One of the most distinctive features of the spondyloarthropathies is the tendency for new bone formation at sites of chronic inflammation. This is important diagnostically because radiographic evidence of ankylosis is often stated as one of the classification criteria, and it is important clinically because loss of spinal mobility over time is a major contributor to disability in this disease. The mechanisms underlying this tendency for ankylosis have not yet been defined. This review updates current concepts of the molecular and cellular basis of normal and abnormal bone formation. A better understanding of this process may open new avenues of therapeutic intervention in these chronic diseases.