PURPOSE

Fat transplantation is a commonly used for the correction of soft tissue deficiencies. While the technique of fat transplantation is quite straightforward, augmentation with fat is unpredictable.  Hence, the search for techniques to enhance graft survival.

The effects of growth factors on cell behavior and graft maintenance have been thoroughly studied (1-4). Recently autologous platelet-rich plasma (PRP) has gained popularity as a clinical treatment in many areas, most notably in the management of chronic non-healing wounds. One of its proposed biological properties is the improvement of healing via delivery of growth factors (PDGF-BB, TGF-β1, VEGF, EGF) to the tissue. These factors also enhance angiogenesis, which is thought to be crucial for fat engrafting. 

We investigated the possibility of enhancing fat graft viability using a single perioperative dose of PRP.

METHOD

48 male Lewis rats were divided into four experimental groups (5 animals each). Fat was harvested from each groin and transplanted into a respective dorsal subcutaneous pocket. Group 1 - control received no PRP. In Groups 2, 3 and 4 the experimental arm (left side) was injected with different aliquots (0.2, 0.4, 0.6cc respectively) of PRP while the opposite pocket was not treated (right side). Animals were sacrificed at 12 weeks (early group) or 24 weeks (late group).

Fat graft survival and volume maintenance were evaluated using immunohistochemistry and weight measurement. CD31 (platelet endothelial adhesion molecule, PECAM-1), an angiogenesis marker strongly expressed on vessel endothelium, was quantified at 3 and 6 months. The vessel density, assessed by expression of CD31, was measured both at the periphery and the center of each fat graft. The presence of vascular endothelial growth factor (VEGF), a potent proangiogenic factor expressed by vessel endothelial cells and secreted by adipocytes, was also assessed. Finally, weight was measured pre and post operatively at both 3 and 6 months.

RESULTS

When the number of CD31 positive vessels were measured on the PRP-treated and non-treated sides at 3 months, no significant differences between the two groups. However, 6 months following fat transplantation the PRP treated side demonstrated a significantly greater number of CD31 positive vessels than the non-treated side (p<0.05).

At both 3 and 6 months after fat transplantation, higher expression of VEGF was observed in all specimens injected with PRP compared to the non-treated side.

Weight measurement reveals no statistical difference between the PRP and the control group at either 3 or 6 months following fat transplantation. However, when analyzing the center of all specimens, a diminished number of vessels expressed the CD31 antigen was noted suggesting impaired angiogenesis, which may explain the non-statistically significant result in weight maintenance.

CONCLUSION PRP enhances revascularization at the periphery of the fat graft. Our model demonstrated poor revascularization at the center of the fat graft suggesting that an “en bloc” fat transfer technique may be less reliable than fat grafted via an injection method such as the Coleman’s technique.