The Role of Simvastatin in Improving Bone Healing in Surgically Created Bony Defects: An Experimental Study

Abstract

The healing of bone defects remains a significant clinical orthopedic challenge. Autologous bone grafts are considered the gold standard. However, these procedures may cause donor-site morbidity, such as hemorrhage, infection, and chronic pain. Bone marrow harbors an abundant source of stem/progenitor cells, which participate in the regeneration of a variety of tissues following injury. Generation of progenitor cells from the bone marrow is one major response during tissue repair. Therefore, an alternative strategy for bone defect healing is to stimulate endogenous stem cell populations from the mature body and actively attract them to the sites of injury. Statins, such as simvastatin, are specific, competitive inhibitors of 3-hydroxy-2-methyl-glutaryl coenzyme A (HMG CoA) reductase. They are widely used in prevention of cardiovascular disease and to lower cholesterol level. In addition to the cholesterol-lowering effect, statins have a series of pleiotropic effects. Among these diverse effects, bone anabolism has been the focus of research for more than a decade. The suggestion that statins can increase bone formation has provided an exciting direction for research as well as providing a greater understanding of the biological importance of cholesterol synthetic pathways.