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<p>Axial spondyloarthritis (axSpA) is a chronic inflammation disorder commonly associated with osteoporosis and fractures. For further information about the pathophysiology of the latter, we analyzed transiliac biopsy samples from n = 21 men with axSpA (age 46 ± 6&#xa0;years, mean ± SD). This cohort comprised patients with (GROUP-1, n = 5) or without increased osteoid thickness and mineralization lag time by histology (GROUP-2, n = 16). We performed quantitative backscattered electron imaging for bone mineralization density distribution (BMDD) and osteocyte lacunae sections (OLS), and Raman microspectroscopy for bone material/compositional properties in cancellous (Cn.) and cortical (Ct.) bone compartments. Patients’ outcomes were compared to different respective reference (REF)/control (CTRL) data. The total cohort and subgroup GROUP-1 (considered separately) showed significant deviations in BMDD versus REF. The average degree of cancellous bone mineralization was decreased by −&#xa0;1.8% (p &lt; 0.05) in the total cohort and decreased by −&#xa0;5.1% (p &lt; 0.01) in GROUP-1, while GROUP-2 had normal BMDD. The total cohort and both subgroups showed abnormal osteocyte OLS-characteristics. Specifically, the respective increases in OLS-area in cancellous and cortical bone were + 14.4% and + 44.5% in GROUP-1 and + 8.8% and + 24.9% in GROUP-2. The total cohort as well as both subgroups showed additionally deviations in organic matrix properties from CTRL with an increased pyridinoline content versus CTRL in both the cohort and subgroups. Our findings showed abnormal bone matrix mineralization in these patients with axSpA, with the largest deviations in the subgroup with histologically defined mineralization defects. The also observed altered osteocyte morphology and pyridinoline content might suggest osteocyte and osteoblast functional abnormalities in axSpA.</p>

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Increased Osteocyte Lacunae Size and Organic Matrix Pyridinoline Content in Transiliac Bone from Patients with Axial Spondyloarthritis (axSpA)

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月1日

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  • Barbara M. Misof,
  • Natalia P. Machado,
  • Shibarjun Mandal,
  • Markus A. Hartmann,
  • Rafaela Ceron,
  • Marcelo M. Pinheiro,
  • Eleftherios P. Paschalis,
  • Stéphane Blouin,
  • Carolina A. Moreira

摘要

Axial spondyloarthritis (axSpA) is a chronic inflammation disorder commonly associated with osteoporosis and fractures. For further information about the pathophysiology of the latter, we analyzed transiliac biopsy samples from n = 21 men with axSpA (age 46 ± 6 years, mean ± SD). This cohort comprised patients with (GROUP-1, n = 5) or without increased osteoid thickness and mineralization lag time by histology (GROUP-2, n = 16). We performed quantitative backscattered electron imaging for bone mineralization density distribution (BMDD) and osteocyte lacunae sections (OLS), and Raman microspectroscopy for bone material/compositional properties in cancellous (Cn.) and cortical (Ct.) bone compartments. Patients’ outcomes were compared to different respective reference (REF)/control (CTRL) data. The total cohort and subgroup GROUP-1 (considered separately) showed significant deviations in BMDD versus REF. The average degree of cancellous bone mineralization was decreased by − 1.8% (p < 0.05) in the total cohort and decreased by − 5.1% (p < 0.01) in GROUP-1, while GROUP-2 had normal BMDD. The total cohort and both subgroups showed abnormal osteocyte OLS-characteristics. Specifically, the respective increases in OLS-area in cancellous and cortical bone were + 14.4% and + 44.5% in GROUP-1 and + 8.8% and + 24.9% in GROUP-2. The total cohort as well as both subgroups showed additionally deviations in organic matrix properties from CTRL with an increased pyridinoline content versus CTRL in both the cohort and subgroups. Our findings showed abnormal bone matrix mineralization in these patients with axSpA, with the largest deviations in the subgroup with histologically defined mineralization defects. The also observed altered osteocyte morphology and pyridinoline content might suggest osteocyte and osteoblast functional abnormalities in axSpA.