Recently, we have further investigated the pathogenesis of ankylosing spondylitis caused by Chlamydia pneumoniae and found that Chlamydia pneumoniae cadavers (antigens) and nucleic acids can be detected in the joints of patients, and proposed a new mechanism by which ankylosing spondylitis can be caused by the deposition of Chlamydia pneumoniae antigens. Chlamydia pneumoniae is a common respiratory pathogen. After infection of humans, some Chlamydia pneumoniae can break the mucosal barrier of the respiratory tract to enter the bloodstream, parasitize in mononuclear phagocytes and lymphocytes, and reach the joint cavity with the bloodstream, causing joint inflammation. Within the joint cavity, the vast majority of these pathogens are killed, and only a very small percentage can survive. These surviving chlamydia can cause inflammation in the joints. Killed chlamydial cadaver components (antigens) can also cause inflammation; they deposit on the synovial membrane of the joint and irritate it causing inflammation. The most prominent component of Chlamydia pneumoniae is probably the lipopolysaccharide component. Our study tentatively suggests that lipopolysaccharides deposited on synovial membranes can stimulate the expression of TLR4 receptors, further activating inflammatory pathways leading to the production of tumor necrosis factor. Some populations are susceptible to recurrent infections with Chlamydia pneumoniae, and the deposition of chlamydial cadaveric components on the synovium continues to activate inflammatory pathways, ultimately leading to the development of ankylosing spondylitis. Chlamydia pneumoniae is a highly prevalent disease, and recurrent or difficult to control ankylosing spondylitis is also associated with recurrent infections with pathogens such as Chlamydia pneumoniae. Therefore , prevention and control of Chlamydia pneumoniae infection is a prerequisite for maintaining stable ankylosing spondylitis.