Formation of Heterotopic Ossification Post-Head Injury

Pathophysiology of Heterotopic Ossification Post-Head Injury

The pathophysiology of HO is not fully understood. Mesenchymal stem cells (osteoblastic cells) can generate cartilage, bone, muscle, tendons, ligaments, or fat (Pape et al. 2004). It is thought that they play a pivotal role in the development of HO (Williams et al. 1999). HO development begins with the formation of osteoid periarticularly and intramuscularly, and progresses to full calcification within a matter of weeks (Pape et al. 2001). Over the next few months, the calcified osteoid remodels into well-organized trabecular bone at which point it is considered to have matured (Pape et al. 2001). Several months after the initial trauma, patients with HO begin to experience restricted range of motion, pain and ankylosis (Banovac & Gonzalez 1997; Garland et al. 1980). The bony lesion has been found to have a high metabolic rate, with a rate of bone formation more than three times greater than that of normal bone, and an osteoclastic density of more than twice the density found in normal bone (Puzas et al. 1987).

Stimulating Factors Related to Head Injury

It is believed that there is likely a neurogenic factor contributing to HO, although this mechanism is not yet understood ( Antiplatelet Trialists’ Collaboration 1994; Hurvitz et al. 1992; Pape et al. 2001; Pape et al. 2004). It has also been noted that circulating factors promoting HO may be present in patients with head injuries (Pape et al. 2004). Many studies have shown enhanced osteogenesis in patients sustaining TBI (Trentz et al. 2005). The presence of certain hormonal factors early post-injury influences the stimulation of osteoprogenitors within skeletal muscles (Ivanhoe et al. 2012). Further, tissue hypoxia, sympathetic changes, immobilization, remobilization, and spasticity are additional risk factors (Ivanhoe et al. 2012). Accelerated fracture healing and HO are well documented phenomena in these patients (Bidner et al. 1990; Keret et al. 1990).

 

 

The pathophysiology of heterotopic ossification is not fully understood.