Physiology and pathophysiology of wound healing in diabetes

Olivera Stojadinovic, Irena Pastar, Katherine A. Gordon, Marjana Tomic-Canic

Research output: Chapter in Book/Report/Conference proceedingChapter

12 Scopus citations

Abstract

Wound healing is an evolutionary conserved process that aims to restore the damaged barrier. This complex process involves many cellular responses including inflammation, proliferation, migration, angiogenesis, and tissue remodeling. Immediately after the injury, blood components are released into the wound site, activating the clotting cascade. The resulting clot induces hemostasis and provides a matrix for the influx of inflammatory cells. Inflammation is characterized by leukocyte migration and arrival to the site of injury. Neutrophils arrive first to remove contaminating bacteria (Singer and Clark, N Engl J Med 341(10):738-746, 1999) and are followed by monocytes, which differentiate into macrophages. Macrophages play an important role in augmenting the inflammatory response and tissue debridement. At the same time, many different cell types respond to initial inflammatory signals and start migrating to the wound site, including keratinocytes, endothelial cells, and circulating and local progenitor cells.

Original languageEnglish (US)
Title of host publicationThe Diabetic Foot
Subtitle of host publicationMedical and Surgical Management: Third Edition
PublisherHumana Press Inc.
Pages127-149
Number of pages23
ISBN (Electronic)9781617797910
ISBN (Print)9781617797903
DOIs
StatePublished - Jan 1 2012

Keywords

  • Angiogenesis
  • Cellular responses
  • Clotting cascade
  • Endothelial cells
  • Fibroblasts
  • Hemostasis
  • Keratinocytes
  • Macrophages
  • Neutrophils
  • Stem and progenitor cells
  • Wound healing

ASJC Scopus subject areas

  • General Medicine

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