio showed no statistically significant association between COX-2 765G>C polymorphism and lichen planus. CONCLUSION: The present evidence thus indicates that variation in the COX-2 gene is unlikely to be of relevance to the aetiology of OLP. As this is the first report concerning the COX-2 -765G>C gene polymorphism and the risk of OLP, additional studies with larger sample size will be required to confirm these findings.
BACKGROUND: Oral lichen planus (OLP) is a chronic inflammatory disorder defined as a precancerous condition. Special attention has been paid to the expression of cyclooxygenase-2 (COX-2) and its potential role in development of oral squamous cell carcinoma. The identification of single nucleotide polymorphisms that affect gene function or expression and contribute to disease predisposition has become a major area of investigation toward understanding the mechanisms for cancer. OBJECTIVE: The objective of this study is to investigate the association between the COX-2 765G>C gene polymorphism, tissue COX-2 expression and the development of OLP as a chronic inflammatory condition. METHODS: This study was done on 50 patients with OLP and 50 healthy controls. COX-2 activity was assessed by measuring tissue prostaglandin E (PGE)2 levels by enzyme immunometric assay kit. COX-2 765G>C gene polymorphism was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR) followed by restricted fragment length polymorphism (RFLP). RESULTS: OLP patients showed statistically significant higher mean PGE2 than the control group. We did not observe any statistically significant differences in genotype distribution or allele frequency between the patients and the control group (P > 0.05). Odds ratio showed no statistically significant association between COX-2 765G>C polymorphism and lichen planus. CONCLUSION: The present evidence thus indicates that variation in the COX-2 gene is unlikely to be of relevance to the aetiology of OLP. As this is the first report concerning the COX-2 -765G>C gene polymorphism and the risk of OLP, additional studies with larger sample size will be required to confirm these findings.