Exploring the Calcitonin Receptor Relationship With Bone Resorption in Odontogenic Cysts

Understanding the pathogenesis of odontogenic cysts (OCs) may facilitate the development of alternative therapeutic strategies and improve patients' quality of life. Given calcitonin's role in regulating bone metabolism and its clinical applications in gnathic bone-destructive lesions, including OCs, this study assessed potential associations between CTR and the bone resorption markers receptor activator of nuclear factor kappa B ligand (RANKL) and tumor necrosis factor alpha (TNF-α) in OCs. Immunohistochemical analyses were performed on 20 radicular cysts (RCs), 20 radicular residual cysts (RRCs), and 27 dentigerous cysts (DCs). RANKL expression in the epithelial lining was significantly higher in RCs and RRCs compared with DCs ( p =0.039 and p =0.046, respectively). In RCs, significant positive correlations were found between epithelial RANKL and capsular CTR ( p =0.039), epithelial TNF-α and capsular TNF-α ( p =0.037), and epithelial TNF-α and capsular CTR ( p =0.005). In RRCs, epithelial RANKL correlated positively with epithelial TNF-α ( p =0.007) and capsular CTR correlated positively with capsular TNF-α ( p =0.041), whereas epithelial RANKL correlated negatively with capsular TNF-α ( p =0.009). In DCs, significant positive correlations were observed between epithelial and capsular RANKL ( p <0.001) and between epithelial and capsular TNF-α ( p =0.019). These findings suggest that CTR contributes to the pathogenesis of DCs, RCs, and RRCs, and highlight the involvement of RANKL and TNF-α in the biological behavior of these cysts. The interplay among these proteins may promote either osteolytic or osteogenic activity depending on the cystic microenvironment.