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Risk Factors and Clinical Presentation

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A case-control study was performed by Citak et al. (2012) among 132 individuals with traumatic spinal cord injury and 132 controls to determine risk factors for HO. The authors reported that the presence of complete neurological deficit was a major risk factor for HO. Moreover, factors such as spasticity, pneumonia, thoracic trauma, tracheostomy, nicotine use, and urinary tract infection increase patients’ risk for HO (Citak et al. 2012). However, another study has reported that patients with fewer comorbidities are also at a higher risk for developing HO. The evaluation of the preceding factors, in combination with early intervention and diagnosis, may reduce incidence of HO or improve a patient’s recovery post-operatively (Citak et al. 2012).

Krauss et al. (2014) reported that males were five times more likely to develop HO; SCI severity was also a risk factor with AIS A patients at greater risk than AIS D patients. Level of injury as a risk factor was highlighted by Ranganathan et al. (2015) whose literature review revealed that injuries to the thoracic and cervical spine are greater risk of developing HO. However, both gender and injury severity as risk factors have been disputed in the literature (Krauss et al. 2014).

Krauss et al. (2014) also investigated the role of hyper-coagulable states and related blood markers as risk factors in the development of HO. D-Dimer was elevated in 24 out of 32 patients with SCI and concurrent HO. Following this, the role of deep vein thrombosis (DVT) and pulmonary embolism (PE) have also been linked to the development of HO. Reznik et al. (2014) reported that DVT/PE were significant predictors of HO along with multiple pressure ulcers and AIS B severity score. Reznik et al. (2014) propose that the association of HO and DVT/PE is due to the link between trauma/surgery/fractures and stimulation/increase in thrombogenic factors such as thromboplastin or factor III. The relationship between HO and pressure ulcers is thought to be due to pressure ulcer infection deep enough to reach the bone. Along with tissue hypoxia, prolonged immobilization and muscle trauma, these factors combine to increase the risk of HO formation (Emami Razavi et al. 2015). Further research is required to solidifythe relationship between HO and pressures sores/ulcers.

Recently, a number of studies have examined potential biological factors that contribute to the development of neurogenic heterotopic ossification (Egan, Duque, Keenan & Pignolo, 2018; Povoroznyuk, Bystrytska, Balatska, 2017). A study by Egan et al. (2018) evaluated the presence of circular osteogenic precursor cells (COP bone marrow-derived type 1 collagen+CD45+) in incidences of non-hereditary HO. All tissue samples collected revealed the presence of COP cells. As these hematopoietic-derived cells were shown to both migrate to inflammatory sites and have osteogenic potential, there is the possibility to use COP cell count as an indicator of the risk for HO development post-SCI (Egan et al., 2018). Another study by Povoroznyuk et al. (2017), identified that the serum marker procollagen type 1 N-terminal propeptide (P1NP) for bone formation was the specific bone turnover marker implicated in HO formation. It was concluded that concentrations of 187.3 ng/mL or higher could be used as an early indicator of HO (Povoroznyuk et al., 2017).

Between 3-12 weeks, symptoms of HO start to appear (Schuetz et al. (2005). The initial clinical signs of inflammation are non-specific for HO (Neal 2003). Individuals typically present with joint and muscle pain, parasthesias and tissue swelling in the involved region, accompanied by a mild fever (Thomas & Amstutz 1987; Orzel & Rudd 1985; Smith 1998; Shehab et al. 2002), and a possible reduction in mobility at the HO site (Brady et al., 2018). Conversely, some SCI patients do not experience any pain. Skeletal bio-markers can help detect development of HO, in particular, ALP serum, CPK, C-reactive protein, prostaglandin E2, and erythrocyte sedimentation rate which have been associated with HO after SCI (Ploumis et al. 2015).