Abstract
Introduction Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disorder with unclear pathogenesis. Bone formation is a hallmark feature of AS, precise mechanisms of which are unknown. The aim of this review was to summarize the current knowledge regarding both clinical significance and pathogenesis of bone formation in AS. Materials and methods Articles, published in the medical literature and chapters in textbooks related to the discussed topic, were critically reviewed and relevant data were selected, collated and organized for the purpose of this manuscript. Results Conventional radiography is the most valuable classical tool for identification of structural changes in AS. The typical manifestations of bone formation in AS usually involve the axial skeleton, including spine, sacroiliac and hip joints, and, if properly recognized, have an important role in diagnosing, classifying and monitoring patients. Molecular pathways leading to bone formation in AS have not been elucidated sufficiently. Abnormally active signalling by wingless-type (wnt)-like and bone morphogenic protein (BMP)-mediated pathways have been suggested as major contributors to diseaserelated ossification in AS. The only medicines, shown currently to delay the process of bone formation in AS patients, are nonsteroidal anti-inflammatory drugs. Conclusion Better understanding and prediction of structural damage would help to improve and individualize management of patients suffering from AS.
Highlights
Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disorder with unclear pathogenesis
Better understanding and prediction of structural damage would help to improve and individualize management of patients suffering from AS
Radiographic features of bone formation in AS Bone formation is a characteristic feature of AS, which, if properly recognized, has an important role in diagnosing, classifying and monitoring patients suffering from the disease
Summary
Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disorder with unclear pathogenesis. The presence of inflammation at the areas of subsequent osseous proliferation is considered to be a necessary trigger; but, on the other hand, the rate of new bone formation in AS does not seem to be a simple function of the inflammatory activity of the disease, and the precise mechanisms of the progressive ankylosis are unknown. It is well appreciated that the rate and course of new bone formation can be individually determined, with some AS patients having radiographic ankylosis already upon first clinical presentation, while others do not develop ankylosis even after longstanding disease. The factors influencing this significant variability in both rate and magnitude of new bone formation in individuals with AS have not been elaborated.
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