ArticleThe American journal of pathology2007
Osteoclasts: what do they do and how do they do it?
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 papers, 2 of them syntheses that pooled it.
What it found
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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.
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
298 citing papers in PubMed, 2 syntheses or guidelines pooled it, 709 citations in OpenAlex.
- Extracellular Vesicles for Treatment of Bone Resorption-Related Diseases in Animal Models: Systematic Review.Calcified tissue international · 2026Pooled it
- Prognostic and therapeutic potential of microRNAs for fracture healing processes and non-union fractures: A systematic review.Clinical and translational medicine · 2023Pooled it
- Circulating osteogenic progenitors and osteoclast precursors are associated with long-term glycemic control, sex steroids, and visceral adipose tissue in men with type 2 diabetes mellitus.Frontiers in endocrinology · 2022Trial
- Fracture healing: from molecular and cellular mechanisms to therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Human parvovirus B19 VP1u‑induced osteoclastogenesis is enhanced by RANKL in RAW264.7 macrophage cells.Molecular medicine reports · 2026Article
- Association of Interleukin 1 Receptor Antagonist (International journal of molecular sciences · 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
- DMXAA accelerates orthodontic tooth movement via macrophage-mediated Rab13-enriched extracellular vesicle release and chemokine secretion.Progress in orthodontics · 2026Article
- Stage-dependent analysis of IL-6, TGF-β, osteocalcin, and sRANKL in the synovial fluid of dogs with osteoarthritis.Scientific reports · 2026Article
- Periodontitis as a Model for Inflammatory Uncoupling of Bone Remodeling.Journal of periodontal research · 2026Review
- Impact of miR-181a-5p and miR-1249-3p treatment on the visceral adipose tissue transcriptome of female mice.GeroScience · 2026Article
- Advances in Bone-on-a-Chips for In Vitro Modeling of Bone Physiology and Pathology.Biomedicines · 2026Review
- Expression of Molecular Markers Associated with Tenosynovial Giant Cell Tumours and Bone Destruction: A Systematic Review.Journal of clinical medicine · 2026Review
- Endothelin-1/endothelin B receptor signalling mediates Prx1Journal of orthopaedic translation · 2026Article
- Dual-action bisphosphonate hydrogel preserves cortical bone integrity and restores healing cascade in osteoporotic fracture-related infection.Nature communications · 2026Article
- Hypergravity reduces F-actin accumulation in osteoclasts, with attenuated bone resorption.PloS one · 2026Article
- HuR Knockdown in MLO-Y4 Osteocyte-like Cells Elevates OPG Expression and Suppresses Osteoclastogenesis In Vitro.International journal of molecular sciences · 2025Article
- Intracellular survival ofVirulence · 2025Review
- Periodontal ligament stem cells in tissue remodeling: from mechanical forces to inflammatory signals.Stem cell research & therapy · 2025Review
- Human platelet-derived extracellular vesicle fractions modulate bone cell metabolism and biologize volume-stable β-TCP matrix in vitro.BMC medicine · 2025Article
238 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
As Americans live longer, degenerative skeletal diseases, such as osteoporosis, become increasingly prevalent. Regardless of cause, osteoporosis reflects a relative enhancement of osteoclast activity. Thus, this unique bone resorptive cell is a prominent therapeutic target. A number of key observations provide insights into the mechanisms by which precursors commit to the osteoclast phenotype and how the mature cell degrades bone. The osteoclast is a member of the monocyte/macrophage family that differentiates under the aegis of two critical cytokines, namely RANK ligand and M-CSF. Tumor necrosis factor (TNF)-alpha also promotes osteoclastogenesis, particularly in states of inflammatory osteolysis such as that attending rheumatoid arthritis. Once differentiated, the osteoclast forms an intimate relationship with the bone surface via the alphavbeta3 integrin, which transmits matrix-derived, cytoskeleton-organizing, signals. These integrin-transmitted signals include activation of the associated proteins, c-src, syk, Vav3, and Rho GTPases. The organized cytoskeleton generates an isolated microenvironment between the cell's plasma membrane and the bone surface in which matrix mineral is mobilized by the acidic milieu and organic matrix is degraded by the lysosomal protease, cathepsin K. This review focuses on these and other molecules that mediate osteoclast differentiation or function and thus serve as candidate anti-osteoporosis therapeutic targets.
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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.