ArticlePloS one2014
Modulation of osteoclastogenesis with macrophage M1- and M2-inducing stimuli.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 42 citations in OpenAlex.
- M-CSF priming enhances the efficiency and reproducibility of hiPSC-derived osteoclast differentiation and pharmacological responsiveness to anti-resorptive agents.Scientific reports · 2026Article
- Macrophages and osteoclasts: similarity and divergence between bone phagocytes.Frontiers in immunology · 2025Review
- Microenvironment of diabetic foot ulcers: Implications for healing and therapeutic strategies.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2025Review
- In Vitro Cell Culture Model for Osteoclast Activation during Estrogen Withdrawal.International journal of molecular sciences · 2024Article
- Article
- Article
- M1/M2 macrophages and their overlaps - myth or reality?Clinical science (London, England : 1979) · 2023Article
- Article
- Review
- Identification of Novel Genes for Cell Fusion during Osteoclast Formation.International journal of molecular sciences · 2022Article
- Integrated computational and in vivo models reveal Key Insights into macrophage behavior during bone healing.PLoS computational biology · 2022Article
- High-mobility group box chromosomal protein-1 deletion alleviates osteoporosis in OVX rat model via suppressing the osteoclastogenesis and inflammation.Journal of orthopaedic surgery and research · 2022Article
- Review
- YAP1 nuclear efflux and transcriptional reprograming follow membrane diminution upon VSV-G-induced cell fusion.Nature communications · 2021Article
- Computational modeling reveals a key role for polarized myeloid cells in controlling osteoclast activity during bone injury repair.Scientific reports · 2021Article
- Hdac3 deletion in myeloid progenitor cells enhances bone healing in females and limits osteoclast fusion via Pmepa1.Scientific reports · 2020Article
- mTOR inhibitor and bone-targeted drugs break the vicious cycle between clear-cell renal carcinoma and osteoclasts in an in vitro co-culture model.Journal of bone oncology · 2019Article
- Tumor necrosis factor receptor-associated factor 6 is required to inhibit foreign body giant cell formation and activate osteoclasts under inflammatory and infectious conditions.Journal of bone and mineral metabolism · 2018Article
- The role of IL-1B in breast cancer bone metastasis.Endocrine-related cancer · 2018Review
- Interleukin-1β induces human cementoblasts to support osteoclastogenesis.International journal of oral science · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Macrophages are generated through the differentiation of monocytes in tissues and they have important functions in innate and adaptive immunity. In addition to their roles as phagocytes, macrophages can be further differentiated, in the presence of receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF), into osteoclasts (multinucleated giant cells that are responsible for bone resorption). In this work, we set out to characterize whether various inflammatory stimuli, known to induce macrophage polarization, can alter the type of multinucleated giant cell obtained from RANKL differentiation. Following a four-day differentiation protocol, along with lipopolysaccharide (LPS)/interferon gamma (IFNγ) as one stimulus, and interleukin-4 (IL-4) as the other, three types of multinucleated cells were generated. Using various microscopy techniques (bright field, epifluorescence and scanning electron), functional assays, and western blotting for osteoclast markers, we found that, as expected, RANKL treatment alone resulted in osteoclasts, whereas the addition of LPS/IFNγ to RANKL pre-treated macrophages generated Langhans-type giant cells, while IL-4 led to giant cells resembling foreign body giant cells with osteoclast-like characteristics. Finally, to gain insight into the modulation of osteoclastogenesis, we characterized the formation and morphology of RANKL and LPS/IFNγ-induced multinucleated giant cells.
Indexed as
Identifiers
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.