Wound healing and its impairment in the diabetic foot.
Optimum healing of a cutaneous wound requires a well-orchestrated integration of the complex biological and molecular events of cell migration and proliferation, and of extracellular matrix deposition and remodelling. Cellular responses to inflammatory mediators, growth factors, and cytokines, and to mechanical forces, must be appropriate and precise. However, this orderly progression of the healing process is impaired in chronic wounds, including those due to diabetes. Several pathogenic abnormalities, ranging from disease-specific intrinsic flaws in blood supply, angiogenesis, and matrix turnover to extrinsic factors due to infection and continued trauma, contribute to failure to heal. Yet, despite these obstacles, there is increasing cause for optimism in the treatment of diabetic and other chronic wounds. Enhanced understanding and correction of pathogenic factors, combined with stricter adherence to standards of care and with technological breakthroughs in biological agents, is giving new hope to the problem of impaired healing.
Falanga
Vincent
V
Department of Dermatology, Boston University, Boston, MA, USA. vfalanga@bu.edu
D000818:Animals; D003646:Debridement; D017719:Diabetic Foot / Q000503:physiopathology*; D006801:Humans; D016023:Integrins / Q000502:physiology*; D015603:Keratinocytes / Q000502:physiology*; D014945:Wound Healing / Q000502:physiology*
D016023:Integrins