ReviewPain reports2021
Reciprocal interactions between osteoclasts and nociceptive sensory neurons in bone cancer pain.
Review in Pain reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Suzetrigine for Cancer-Related Bone Pain: A Three-Patient Case Series.Orthopedic reviews · 2026Article
- Extracellular vesicle-based therapeutic strategies for spinal tumors and associated nerve damage: advances, challenges, and future directions.Frontiers in cell and developmental biology · 2026Review
- Pain in Osteoporosis: Current and Future Strategies.Drugs & aging · 2025Review
- Article
- GPR37 Activation Alleviates Bone Cancer Pain via the Inhibition of Osteoclastogenesis and Neuronal Hyperexcitability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanism of the analgesic effect of electroacupuncture on bone cancer pain through the neuro-immune system: progress based on animal experiments.Frontiers in neurology · 2025Review
- Article
- Macrophage heterogeneity in bone metastasis.Journal of bone oncology · 2024Article
- Altered gut microbiome drives heightened pain sensitivity in a murine model of metastatic triple-negative breast cancer.American journal of cancer research · 2024Article
- Nociceptor mechanisms underlying pain and bone remodeling via orthodontic forces: toward no pain, big gain.Frontiers in pain research (Lausanne, Switzerland) · 2024Review
- Macrophages and microglia in inflammation and neuroinflammation underlying different pain states.Medical review (2021) · 2023Article
- Immunotherapies in chronic pain through modulation of neuroimmune interactions.Pharmacology & therapeutics · 2023Review
- Engineered Sensory Nerve Guides Self-Adaptive Bone Healing via NGF-TrkA Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Cancer aggravation due to persistent pain signals with the increased expression of pain-related mediators in sensory neurons of tumor-bearing mice.Molecular brain · 2023Article
- Ion channels in cancer-induced bone pain: from molecular mechanisms to clinical applications.Frontiers in molecular neuroscience · 2023Review
- Prostate cancer induced bone pain: pathobiology, current treatments and pain responses from recent clinical trials.Discover oncology · 2022Review
- Activation of GDNF-ERK-Runx1 signaling contributes to P2X3R gene transcription and bone cancer pain.iScience · 2022Article
- Glycogen synthase kinase-3β inhibition decreases inflammation and relieves cancer induced bone pain via reducing Drp1-mediated mitochondrial damage.Journal of cellular and molecular medicine · 2022Article
- A metastasis-on-a-chip approach to explore the sympathetic modulation of breast cancer bone metastasis.Materials today. Bio · 2022Article
- Neuroimmunology of cancer and associated symptomology.Immunology and cell biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many common cancers such as breast, prostate, and lung cancer metastasize to bones at advanced stages, producing severe pain and functional impairment. At present, the current pharmacotherapies available for bone cancer pain are insufficient to provide safe and efficacious pain relief. In this narrative review, we discuss the mechanisms used by cancer cells within the bone tumor microenvironment (TME) to drive bone cancer pain. In particular, we highlight the reciprocal interactions between tumor cells, bone-resorbing osteoclasts, and pain-sensing sensory neurons (nociceptors), which drive bone cancer pain. We discuss how tumor cells present within the bone TME accelerate osteoclast differentiation (osteoclastogenesis) and alter osteoclast activity and function. Furthermore, we highlight how this perturbed state of osteoclast overactivation contributes to bone cancer pain through (1) direct mechanisms, through their production of pronociceptive factors that act directly on sensory afferents; and (2) by indirect mechanisms, wherein osteoclasts drive bone resorption that weakens tumor-bearing bones and predisposes them to skeletal-related events, thereby driving bone cancer pain and functional impairment. Finally, we discuss some potential therapeutic agents, such as denosumab, bisphosphonates, and nivolumab, and discuss their respective effects on bone cancer pain, osteoclast overactivation, and tumor growth within the bone TME.
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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.