Histologic analysis of angiogenesis and lymphangiogenesis in acellular human dermis. Academic Article uri icon

Overview

abstract

  • BACKGROUND: Acellular dermal matrix (AlloDerm) is used frequently in a variety of reconstructive procedures. Although it is clear that AlloDerm is revascularized by host tissues, the mechanisms by which vascularization and tissue incorporation occur remain essentially unknown. The purpose of this experiment was to delineate the time course and composition of host cell infiltrate into the matrix of an AlloDerm composite flap. METHODS: A flap based on the superficial inferior epigastric pedicle in the rat was developed and used to obtain tissue specimens at 3, 7, and 14 days after implantation of AlloDerm. Histology, bromodeoxyuridine incorporation, and immunohistologic assays were used to temporally characterize the appearance of myofibroblasts, endothelial cells, and lymphatic endothelial cells within the matrix. RESULTS: Active host cell proliferation occurs within the matrix at 7 days after implantation. The total number of both host cells and myofibroblasts increased by 8-fold between days 3 and 14. There was a 4-fold increase in endothelial cells between days 3 and 7 but no significant increase at day 14. Putative lymphatic channels were identified within the matrix by 14 days and confirmed using immunohistochemistry for Prox-1, a well-established lymphatic endothelial cell marker. CONCLUSIONS: The host response to AlloDerm parallels normal wound healing. Host cell infiltrate increases steadily over a 14-day period. By 7 days after implantation, a large number of CD31 endothelial cells have infiltrated the matrix and early vessels are abundantly present. These vessels continue to mature by day 14. Finally, the authors show that AlloDerm composite flaps also support infiltration and development of a lymphatic network.

publication date

  • April 1, 2008

Research

keywords

  • Collagen
  • Lymphangiogenesis
  • Neovascularization, Physiologic
  • Skin

Identity

Scopus Document Identifier

  • 42649107651

Digital Object Identifier (DOI)

  • 10.1097/01.prs.0000302505.43942.07

PubMed ID

  • 18349631

Additional Document Info

volume

  • 121

issue

  • 4