Increased Concentrations of Prostaglandin D2 During Post-Fracture Bone Remodeling

Objective To test the hypothesis that increased concentrations of prostaglandin D2 (PGD2) correlate with bone remodeling. Studies using isolated bone cells indicate that PGD2 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 11s-PGF2α, a PGD2 metabolite, and PGE2 metabolites (PGEM), serum lipocalin-type PGD2 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, 11s-PGF2α, 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 11s-PGF2α and bone ALP were positively correlated, suggesting that PGD2 may be implicated in fracture repair. Conclusion These results support our working hypothesis that PGD2 could be implicated in the control of bone anabolism in humans.