ArticleBone2021
Low bone mass resulting from impaired estrogen signaling in bone increases severity of load-induced osteoarthritis in female mice.
Article in Bone, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.
- Association between physical activity and knee osteoarthritis: a comprehensive systematic review and meta-analysis.Journal of global health · 2025Pooled it
- Uncovering the "riddle of femininity" in osteoarthritis: a systematic review and meta-analysis of menopausal animal models and mathematical modeling of estrogen treatment.Osteoarthritis and cartilage · 2023Pooled it
- A Thematic Narrative Review of Osteoarthritis Risk Factors Across the Female Life Course.International journal of molecular sciences · 2026Review
- Micro-CT-based analysis of the murine osteochondral unit: a review and recommendations for standardized subchondral bone assessment.JBMR plus · 2026Review
- Estrogen deficiency as a common driver and integrative mechanism in osteoporosis‑osteoarthritis comorbidity (Review).Molecular medicine reports · 2026Review
- Joint damage is more severe following a single bout than multiple bouts of high magnitude loading in mice.Osteoarthritis and cartilage · 2026Article
- Immunometabolic reprogramming in osteoporosis-osteoarthritis comorbidity: from inflammaging to osteochondral unit degeneration.Frontiers in immunology · 2026Review
- Deciphering bisphenol A (BPA)-elicited osteoarthritis mechanisms through network toxicology and molecular docking, then de novo generation of novel therapeutic candidates.BMC pharmacology & toxicology · 2025Article
- Exploring the mechanism of action of astragaloside in the treatment of osteoarthritis based on network pharmacology.Biomedical engineering online · 2025Article
- Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.Biomedicines · 2025Review
- Review
- Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression.Nature communications · 2025Article
- Toward a clear relationship between mechanical signals and bone adaptation.Mechanobiology in medicine · 2025Review
- Single-cell transcriptomics reveals novel chondrocyte and osteoblast subtypes and their role in knee osteoarthritis pathogenesis.Signal transduction and targeted therapy · 2025Article
- Association of organs-crosstalk with the pathogenesis of osteoarthritis: cartilage as a key player.Frontiers in endocrinology · 2025Review
- Exploring the mechanism of action ofHeliyon · 2024Article
- PTH treatment before cyclic joint loading improves cartilage health and attenuates load-induced osteoarthritis development in mice.Science advances · 2024Article
- Mechanical loading of joint modulates T cells in lymph nodes to regulate osteoarthritis.Osteoarthritis and cartilage · 2024Article
- Ferroptosis and its role in osteoarthritis: mechanisms, biomarkers, and therapeutic perspectives.Frontiers in cell and developmental biology · 2024Review
- Wnt5a deficiency in osteocalcin-expressing cells could not alleviate the osteoarthritic phenotype in a mouse model of post-traumatic osteoarthritis.Iranian journal of basic medical sciences · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveReduced subchondral bone mass and increased remodeling are associated with early stage OA. However, the direct effect of low subchondral bone mass on the risk and severity of OA development is unclear. We sought to determine the role of low bone mass resulting from a bone-specific loss of estrogen signaling in load-induced OA development using female osteoblast-specific estrogen receptor-alpha knockout (pOC-ERαKO) mice.
methodsOsteoarthritis was induced by cyclic mechanical loading applied to the left tibia of 26-week-old female pOC-ERαKO and littermate control mice at peak loads of 6.5N, 7N, or 9N for 2 weeks. Cartilage damage and thickness, osteophyte development, and joint capsule fibrosis were assessed from histological sections. Subchondral bone morphology was analyzed by microCT. The correlation between OA severity and intrinsic bone parameters was determined.
resultsThe loss of ERα in bone resulted in an osteopenic subchondral bone phenotype, but did not directly affect cartilage health. Following two weeks of cyclic tibial loading to induce OA pathology, pOC-ERαKO mice developed more severe cartilage damage, larger osteophytes, and greater joint capsule fibrosis compared to littermate controls. Intrinsic bone parameters negatively correlated with measures of OA severity in loaded limbs.
conclusionsSubchondral bone osteopenia resulting from bone-specific loss of estrogen signaling was associated with increased severity of load-induced OA pathology, suggesting that reduced subchondral bone mass directly exacerbates load-induced OA development. Bone-specific changes associated with estrogen loss may contribute to the increased incidence of OA in post-menopausal women.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.