| dc.description.abstract | Spinal contusion injuries are characterized by an increased excitation of the immune system that results in inflammation and heightened expression levels of pro-inflammatory cytokines in the central nervous system (CNS) (Donnelly et al. 2008). These inflammatory cytokines impair bone homeostasis to favor bone resorption over the secretion of bone matrix, thus contributing to an overall decline in bone mineral density (BMD) (Perez-Castrillon et al. 2000, Schett 2011). Maintenance of bone integrity following spinal cord injury (SCI) is critical because low BMD compromises locomotor and sensory recovery, and is a predictor of bone pain, future fractures, and osteoporosis. We proposed that minocycline, an FDA-approved anti-inflammatory drug (Kobayashi et al. 2013), may protect against the BMD deterioration routinely observed after SCI. To test this, male Sprague Dawley rats were given a moderate spinal contusion injury and then treated with 0 or 0.33 mg/kg/ml of minocycline from days 1-14 following injury. Recovery of function was assessed for 28 days post injury. At the end of the experiment, bone samples werecollected to assess BMD and changes in amount of mineralization. Administration of minocycline significantly enhanced active bone mineralization and overall new bone formation rates in a rodent SCI model compared to vehicle-treated SCI controls. A more comprehensive understanding of the effects of different therapeutic strategies for alleviating post-injury bone loss is important for the development of effective treatment strategies to improve long-term rehabilitation following SCI. | en |
