Aberrant bone formation and dysregulated bone homeostasis in ankylosing spondylitis

Ankylosing spondylitis (AS) is a chronic, progressive, systemic autoimmune disease characterised by spinal stiffness and ocular, cardiac, intestinal, and peripheral joint involvements. Genetics, infectious agents, and immune-mediated inflammatory processes have all been hypothesized to contribute to AS pathogenesis, but the precise aetiology remains elusive. Recent studies have identified biological and cellular factors that correlate with the onset and progression of AS. This has provided avenues of research that may help elucidate disease mechanisms and lead to advances in therapeutic interventions. This study aimed to examine some of the findings from recent molecular studies, focusing on the molecular mechanism and associated factors such as interleukin-17, tumor necrosis factor-alpha, receptor activator of nuclear factor-kappa B/receptor activator of nuclear factor-kappa B ligand/osteoprotegerin pathway, and related microRNAs to gain insight into aberrant bone formation in AS and potential approaches to its prevention. This editorial also addresses the contribution of osteoclasts to bone pathology in AS. The author examined the molecular pathways governing osteoclast differentiation and activity, with particular emphasis on relevant cytokines and immune cell interactions. A comprehensive understanding of these mechanisms is essential for the development of targeted therapies to mitigate excessive bone resorption and pathological skeletal remodeling in AS.