Ankylosing spondylitis (AS) is the most common form of spondyloarthritis and its pathogenesis is not clear. It primarily affects the sacroiliac joints and spine, and could cause stiffness and deformity in severe cases. A typical manifestation at the axial skeleton is inflammatory back pain which is typically at its worst in the early morning and disappears or subsides after limbering up. The incidence of AS in males is higher than females. In males it mainly causes axial joint changes, whereas in females mainly caused peripheral joints changes. Treatment with tumour necrosis factor blockers has been proven to be an important step forward in the treatment of this disease. It influences the progression of the disease by inhibiting inflammation, but whether it can stop heterotopic ossification has not to be affirmed by sufficient evidence. This review focuses on the advances in genetic, signal-ing pathways and cellular research to explore the cause of AS. Recent research found that abnormal genes like LRP5, ANTXR2, PTGER4 and ANKH can activate the signaling pathways of bone formation, then under the directly or indirectly action of cytokines and related proteins (such as Noggin, DKK, TGF-β, BMP and CA1), the signal passes the surface of the target cells to the nucleus. This process can change the normal metabolism of the target cells, resulting in heterotopic ossification. Recently clinical imaging of AS also suggests that mechanical forces may play an important role in heterotopic ossification. In this review, literatures on heterotopic ossification were summarized, in order to further understand this disease and to provide new ideas for the treatment of AS. |