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Updated: May 3, 2026

Direct Mouse Trauma/Burn Model of Heterotopic Ossification
Published on: August 6, 2015
Association of vitamin D deficiency, secondary hyperparathyroidism, and heterotopic ossification in spinal cord
Christina V Oleson1, Benjamin J Seidel, Tingting Zhan
1Jefferson Medical College of Thomas Jefferson University, Department of Rehabilitation Medicine, 132 South 10th St, Regional SCI Center of the Delaware Valley, TJUH, 375 Main Building, Philadelphia, PA 19107. christinavoleson@msn.com.
Abstract:
Our objective was to explore the relationship between low vitamin D, secondary hyperparathyroidism, and heterotopic ossification (HO) in patients with spinal cord injury (SCI). Ninety-six subjects with acute or chronic motor complete SCI participated. Levels of serum vitamin D25(OH), calcium, and intact parathyroid hormone (PTH) were collected, and information regarding nutritional patterns and fracture history was obtained from subjects. Evidence of current or previous HO was ascertained through chart review. Of the 96 subjects, 12 were found to have developed HO, 11 with serum vitamin D25(OH) between 5 and 17 ng/mL. Nine subjects exhibited secondary hyperparathyroidism in the range of 72 to 169 pg/mL. Only one subject demonstrated HO in the absence of low vitamin D. However, many subjects with low vitamin D (5-31 ng/mL) did not have hyperparathyroidism or HO. Statistical testing demonstrated a correlation between hyperparathyroidism and HO (p < 0.001) as well as hyperparathyroidism and vitamin D deficiency (<20 ng/mL). Direct correlation between HO and low vitamin D was not observed, but hyperparathyroidism may increase this risk. We believe that those patients who demonstrate low vitamin D and elevated PTH should be screened for HO in addition to beginning vitamin supplementation. Initiating early treatment of low vitamin D to restore therapeutic levels may prevent development of HO.
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