Osteoporosis is a frequent complication of chronic inflammatory diseases and increases in the pro-inflammatory
cytokines make an important contribution to bone loss by promoting
bone resorption and impairing bone formation. Omentin-1 is a newly identified
adipocytokine that has anti-inflammatory effects, but little is known about the role of omentin-1 in inflammatory
osteoporosis. Here we generated global omentin-1 knockout (omentin-1-/-) mice and demonstrated that depletion of omentin-1 induces inflammatory bone loss-like phenotypes in mice, as defined by abnormally elevated pro-inflammatory
cytokines, increased osteoclast formation and bone tissue destruction, as well as impaired osteogenic activities. Using an inflammatory cell model induced by
tumor necrosis factor-α (TNF-α), we determined that recombinant omentin-1 reduces the production of pro-inflammatory factors in the TNF-α-activated macrophages, and suppresses their anti-osteoblastic and pro-osteoclastic abilities. In the
magnesium silicate-induced inflammatory
osteoporosis mouse model, the systemic administration of adenoviral-delivered omentin-1 significantly protects from osteoporotic bone loss and
inflammation. Our study suggests that omentin-1 can be used as a promising therapeutic agent for the prevention or treatment of inflammatory
bone diseases by downregulating the pro-inflammatory
cytokines.