ArticleBioMed research international2019
SOST Deficiency Aggravates Osteoarthritis in Mice by Promoting Sclerosis of Subchondral Bone.
Article in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- [Pathology of Cartilage-to-Bone Crosstalk: A New Angle for Animal Experimental Studies on Osteoarthritis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Review
- Comparative review: clinical and pathological heterogeneity in kneeFrontiers in bioengineering and biotechnology · 2025Review
- Mechanotransduction in subchondral bone microenvironment and targeted interventions for osteoarthritis.Mechanobiology in medicine · 2024Review
- Role and Mechanism of Mechanical Load in the Homeostasis of the Subchondral Bone in Knee Osteoarthritis: A Comprehensive Review.Journal of inflammation research · 2024Review
- Hypoxia-induced Wnt/β-catenin signaling activation in subchondral bone osteoblasts leads to an osteoarthritis-like phenotype of chondrocytes in articular cartilage.Frontiers in molecular biosciences · 2023Article
- Senescent skeletal cells cross-talk with synovial cells plays a key role in the pathogenesis of osteoarthritis.Arthritis research & therapy · 2022Review
- Competitive blocking of LRP4-sclerostin binding interface strongly promotes bone anabolic functions.Cellular and molecular life sciences : CMLS · 2022Article
- Osteoclasts secrete leukemia inhibitory factor to promote abnormal bone remodeling of subchondral bone in osteoarthritis.BMC musculoskeletal disorders · 2022Article
- Light on osteoarthritic joint: from bench to bed.Theranostics · 2022Review
- Sclerostin Suppression Facilitates Uveal Melanoma Progression Through Activating Wnt/β-Catenin SignalingFrontiers in oncology · 2022Article
- The role of miR-29 family in disease.Journal of cellular biochemistry · 2021Review
- Osteocyte Dysfunction in Joint Homeostasis and Osteoarthritis.International journal of molecular sciences · 2021Review
- Microenvironment in subchondral bone: predominant regulator for the treatment of osteoarthritis.Annals of the rheumatic diseases · 2021Review
- From Pathogenesis to Therapy in Knee Osteoarthritis: Bench-to-Bedside.International journal of molecular sciences · 2021Review
- WNT Signalling in Osteoarthritis and Its Pharmacological Targeting.Handbook of experimental pharmacology · 2021Review
- Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As the initial part in the development of osteoarthritis (OA), subchondral bone sclerosis has been considered to be initiated by excess mechanical loading and proven to be correlated to other pathological changes. Sclerostin, which is an essential mechanical stress response protein, is encoded by the SOST gene. It is expressed in osteocytes and mature chondrocytes and has been proven to be closely correlated to OA. However, the relationship and mechanism between the SOST gene and the development of OA remain unclear. The aim of the present study was to investigate the role of the SOST gene in OA pathogenesis in the subchondral bone. A knee anterior cruciate ligament transection (ACLT) mouse osteoarthritis (OA) model on SOST-knockout (SOST KO) and wild-type (WT) mice was established. The pathogenic and phenotypic changes in the subchondral bone were investigated by histology, micro-CT, immunohistochemistry, TRAP staining, Masson staining, and Toluidine blue staining. It was found that sclerostin expression decreased in both the calcified cartilage and mineralized subchondral structures during the development of OA. Joint instability induced a severe cartilage degradation phenotype, with higher OARSI scores in SOST KO mice, when compared to WT mice. SOST KO mice with OA exhibited a higher BMD and BV/TV ratio, as well as a higher rate of bone remodeling and TRAP-positive cell number, when compared to the WT counterparts, but the difference was not significant between the sham-operation groups. It was concluded that loss of sclerostin aggravates knee OA in mice by promoting subchondral bone sclerosis and increasing catabolic activity of cartilage.
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