Fracture healing is a process of recovering injured bone tissue forms and functions. Osteoporosis can delay the
healing process, which contributes to personal suffering and loss of activities. Osteoporosis patients tend to lose bone
mass at the metaphyseal region which require treatment to increase bone mass. Postmenopausal osteoporosis is the most
common osteoporosis that occurs in women which subsequently resulted in fractures even under slight trauma. Estrogen
Replacement Therapy (ERT), the recommended therapy for postmenopausal osteoporosis, is associated with higher risk of
breast cancer, ovarian cancer and cardiovascular diseases. As osteoporotic fractures are becoming a public health issue, alternative
treatment is now being thoroughly explored. The potential agent is statins, the HMG-CoA reductase inhibitor
which is widely used for hypercholesterolemia treatment. Statins have been found to increase bone mass by stimulation of
Bone morphogenetic protein-2 (BMP-2) expression and Vascular Endothelial Growth Factor (VEGF) production. However,
these bone forming effects were achieved at very high systemic doses. Therefore, studies on locally applied statins
are required to further explore the ability of statins to stimulate bone formation at acceptable doses for better fracture healing.
This review highlights the animal and clinical studies on fracture healing promotions by statins and the mechanisms
Keywords: Fracture healing, osteoporosis, HMG-CoA reductase inhibitor, BMP-2, VEGF.
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