Oral lichen planus (OLP) is a chronic, immune-mediated inflammatory disease of the oral mucosa that can cause persistent pain and has a recognized, though relatively low, risk of malignant transformation. Recent studies have identified oxidative and nitrosative stress as key contributors to the pathophysiology of OLP. Excessive production of reactive oxygen and nitrogen species, combined with reduced antioxidant defenses, leads to cellular damage, including lipid peroxidation, protein modification, and DNA injury. This oxidative imbalance drives keratinocyte apoptosis and sustains inflammatory signaling, creating a pro-inflammatory tissue environment. In parallel, metabolic dysfunction is increasingly recognized in OLP, characterized by altered energy production and nutrient utilization that disrupt tissue homeostasis. These two processes are closely linked, as oxidative stress impairs metabolic pathways, while metabolic alterations further increase oxidative burden, forming a self-reinforcing cycle that perpetuates mucosal injury and chronic inflammation. Clinically, markers of oxidative stress and metabolic imbalance, particularly those detectable in saliva, show promise for non-invasive diagnosis and risk assessment. Therapeutic strategies aimed at restoring redox balance and improving metabolic regulation represent emerging avenues beyond conventional symptom management. Understanding the crosstalk between oxidative stress and metabolism offers new opportunities for precision medicine approaches to improve the diagnosis, treatment, and long-term outcomes of patients with OLP.
Song et al. (2026) studied this question.