Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMedOpen access

How Fat Grafting Works.

Evans BGA., Gronet EM., Saint-Cyr MH.

Laboratory Study on Chronic Inflammation, published in Plast Reconstr Surg Glob Open (2020) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Plast Reconstr Surg Glob Open (2020)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
32802628
PMCID
PMC7413772
DOI
10.1097/GOX.0000000000002705
Citations
19

Abstract (original English)

Fat grafting has been shown to improve diseased soft issue. Although the mechanism behind fat grafting's regenerative properties is currently debated, published studies agree that there is an associated vasculogenic effect. A systematic literature review was conducted to elucidate the biochemical pathways responsible for establishing neo-vasculature to grafted fat. Methods A systematic literature review was conducted by searching PubMed for current basic science and clinical research relating to fat grafting. In total, 144 of 269 (54%) articles met the inclusion criteria for our literature review. These 144 articles were summarized, with 86 of them (60%) used to construct this article at the authors' discretion. Results Fat grafting-induced neovascularization can be divided into 3 parts. First, tissue trauma induced via fat injection activates a host inflammatory response necessary for cellular recruitment. Recruited cells promote the formation of connective tissue and neo-vasculature at the graft site. Second, cellular elements within the lipoaspirate contribute to neovascularization through a cytokine burst. Third, a synergistic relationship is established between recruited inflammatory cells and the cytokine burst of grafted fat. The end product of these processes is the differentiation of progenitor cells and the creation of neo-vasculature at the graft site. Conclusions Es

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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