Post-stroke bilateral heterotopic ossification: An acute problem with long-lasting consequences

Özen, Selin; Şenlikçi, Huma Bölük; Yemişçi, Oya Ümit

doi:10.5606/ehc.2020.72081

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…Neurogenic forms of tHO have been documented after insults to the central nervous system. Cerebral vascular accidents have been implicated in the development of nHO [ 196 , 197 ], and both traumatic brain injury (TBI) and SCI have been reported to significantly increase the risk of nHO [ 3 , 198 , 199 ]. Additionally, patients suffering from TBI with concurrent fractures report increased fracture healing rates [ 200 ], suggesting a pro-osteogenic effect following nervous system injury.…”

Section: Nervous System Involvement In Homentioning

confidence: 99%

Intersections of Fibrodysplasia Ossificans Progressiva and Traumatic Heterotopic Ossification

Juan,

Bancroft,

Choi

et al. 2024

Biomolecules

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Heterotopic ossification (HO) is a debilitating pathology where ectopic bone develops in areas of soft tissue. HO can develop as a consequence of traumatic insult or as a result of dysregulated osteogenic signaling, as in the case of the orphan disease fibrodysplasia ossificans progressiva (FOP). Traumatic HO (tHO) formation is mediated by the complex interplay of signaling between progenitor, inflammatory, and nerve cells, among others, making it a challenging process to understand. Research into the pathogenesis of genetically mediated HO (gHO) in FOP has established a pathway involving uninhibited activin-like kinase 2 receptor (ALK2) signaling that leads to downstream osteogenesis. Current methods of diagnosis and treatment lag behind pre-mature HO detection and progressive HO accumulation, resulting in irreversible decreases in range of motion and chronic pain for patients. As such, it is necessary to draw on advancements made in the study of tHO and gHO to better diagnose, comprehend, prevent, and treat both.

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