ArticleBone research2019
Osteocyte dysfunction promotes osteoarthritis through MMP13-dependent suppression of subchondral bone homeostasis.
Article in Bone research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 112 citations in OpenAlex.
- hMSCs form Osteocyte-like Cell Networks within Strain-Stiffening Bottlebrush Polymer Hydrogels.bioRxiv : the preprint server for biology · 2026Article
- A bone histological approach to distinguish periprosthetic joint infection from aseptic osteolysis in revision joint replacement.Bone & joint research · 2026Article
- Semaglutide alleviates osteoarthritis independent of weight loss via GLP-1R-mediated activation of autophagy through AKT/mTOR inhibition.Journal of orthopaedic translation · 2026Article
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PLGA Nanoparticle-Mediated Sustained Release of Fisetin for Intra-Articular Therapy of Temporomandibular Joint Osteoarthritis.International journal of molecular sciences · 2026Article
- Osteocyte-Intrinsic MMP13 exacerbates injury-induced temporomandibular joint osteoarthritis.Osteoarthritis and cartilage · 2026Article
- Inflammatory cytokines secreted from senescent periodontal ligament cells influence the osteocyte network in alveolar bone.JBMR plus · 2026Article
- Tissue and extracellular matrix remodeling of the subchondral bone during osteoarthritis of knee joints as revealed by spatial mass spectrometry imaging.Bone research · 2026Article
- Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.Frontiers in immunology · 2026Review
- Stage-dependent effects of moderate treadmill exercise on cartilage preservation and subchondral bone remodeling in mouse osteoarthritis progression.Osteoarthritis and cartilage · 2025Article
- Osteoarthritis: Mechanisms and Therapeutic Advances.MedComm · 2025Review
- Osteocyte-derived extracellular vesicles mediate the bone-to-cartilage crosstalk and promote osteoarthritis progression.Nature communications · 2025Article
- Callus organoids reveal distinct cartilage to bone transition mechanisms across donors and a role for biological sex.Bone research · 2025Article
- Targeting Long Noncoding RNA H19 in Subchondral Bone Osteocytes and the Alleviation of Cartilage Degradation in Osteoarthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Articular cartilage degeneration and aberrant osteocyte perilacunar/canalicular remodeling in subchondral bone of patients with developmental dysplasia of the hip.BMC musculoskeletal disorders · 2025Article
- Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis.Bone research · 2025Article
- Osteocytes: master orchestrators of skeletal homeostasis, remodeling, and osteoporosis pathogenesis.Frontiers in cell and developmental biology · 2025Review
- IL-19 suppresses Hippo signaling via modulating YAP1 phosphorylation in osteoarthritis.Frontiers in immunology · 2025Article
- A novel optimized silver nitrate staining method for visualizing the osteocyte lacuno-canalicular system.Frontiers in endocrinology · 2025Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Osteoarthritis (OA), long considered a primary disorder of articular cartilage, is commonly associated with subchondral bone sclerosis. However, the cellular mechanisms responsible for changes to subchondral bone in OA, and the extent to which these changes are drivers of or a secondary reaction to cartilage degeneration, remain unclear. In knee joints from human patients with end-stage OA, we found evidence of profound defects in osteocyte function. Suppression of osteocyte perilacunar/canalicular remodeling (PLR) was most severe in the medial compartment of OA subchondral bone, with lower protease expression, diminished canalicular networks, and disorganized and hypermineralized extracellular matrix. As a step toward evaluating the causality of PLR suppression in OA, we ablated the PLR enzyme MMP13 in osteocytes while leaving chondrocytic MMP13 intact, using Cre recombinase driven by the 9.6-kb DMP1 promoter. Not only did osteocytic MMP13 deficiency suppress PLR in cortical and subchondral bone, but it also compromised cartilage. Even in the absence of injury, osteocytic MMP13 deficiency was sufficient to reduce cartilage proteoglycan content, change chondrocyte production of collagen II, aggrecan, and MMP13, and increase the incidence of cartilage lesions, consistent with early OA. Thus, in humans and mice, defects in PLR coincide with cartilage defects. Osteocyte-derived MMP13 emerges as a critical regulator of cartilage homeostasis, likely via its effects on PLR. Together, these findings implicate osteocytes in bone-cartilage crosstalk in the joint and suggest a causal role for suppressed perilacunar/canalicular remodeling in osteoarthritis.
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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.