BackgroundHypertrophic scars cause cosmetic and functional problems for patients, and their treatment remains challenging. Mechanical micronization of adipose tissue can remove adipocytes and concentrate functional cells. Stromal vascular fraction (SVF)-gel is obtained by a series of simple mechanical processes, including shifting between syringes and centrifugation. This study aimed to assess the therapeutic effect of SVF-gel on hypertrophic scars.MethodsA model of hypertrophic scars was established in rabbit ears. SVF-gel and SVF cells were obtained from rabbit inguinal fat pads and injected into scars. Phosphate-buffered saline (PBS) was used as a control. Scars were structurally characterized by histologic and immunohistochemical analyses. Expression of inflammatory and fibrogenic genes was evaluated.ResultsHypertrophic scars became less visible and softer following injection of SVF-gel or SVF cells. Dermal thickness was significantly lower in the groups treated with SVF-gel and SVF cells than in the PBS-treated group. Treatment with SVF-gel restored subcutaneous fat tissue in scars, while treatment with SVF cells and PBS did not. Injection of SVF-gel and SVF cells reduced macrophage infiltration in the dermal layer and decreased mRNA expression of interleukin-6 and monocyte chemoattractant protein-1. In addition, the level of myofibroblasts and collagen deposition were reduced in the groups treated with SVF-gel and SVF cells.ConclusionsSVF-gel has therapeutic effects on hypertrophic scars. Injection of SVF-gel into hypertrophic scars restores subcutaneous fat tissue and reduces the levels of macrophages and myofibroblasts; thus, it decreased the dermal thickness of the scar.

Inflammatory responses mediated by macrophages play a role in tissue repair. However, it is unclear whether the repair in the donor site after liposuction would have any effects on fat graft retention in the recipient site. This study is designed to evaluate the effects of a macrophage‐mediated inflammatory response in donor sites on long‐term retention of fat grafting. In this study, mice were randomly divided into two groups. One underwent simulated liposuction, called the fat procurement plus grafting (Pro‐Grafting) group, and the other underwent sham surgery, called the fat grafting only (Grafting Only) group. The prepared fat (0.3 ml each) was engrafted and cellular events over a 90‐day period were assessed. We found macrophages were infiltrated into adipose tissue at the recipient site in the Grafting Only group within 7 days and the repair essentially completed within 30 days. By contrast, few macrophages infiltrated the recipient site in the Pro‐Grafting group within 7 days and the entire remodeling process took 30 days longer in the Pro‐Grafting than the Grafting Only group. Moreover, C‐reactive protein levels were immediately upregulated after surgery, and the inflammatory factors' expression was higher at the donor rather than the recipient site. However, the repair processes and the long‐term retention rate became normal when the adipose tissue was grafted after the donor site did not require macrophages for repair. Therefore, we suggest higher inflammatory factors promote macrophage infiltration and the adipose tissue regeneration process at the donor site. This process is delayed at the recipient site, which may affect long‐term retention of fat grafts.

No abstract

No abstract