###### Abstract  
Despite extensive research, the exact cause of oral lichenoid lesions remains unknown. The chronic inflammatory tissue reaction mediated by T cells is the basis of the etiological process. However, oral lichenoid lesions often occur in the presence of certain drugs. Our aim was to conduct a preliminary retrospective study to assess the correlation between the administration of statins or HMG-inhibitor CoA reductase, which are commonly used for treating hypercholesterolemia, and the satrans or blockers of the angiotensin II receptor, which are used for treating hypertension, in relation to the occurrence of oral lichenoid lesions. This preliminary retrospective study included 2158 patients who attended the Oral Medicine and Maxillofacial Surgery (Mo-Max) Department of Oral Science and Maxillofacial Surgery, Sapienza University of Rome, from 2019 to 2022. A significant association was found between the presence of oral lichenoid lesions and the simultaneous administration of satrans and statins (\(\chi^{2}=46.49\); \(p<0.001\)). Of the 2158 patients, 118 (5.5%) were diagnosed with oral lichenoid lesions. In the analysis of standardized residues, we found that pathology developed in 16.3% of patients taking statins and 15.9% of those taking satrans. Oral lichenoid lesions only developed in 4.4% of those not taking these drugs. os 202  
and methyldopa, have also been implicated, the evidence is often limited to isolated cases [1; 2; 3; 4; 5; 6; 7; 8]. Clinically, OLLs tend to appear as unilateral or localized lesions near an identifiable trigger, whereas OLP typically presents with a bilateral and symmetrical distribution. Both conditions present with various lesion types, including whitish lesions such as striae, plaques, and papules, as well as reddish alterations indicative of atrophy, erosion/ulceration, or bullae (Figures 1 and 2). These manifestations may occur independently or in various combinations. OLLs may also display more intense erythema and isolated erosions. Histologically, OLLs and OLP share features, such as a lichenoid inflammatory infiltrate and basal cell degeneration. However, OLLs often demonstrate a more diffuse lymphocytic infiltrate and include inflammatory cells like eosinophils and plasma cells, which are less common in OLP [9; 10; 11; 12; 13]. These characteristics suggest greater epithelial instability in OLLs, including cellular atypia, hyperplasia, and neovascularization, potentially increasing its risk of malignant transformation. This epithelial instability, combined with chronic inflammation, creates a pro-oncogenic environment characterized by oxidative DNA damage and cytokine-driven immune dysregulation. Recent studies have indicated that the risk of malignant transformation is higher in OLLs than in OLP, which is driven by a combination of factors such as etiology, histopathology, and inflammation. These findings underline the necessity for the vigilant, long-term monitoring of patients with OLLs, particularly those with additional risk factors like tobacco use, alcohol consumption, hepatitis C infection, or the presence of red-type lesions (atrophic, erosive, or bullous forms) [14; 15; 16]. Despite overlapping clinical presentations, OLLs and OLP require different management approaches. In OLLs, addressing the underlying trigger, such as replacing dental materials or discontinuing drugs, can resolve the condition. Conversely, OLP often necessitates long-term treatment, with topical corticosteroids being the first-line therapy. Emerging treatments such as photobiomodulation (PBM) have shown promise in cases unresponsive to corticosteroids, offering anti-inflammatory and biostimulatory benefits [17; 18; 19; 20]. In conclusion, while OLLs and OLP share certain similarities, they are distinct entities with differing etiologies and treatment protocols. Proper differentiation is essential for effective management and improved patient outcomes.