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Introduction <p>Spondyloarthropathies (SpA) are chronic inflammatory disorders characterized by the paradoxical coexistence of bone loss and pathological new bone formation, leading to syndesmophytes, ankylosis, erosions, and osteoporosis. These skeletal changes severely impair mobility and heighten fracture risk.</p> Methodology <p>This narrative review was conducted by non-systematically searching PubMed, Scopus, Google Scholar, and Web of Science databases up to September 2025 for studies addressing the molecular mechanisms, imaging correlates, and therapeutic strategies in bone disease of SpA. Reference lists were manually screened to include additional relevant literature.</p> Discussion <p>Evidence highlights the pathogenic role of cytokines such as tumor necrosis factor (TNF), interleukin (IL)-17, and IL-23 in orchestrating crosstalk between immune and bone cells. Dysregulation of the Wnt/β-catenin pathway and the receptor activator of nuclear factor-κB (RANK)–RANK ligand (RANKL)–osteoprotegerin (OPG) axis underpins the imbalance between osteoclast-mediated resorption and osteoblast-driven ossification. Imaging modalities, including MRI and high-resolution quantitative CT, have advanced early detection and monitoring of structural lesions. Biologic and targeted synthetic agents, notably TNF inhibitors, IL-17 antagonists, and Janus kinase inhibitors, effectively reduce inflammation and bone loss but show limited impact on syndesmophyte progression.</p> Future directions <p>Integration of molecular biomarkers, multi-omics profiling, and advanced imaging may enable precision medicine approaches. Therapeutic strategies directly targeting Wnt and BMP signaling represent promising avenues to prevent pathological ossification.</p> Conclusion <p>Bone disease in SpA arises from intertwined inflammatory, genetic, and mechanical mechanisms. Despite therapeutic advances, structural progression remains unresolved. Future research should focus on interventions that couple anti-inflammatory activity with modulation of bone remodeling to prevent fractures and ankylosis.</p>

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A narrative review of bone disease in spondyloarthropathy: molecular mechanisms and emerging advances

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月8日

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  • Yuliasih Yuliasih,
  • Betty Rachma,
  • Awalia Awalia,
  • Lita Diah Rahmawati,
  • Cahyo Wibisono Nugroho,
  • Arinditia Triasti Putri,
  • Henry Sutanto

摘要

Introduction

Spondyloarthropathies (SpA) are chronic inflammatory disorders characterized by the paradoxical coexistence of bone loss and pathological new bone formation, leading to syndesmophytes, ankylosis, erosions, and osteoporosis. These skeletal changes severely impair mobility and heighten fracture risk.

Methodology

This narrative review was conducted by non-systematically searching PubMed, Scopus, Google Scholar, and Web of Science databases up to September 2025 for studies addressing the molecular mechanisms, imaging correlates, and therapeutic strategies in bone disease of SpA. Reference lists were manually screened to include additional relevant literature.

Discussion

Evidence highlights the pathogenic role of cytokines such as tumor necrosis factor (TNF), interleukin (IL)-17, and IL-23 in orchestrating crosstalk between immune and bone cells. Dysregulation of the Wnt/β-catenin pathway and the receptor activator of nuclear factor-κB (RANK)–RANK ligand (RANKL)–osteoprotegerin (OPG) axis underpins the imbalance between osteoclast-mediated resorption and osteoblast-driven ossification. Imaging modalities, including MRI and high-resolution quantitative CT, have advanced early detection and monitoring of structural lesions. Biologic and targeted synthetic agents, notably TNF inhibitors, IL-17 antagonists, and Janus kinase inhibitors, effectively reduce inflammation and bone loss but show limited impact on syndesmophyte progression.

Future directions

Integration of molecular biomarkers, multi-omics profiling, and advanced imaging may enable precision medicine approaches. Therapeutic strategies directly targeting Wnt and BMP signaling represent promising avenues to prevent pathological ossification.

Conclusion

Bone disease in SpA arises from intertwined inflammatory, genetic, and mechanical mechanisms. Despite therapeutic advances, structural progression remains unresolved. Future research should focus on interventions that couple anti-inflammatory activity with modulation of bone remodeling to prevent fractures and ankylosis.