Vitamin D and spondyloarthritis

Abstract

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::

• disease activity
• gut inflammation
• IL-23
• sclerostin
• spondyloarthritis
• VDR
• vitamin D

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• In vitro studies show that vitamin D might interfere with key molecular pathways involved in SpA onset, activity and radiologic progression.

• Vitamin D supplementation might notably down-regulate IL-23 and up-regulate sclerostin pathways.

• Vitamin D deficiency could also be involved in SpA-associated gut and periodontal inflammation.

• Many cross-sectional studies show that vitamin D deficiency is frequent in SpA patients and suggest an inverse correlation between 25OHD levels and SpA activity, radiological progression.

• However, many confounders should be assessed (sunlight exposure, functional impairment, BMI, malabsorption, vitamin D supplementation) in longitudinal controlled studies (cohort studies and interventional studies).

• Vitamin D receptor selective agonists such as paricacitol and BXL-62 could exert immunomodulatory properties in the immune cell microenvironment without inducing hypercalcemia and should be evaluated as a potential therapeutic option in this pathology.

Notes