### Theories  
OLLs are increasingly recognized as adverse reactions to a wide variety of medications, including antihypertensives, lipid-lowering agents, antimalarials, diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), and antibiotics. Among antihypertensives, satrans (angiotensin receptor blockers, ARBs) and ACE inhibitors are frequently implicated due to their potential to modulate inflammatory pathways and trigger immune dysregulation. Beta blockers, calcium channel blockers (e.g., amlodipine), and diuretics (e.g., hydrochlorothiazazide) have also been associated with OLLs, primarily through mechanisms involving T cell activation, oxidative stress, and delayed hypersensitivity reactions [21; 22; 23]. Statins, widely used for lipid management, are also notable for their pleiotropic effects on inflammation and T cell modulation, which may contribute to OLL development in predisposed individuals. Elevated cholesterol levels modulate the immune responses of T cells because cholesterol is a key component of the cell membrane. Lymphocyte responses to external signals are coordinated by many molecules that accumulate in the cholesterol-rich regions of the cell membrane called lipid rafts. These lipid rafts serve as platforms for immune cell activation and the inhibition of cholesterol synthesis. Statins interrupt these lipid rafts, affecting the functioning of lymphocytes [24; 25; 26; 27]. OLP, which shares histopathological features with OLLs, is caused by a change in the immune response, in which the T helper 1 lymphocytes no longer intervene. Instead, T helper 2 cells trigger the reactivity of B cells, leading to the production of pathogenic self-antibodies. Although the exact mechanisms linking statins to OLLs remain unclear, their immunomodulatory properties suggest a possible role in triggering or exacerbating these lesions. Histopathological findings in statin-induced OLLs often reveal lymphocytic infiltrates along the basal membrane, apoptotic keratinocytes, and eosinophilic infiltrates, indicating an immune-mediated cytotoxic reaction similar to that observed in drug-induced lichenoid eruptions [28; 29]. Antihypertensives contribute to OLLs through multiple mechanisms. Type IV hypersensitivity reactions play a crucial role, in which drugs such as ACE inhibitors, satrans, beta blockers, and calcium channel blockers alter antigen presentation and activate CD8+ T lymphocytes, leading to basal keratinocyte apoptosis and chronic mucosal inflammation. Oxidative stress is another significant factor, particularly with beta blockers and calcium  
Figure 2: A clinical intraoral image showing a unilateral whitish, reticulated lesion on the buccal mucosa, accompanied by areas of erythema. The lesion presents a slightly irregular but well-defined pattern, consistent with lichenoid mucosal alterations. antagonists, which can increase reactive oxygen species (ROS), disrupt epithelial integrity, and amplify inflammatory responses. Furthermore, the immunomodulatory effects of antihypertenives, especially satrans, can interfere with cytokine signaling and induce an autoimmune-like response, further exacerbating oral mucosal damage (Figure 3) [30]. A key concern in patients undergoing polydrug therapy is the risk of drug-drug interactions (DDIs), which can amplify adverse effects. DDIs occur when the pharmacokinetics or pharmacodynamics of a drug are altered by the concomitant administration of another medication, potentially intensifying the risk of lichenoid reactions. Sartans, which already exhibit immunomodulatory properties, may further contribute to this risk when combined with statins. A well-known example of drug-induced lichenoid reactions is Grinspan syndrome, in which the concurrent use of antihypertensive and antidiabetic medications has been associated with OLL onset [31]. Diagnosing drug-induced OLLs requires a meticulous evaluation of the patient's medication history, particularly focusing on recent changes or the long-term use of high-risk drugs.