Tang Howard H, Han Xiao-Lian, Debels Heidi, Tan Beryl, Palmer Jason, Poon Christopher, Abberton Keren, Morrison Wayne
From the O'Brien Institute Department, St. Vincent's Institute; the Faculty of Health Sciences, Australian Catholic University; the Free University Brussels, Campus Jette; and the Department of Plastic and Reconstructive Surgery, University Hospital Brussels; Murdoch Children's Research Institute; and the Departments of Paediatrics and Surgery, University of Melbourne.
Plast Reconstr Surg. 2018 Oct;142(4):939-950. doi: 10.1097/PRS.0000000000004739.
Free fat grafting is popular, but it is still unclear how it works. Although focusing on graft survival seems an obvious direction for improving clinical results, the authors' research suggests that long-term volume retention is in part attributable to new fat regeneration. Measures to facilitate adipogenesis may therefore be equally important.
To investigate the relative roles of survival and regeneration of fat grafts, the authors measured the fate of human lipoaspirate implanted into the scalps of immunodeficient mice, with and without stromal vascular fraction and a porcine extracellular matrix (Adipogel). Specifically, the authors were interested in volume retention, and the composition of implanted or regenerated tissue at 6 and 12 weeks.
Free fat grafts exhibited poor volume retention and survival. Almost all of the injected human adipocytes died, but new mouse fat formed peripheral to the encapsulated fat graft. Adipogel and stromal vascular fraction improved proliferation of murine fat and human vasculature. Human CD34 stromal cells were present but only in the periphery, and there was no evidence that these cells differentiated into adipocytes.
In the authors' model, most of the implanted tissue died, but unresorbed dead fat accounted substantially for the long-term, reduced volume. A layer of host-derived, regenerated adipose tissue was present at the periphery. This regeneration may be driven by the presence of dying fat, and it was enhanced by addition of the authors' adipogenic adjuncts. Future research should perhaps focus not only on improving graft survival but also on enhancing the adipogenic environment conducive to fat regeneration.
游离脂肪移植很常见，但它的作用机制仍不清楚。尽管关注移植物存活似乎是改善临床效果的一个明显方向，但作者的研究表明，长期的体积维持部分归因于新脂肪的再生。因此，促进脂肪生成的措施可能同样重要。
为了研究脂肪移植物存活和再生的相对作用，作者将人抽脂物植入免疫缺陷小鼠的头皮中，分别植入有或没有基质血管成分和猪细胞外基质（脂肪凝胶）的抽脂物。具体而言，作者关注6周和12周时的体积维持情况以及植入或再生组织的组成。
游离脂肪移植物的体积维持和存活情况较差。几乎所有注入的人脂肪细胞都死亡了，但在包裹的脂肪移植物周围形成了新的小鼠脂肪。脂肪凝胶和基质血管成分促进了小鼠脂肪和人血管的增殖。人CD34基质细胞存在，但仅存在于周边，没有证据表明这些细胞分化为脂肪细胞。
在作者的模型中，大多数植入组织死亡，但未吸收的死亡脂肪在很大程度上导致了长期体积减小。周边存在一层宿主来源的再生脂肪组织。这种再生可能由死亡脂肪的存在驱动，并且通过添加作者的脂肪生成辅助剂而增强。未来的研究或许不仅应关注提高移植物存活，还应关注增强有利于脂肪再生的脂肪生成环境。
