Objective. To investigate the effect of etanercept therapy on radiographic progression in patients with ankylosing spondylitis (AS).Methods Conclusion. Unlike other inflammatory rheumatic diseases such as rheumatoid arthritis and psoriatic arthritis, structural progression in AS seems to be independent of TNF, despite the fact that TNF is responsible for the signs and symptoms due to inflammation in this disease.Ankylosing spondylitis (AS) belongs to a family of rheumatic diseases known as spondylarthritides that characteristically cause spinal joint inflammation and bony fusion of the spine. AS is the prototype of the spondylarthritides and is typified by ankylosis of the axial skeleton. Radiographic damage known to result from AS primarily includes fusion of entheses of the sacroiliac joints and of the posterior articulations and ligaments of the spine. These fusions can lead to impaired spinal mobility and in turn decreased ability to perform daily activities and severely reduced healthrelated quality of life (1).Tumor necrosis factor ␣ (TNF␣) has been shown to play an important role in the inflammatory response observed in AS. It has been found at increased levels in the serum and synovium of patients with AS (2,3), and treatment with TNF␣-blocking agents (etanercept, adalimumab, and infliximab) has been shown to safely and effectively reduce the signs and symptoms of AS (4-6) and significantly improve health-related quality of life (1). In addition, these agents have been shown to ClinicalTrials.gov identifier: NCT00356356.

Patients with AS have an increased risk of clinical vertebral fracture but not of non-vertebral fractures, while the risk of any clinical fracture is increased in patients with concomitant inflammatory bowel disease. The mechanism by which non-steroidal anti-inflammatory drugs reduce the risk of any clinical fracture warrants further research.

A considerable proportion of AS patients will experience a vertebral fracture during the course of the disease, in particular if peripheral joints are also involved.

In AS, cartilage degradation plays a role in explaining radiological-damage and -progression in the spine.

Patients with AS have a 5-fold higher risk of clinical spine fracture and a 35% increased risk of non-vertebral fracture. This excess risk peaks early, in the first 2.5 years of AS disease. Patients should be assessed for fracture risk early after AS diagnosis.