Abstract
Wound healing is an ever-changing field, as new insights are made into its mechanisms through basic science research, thus driving development of new therapies. In this paper, we present the current molecular models of wound healing and scar formation in the three phases: inflammation, proliferation and remodeling. New cellular signaling pathways such as mechanotransduction through the transforming growth factor-beta and integrin pathways have opened up various targets for wound therapy. Other therapies such as negative pressure devices and anti-microbial peptides are being improved as more data becomes available. Cutting edge treatments in gene therapy like Regranex are under heavy investigation, as are various treatments whose molecular mechanisms remain to be elucidated such as electrostimulation and Substance P. A promising area in wound treatment research is the use of bone marrow derived stem cell therapy, where research in animal models has shown these stem cells are able to differentiate into keratinocytes. The field of wound therapy is at an exciting junction where advances in basic science will no doubt lead to many improvements in scar prevention and wound healing in the upcoming years.
Acknowledgements
The authors thank T Jow and B Reddy for their assistance in researching and editing of the manuscript.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Key issues
• Normal wound healing includes three phases: inflammation, cell proliferation, and remodeling.
• Cell proliferation, which lasts approximately 4–14 days, is the period during which tissue continuity is re-established.
• The increase in tensile strength, which occurs most prolifically 1–8 weeks post-wound formation, correlates with collagen cross-linking by lysl oxidase.
• Transforming growth factor-beta, a crucial growth factor in wound healing, exerts biologic activity within target cells primarily through the SMAD pathway.
• In spite of appropriate treatments, chronic wounds frequently require surgical intervention.
• Approximately 80–90% of lower extremity wounds result from venous insufficiency secondary to venous valvular disease.
• Maximum tensile strength may require 6–12 months, and at best reaches 80% of normal skin tensile strength.
• Chronic wounds are the result of an inadequate repair process that renders an inability to restore anatomic and functional skin integrity in an appropriate length of time.
• The ideal wound dressing maintains a moist, clean environment that prevents pressure and mechanical trauma, reduces edema, stimulates repair, and limits wound disruption by reducing the number of dressing changes.