Table 1.

Effect of immune cells on bone metabolism in RA and SpA.

Cells	Effect on Bone Metabolism
DC	Differentiate into osteoclast-like cells stimulated by RANKL and M-CSF [23]
Th1 cells	Reduce osteoclastogenesis inhibiting RANK expression [23]
Th2 cells	Reduce osteoclastogenesis inhibiting RANK expression [23]
Th17 cells	Dual effect on bone metabolism (bone loss/bone formation) depending on the microenvironment, via IL-17 production
Th23 cells	Polarization into Th17 via IL23 production [27]
FLS	Promote bone loss via both RANKL-dependent and RANKL-independent pathways [28]

DC: dendritic cells; FLS: fibroblast-like synoviocytes; IL: interleukin; M-CSF: macrophage colony stimulating factors; RA: rheumatoid arthritis; RANK: receptor activator of NF-κB; RANKL: receptor activator of NF-κB ligand; SpA: spondyloarthritis; Th: T helper.