骨ルポ
IFMRS 2025 レポート
Karishma Desai(Oral Health Science Center, Tokyo Dental College)

I am honored and grateful to have received the IFMRS Herbert Fleisch workshop - Asia pacific 2025 Travel Award from the Japan Society for Bone and Mineral Research, which provided the opportunity to present my work and engage with leading experts in the field. My work received valuable feedback, opening new avenues for future research.
紹介演題 [1]
Skeletal stem cell functions in bone development, repair and disease
キーワード
Skeletal Stem cells, Progenitors, Bone development Research Group
研究グループ
Christa Maes
Laboratory of Skeletal Cell Biology and Physiology, Skeletal Biology and Engineering Research, Department of Development and Regeneration, KU Leuven, Belgium
サマリー
The keynote presentation by Dr. Maes on the first day of the workshop provided an overview of the role of skeletal stem and progenitor cells (SSPCs) in bone development, repair and disease. Dr. Maes discussed her extensive work on SSPCS, emphasizing the key contribution of Osterix (Osx). The presentation also expanded current understanding of platelet-derived growth factor receptor-beta (PDGFR+) in regulating SSPCs during bone repair. Using lineage tracing and genetic targeting with Osx-Cre; GFP mice, her group demonstrated that Osx-expressing subsets, including bone marrow reticular stromal and perivascular skeletal progenitors contribute to bone formation and exhibit multilineage differentiation potential toward osteogenic and adipogenic fates. In reponse to Injury, multiple Osx+ subsets including PDGFR+-expressing progenitors in perivascular niches collectively expand, migrate and contribute to the regenerating callus. Conditional inactivation of PDGFR+ in Osx+ cells resulted in impaired SSPC proliferation and differentiation, reduced angiotropism, and led to undersized, poorly vascularized callus, demonstrating the importance of PDGFR+ for effective fracture healing. PDGF-PDGFR+ signaling promotes SSPC proliferation, migration and angio-osteogenic crosstalk with endothelial cells, in part via downstream effectors MMP9 and VCAM1, which mediate remodeling and vascular affinity. On the second day, Dr. Besold, PhD research scholar and a member of Dr. Maes’ group, further elaborated on the functional role of PDGFR+ in bone metabolism. Administration of iPTH in mice for 10 days (80µg/Kg) increased the proliferation of PDGFRβ/Ai9+ SSPCs. Overall, their work identifies the PDGF-PDGFR pathway as a molecular target of iPTH, suggesting possible therapeutic potential.
コメント
The work of Dr. Maes’ group highlights PDGFR+ as a key regulator of reparative SSPC activation and vascular integration. The elucidated trajectory positions PDGFR+-regulated SSPCs as a unifying axis linking bone biology, vascular biology and regenerative medicine.
紹介演題 [2]
Cortical bone in older women has greater collagen compaction and less osteocyte connectivity at the time of deposition
キーワード
Bone fragility, Bone Fracture, Osteon, Collagen Research Group
研究グループ
Haniyeh Hemmatian et al
Natalie A.Sims Group, St.Vincent Institute, Fitzroy, VIC, Australia; Department of Medicine at St.Vinvent Hospital, The University at Melbourne, Melbourne; St.Vincent Institute of Medical Research, Melbourne; Australian Catholic University, Melbourne
サマリー
Dr Hemmatian’s research explored factors associated with bone fragility in aging women. It is known that in aging women, increased bone fragility and fractures can occur despite normal bone mineral density. They tested the hypothesis that older women have an intrinsic defect in bone remodeling. They analyzed osteons from mid-diaphysis of femur in two age groups – healthy young (19-40 years) and older (77-95 years) women (n = 10/group). Femoral cortical bone at mid-diaphysis was examined using advanced imaging techniques such as synchrotron-based FTIRM, qBEI, and 3D confocal microscopy. As their samples lacked fluorochrome labels, they developed a histological method to classify osteons into four maturation stages – early, mid, late and stable. Their analysis revealed that mineralization process was similar in both groups. However, older women exhibited compact collagen in mid-to-stable osteons and ~40% lower osteocyte connectivity (canalicular density) in new osteons. Their work highlighted that reduced osteocyte connectivity in new bone and the altered collagen structure rather than degradation of existing bone contribute to bone fragility.
コメント
Their work is useful for understanding bone remodeling in the aging population, especially the factors implicated for increased bone fragility. Research on osteocytes particularly their dendrites and connectivity networks is expanding. Future research directed towards improving bone quality including osteocyte network connectivity may help to improve bone health in elderly women.

Post workshop picture with experts and JSBMR travel awardees at the IFMRS workshop


