In cross-sectional studies, vitamin D deficiency is frequent in spondyloarthritic patients and associated with increased spondyloarthritis (SpA) activity and structural damage. Experimental studies also show that vitamin D interferes with molecular pathways critically involved in SpA, especially regarding entheseal inflammation and ossification (involving cytokines such as IL-23 and sclerostin). Vitamin D deficiency might also affect the course of the disease through periodontal and gut inflammation, leading to increased functional impairment. Therefore, Vitamin D receptor selective agonists could represent a promising therapeutic pathway in this pathology. Randomised-controlled intervention studies are required in order to further elucidate complex relationships between vitamin D deficiency and SpA.
Keywords: IL-23; VDR; disease activity; gut inflammation; sclerostin; spondyloarthritis; vitamin D.