SKELETAL BONE LOSS IN RESPONSE TO REMOTE BONE DEFECT HEALING
Alejandro Morales Betancourt, Mark Appleford.
The University of Texas at San Antonio, San Antonio, TX.
In the U. S., 2.4% of the population suffers bone fractures annually. During the fracture healing process, the lacunar-canalicular network (LCN) triggers basic multicellular units (BMUs) that are composed of osteoclasts and osteoblasts. BMUs are responsible for the activation-resorption-formation sequence, also called remodeling. Initial fractures could lead to secondary fractures due to loss of bone density, but the underlying mechanism relating them to the healing process is unclear. This study strives to find a correlation between bone density reduction and LCN activity to maintain skeletal homeostasis. A critical-sized (6 mm) defect was created in the right femur of 42 rats. The animals were treated by 1 of 3 implants with varying mineral concentration and evaluated after 2 and 4 weeks. Eight bones were harvested from each rat at different skeletal sites. An early assessment of the 42 samples using microCT revealed that bone loss occurred primarily in long bones. Samples were treated with histological techniques. Cellular mechanisms will be evaluated by quantifying bone remodeling parameters using BioQuant software. The expected results are that remodeling activity will be greater in those areas that presented a reduction in bone density. This will support the hypothesis of a correlation between local bone defect healing and loss of bone density due to comprehensive skeletal remodeling activity performed through the LCN. This investigation will provide the possibility of anticipating mineral deficit at certain skeletal sites as a result of fracture healing and the potential ability to alleviate remote secondary fracture risks through techniques such as calcium supplementation.