ArticleJournal of dental research2018
Resolving Macrophages Counter Osteolysis by Anabolic Actions on Bone Cells.
Article in Journal of dental research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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.
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Who cites it
52 citing papers in PubMed, 92 citations in OpenAlex.
- B10 Adoptive Transfer Ameliorates Inflammation and Bone Loss in Experimental Periodontitis Through Promoting Macrophage-Mediated Pro-Resolving Functions.Inflammation · 2026Article
- Periodontitis induces skeletal muscle atrophy by increasing circulating levels of activin A.Nature communications · 2026Article
- Immunometabolism of macrophages in the bone microenvironment: a new perspective for bone healing therapy.Journal of advanced research · 2026Review
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- Young plasma-derived exosomes deliver YOD1 to induce M2 polarization and ameliorate osteoporosis via mTOR signaling pathways.International journal of biological sciences · 2026Article
- Functions of Macrophages in Periodontal Disease Progression and Gingival Tissue Homeostasis.Advances in experimental medicine and biology · 2026Review
- Fluvastatin enhances healing of medication-related osteonecrosis of the jaw (MRONJ) via macrophage polarization in a rat MRONJ-like model.Journal of dental sciences · 2026Article
- Periodontal ligament stem cells in tissue remodeling: from mechanical forces to inflammatory signals.Stem cell research & therapy · 2025Review
- Metal-phenolic encapsulation of carbon monoxide releasing molecule for enhanced gas therapy of periodontitis.Materials today. Bio · 2025Article
- Macrophage Depletion Reduces Bone Loss and Alters Inflammatory Responses: A Mouse Peri-Implantitis Model.Journal of clinical periodontology · 2025Article
- Hyperfunctional Neutrophils in Aged Mice Are Linked to Enhanced Bone Loss in Ligature-Induced Periodontitis.Dentistry journal · 2025Article
- Natural and induced immune responses in oral cavity and saliva.BMC immunology · 2025Review
- Article
- Geniposide Stabilized Atherosclerosis Plaque by Induced M2 Polarization via PPARγ Signaling Pathway.Drug design, development and therapy · 2025Article
- Unveiling research hotspots: a bibliometric study on macrophages in musculoskeletal diseases.Frontiers in immunology · 2025Review
- Local Controlled Delivery of IL-4 Decreases Inflammatory Bone Loss in a Murine Model of Periodontal Disease.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Therapeutic delivery of CCL2 modulates immune response and restores host-microbe homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Macrophage Polarization during MRONJ Development in Mice.Journal of dental research · 2024Article
- A new direction in periodontitis treatment: biomaterial-mediated macrophage immunotherapy.Journal of nanobiotechnology · 2024Review
- Tim4 deficiency reduces CD301bInternational journal of oral science · 2024Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Progression of inflammatory osteolytic diseases, including rheumatoid arthritis and periodontitis, is characterized by increased production of proinflammatory mediators and matrix-degrading enzymes by macrophages and increased osteoclastic activity. Phenotypic changes in macrophages are central to the healing process in virtually all tissues. Using a murine model of periodontitis, we assessed the timing of macrophage phenotypic changes and the impact of proresolving activation during inflammatory osteolysis and healing. Proinflammatory macrophage activation and TNF-α overproduction within 3 wk after induction of periodontitis was associated with progressing bone loss. Proresolving activation within 1 wk of stimulus removal and markers of resolving macrophages (IL-10, TGF-β, and CD206) correlated strongly with bone levels. In vivo macrophage depletion with clodronate liposomes prevented bone resorption but impaired regeneration. Induction of resolving macrophages with rosiglitazone, a PPAR-γ agonist, led to reduced bone resorption during inflammatory stimulation and increased bone formation during healing. In vitro assessment of primary bone marrow-derived macrophages activated with either IFN-γ and LPS (proinflammatory activation) or IL-4 (proresolving activation) showed that IL-4-activated cells have enhanced resolving functions (production of anti-inflammatory cytokines; migration and phagocytosis of aged neutrophils) and exert direct anabolic actions on bone cells. Cystatin C secreted by resolving but not inflammatory macrophages explained, in part, the macrophage actions on osteoblasts and osteoclasts. This study supports the concept that therapeutic induction of proresolving functions in macrophages can recouple bone resorption and formation in inflammatory osteolytic diseases.
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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.