Neuropathy-induced osteopenia in rats is not due to a reduction in weight born on the affected limb

Whiteside, Garth T.; Boulet, Jamie; Sellers, Rani S.; Bunton, Tracie E.; Walker, Katharine

doi:10.1016/j.bone.2005.08.017

Cited by 22 publications

(13 citation statements)

References 39 publications

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“…Adults with fibromyalgia [102] or rheumatoid arthritis [103] demonstrate lower BMD than healthy adults, while individuals with upper or lower extremity reflex sympathetic dystrophy demonstrate lower BMD in the affected limb [104] and unaffected limb [105]. Notably, data from animal models suggest that BMD deficits observed in the context of neuropathic pain is a consequence of disruptions in bonenerve signalling rather than reduced mechanical loading [106]. Bogdanffy et al [107] described a systematic decrease in areal BMD in the lumbar spine measured by DXA in patients who had undergone lumbar spinal fusion surgery due to intractable back pain.…”

Section: Discrete Clinical Groups (Adults)mentioning

confidence: 99%

Bone health and back pain: What do we know and where should we go?

2008

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Bone health is generally not considered in patients who present with chronic back pain. Nonetheless, bone health and back pain share common genetic and environmental correlates suggesting a co-dependence. Evidence exists for a relationship between back pain and impaired bone health. Here we present the evidence, theoretic framework and clinical relevance. Bone health and back pain are important determinants of musculoskeletal health. Back pain experienced in youth is a risk factor for future back pain, while suboptimal bone health during development increases the risk of skeletal fragility in later life. Generally, bone health is not considered in patients with chronic back pain who do not demonstrate other well-recognised bone health risk factors or associated conditions. Nonetheless, evidence suggests that back pain and impaired bone health share common environmental and genetic correlates, indicating that bone health ought to be considered in the context of back pain in otherwise healthy individuals. This review describes the likely mechanisms explaining the relationship between back pain and impaired bone health, evidence concerning the relationship and suggestions for future research. A narrative literature search was conducted using CINAHL, Medline, PubMed and Web of Science electronic databases. A history of back pain is associated with decreased bone mineral density in adults, yet this tends to be site-specific. No studies were identified examining this association in youth, yet the negative effects of childhood skeletal trauma and obesity on bone and spinal health provide indirect evidence for an association. Further research is required to clarify the impact of back pain on bone health at different lifespan stages using prospective cohort designs.

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Section: Discrete Clinical Groups (Adults)mentioning

confidence: 99%

Bone health and back pain: What do we know and where should we go?

2008

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“…Previous work has demonstrated a neural component in several aspects of bone physiology (Imai and Matsusue, 2002;Spencer et al, 2004;Elefteriou, 2008). Specifically, Sample et al (2008) recently demonstrated a neural contribution in the regulation of functional adaptation to loading, and Whiteside et al (2006) showed that neuropathy-induced reduction in bone mineral density is not strictly a result of reduced weight bearing on the affected limb. More closely related to the research covered here, sciatic nerve resection has experimentally been shown to influence fracture healing in the tibia, yielding a larger, less dense fracture callus with diminished mechanical properties (Nordsletten et al, 1994;Madsen et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Characterization of a composite injury model of severe lower limb bone and nerve trauma

Uhrig

Clements

Boerckel

et al. 2012

J Tissue Eng Regen Med

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Severe extremity trauma often results in large zones of injury comprising multiple types of tissue and presents many clinical challenges for reconstruction. Considerable investigation is ongoing in tissue engineering and regenerative medicine therapeutics to improve reconstruction outcomes; however, the vast majority of musculoskeletal trauma models employed for testing the therapeutics consist of single-tissue defects, offering limited utility for investigating strategies for multi-tissue repair. Here we present the first model of composite lower limb bone and nerve injury, characterized by comparison to well-established, single-tissue injury models, using biomaterials-based technologies previously demonstrated to show promise in those models. Quantitative functional outcome measures were incorporated to facilitate assessment of new technologies to promote structural and functional limb salvage following severe extremity trauma. Nerve injury induced significant changes in the morphology and mechanical properties of intact bones. However, BMP-mediated segmental bone regeneration was not significantly impaired by concomitant nerve injury, as evaluated via radiographs, microcomputed tomography (μCT) and biomechanical testing. Neither was nerve regeneration significantly impaired by bone injury when evaluated via histology and electrophysiology. Despite the similar tissue regeneration observed, the composite injury group experienced a marked functional deficit in the operated limb compared to either of the single-tissue injury groups, as determined by quantitative, automated CatWalk gait analysis. As a whole, this study presents a challenging, clinically relevant model of severe extremity trauma to bone and nerve tissue, and emphasizes the need to incorporate quantitative functional outcome measures to benchmark tissue engineering therapies.

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“…In fact, animal studies have shown bisphosphonates are effective in preserving CRPS associated bone loss. Chronic administration of zoledronate acid can lead to increased BMD in CCI animal models (Whiteside et al, 2006). The efficacy of alendronate in limiting bone loss in CCI rat model has been shown in a recent study (Im et al, 2010).…”

Section: Bisphosphonate 531 Mechanism Of Bisphosphonate Through Expmentioning

confidence: 97%

“…They have suggested that one possible mechanism would be the increase of bone resorption with immobilization. Another possible mechanism suggested by others (Whiteside et al, 2006) would be that bone loss in CRPS models may be due to altered nerve signaling and not attributable to limb disuse or reduced mechanical loading associated with pain. Experimental studies have shown that substance P release is involved in the pathogenesis of bony changes induced by CRPS (Gaus et al, 2003).…”

Section: Pathomechanismmentioning

confidence: 98%

“…Because the activation of bony osteoclasts is known to play significant role in CRPS pain generation, it is not surprising that aside from these central pain modulating medications, bone modulating agents are used in CRPS. These agents are known not only to alleviate pain but also to reverse and inhibit CRPS associated osteopenia (Whiteside et al, 2006). The two bone modulating agents in reference are calcitonin and bisphosphonate agents.…”

Section: Treatment Of Patchy Osteoporosis In Crpsmentioning

confidence: 99%

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