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<p>Inflammatory bowel disease (IBD) represents a group of chronic inflammatory conditions that extend beyond the gastrointestinal tract, with profound systemic effects on the musculoskeletal system. This review comprehensively examines the experimental models that have elucidated the intricate relationship between intestinal inflammation and the development of osteosarcopenia—the concurrent deterioration of bone and muscle tissues. We analyze chemically-induced models (DSS, TNBS), genetically engineered models (T-cell transfer, IL-10 knockout, IL-2 knockout), and the Winnie mouse model of spontaneous colitis, highlighting their contributions to our understanding of IBD-associated musculoskeletal complications. The review emphasizes how these models have revealed critical molecular mediators, particularly gut-derived serotonin and vitamin D signaling pathways, that connect intestinal pathology to distant skeletal deterioration. Notably, pro-inflammatory cytokines including TNF-α, IL-6, and IL-17 emerge as central regulators affecting both bone and muscle homeostasis, explaining the synchronized pattern of deterioration observed clinically. The findings from these experimental models highlight potential therapeutic targets and intervention strategies beyond conventional approaches, including gut-derived serotonin inhibition and vitamin D modulation. This review underscores the value of chronic colitis models in elucidating the complex pathophysiology of IBD-associated osteosarcopenia and provides direction for translational research to develop integrated treatment approaches for this debilitating extraintestinal manifestation.</p>

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Cross-talk of gut-bone-muscle: osteosarcopenia in experimental colitis models

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月14日

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  • Shilpa Sharma

摘要

Inflammatory bowel disease (IBD) represents a group of chronic inflammatory conditions that extend beyond the gastrointestinal tract, with profound systemic effects on the musculoskeletal system. This review comprehensively examines the experimental models that have elucidated the intricate relationship between intestinal inflammation and the development of osteosarcopenia—the concurrent deterioration of bone and muscle tissues. We analyze chemically-induced models (DSS, TNBS), genetically engineered models (T-cell transfer, IL-10 knockout, IL-2 knockout), and the Winnie mouse model of spontaneous colitis, highlighting their contributions to our understanding of IBD-associated musculoskeletal complications. The review emphasizes how these models have revealed critical molecular mediators, particularly gut-derived serotonin and vitamin D signaling pathways, that connect intestinal pathology to distant skeletal deterioration. Notably, pro-inflammatory cytokines including TNF-α, IL-6, and IL-17 emerge as central regulators affecting both bone and muscle homeostasis, explaining the synchronized pattern of deterioration observed clinically. The findings from these experimental models highlight potential therapeutic targets and intervention strategies beyond conventional approaches, including gut-derived serotonin inhibition and vitamin D modulation. This review underscores the value of chronic colitis models in elucidating the complex pathophysiology of IBD-associated osteosarcopenia and provides direction for translational research to develop integrated treatment approaches for this debilitating extraintestinal manifestation.