ArticleWorld journal of orthopedics2025
Altered lineage commitment of bone marrow mesenchymal stem cells in idiopathic osteonecrosis of the femoral head.
Article in World journal of orthopedics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Bone marrow mesenchymal stem cell exosomes in osteonecrosis: pathological mechanisms and therapeutic strategies.Molecular biology reports · 2026Review
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5 authors.
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Abstract
backgroundOsteonecrosis of the femoral head (ONFH) is an ischaemic disorder often leading to collapse of the femoral head and severe hip dysfunction. Mesenchymal stem cells (MSCs) have a key role in bone repair, through their ability to differentiate into osteoblasts and their paracrine regulation of the bone microenvironment. While altered MSCs behaviour has been reported in some secondary forms of ONFH, the proliferative and differentiation programmes of MSCs in human idiopathic ONFH have not been previously characterized.
aimTo compare the proliferative capacity, differentiation potential and nuclear factor kappa B (NF-κB) pathway activation of bone marrow MSCs (BM-MSCs) from idiopathic ONFH patients with those from osteoarthritis controls.
methodsFemoral heads were collected during total hip replacement surgeries. Idiopathic ONFH was defined by imaging and histological criteria. Secondary causes were excluded. BM-MSCs were isolated from trabecular bone cylinders and expanded to passage 2 prior characterizations. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay at various seeding densities. Osteogenic potential was assessed by alkaline phosphatase activity, osteogenic gene expression (
resultsIdiopathic ONFH MSCs exhibited significantly higher proliferation rates than osteoarthritis controls. However, they showed reduced alkaline phosphatase activity and osteogenic gene expression but paradoxically, increased mineralization, suggesting non-canonical mineral deposition mechanisms. These cells also display increased adipogenic differentiation. Importantly, ONFH-MSCs expressed higher, although non-significant levels of certain NF-κB target gene genes, consistent with an activated inflammatory state.
conclusionHuman BM-MSCs from idiopathic ONFH display a paradoxical phenotype: Hyperproliferative yet osteogenically impaired with greater adipogenesis and activation of NF-κB signalling. This functional compromise and inflammatory bias may underline the failure of bone regeneration in ONFH, highlighting the need for therapies re-directing MSCs fate and modulating the bone marrow niche.
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