Chen X, Kuang SX, Zhou FG, Zhang CG. Neuroinflammatory regulation of fracture healing after traumatic brain injury: Clinical evidence and emerging mechanistic insights. World J Orthop 2026; 17(7): 120345 [DOI: 10.5312/wjo.120345]
Corresponding Author of This Article
Cheng-Gui Zhang, MD, PhD, Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, No. 9677 Jingshi Road, Jinan 250000, Shandong Province, China. chenggui1214@pku.edu.cn
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Orthopedics
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review-article
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Xi Chen, Shou-Xiang Kuang, Cheng-Gui Zhang, Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250000, Shandong Province, China
Feng-Ge Zhou, Tumor Research and Therapy Center, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250000, Shandong Province, China
Author contributions: Chen X contributed to the conceptual development of the manuscript and drafted the initial version; Kuang SX contributed to refining the discussion of key clinical challenges; Zhou FG provided interdisciplinary expertise that helped shape the perspective of the manuscript; Zhang CG conceived the central perspective and overall framework of this opinion review and supervised the writing and revision process; and all authors have read and approved the final manuscript.
AI contribution statement: ChatGPT (OpenAI, GPT-4) was used during manuscript and answering-reviewers document preparation. ChatGPT (OpenAI, GPT-4) was used only to assist with literature search and language polishing. All content was verified by the authors. The manuscript’s writing, scientific content, and study design were independently completed by the authors. No AI-generated figures were used.
Supported by National Natural Science Foundation of China, No. 82202701; Natural Science Foundation of Shandong Province, China, No. ZR2022QH184; and Taishan Scholars Program.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Cheng-Gui Zhang, MD, PhD, Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, No. 9677 Jingshi Road, Jinan 250000, Shandong Province, China. chenggui1214@pku.edu.cn
Received: February 24, 2026 Revised: April 18, 2026 Accepted: May 22, 2026 Published online: July 18, 2026 Processing time: 140 Days and 12.3 Hours
Abstract
Evidence accumulated over the past decades indicates that traumatic brain injury (TBI) may influence the biological process of fracture repair. Orthopedic observations indicate increased callus formation and shorter time to union in fractures accompanied by brain injury. Several clinical studies have confirmed this association and described larger callus volume, earlier radiographic consolidation, and altered systemic biochemical profiles compared with isolated fractures. Experimental research has provided further mechanistic insight. TBI induces sympathetic activation, neuroinflammatory signaling, and endocrine alterations that influence peripheral bone repair. These neuroimmune interactions reshape the inflammatory and reparative phases of healing. Multiple mediators participate in this process, including growth hormone, parathyroid hormone, inflammatory cytokines such as interleukin-6, neuropeptides, and adrenergic pathways. Their effects are temporally regulated and context dependent, and no single factor appears to dominate the response. In this paper, we synthesize current clinical and experimental evidence and discuss the integrated neuroimmune and neuroendocrine networks that may underlie TBI-associated fracture healing.
Core Tip: Accelerated fracture healing associated with traumatic brain injury represents a distinct biological phenomenon that cannot be explained by single factor mechanisms. This paper proposes that an integrated regulatory network involving the nervous, immune, and endocrine systems underlies this process. By synthesizing clinical observations and experimental evidence, it highlights a system level framework and provides insight into the potential mechanisms of neuroendocrine and immune interactions in fracture repair.
Citation: Chen X, Kuang SX, Zhou FG, Zhang CG. Neuroinflammatory regulation of fracture healing after traumatic brain injury: Clinical evidence and emerging mechanistic insights. World J Orthop 2026; 17(7): 120345
The phenomenon of accelerated fracture healing in patients with concomitant traumatic brain injury (TBI) has been consistently documented in both clinical and preclinical research, yet it remains one of the most intriguing and complex intersections between neurology and orthopaedics[1-3]. Orthopedic surgeons have consistently observed exuberant callus formation and accelerated union in patients with concomitant brain injury, highlighting the systemic influence of central nervous system trauma on skeletal repair and raising questions about the underlying cellular and molecular mechanisms[2,4,5].
A growing body of clinical evidence supports the association between TBI and accelerated fracture healing. Across cohort studies and retrospective series, fractures accompanied by brain injury exhibit larger callus formation, accelerated radiographic union, and systemic biochemical alterations compared with isolated fractures[4-6]. Despite these consistent observations, heterogeneity in study design, injury severity, fracture characteristics, and timing of assessment limits direct comparisons across studies[1,7]. Thus, while the clinical phenomenon is well established, the underlying biological drivers and their relative contributions remain incompletely defined, highlighting the need for more standardized and mechanistically integrated clinical investigations[8].
Beyond clinical observations, experimental studies have begun to elucidate the mechanistic basis of accelerated fracture healing following TBI. These investigations indicate that TBI triggers sympathetic nervous system activation, neuroinflammatory signaling, and systemic endocrine alterations, which collectively influence peripheral tissues, including bone[9,10]. However, despite these advances, the relative contributions of individual pathways and their temporal dynamics remain incompletely understood[1,11]. Elucidating how these systemic signals are integrated within the local fracture microenvironment will be critical for translating mechanistic insights into targeted therapeutic strategies[1].
Within this complex regulatory network, multiple mediators have been implicated, including growth hormone (GH), parathyroid hormone (PTH), inflammatory cytokines such as interleukin-6 (IL-6)[6,12-14], catecholamines, leptin, brain-derived neurotrophic factor, nerve growth factor (NGF), norepinephrine, substance P, calcitonin gene-related peptide (CGRP), small extracellular vesicles, and other humoral and neural factors[9,10,15,16]. Rather than functioning independently, these mediators are coordinately regulated following TBI[17]. In light of these evolving findings, this opinion review aims to synthesize current clinical and mechanistic evidence and discusses the integrated neuroendocrine and neuroimmune factors that may underlie TBI-associated fracture healing.
CLINICAL STUDIES ON TBI AND FRACTURE HEALING
Clinical investigations into TBI-associated fracture healing have primarily been derived from observational studies, including prospective cohorts and retrospective analyses, which together provide important but inherently heterogeneous evidence[4,6,18,19]. These studies have focused on quantifiable clinical endpoints such as time to union, callus formation, and systemic biochemical alterations, forming the basis for current understanding of this phenomenon[4-6]. For instance, a prospective study by Mollahosseini et al[6] reported a significantly shorter time to union in patients with femoral fractures and TBI, accompanied by elevated circulating levels of osteogenic and inflammatory mediators, suggesting a role for systemic humoral regulation. Similarly, Shim et al[4] observed earlier callus formation and higher callus ratios in tibial fracture patients with TBI, along with hematological changes indicative of an enhanced proinflammatory state. Mounisamy et al[20] recently compared neuroendocrine and inflammatory profiles, as well as callus volume formation, in patients with long-bone fractures with or without concomitant TBI, providing further clinical evidence linking neuroendocrine and immune responses to enhanced skeletal repair.
However, not all studies have yielded consistent findings, and discrepancies remain a notable feature of the current clinical literature[15,18]. Variability in fracture type, fixation strategy, injury severity, patient demographics, and timing of outcome assessment, together with the predominance of retrospective designs and limited sample sizes, complicates direct comparisons across studies[4,7,18]. As highlighted in recent syntheses, TBI appears to exert a dual effect on the skeletal system, characterized by long-term bone loss yet paradoxically accelerated healing in the setting of acute fractures[15].
Taken together, existing clinical studies suggest that brain injury modifies the trajectory of fracture repair, but the underlying mechanisms and causal relationships remain incompletely defined[15,19]. These observations provide a critical clinical framework for further exploration of the neuroendocrine and neuroimmune pathways involved in this process[2,9]. To provide a structured overview of the clinical evidence supporting TBI-associated alterations in fracture healing, the key study characteristics are summarized in Table 1.
Table 1 Summary of clinical studies investigating fracture healing in patients with traumatic brain injury.
Beyond clinical observations, accumulating experimental evidence has begun to elucidate the mechanistic basis of TBI-associated fracture repair, shifting the field from descriptive phenomena toward an integrated framework of brain-bone crosstalk[9,21,22].
In a representative mechanistic study, Xia et al[23] identified neuron-derived extracellular vesicles as key mediators linking central injury to peripheral osteogenesis. Following TBI, hippocampal neurons released small extracellular vesicles enriched in osteogenic miRNAs, which preferentially accumulated in bone tissue and modulated osteoprogenitor activity[23,24]. Among these cargos, miRNA-328a-3p and miRNA-150-5p promoted osteogenic differentiation via suppression of forkhead box O4 and Casitas B-lineage lymphoma signaling pathways[23]. Consistently, circulating miRNA signatures associated with hypertrophic callus formation in TBI patients support their clinical relevance[25]. Moreover, biomaterial-assisted delivery of these vesicles enhances bone defect repair in vivo, highlighting their translational potential[23,26,27]. Consistent with the emerging role of extracellular vesicles, Lin et al[28] demonstrated that circulating miRNA-21-enriched vesicles derived from TBI patients facilitate bone remodeling by targeting mothers against decapentaplegic homolog 7, thereby promoting osteogenic differentiation. Pre-administration of TBI-derived exosomes further enhanced bone formation in murine fracture models, supporting a systemic pro-osteogenic effect of brain injury-induced circulating factors[28].
In parallel, experimental models highlight a key role for neuroimmune modulation. Ritter et al[29] reported elevated plasma osteopontin and progranulin in mice with combined TBI and femoral fracture, indicating systemic inflammation and repair activity. Consistently, Liu et al[9] showed that TBI-induced sympathetic activation enhances bone marrow myelopoiesis and fracture healing, β2-adrenergic receptor (ADRB2) signaling promoting M2 macrophage infiltration in the callus. Complementing these findings, Haffner-Luntzer et al[2] reported reduced neutrophil and mast cell infiltration and decreased C-X-C motif chemokine ligand 10 expression in the early fracture hematoma of combined trauma models, indicating a tightly regulated, temporally distinct inflammatory response.
Adrenergic signaling has emerged as a central regulatory axis in this process[30]. Sympathetic activation following TBI leads to increased release of norepinephrine, which acts on β-adrenergic receptors (e.g., ADRB2) to regulate immune cell dynamics, angiogenesis, and osteogenesis during fracture repair[9,10]. Jahn et al[10] identified ADRB2 as a key mediator of TBI-enhanced fracture healing, demonstrating that pharmacological blockade with propranolol impaired bone repair, whereas activation with formoterol improved callus vascularization and regeneration. These findings further support the concept that sympathetic signaling not only modulates immune cell dynamics but also directly influences angiogenesis and osteogenesis[9,10,31,32].
Beyond individual pathways, integrative analyses emphasize that TBI-induced fracture repair arises from the convergence of multiple systemic signals[6,15,33]. As summarized by Zhang et al[15], neurohormones, neuropeptides, neurotransmitters, and mechanical factors collectively orchestrate the brain-bone axis, highlighting the bidirectional and dynamic nature of this interaction.
Taken together, these experimental studies delineate a multifaceted regulatory network involving extracellular vesicle signaling, sympathetic activation, and immune modulation, which collectively underpin TBI-accelerated fracture healing[9,10,15,23]. However, variability in experimental models, injury severity, and temporal assessment remains a challenge, underscoring the need for standardized approaches and deeper mechanistic dissection to enable clinical translation[18,33,34]. A systematic summary of representative experimental models, key signaling pathways, and mechanistic insights into TBI-accelerated fracture healing is presented in Table 2.
Table 2 Experimental evidence and mechanistic insights into traumatic brain injury-accelerated fracture healing.
NEUROENDOCRINE AND IMMUNE FACTORS UNDERLYING TBI-ASSOCIATED FRACTURE HEALING
Neuroendocrine and immune signaling pathways are increasingly recognized as key mediators linking TBI to accelerated fracture healing, primarily through coordinated modulation of osteogenesis, angiogenesis, and inflammation[1,9,17].
Neuropeptides, particularly CGRP, appear to play a central role in this process[35,36]. Elevated CGRP levels following TBI have been associated with accelerated fracture healing and enhanced callus formation[37]. CGRP exerts these effects through multiple coordinated mechanisms, including promoting macrophage M2 polarization to create a favorable osteoimmune microenvironment[38], directly acting on endothelial cells to stimulate angiogenesis[39,40], and binding to the calcitonin receptor-like receptor/receptor activity-modifying protein 1 receptor complex on osteoblasts to promote osteogenic differentiation and bone formation[35]. These coordinated actions on immune cells, vascular cells, and bone-forming cells collectively accelerate fracture healing. Conversely, genetic deficiency of α-CGRP leads to reduced osteoblast numbers, impaired callus bridging, and increased rates of non-union[41-43]. Vasoactive intestinal peptide exhibits context dependent and sometimes opposing effects on fracture healing. Although inhibitory effects on osteoblastic differentiation and potential negative impacts on healing have been reported[16], vasoactive intestinal peptide can also promote bone marrow mesenchymal stem cell osteogenesis via Wnt/β-catenin signaling and improve fracture repair under specific conditions, such as sympathetic denervation[44,45], emphasizing the complexity of neuropeptide-mediated regulation of bone regeneration.
Following TBI, increased levels of NGF have been observed in both serum and fracture callus tissue, correlating with accelerated fracture healing[46,47]. Mechanistically, NGF promotes osteoblast proliferation, migration, and endochondral ossification via TrkA-mediated signaling pathways[48-50], supporting a neurogenic link between central nervous system injury and enhanced bone regeneration.
TBI profoundly alters the neuroendocrine milieu, with growing evidence implicating the GH/insulin-like growth factor-1 (IGF-1) axis and PTH signaling in accelerated fracture healing[15,51]. Clinical and prospective studies indicate that patients with TBI exhibit an early increase in circulating GH and PTH during the fracture repair process, suggesting a systemic osteoanabolic shift following neurotrauma[20,52]. The accelerated fracture healing associated with these hormonal elevations following TBI is mechanistically plausible, as GH promotes osteoblast differentiation and matrix deposition primarily through activation of the IGF-1 pathway[53], whereas intermittent PTH administration enhances callus formation and accelerates endochondral ossification, promoting cartilaginous callus conversion to bony callus through activation of the Indian hedgehog signaling pathway and multiple anabolic pathways including cyclic adenosine monophosphate/protein kinase A pathway and Wnt signaling pathway[13,54]. PTH also stimulates local IGF-1 production, which acts as a key mediator of PTH’s anabolic effects on bone formation and fracture repair through autocrine and paracrine mechanisms[13]. Notably, the persistence of these hormonal changes has been associated with enhanced callus formation, providing human evidence for a neuroendocrine contribution to fracture repair[20]. These observations raise the possibility that, despite the well-recognized risk of post-traumatic hypopituitarism, a subset of TBI patients may exhibit early hormonal hypersecretion or altered pulsatility that is permissive for bone regeneration[15,20,51]. However, the causal relationships, clinical significance, and reproducibility of these early hormonal elevations remain to be fully elucidated, and further prospective studies with serial hormonal measurements are needed to reconcile these apparently conflicting observations.
Leptin, an adipocyte-derived hormone involved in energy metabolism and bone homeostasis, has emerged as a key mediator of TBI-enhanced fracture healing[15]. Following TBI, serum and cerebrospinal fluid leptin levels are significantly elevated and positively correlated with GH and IGF-1 concentrations[55]. Critically, leptin-deficient mice fail to exhibit accelerated fracture healing after TBI[15]. These findings suggest that the osteoanabolic effects observed post-TBI may be dependent on intact leptin signaling.
Beyond neuroendocrine mediators, TBI triggers a systemic release of growth factors and inflammatory cytokines that collectively contribute to accelerated fracture healing[6,9]. Clinical studies demonstrate that patients with concomitant TBI and fracture exhibit significantly elevated serum levels of bone morphogenetic protein-2 (BMP-2), fibroblast growth factor-2 (FGF-2), platelet-derived growth factor (PDGF), and IL-1β at both 12 hours and 4 weeks post-injury, with sustained elevation correlating with shorter time to fracture union[6]. Mechanistically, TBI-induced sympathetic hyperactivity not only modulates bone marrow myelopoiesis toward anti-inflammatory M2 macrophage polarization, but also creates a permissive microenvironment enriched in osteogenic growth factors (BMP-2, PDGF) and angiogenic mediators (FGF-2), while the early surge in IL-1β may prime the inflammatory cascade essential for fracture repair initiation[6,9]. BMP-2 promotes osteogenic differentiation of mesenchymal stem cells through activation of BMP type I receptors, initiating early osteogenic lineage commitment[56,57]. FGF-2 expands periosteal progenitor cells and enhances their endochondral ossification potential, predominantly through increased BMP-2 production[58], while PDGF promotes migration and proliferation of mesenchymal stem cells via platelet-derived growth factor receptor beta signaling[59,60].
IL-6 exhibits a complex and context-dependent role in fracture healing. Classical IL-6 signaling appears to be essential during the early phase of repair, as IL-6 deficiency or inhibition impairs systemic inflammation, immune cell recruitment, and subsequent bone regeneration[61,62]. However, paradoxically, IL-6 deficiency has also been shown to enhance callus formation under specific conditions, suggesting a potential inhibitory effect on intramembranous ossification[63]. Notably, our previous work observed that local blockade of IL-6 signaling at the fracture site accelerates bone healing by modulating sensory nerve-derived CGRP activity, downregulating pro-inflammatory cytokines (tumor necrosis factor-α, IL-1β) and M1 macrophage markers, while upregulating anti-inflammatory mediators and promoting M2 macrophage polarization[64]. Taken together, we propose that IL-6 functions as a context-dependent immunoregulatory switch, with its effects determined by temporal dynamics and local vs systemic signaling. In the setting of TBI, where neuroimmune activation is profoundly altered, IL-6 blockade may potentially shift the inflammatory balance toward a pro-regenerative state, thereby contributing to accelerated fracture healing. However, this hypothesis requires further validation in TBI models. To integrate these findings into a coherent conceptual framework, the major neuroimmune and neuroendocrine regulators, their mechanistic roles, temporal dynamics, and potential translational implications are systematically summarized in Table 3. These interconnected neural, endocrine, and immune mechanisms likely operate as an integrated regulatory network to drive the accelerated fracture healing observed after TBI, as illustrated in Figure 1.
Elevated CGRP levels in serum after TBI correlate with accelerated fracture healing; CGRP may be released from brain tissue into serum; α-CGRP deficiency leads to impaired callus bridging, reduced osteoblast numbers, and high rate of non-union
Promotes osteoblast proliferation and differentiation via cAMP signaling pathway; modulates bone remodeling through CGRP receptor (CRLR/RAMP1) activation; induces expression of genes linked to ossification and bone remodeling
Inflammatory and reparative phases
CGRP receptor agonism represents potential therapeutic approach to stimulate bone regeneration; neurologic regulation of bone metabolism
No direct TBI-related evidence; however, VIP exhibits context-dependent effects on fracture healing and may interact with altered sympathetic tone
Promotes BMSC osteogenic differentiation via activation of Wnt/β-catenin signaling; interacts with neuroendocrine environment
Reparative phase
Potential therapeutic candidate for bone regeneration; biomaterial-based delivery may enhance repair, but efficacy depends on local neuroendocrine and sympathetic status
Leptin levels are elevated in serum and cerebrospinal fluid after TBI, positively correlated with GH and IGF-1, and associated with accelerated callus formation
Leptin signaling appears necessary for TBI-induced acceleration of fracture healing; involved in regulation of energy metabolism, fat storage, and bone homeostasis
Early inflammatory and reparative phases
Intact leptin signaling is critical for TBI-mediated bone regeneration
THERAPEUTIC IMPLICATIONS OF TARGETING NEUROIMMUNE AND NEUROENDOCRINE PATHWAYS IN FRACTURE HEALING
Building upon evidence that TBI reshapes fracture healing through integrated neuroimmune and neuroendocrine networks, its therapeutic relevance lies not in replicating brain injury, but in extracting the regulatory principles it reveals[15,65,66]. TBI exposes coordinated signaling programs that govern the inflammatory, reparative, and remodeling phases of bone healing[18]. Emerging evidence suggests that sympathetic signaling, neuropeptides, endocrine mediators, and inflammatory cytokines function as an interconnected network regulating fracture repair[9,67,68].
We propose that, for the accelerated fracture healing observed after TBI, further exploration of upstream triggers and downstream signaling cascades is warranted. Future therapeutic strategies should emphasize temporal precision and integrated modulation of the neuroimmune-neuroendocrine network, shifting from single-target approaches toward temporally controlled and system-level regulation of the fracture microenvironment. For example, sequential or localized delivery of key mediators could promote bone repair in a controlled and reproducible manner. Stage specific intervention, precise local regulation, and minimization of systemic adverse effects are critical for clinical translation[69,70].
CONCLUSION
Converging lines of evidence support the concept that TBI accelerates fracture healing not through a single dominant pathway, but via the coordinated activation of neuroimmune and neuroendocrine networks. Sympathetic signaling, endocrine modulation, inflammatory mediators, and immune cell reprogramming operate in a temporally regulated and context dependent manner to reshape the biological milieu of skeletal repair. We propose that this network level coordination underlies the altered trajectory of bone regeneration after brain injury. Elucidating the temporal hierarchy, regulatory interactions, and systemic consequences of these pathways will be critical for translating mechanistic insights into rational therapeutic strategies. Future efforts should prioritize system level interventions that modulate multiple components of the neuroimmune and neuroendocrine network in a stage specific manner to achieve controlled and reproducible enhancement of fracture repair.
ACKNOWLEDGEMENTS
The authors sincerely thank all the individuals and institutions that have contributed to this research.
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