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Introduction The success of fracture healing relies on coordinated stages of inflammation,callus formation and remodeling.The delay in osteoporotic fracture is believed to be related to impairments in these stages.Estrogen deficiency-related osteoporosis is the most prevalent type and estrogen has both immune-supportive and pro-inflammatory effects [1] and the inflammatory response to injury was lowered in ovariectomized animal models [2],these suggest a possible altered initial inflammatory response in osteoporotic fractures.Therefore,it is hypothesized that osteoporotic fracture healing exhibits a differential inflammatory stage in the fracture healing process. Methods SD rats were SHAM-operated and ovariectomized at 6-months old and received closed femoral fracture model 3 months later(n=3/group/time-point).Callus width & area were recorded by weekly x-ray assessment.Histological sections at 5 micrometers at the callus were prepared.Immunohistochemistry of pro-inflammatory markers of tumor necrosis factor(TNF)-a,interleukin(IL)-6 were stained at 2,4,8 weeks post-fracture and quantified by image analysis software. Results Difference was observed between groups at week 2 and 4 post-fracture.Area fraction of TNF-a positive signals was found to be higher at 57±9%in SHAM rats versus 32±5%in OVX group at week 2 post-fracture(n=3,p=0.012).IL-6 was found to be higher at 40±6%in SHAM than 10±2%in OVX group at week 2(n=3,p=0.001).Qualitatively,TNF-a and IL-6 were detected to express at higher levels during the earlier phase of the healing process in the marrow space and also the periosteum lining cells during the healing process. Conclusions Processes in fracture healing are triggered and initiated by the inflammation.Our results demonstrate that the inflammatory response is impaired in osteoporotic fracture as shown by decreased TNF-a and IL-6 protein expression at the callus,suggesting possible relationship among other factors including MSC recruitment,angiogenesis,level of endochondral ossification and callus remodeling in ovariectomy-induced osteoporotic rat fractures. Acknowledgement NSFC(A.03.15.02401),AADO Research Fund(AADO-RF2015-2Y),OTC Research Fund(2015-SCNT). References 1.Straub RH,Endocr Rev 2007.2.Torres et al,Respir Physiol Neurobiol,2014.