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Purpose of Review <p>Traumatic brain injury (TBI) is increasingly recognized as a systemic disorder with significant effects on skeletal biology. This review summarizes current evidence describing how TBI impacts fracture healing, heterotopic ossification, and long-term bone remodeling.</p> Recent Findings <p>Clinical observations and experimental models demonstrate that TBI can accelerate early fracture callus formation and increase the risk of heterotopic ossification, suggesting a transient pro-osteogenic state following injury. Proposed mechanisms include neuroinflammatory cytokine release, sympathetic nervous system activation, neuroendocrine dysregulation, and mobilization of osteoprogenitor cells. Conversely, persistent neuroinflammation, hypothalamic–pituitary axis dysfunction, oxidative stress, and altered autonomic signaling are associated with impaired fracture remodeling, increased bone resorption, and progressive bone loss. Emerging data implicate extracellular vesicle-mediated signaling as a key pathway linking brain injury to skeletal outcomes.</p> Summary <p>TBI induces a contextual, biphasic skeletal response with both osteogenic and degenerative consequences. Understanding this duality is essential for optimizing fracture care and preserving bone health after neurotrauma.</p>

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Brain–bone Crosstalk after Neurotrauma: Dual Effects of Traumatic Brain Injury on Skeletal Remodeling

  • 期刊论文

  • 发表日期：

    2026年5月7日

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  • Vetriganesh Maduraiveeran,
  • Shivum Lal,
  • Carlos Isales,
  • Krishnan Dhandapani,
  • Sadanand Fulzele

摘要

Purpose of Review

Traumatic brain injury (TBI) is increasingly recognized as a systemic disorder with significant effects on skeletal biology. This review summarizes current evidence describing how TBI impacts fracture healing, heterotopic ossification, and long-term bone remodeling.

Recent Findings

Clinical observations and experimental models demonstrate that TBI can accelerate early fracture callus formation and increase the risk of heterotopic ossification, suggesting a transient pro-osteogenic state following injury. Proposed mechanisms include neuroinflammatory cytokine release, sympathetic nervous system activation, neuroendocrine dysregulation, and mobilization of osteoprogenitor cells. Conversely, persistent neuroinflammation, hypothalamic–pituitary axis dysfunction, oxidative stress, and altered autonomic signaling are associated with impaired fracture remodeling, increased bone resorption, and progressive bone loss. Emerging data implicate extracellular vesicle-mediated signaling as a key pathway linking brain injury to skeletal outcomes.

Summary

TBI induces a contextual, biphasic skeletal response with both osteogenic and degenerative consequences. Understanding this duality is essential for optimizing fracture care and preserving bone health after neurotrauma.