The chronic disease of ankylosing spondylitis is not well understood in our lives. In particular, the pathological changes of ankylosing spondylitis are not clear. This makes it difficult for many people with ankylosing spondylitis to be treated. Experts have provided comprehensive explanations for this complex disease. Here’s what we know about ankylosing spondylitis pathology. The complication of ankylosing spondylitis is the attachment of ligaments and joint capsules. The characteristic changes in the pathology of ankylosing spondylitis are ligament attachment end disease, which leads to ligamentous bone formation, squared-off vertebral body changes, destruction of the vertebral endplates, Achilles tendinitis and other changes. Because the tendon end is a metabolically active site, at least during the growth phase, it is a plausible area for the development of AS in early childhood, and it remains unknown why the tendon end is preferred. The synovial changes in the joints surrounding AS are characterized by granulomatous synovial fire. There is infiltration of macrophages, lymphocytes and plasma cells around the small synovial vessels, thickening of the synovium, and after months or years, granulation tissue formation in the affected synovium. There is obvious calcification and ossification of the soft tissues around the joints, and ligamentous redundancies can be formed at the ligamentous attachments, which continuously extend longitudinally and become two direct bony bridges adjacent to the vertebral body, and calcification of the paravertebral ligament and the anterior vertebral ligament, making the spine “bamboo-like”. As the lesion progresses, there is a significant tendency for ossification in and around the joints. In the early stages, the ligaments, fibrous rings, intervertebral discs, periosteum and trabeculae are invaded by vascular and fibrous tissue and replaced by granulation tissue, leading to destruction of the entire joint and sclerosis of the adjacent bone; after repair, fibrous and bony ankylosis of the joint eventually occurs, with vertebral osteoporosis, muscle atrophy and thoracic kyphosis. Inflammation of the vertebral cartilage endplates and intervertebral disc margins eventually causes local ossification. Cardiac lesions are characterized by invasion of the aortic valve, thickening of the aortic adventitia, shortening due to fibrosis but not fusion, and enlargement of the aortic annulus, sometimes with fibrosis reaching inferior to the basal part of the aorta. Occasionally, pericardial and myocardial fibrosis is seen, and histology reveals chronic inflammatory cell infiltration of epicardial vessels and endarteritis; the middle elastic tissue of the aortic wall is destroyed and replaced by fibrous tissue, and fibrotic tissue that invades the atrioventricular bundle causes atrioventricular block. The complications of ankylosing spondylitis can also cause pulmonary lesions, which are characterized by patchy inflammation of the lung tissue with round cell and fibroblast infiltration, and eventually develop into interalveolar fibrosis with vitreous changes. The reason why ankylosing spondylitis is a very special disease is that it causes many complications and has a great impact on the life of the patient. This is because patients with ankylosing spondylitis should be actively treated and have a good attitude towards the disease.