Introduction: Abnormal fracture healing in aged, post-menopausal or ovariectomised patients remains a clinical problem. Understanding the distribution and regulation of biomolecular factors in fracture healing in oestrogen deficient rats may have clinical implications for developing novel therapeutic strategies for enhancing osteoporotic fracture healing. Our previous work demonstrated that bone morphogenetic proteins (BMPs), transforming growth factor beta (TGF-ß) and their signal transducers, Smads, played important roles in normal fracture healing. Insulin-like growth factor I (IGF-I) has been indicated playing a role in the maintenance of bone mass. Matrix metalloproteinases (MMPs) has been indicated to play a role in bone matrix degradation. Those factors in ovariectomised fracture healing have not yet been reported.

Aim: To investigate the expression of BMP-2, 7, TGF-ß, Smads1–7, IGF-I, IGF-I receptor 1a (IGF-IR1), MMPs and TIMPs by a quantitative immunohistochemistry in a fracture model in an ovariectomised rodent (OVX).

Methods: Age-matched, normal, female rats served as controls. The animals were sacrificed in groups of six at one, two, three, four and six weeks after the fracture.

Results: The highlights of our results were the lack of IGF-I in the early stage of fracture healing (up to two weeks) in OVX rats and the greater expression of MMP-1 in OVX rats at all groups when compared with the normal rats.

Conclusions: Our data suggested that the regulation downward of IGF-I in the OVX fractures resulted from estrogen deficiency and may have the function to stimulate MMP-1 activity. Over-expressed MMP-1 degraded collagen matrix in the cortex and inhibited the woven bone matrix formation during OVX fracture healing.