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Further evidence for the role of IL-17 in RA is provided by its biological properties in vitro and in vivo, as it induces monocyte- and fibroblast-derived pro-inflammatory cytokines (TNFα, IL-1β, IL-8), mediators of bone and cartilage damage such as matrix metalloproteinases and RANK-ligand (RANKL) [4], [5], [6], neutrophil and monocyte recruitment [7], [8], and osteoclastogenesis [9].
Pro-inflammatory cytokines are potent mediators of bone loss.
Importantly, this study demonstrates that both tumor cells and osteoblasts are potential mediators of bone formation.
Prostaglandins are important mediators of bone repair, and cyclooxygenases are required for prostaglandin production.
Furthermore, age and estrogen status, two other mediators of bone metabolism, correlate with cytokine secretion by the bone marrow [ 68].
This work has shown that systemic expression of soluble mediators of bone remodeling is disordered in PsA.
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Lately, bone regulatory proteins such as: osteoprotegerin (OPG) and Receptor Activator for Nuclear Factor κB Ligand (RANKL) has attracted attention of researchers as a possible key mediators of bone-vascular calcification imbalance.
IL-6 is a critical mediator of bone marrow cell expansion and is responsible for PTH actions in hematopoietic cell expansion.
RANKL is an essential mediator of bone resorption.
The second major mediator of bone remodelling is the parathyroid hormone (PTH).
Cathepsin K is the major mediator of bone resorption, controlling the osteoclast portion of the vicious cycle.
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mediation of bone
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mediators of interest
mediators of inflammation
mediators of host
mediators of change
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