The mechanism underlying HO following spinal cord injury is not fully understood creating challenges in early diagnostic and therapeutic interventions. It appears to be initiated by metaplasia of mesenchymal cells in the peri articular hematoma and micro-hematomainto bone precursor cells (Schuetz et al. 2005). With time after a SCI, these cells calcify and ossify into bone cells (Emami Razavi et al. 2015). Pape et al. (2004) has noted that mesenchymal stem cells can differentiate into osteogenic cells given the right stimuli and within the right environment (even soft tissue; Chalmers et al. 1975). These mesenchymal stem cells can generate cartilage, muscles, tendons, ligaments or fat, besides bone (Williams et al. 1999) and are thought to play a pivotal role in the development of HO (Pape et al. 2004). After mesenchymal cell differentiation to osteogenic cells, a protein mixture created by bone cells (osteoid) calcifies within a matter of weeks (Pape et al. 2001). Over the next few months, the calcified osteoid remodels and matures into well-organized trabecular bone (Pape et al. 2001). Months following the initial trauma, patients develop bone formation in muscle and soft tissues in a periarticular location with resultant restriction in range of motion, pain and ankylosis (Banovac & Gonzalez 1997; Garland et al. 1980). The bony lesion has a high metabolic rate, adding new bone at more than three times the rate of normal bone. Osteoclastic (bone removal cells) density is more than twice that found in healthy bone (Puzas et al. 1987). It is suspected there may be a neurogenic factor contributing to HO but the mechanism is poorly understood (Hurvitz et al. 1992; Pape et al. 2001; Pape et al. 2004).