Complications of Fat Grafting and Repositioning for Correction of Lower Eyelid Pouch With Tear Trough Deformity or Lid-Cheek Junction: A Systematic Review.

BACKGROUND: Fat grafting and repositioning may serve as a convenient, economical, and effective surgical method for correcting lower eyelid pouch with a tear trough deformity or lid-cheek junction. However, comprehensive systematic reviews and meta-analyses investigating the complications associated with this technique are lacking. OBJECTIVE: This study aimed to summarize and gather data on complications related to fat grafting and repositioning for the correction of tear trough deformity or lid-cheek junction in lower eyelid blepharoplasty. METHODS: A thorough search was performed across multiple databases including PubMed, Cochrane, Embase, ProQuest, Ovid, Scopus, and Web of Science. Specific inclusion and exclusion criteria were applied to screen the articles. The occurrence of complications was analyzed using a random-effects model. RESULTS: A total of 33 studies involving 4671 patients met the criteria for systematic evaluation and were included in this meta-analysis. The overall complication rates were 0.112 (95% confidence interval [CI]: 0.060-0.177) for total complications, 0.062 (95% CI: 0.003-0.172) for unsatisfactory correction or contour irregularity, 0.062 (95% CI: 0.009-0.151) for hematoma, swelling (not specified as bulbar conjunctiva), ecchymosis, or oozing of blood, and 0.024 (95% CI: 0.013-0.038) for reoperation. CONCLUSIONS: Fat grafting and repositioning for correcting a lower eyelid pouch with tear trough deformity or lid-cheek junction was associated with high rates of complications. Therefore, it is crucial to closely monitor the rates of unsatisfactory correction or contour irregularity, hematoma, swelling (not specified as bulbar conjunctiva), ecchymosis, or oozing of blood, and reoperation. In addition, effective communication with patients should be prioritized.

Effects of adipose-derived stromal cells and endothelial progenitor cells on adipose transplant survival and angiogenesis.

BACKGROUND: A paracrine mechanism is thought to mediate the proangiogenic capacity of adipose-derived stromal/stem cells (ASCs). However, the precise mechanism by which ASCs promote the formation of blood vessels by endothelial progenitor cells (EPCs) is unclear. METHODS: The EPCs-ASCs cocultures prepared in different ratios were subjected to tube formations assay to verify whether ASCs could directly participate in the tube genesis. The supernatant from cultured ASCs was used to stimulate EPCs to evaluate the effects on the angiogenic property of EPCs, as well as capacity for migration and invasion. A coculture model with transwell chamber were used to explore the regulation of angiogenesis markers expression in EPCs by ASCs. We then mixed ASCs with EPCs and transplanted them with adipose tissue into nude mice to evaluate the effects on angiogenesis in adipose tissue grafts. RESULTS: In the EPCs-ASCs cocultures, the tube formation was significantly decreased as the relative abundance of ASCs increased, while the ASCs was found to migrate and integrated into the agglomerates formed by EPCs. The supernatant from ASCs cultures promoted the migration and invasion of EPCs and the ability to form capillary-like structures. The expression of multiple angiogenesis markers in EPCs were significantly increased when cocultured with ASCs. In vivo, ASCs combined with EPC promoted vascularization in the fat transplant. Immunofluorescence straining of Edu and CD31 indicated that the Edu labeled EPC did not directly participate in the vascularization inside the fat tissue. CONCLUSIONS: ADSC can participate in the tube formation of EPC although it cannot form canonical capillary structures. Meanwhile, Soluble factors secreted by ASCs promotes the angiogenic potential of EPCs. ASCs paracrine signaling appears to promote angiogenesis by increasing the migration and invasion of EPCs and simultaneously upregulating the expression of angiogenesis markers in EPCs. The results of in vivo experiments showed that ASCs combined with EPCs significantly promote the formation of blood vessels in the fat implant. Remarkably, EPCs may promote angiogenesis by paracrine regulation of endogenous endothelial cells (ECs) rather than direct participation in the formation of blood vessels.