Spondyloarthritis (SpA) is a form of chronic inflammatory arthritis affecting axial and peripheral joints, which may be initiated by inflammation of joint subchondral bone marrow or enthesitis. Invasive fibrous tissue which substitutes bone marrow, entheseal innate-like T lymphocytes and proinflammatory cytokines: tumor necrosis factor (TNF), interleukins 23, 17 and 22, all contribute to these local pathological processes. Joint inflammation, joint cartilage and bone destruction are mediated by mechanisms that are molecularly similar to rheumatoid arthritis. These pathologic processes are halted by effective anti-inflammatory therapy, including anti-TNF biological agents. By contrast, anti-TNF therapy fails to inhibit pathologic new bone formation, which is a unique hallmark of SpA and results, among others things, in syndesmophyte formation followed by spine ankylosis. The molecular mechanisms driving pathologic bone remodeling in SpA patients and interaction of this process with inflammatory pathways are not fully understood. Three hypotheses, discussed in the article, have been proposed to explain this issue
