ReviewTrends in molecular medicine2014
Osteoclasts: more than 'bone eaters'.
Review in Trends in molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 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
190 citing papers in PubMed.
- Decoding Skeletal Biology Through Transcriptomics: Insights from Bulk, Single-Cell, Spatial, and Multi-Omics Approaches.International journal of molecular sciences · 2026Review
- Early bone-formation response to sclerostin antibody is altered by prior antiresorptive treatment in ovariectomized rats.JBMR plus · 2026Article
- The molecular and functional interplay between the osteopetrosis-associated proteins SNX10, OSTM1, and CLC-7 during mouse osteoclastogenesis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- KPT-330 alleviates osteoarthritis by inhibiting subchondral bone osteoclastogenesis via the NF-κB and MAPK signaling pathways.iScience · 2026Article
- Apoptotic bodies in bone homeostasis and skeletal disease: biology and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Exosomes in bone health and disease: cellular crosstalk, systemic signaling, and AI-driven advances in regenerative therapy.Stem cell research & therapy · 2026Review
- Intermittent parathyroid hormone employs autonomous and non-autonomous mechanisms to drive osteogenesis from Ebf3-expressing skeletal progenitor cells.bioRxiv : the preprint server for biology · 2026Article
- The TLR10-Vitamin D Axis Facilitates Osteogenic Differentiation of Mesenchymal Stem Cells In Vitro.Cells · 2026Article
- Aebp1 loss in osteoprogenitors leads to skeletal defects resembling Ehlers-Danlos Syndrome by diminishing Wnt/β-catenin signaling.JCI insight · 2026Article
- Plants used in medicines and foods in osteoporosis: mechanistic insights into bone-remodeling homeostasis and clinical evidence.Frontiers in pharmacology · 2026Review
- Tissue Factor-inhibited Beclin1-autophagy via BCL2 overexpression suppresses the differentiation of human monocytes into mature osteoclasts.Genetics and molecular biology · 2026Article
- Article
- Loss of Stat3 in Prx1Advanced biology · 2025Article
- Yougui pills prevent ovariectomy-induced bone loss by suppressing Th17 response and IL-17/NF-κB pathway.Annals of medicine · 2025Article
- Brain-Bone Axis in Physiological and Pathological Conditions.International journal of molecular sciences · 2025Review
- Article
- The shoulder girdle of early chondrichthyans grew by skeletal remodelling.Biology letters · 2025Article
- BMP9 attenuates microgravity-related disuse osteoporosis by modulating TGFβ and BMP signaling.NPJ microgravity · 2025Article
- The Role of Osteoporosis in Total Hip Arthroplasty Periprosthetic Fractures and Current Management Strategies: a Review.Current osteoporosis reports · 2025Review
- Age-related alterations of angiogenesis, inflammation and bone microarchitecture during fracture healing in mice.GeroScience · 2025Article
130 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.
Funding
Abstract
As the only cells definitively shown to degrade bone, osteoclasts are key mediators of skeletal diseases including osteoporosis. Bone-forming osteoblasts, and hematopoietic and immune system cells, each influence osteoclast formation and function, but the reciprocal impact of osteoclasts on these cells is less well appreciated. We highlight here the functions that osteoclasts perform beyond bone resorption. First, we consider how osteoclast signals may contribute to bone formation by osteoblasts and to the pathology of bone lesions such as fibrous dysplasia and giant cell tumors. Second, we review the interaction of osteoclasts with the hematopoietic system, including the stem cell niche and adaptive immune cells. Connections between osteoclasts and other cells in the bone microenvironment are discussed within a clinically relevant framework.
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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.