Salivary MMP-9 Level: Association with Tissue Remodeling in Oral Lichen Planus

Background: Oral lichen planus (OLP) is a chronic inflammatory disorder characterized by lesions in the oral mucosa. Matrix metalloproteinase-9 (MMP-9), a key enzyme in tissue remodeling, is implicated in various inflammatory diseases, but its role in OLP pathogenesis remains unclear. This study aims to investigate salivary MMP-9 levels in patients with OLP and correlate them with the clinical characteristics of the disease, specifically considering their potential association with tissue remodeling. Methods: A case-control study was conducted, including 40 patients with clinically and histopathologically confirmed OLP and 40 healthy controls. Unstimulated saliva samples were collected from all participants. MMP-9 levels were measured using an ELISA kit. Data were analyzed using independent t-tests and correlation analysis using SPSS 20. The correlation between salivary MMP-9 levels and OLP clinical features were investigated. Results: Salivary MMP-9 levels were significantly higher in OLP patients compared to healthy controls (p < 0.001). When categorizing the subtypes of OLP, erosive and atrophic lesions presented with significantly higher MMP-9 levels than reticular lesions and healthy control group (p < 0.01). A moderate positive correlation was observed between salivary MMP-9 levels and disease severity. No correlation was observed between patients’ age and sex with MMP-9 levels. Conclusion: This study suggests that elevated salivary MMP-9 levels are associated with OLP, especially in erosive and atrophic subtypes, indicating its role in the tissue remodeling process during the progression of OLP. Our findings suggest that MMP-9 could be a useful biomarker for OLP diagnosis and potentially a target for therapeutic interventions aimed at controlling the excessive tissue remodeling associated with this disease. Further studies are necessary to validate our findings and determine the specific mechanisms through which MMP-9 contributes to OLP pathogenesis.