How Fat Grafting Works

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.

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.

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.

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.