How Fat Grafting Works

Brogan G A Evans, Edward M Gronet, Michel H Saint-Cyr, Brogan G A Evans, Edward M Gronet, Michel H Saint-Cyr

Abstract

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: Establishing neovasculature is paramount for the survival of grafted fat. Fat graft take can be divided into 2 steps: imbibition and neovascularization. We believe this process occurs through 3 distinct concepts: host inflammation via graft injection, hypoxic response of lipoaspirate-derived cellular elements, and a synergistic relationship between host inflammation and grafted fat.

Copyright © 2020 The Author. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons.

Figures

Fig. 1.
Fig. 1.
A literature search was made to identify fat grafting articles relating to plastic surgery. Additional screening at the authors’ discretion was used to identify the 86 articles referenced to construct this article.
Fig. 2.
Fig. 2.
Tissue trauma induces platelet, monocyte, and BM-MSC migration to the graft site. After hemostasis, platelets (Plt) help remodel the ECM and recruit pericytes to growing vessels. Recruited BM-MSCs differentiate into endothelial cells and recruit monocytes. Monocytes are polarized from M1 to M2 macrophages. Each process facilitates neovascularization.
Fig. 3.
Fig. 3.
Harvest forces hypoxia on grafted adipocytes and ASCs. As hypoxic adipocytes lyse, they release FGF-2 to the recipient site. ASCs secrete TNF-α and HIF-1α when hypoxic. TNF-α acts on ASCs and adipocytes to increase FGF-2 levels at the graft site. HIF-1α and FGF-2 upregulate VEGF levels, which promote EC proliferation and EC migration. IGF-1 is released to promote preadipocyte maturation (regenerative).
Fig. 4.
Fig. 4.
Cellular elements within the lipoaspirate act in synergy with the tissue’s response to injection to drive neovascularization at the graft site.

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Source: PubMed

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