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Background The mechanism for the new bone formation in ankylosingspondylitis (AS) is still unclear. Although it has been demonstrated thatIL-23 plays a pivotal role in the pathophysiology of AS, IL-23 has no directeffects on osteoblasts but modulates the function of osteoclasts.  Aims To explore whether IL-23 indirectly facilitates new boneformation through osteoclasts in AS, here we analyzed whether IL-23 enhancesthe expression levels of pro-osteogenic factors by osteoclasts.  Methods Mononuclear cells were harvested from mouse bone marrow andcultured in the presence of M-CSF (50 ng/ml) and RANKL(30 ng/ml) to trigger the production of osteoclasts. Proteinand mRNA expression levels of Semaphorin 4D, Ephrin B2, BMP2, BMP6, SPHK1,HtrA1 and Wnt10b were measured using Western blot and qRT-PCR.  Results Primary mononuclear cells were transformed into osteoclastswith RANKL and M-CSF. The increased expression of NFATc1 and TRAP togetherwith TRAP staining of&gt;3 nuclei were used to identify matureosteoclasts. The mRNA expression levels of BMP2, Ephrin B2 and SPHK1 wereenhanced by 1.46, 2.1 and 2.46 folds after exposure to IL-23. Confirmationof increased levels of Ephrin B2 and SPHK1 in IL-23-stimulated osteoclastswas provided by Western blot analysis. IL-23 had no effects on theexpression of BMP6 or Wnt10b, or on the anti-osteogenic factors Semaphorin4D or HtrA1.  Conclusions IL-23 induces osteoclasts to express pro-osteogenicfactors rather than anti-osteogenic factors, suggesting IL-23 mightindirectly promote the differentiation of osteoblasts through activatedosteoclasts in ankylosing spondylitis.

IL-23 induces the expression of pro-osteogenic factors in osteoclasts