Abstract
Recent experimental evidence suggests that IL-23 may induce spondyloarthropathy by acting on entheseal resident "innate-like" T cells. These cells express IL-23R and respond to IL-23 by secreting inflammatory cytokines such as IL-6 and IL-17 as well as IL-22 which acts on osteoblasts and regulates bone remodeling. Moreover, a large amount of evidence indicates that new bone formation in the form of osteophytes is mainly driven by reactivation of developmental pathways such as the Wnt and the Hedgehog pathway. We hypothesize that IL-23/IL-17 may mediate bone remodeling by affecting the expression of developmental pathways.