Introduction In reconstructive surgery, fat volume augmentation is often necessary for esthetic or functional reasons. As an alternative to synthetic and xenogeneic materials, autologous fat grafting (AFG) based on liposuction is gaining popularity, yet successful transplantation and long-term volume maintenance are difficult. Standard tumescent solution formulations neglect adipocyte and stromal vascular fraction (SVF) cell survival during extraction, as well as SVF differentiation into adipocytes thereafter, all of which are crucial for the success of AFG. Here we hypothesized that addition of ascorbic acid (AA) to the tumescent solution could prevent liposuction-induced cell damage. Materials and Methods The effect of 0.1 mmol/L AA in tumescent solution was investigated in a previously described ex vivo model of AFG. Briefly, excision fat was infiltrated with tumescent solution, with or without AA, and incubated for 20 minutes at 37°C. Hand-assisted liposuction was then performed with a blunt cannula. Total cell viability, clonogenicity, and differentiation capacity of the SVF cells were assessed. Results With AA, 10.3% more cells and in particular 14.9% more adipocytes survived liposuction. Clonogenicity, adipocyte and osteoblast differentiation by SVF cells remained unchanged. Conclusions Addition of AA successfully improved survival of adipocytes during liposuction without affecting SVF growth and differentiation. This study therefore identified a useful supplement to the tumescent solution which may lead to improving AFG success.

Background: As part of the engineering of bone grafts, wrapping constructs in well-vascularized tissue, such as fascial flaps, improves bone formation. Our aim was to understand the cross-sectional vascularization pattern of human adipofascial flaps for this application. Methods: Seven adipofascial anterolateral thigh (ALT) flaps were harvested from five human cadaveric specimens. Axial vessel density was analyzed by immunohistochemistry and quantitative histology. Results: We found a high density of blood vessels directly superficial to and close to the fascia. A secondary plexus in between this first suprafascial plexus and the subdermal plexus was also identified. In all specimens, this second plexus showed less vascular density, and appeared to be at a constant level within the suprafascial fat throughout the flaps. The peak measurements for this secondary plexus varied between 1.2 and 2 mm above the deep fascia, depending on the donor’s body mass index. Conclusions: Quantitative immunohistochemistry is a reliable method to quantify and locate vessel density in an adipofascial flap. This is vital information before wrapping nonvascularized material into such a flap to estimate the inosculation potential of these vessels and likelihood of survival of the tissue. To profit from both suprafascial vascular plexuses, a correlation between subcutaneous tissue thickness and distance of the second plexus to the fascia should be further investigated. For the moment, we recommend maintaining at least 2–3 mm of subcutaneous fatty tissue on the fascia, to profit from both plexuses. Engineered constructs should be wrapped on the superficial medial side of the fascial flap to enhance vascularization.

Pressure injuries (PI) are a common issue among individuals with spinal cord injury (SCI), especially in the sitting areas of the body. Considering the risk of infections occurring to PI during the wound healing process, the skin microbiome is likely to be a source of bacteria. We investigated the relationship between skin and PI microbiomes, and assessed any correlation with clinically relevant outcomes related to PI. Samples were isolated from SCI patients undergoing reconstructive surgery of PI, severity grades III and IV. DNA samples from skin and PI were analysed using 16S rRNA gene sequencing. Our results showed disparities in microbiome composition between skin and PI. The skin had lower diversity, while PI showed increased bacterial homogeneity as the severity grade progressed. The skin bacterial composition varied based on its location, influenced by Cutibacterium. Compositional differences were identified between PI grades III and IV, with clusters of bacteria colonizing PI, characterized by Pseudomonas, Proteus and Peptoniphilus. The skin and PI microbiomes were not affected by the level of the SCI. Our study highlights the differences in the microbiome of skin and PI in SCI patients. These findings could be used to target specific bacteria for PI treatment in clinical practice.