Platelet-Rich Fibrin Matrix Shots Induce Cellular Changes

PRFM injection induces fibroblast activation, collagen deposition, angiogenesis, adipogenesis

THURSDAY, Oct. 20 (HealthDay News) -- Administration of platelet-rich fibrin matrix (PRFM) into the deep dermis and immediate subdermis stimulates cellular changes, including activated fibroblasts, new collagen deposition, new blood vessel development, intradermal adipocyte collection, and subdermal adipocyte stimulation, according to a study published online Oct. 17 in the Archives of Facial Plastic Surgery.

Anthony P. Sclafani, M.D., and Steven A. McCormick, M.D., from the New York Eye and Ear Infirmary in New York City, evaluated the histological changes induced in human skin by injection of autologous PRFM. A proprietary system was used to prepare PRFM from 9 mL of autologous blood. This PRFM was injected into the deep dermis and immediate subdermis of the upper arms of four healthy adult volunteers. Histological evaluation was performed for full-thickness skin biopsy specimens taken from the treated areas over a 10-week period.

The investigators found that activated fibroblasts and new collagen deposition were noted seven days after treatment, and remained evident throughout the study. New blood vessels developed by 19 days, and at this time, intradermal adipocyte collection and subdermal adipocyte stimulation were seen. All of these findings became more pronounced over the study duration except the fibroblastic response, which became less evident. A very mild chronic inflammatory response was observed only at the earliest time points of the study, and there were no abnormal mitotic figures during the study.

"Injection of PRFM into the deep dermis and subdermis of the skin stimulates a number of cellular changes that can be harnessed for use," the authors write.

The study was funded by Aesthetic Factors Inc., which developed the proprietary system used to prepare the PRFM in this study.

Abstract
Full Text

Copyright © 2011 HealthDay. All rights reserved.

Powered by