Evidence map›Paper›PMID 22293759›Full record

ReviewNature reviews. Rheumatology2012

Fracture healing under healthy and inflammatory conditions.

Lutz Claes, Stefan Recknagel, Anita Ignatius

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 657 papers.

0numbers the graph read from it
0cells of the map it votes in
657citing papers in PubMed
–field-weighted citation impact
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

657 citing papers in PubMed.

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597 more citing papers are in PubMed but not listed here.

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.

Lutz ClaesInstitute of Orthopedic Research and Biomechanics, Center of Musculoskeletal Research, University of Ulm, Helmholtzstraße 14, 89081 Ulm, Germany. lutz.claes@uni-ulm.de
Stefan Recknagel
Anita Ignatius

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Optimal fracture treatment requires knowledge of the complex physiological process of bone healing. The course of bone healing is mainly influenced by fracture fixation stability (biomechanics) and the blood supply to the healing site (revascularization after trauma). The repair process proceeds via a characteristic sequence of events, described as the inflammatory, repair and remodeling phases. An inflammatory reaction involving immune cells and molecular factors is activated immediately in response to tissue damage and is thought to initiate the repair cascade. Immune cells also have a major role in the repair phase, exhibiting important crosstalk with bone cells. After bony bridging of the fragments, a slow remodeling process eventually leads to the reconstitution of the original bone structure. Systemic inflammation, as observed in patients with rheumatoid arthritis, diabetes mellitus, multiple trauma or sepsis, can increase fracture healing time and the rate of complications, including non-unions. In addition, evidence suggests that insufficient biomechanical conditions within the fracture zone can influence early local inflammation and impair bone healing. In this Review, we discuss the main factors that influence fracture healing, with particular emphasis on the role of inflammation.

Indexed as

AnimalsBiomechanical PhenomenaBone RemodelingDisease Models, AnimalFracture FixationFracture HealingHumansInflammationSheep

Identifiers

PMID22293759

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.