ReviewPharmacology & therapeutics2017
Macrophages and skeletal health.
Review in Pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
92 citing papers in PubMed, 169 citations in OpenAlex.
- Macrophage-MSCs Interplay in Orthodontic Bone Remodelling: Mechanics-Immunity-Stem Cell Axis.International dental journal · 2026Review
- The NLRP12 Osteoimmune Checkpoint: Coordinating Inflammatory Signaling and Bone Remodeling.Biomedicines · 2026Review
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Electric field stimulation-responsive hydrogels for bone regeneration: from mechanisms to applications.Bone research · 2026Review
- Cellular mechanisms of osteoporosis: A comprehensive perspective on ferroptosis, cuproptosis and lipid metabolism abnormalities.Biomaterials translational · 2026Review
- The regulatory networks and mechanisms of bone microenvironment in tumorigenesis and metastasis.Journal of bone oncology · 2025Review
- BPAG1 promotes osteoclastogenesis and postmenopausal osteoporosis via activating ERK signaling pathway.iScience · 2025Article
- Targeting APJ drives BNIP3-PINK1-PARKIN induced mitophagy and improves systemic inflammatory bone loss.Journal of advanced research · 2025Article
- Engineering Efferocytosis for Bone Regeneration.Macromolecular bioscience · 2025Review
- Dynamics of Macrophage Polarization Reveal Unique Phenotypes During Mouse Postpartum Uterine Remodeling.bioRxiv : the preprint server for biology · 2025Article
- The multifaceted biomimetic titanium implant promotes bone integration with sequential antibacterial and immune modulation properties.Bioactive materials · 2025Article
- An engineered M2 macrophage-derived exosomes-loaded electrospun biomimetic periosteum promotes cell recruitment, immunoregulation, and angiogenesis in bone regeneration.Bioactive materials · 2025Article
- Macrophage ATF6 accelerates corticotomy-assisted orthodontic tooth movement through promoting Tnfα transcription.International journal of oral science · 2025Article
- Osteosarcoma biomarker analysis and drug targeting prediction based on pyroptosis-related genes.Medicine · 2025Article
- Macrophages in osteoporotic fractures: from immunometabolic mechanisms to precision therapeutic approaches.Frontiers in endocrinology · 2025Review
- Efferocytosis-induced metabolic shift in bone macrophages drives lactate production and modulates inflammation and osteoclastogenesis.Frontiers in immunology · 2025Article
- Targeting dipeptidyl peptidase-8/9 to combat inflammation-induced osteoclastogenesis in RAW264.7 macrophages and analysis of anti-osteoclastogenesis potential of chrysin.Iranian journal of basic medical sciences · 2025Article
- Inflammation and mechanical force-induced bone remodeling.Periodontology 2000 · 2024Review
- Dynamic transcriptome analysis of osteal macrophages identifies a distinct subset with senescence features in experimental osteoporosis.JCI insight · 2024Article
- CCL2/CCR2 Signalling in Mesenchymal Stem/Progenitor Cell Recruitment and Fracture Healing in Mice.Journal of cellular and molecular medicine · 2024Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bone is in a constant state of remodeling, a process which was once attributed solely to osteoblasts and osteoclasts. Decades of research has identified many other populations of cells in the bone that participate and mediate skeletal homeostasis. Recently, osteal macrophages emerged as vital participants in skeletal remodeling and osseous repair. The exact mechanistic roles of these tissue-resident macrophages are currently under investigation. Macrophages are highly plastic in response to their micro-environment and are typically classified as being pro- or anti-inflammatory (pro-resolving) in nature. Given that inflammatory states result in decreased bone mass, proinflammatory macrophages may be negative regulators of bone turnover. Pro-resolving macrophages have been shown to release anabolic factors and may present a target for therapeutic intervention in inflammation-induced bone loss and fracture healing. The process of apoptotic cell clearance, termed efferocytosis, is mediated by pro-resolving macrophages and may contribute to steady-state bone turnover as well as fracture healing and anabolic effects of osteoporosis therapies. Parathyroid hormone is an anabolic agent in bone that is more effective in the presence of mature phagocytic macrophages, further supporting the hypothesis that efferocytic macrophages are positive contributors to bone turnover. Therapies which alter macrophage plasticity in tissues other than bone should be explored for their potential to treat bone loss either alone or in conjunction with current bone therapeutics. A better understanding of the exact mechanisms by which macrophages mediate bone homeostasis will lead to an expansion of pharmacologic targets for the treatment of osteoporosis and inflammation-induced bone loss.
Indexed as
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What OpenQuestion holds
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.