| Ankylosing spondylitis (AS) is a disease characterized by chronic inflammatory arthritis caused by abnormal autoimmune function, which can develop into spinal arthritis. Chronic inflammation and pathological bone formation are its two main pathological features. Progressive spinal dyskinesia is the most important complaint in patients. So the pathological mechanism of abnormal osseous hyperplasia of the spinal joint is widely concerned. However, with the further study of AS, it is found that partial ossification of the spinal column often accompanied by systemic bone loss. This indicated that pathogenesis of AS is not due to the occurrence of abnormal osteogenesis or bone resorption alone, but because of an unbalanced environment of bone metabolism with both. Recent studies have shown Wnt, BMP signaling pathway and inflammatory reaction in AS disease not only promote osteogenesis, but also affect osteoclast formation. Nevertheless osteoclast plays a role in bone resorption, while its products participate in new bone formation. However, most studies have only focused on describing a single mechanism of osteogenesis or osteoclasts in the AS, and have not clearly elucidated how they contribute to bone mass loss in the whole body while causing bone hyperplasia around the spine. In the pathological process of AS, whether the inflammatory factors play different roles in different parts of the body, and how to control the formation of new bone and reduce the risk of osteoporosis, need to be further explored. |