ArticleNature communications2022
Osteocytes directly regulate osteolysis via MYD88 signaling in bacterial bone infection.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Host insulin resistance caused byFrontiers in cellular and infection microbiology · 2023Pooled it
- Dissecting Hypoxia Inducible Factor-Driven High Bone Mass Phenotype in Mice Lacking Osteocytic Von Hippel-Lindau.JBMR plus · 2026Article
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Neuroimmune Regulation in Posttraumatic Bone Repair: From Inflammatory Transition to Neurovascular Coupling and Functional Recovery.Journal of cellular physiology · 2026Review
- Extreme PTH-Independent Hypercalcemia Mediated by a Rare Non-Osteoclastic Osteolysis Mechanism in Newly Diagnosed High-Risk Biclonal IgA Multiple Myeloma: Temporal Association with the Second Dose of Moderna mRNA-1273 COVID-19 Vaccine.International journal of molecular sciences · 2026Article
- Review
- ROR2 preserves alveolar bone homeostasis by orchestrating IRAK4-dependent suppression of CXCL8-driven osteolysis.Cell communication and signaling : CCS · 2026Article
- Turmeric-derived nanovesicles reprogram pathological NETosis to mitigate inflammatory bone loss.Journal of nanobiotechnology · 2026Article
- Clinical Outcome After Surgery for Fracture-Related Infection Is Dependent on Both Microbiology and the Host Inflammatory Response.Pathogens (Basel, Switzerland) · 2026Article
- Establishment of a coculture system for Porphyromonas gingivalis and head and neck squamous cell carcinoma using spheroid culture and LATS inhibition.FEBS open bio · 2026Article
- Bone and Infections: An Osteoimmunological Interplay.International journal of molecular sciences · 2026Review
- Punicalagin with anti-inflammatory activities affects Brd-4 mediated chromatin remodeling for attenuating inflammatory osteolysis.Scientific reports · 2026Article
- Article
- Dual-action bisphosphonate hydrogel preserves cortical bone integrity and restores healing cascade in osteoporotic fracture-related infection.Nature communications · 2026Article
- Pharmacovigilance-Based Identification and Mechanistic Exploration of Periodontitis-Related Drugs.Journal of clinical periodontology · 2026Article
- Osteomyelitis related lameness across animal species: pathophysiology, etiology, epidemiology and experimental model approaches.Frontiers in veterinary science · 2026Review
- Combined analysis of host immune response, biofilm genes, and 16S rRNA detection in fracture-related infection: an observational cohort study.Journal of bone and joint infection · 2026Article
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- Electrosensitive Heterogeneous Short Fibers via Acousto-Electric Coupling for Sequential Bone Regeneration in Infectious Defects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The impact of bone cell activation on bacterially-induced osteolysis remains elusive. Here, we show that matrix-embedded osteocytes stimulated with bacterial pathogen-associated molecular patterns (PAMPs) directly drive bone resorption through an MYD88-regulated signaling pathway. Mice lacking MYD88, primarily in osteocytes, protect against osteolysis caused by calvarial injections of bacterial PAMPs and resist alveolar bone resorption induced by oral Porphyromonas gingivalis (Pg) infection. In contrast, mice with targeted MYD88 restoration in osteocytes exhibit osteolysis with inflammatory cell infiltration. In vitro, bacterial PAMPs induce significantly higher expression of the cytokine RANKL in osteocytes than osteoblasts. Mechanistically, activation of the osteocyte MYD88 pathway up-regulates RANKL by increasing binding of the transcription factors CREB and STAT3 to Rankl enhancers and by suppressing K48-ubiquitination of CREB/CREB binding protein and STAT3. Systemic administration of an MYD88 inhibitor prevents jawbone loss in Pg-driven periodontitis. These findings reveal that osteocytes directly regulate inflammatory osteolysis in bone infection, suggesting that MYD88 and downstream RANKL regulators in osteocytes are therapeutic targets for osteolysis in periodontitis and osteomyelitis.
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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.