Objective: To test the hypothesis that increased concentrations of prostaglandin D(2) (PGD(2)) correlate with bone remodeling. Studies using isolated bone cells indicate that PGD(2) may be implicated in the regulation of bone homeostasis, with a positive influence on bone anabolism. We studied patients with traumatic fractures and age- and sex-matched healthy controls as an in vivo model of increased bone remodeling.
Methods: Thirty-five patients with bone fracture and matched controls were recruited. Urine and sera samples were collected. Urinary 11ss-PGF(2alpha), a PGD(2) metabolite, and PGE(2) metabolites (PGEM), serum lipocalin-type PGD(2) synthase (L-PGDS), bone alkaline phosphatase (bone ALP), and crosslinked C-telopeptides of type I collagen (CTX) were measured.
Results: At 5-6 weeks post-fracture, 11ss-PGF(2alpha), L-PGDS, bone ALP, and CTX were significantly increased in the fracture patients compared to controls. PGEM levels were not different between groups. Levels of 11ss-PGF(2alpha) and bone ALP were positively correlated, suggesting that PGD(2) may be implicated in fracture repair.
Conclusion: These results support our working hypothesis that PGD(2) could be implicated in the control of bone anabolism in humans.