Evidence map›Paper›PMID 24356518›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2014

Nitric oxide-mediated vasodilation increases blood flow during the early stages of stress fracture healing.

Ryan E Tomlinson, Kooresh I Shoghi, Matthew J Silva

Abstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Review
  3. The role of sympathetic control in bone vasculature: insights from spinal cord injury.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Inhibition of 15-PGDH prevents ischemic renal injury by the PGEAmerican journal of physiology. Renal physiology · 2020
    Article
  9. Review
  10. Molecular pathogenesis of fracture nonunion.Journal of orthopaedic translation · 2018
    Review
  11. Review
  12. Antagonizing the αv β3 integrin inhibits angiogenesis and impairs woven but not lamellar bone formation induced by mechanical loading.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014
    Article
  13. Article
  14. Review
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

3 authors at 1 institution in 1 country.

Ryan E TomlinsonDepartment of Orthopaedic Surgery, Washington University in St. Louis, St. Louis, Missouri;
Kooresh I Shoghi
Matthew J Silva
Washington University in St. Louis · US

Funding

The Role of the Osteoblast Secretome in Bone FormationP30AR057235 · NIAMS · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2009 to 2018
$5.7M
OSTEOGENIC AND ANGIOGENIC RESPONSE TO SKELETAL LOADINGR01AR050211 · NIAMS · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2003 to 2020
$5.0M
NIAMS NIH HHS P30 AR057235NIAMS NIH HHS R01 AR050211
6 · The paper itself

Abstract

Despite the strong connection between angiogenesis and osteogenesis in skeletal repair conditions such as fracture and distraction osteogenesis, little is known about the vascular requirements for bone formation after repetitive mechanical loading. Here, established protocols of damaging (stress fracture) and nondamaging (physiological) forelimb loading in the adult rat were used to stimulate either woven or lamellar bone formation, respectively. Positron emission tomography was used to evaluate blood flow and fluoride kinetics at the site of bone formation. In the group that received damaging mechanical loading leading to woven bone formation (WBF), (15)O water (blood) flow rate was significantly increased on day 0 and remained elevated 14 days after loading, whereas (18)F fluoride uptake peaked 7 days after loading. In the group that received nondamaging mechanical loading leading to lamellar bone formation (LBF), (15)O water and (18)F fluoride flow rates in loaded limbs were not significantly different from nonloaded limbs at any time point. The early increase in blood flow rate after WBF loading was associated with local vasodilation. In addition, Nos2 expression in mast cells was increased in WBF-, but not LBF-, loaded limbs. The nitric oxide (NO) synthase inhibitor N(ω)-nitro-l-arginine methyl ester was used to suppress NO generation, resulting in significant decreases in early blood flow rate and bone formation after WBF loading. These results demonstrate that NO-mediated vasodilation is a key feature of the normal response to stress fracture and precedes woven bone formation. Therefore, patients with impaired vascular function may heal stress fractures more slowly than expected.

Indexed as

Fracture HealingOsteogenesisVasodilationAnimalsBlood Flow VelocityDisease Models, AnimalEnzyme InhibitorsFractures, StressMaleMast CellsNitric OxideNitric Oxide Synthase Type IIPositron-Emission TomographyRatsRats, Inbred F344Regional Blood FlowEnzyme InhibitorsNitric OxideNitric Oxide Synthase Type IINos2 protein, ratbone formationl-NAMEstress fracturevasodilationwoven

Identifiers

PMID24356518
PMCPMC3921351
OpenAlexW2055754630

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.