Ankylosing spondylitis is a chronic inflammatory rheumatic disease, characterized by axial pain and osteoproliferation, leading to painful rigidity of the spine and disability. In contrast with this bone formation, bone loss is an early event in this disease, and an increased vertebral fracture risk (but not non-vertebral fracture risk) has been reported in these patients.
Prospective studies have shown that potent anti-inflammatory drugs, such as anti-TNF therapies, can prevent bon loss and low bone density without effect on bone proliferation, i.e. without evidence of prevention of ossification of ligamentous structures. Ankylosing spondylitis is a relevant model for assessing the effect of inflammation on bone. Data suggest that low sclerostin levels may participate to the structural change. Recent evidence of the presence of enthesis-resident T cells which can be activated by IL-23 and promote lesions that are characteristic of ankylosing spondylitis can open new therapeutic pathways.
18 May 2013 - 22 May 2013