Evidence map›Paper›PMID 30357885›Full record

ReviewBritish journal of clinical pharmacology2019

Mechanisms that drive bone pain across the lifespan.

Patrick W Mantyh

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of clinical pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 3 pooled it
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 3 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
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  11. Review
  12. Review
  13. Bone pain in fibrous dysplasia does not rely on aberrant sensory nerve sprouting or neuroma formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Article
  14. Review
  15. Extensive Periosteal Injury During Fracture Induces Long-Term Pain in Mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Patrick W MantyhDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA.ORCID 0000-0002-0126-138X
University of Arizona · US

Funding

Peripheral Nociceptors in Persistent PainR01NS023970 · NINDS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MANTYH, PATRICK WILLIAM · 1987 to 2019
$3.7M
PERIPHERAL NOCICEPTORS IN PERSISTENT PAINR37NS023970 · NINDS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MANTYH, PATRICK WILLIAM · 2001 to 2007
$2.9M
Preventive Analgesia for Bone Cancer PainR01CA154550 · NCI · UNIVERSITY OF ARIZONA · PI MANTYH, PATRICK WILLIAM · 2011 to 2015
$1.6M
METASTATIC PROSTATE CANCER-INDUCED BONE PAINR01CA157449 · NCI · UNIVERSITY OF ARIZONA · PI MANTYH, PATRICK WILLIAM · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA154550NCI NIH HHS R01 CA157449NINDS NIH HHS R01 NS023970NINDS NIH HHS R37 NS023970
6 · The paper itself

Abstract

Disorders of the skeleton are frequently accompanied by bone pain and a decline in the functional status of the patient. Bone pain occurs following a variety of injuries and diseases including bone fracture, osteoarthritis, low back pain, orthopedic surgery, fibrous dysplasia, rare bone diseases, sickle cell disease and bone cancer. In the past 2 decades, significant progress has been made in understanding the unique population of sensory and sympathetic nerves that innervate bone and the mechanisms that drive bone pain. Following physical injury of bone, mechanotranducers expressed by sensory nerve fibres that innervate bone are activated and sensitized so that even normally non-noxious loading or movement of bone is now being perceived as noxious. Injury of the bone also causes release of factors that; directly excite and sensitize sensory nerve fibres, upregulate proalgesic neurotransmitters, receptors and ion channels expressed by sensory neurons, induce ectopic sprouting of sensory and sympathetic nerve fibres resulting in a hyper-innervation of bone, and central sensitization in the brain that amplifies pain. Many of these mechanisms appear to be involved in driving both nonmalignant and malignant bone pain. Results from human clinical trials suggest that mechanism-based therapies that attenuate one type of bone pain are often effective in attenuating pain in other seemingly unrelated bone diseases. Understanding the specific mechanisms that drive bone pain in different diseases and developing mechanism-based therapies to control this pain has the potential to fundamentally change the quality of life and functional status of patients suffering from bone pain.

Indexed as

LongevityPain ThresholdAge FactorsAnalgesicsAnimalsBone and BonesCentral Nervous System SensitizationChemoreceptor CellsHumansMechanoreceptorsMusculoskeletal PainPain PerceptionQuality of LifeRisk FactorsSympathetic Nervous SystemAnalgesicsagingneuropathicNGFnociceptorspaediatricTrkA

Identifiers

PMID30357885
PMCPMC6533434
OpenAlexW2898114053

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.