Collagen and Wound Healing

When the skin is injured, collagen becomes a comment denominator in the body’s healing response. Collagen helps the body heal itself by preparing the wound bed, balancing wound chemistry, causing cell migration and growth, inducing granulation tissue, and improving overall skin strength. Collagen’s role in these various chemical, mechanical, and biological factors form an environment conducive to wound healing, and ultimately to wound closure.
For many years, the scientific community has identified collagen as a common element in wound healing. Research indicates that collagen plays an important role in the body’s natural healing response.

The Role of Collagen in Wound Healing

Stops Bleeding

Hemostasis

  • Collagen binds to specific receptor sites on platelet membranes [1] which swell and release substances to initiate hemostasis.[2.3]
  • Collagen binds to fibronectin,[4,5] causing platelet adhesion and aggregation.6]

Wound Debridement

  • Collagen is chemotactic to monocytes and leukocytes.[7,8] Monocytes transform into macrophages which scavenge and phagocytize foreign bodies and debris.[9,10]

Cleanses the Wound

Establishes New Tissue and Blood Vessels

Granulation and Angiogenesis

  • Collagen attracts monocytes [7,8] which transform into macrophages.Macrophages release substances that result in fibroplasia and angiogenesis.[11]
  • Collagen provides support for the growth of new capillaries.[11,12] The presence of capillaries is essential for the deposition of new fibers.[11]

Fibroblastic Activity

  • Collagen binds with fibronectin, [4,5} which promotes cell binding and fibrillogenesis, [15] influences bibarel dimensions, and stimulates fibroblast proliferation and migration.[16]
  • Collagen is chemotactic to fibroblasts, [17] which govern the restoration of new tissue by depositing oriented and organized fibers.[19.2] Collagen provides a substrate for directed migration and permeation of fibroblasts.[21]

Create Structural Matrix

Closes the Wound

Re-epithelialization

  • Collagen directly supports the growth, [22,23 attachment,[24] differentiation,[23,24] and migration [25] of keratinocytes.
  • By binding with fibronectin, [4,5,26,27] collagen provides a provisional matrix for keratinocytesmigration [28].

Wound Remodeling

  • Collagen and reduce the scarring by depositing oriented and organized fibers [29] and by regulating the amount of collagenase expressed by keratinocytes.[30,32]

Regains Original Integrity

Collagen; The Common Denominator and Wound Healing

Wounds should follow the same healing response, but factors such as clinical conditions and complications may alter or help the ideal healing process. In these cases collagen-related activity redirects the wound to the normal healing path.

Injury Occurs and Follows the Normal Healing Path to a Healed Wound

Clinical Condition / Complication

Symptoms

Collagen Related Activity

References

  1. Chiang TM, et al., J of Bio Chem. 1982;257(13):7581 7586.
  2. Hovig T, et al., J. Lab & Clin. Med. 1968;71(1)29-39.
  3. Zucker MB, et al., Proc. Soc. Exp. Bio. Med. 1962;109:779-787.
  4. Kleinman HK, et al., BioChem. 1981;20:2325-2330.
  5. Mosher DF, et al., J. Clin. Invest. 1979;64:781-787.
  6. Yamada KM, et al., Nature 1978;275:179-184.
  7. Postlethwaite AE, et al., Proc. Nat. Acad. Sci. USA 1978;75(2):871-875.
  8. Postlethwaite AE, et al., J Exper. Med. 1976;143:1299 1307.
  9. Bryant R, J. Enter. Ther. 1987;14(6):262-266.
  10. Leibovich, SJ, Amer. J Pathol. 1975;78(1):71 91.
  11. Gogia PP, Ost/Wound Mngt. 1992;38(9):12-20.
  12. Schor, AM, et al., Int’l J Cancer 1979;24:225 234.
  13. Yamada KM, et al., Proc. Nat. Acad. Sci. USA 1976;73(4):1217-1221.
  14. Mosher, DF, Prog. Hemo. Thromb. 1980;5:111-131.
  15. Grinnell F, et al., J Inves. Derm. 1981,76:181-189.
  16. Clark RAF, et al., Clin. Res. 1981;29(2):590A.
  17. Chiang TM, et al., J Clin Invest. 1978;62:916-922.
  18. Ross R. Biol. Reviews 1968;43(1):51 98.
  19. Dunn GA, Exp. Cell Res. 1978;111:475-479.
  20. Tomaseck JT, et al., Dev. Bio. 1982;92:107-122.
  21. .Burton JL, et al., J Enter. Ther. 1987;14(6):262-266.
  22. Morykwas MJ, et al., J Trauma 1989;29(8):1163-1167.
  23. Karasek, MA, et al., J Inves. Derm. 1968;51(4):247 252.
  24. Murray JC, et al., Cell Bio. 1979;80:197-202.
  25. Emerman JT, et al., In Vitro 1977;13(5):316-327.
  26. Rouslahti E, et al., BioChem. et Biophys. Acta 1980;631:350-358.
  27. Engvall E, et al., Int’l J Cancer 1977:20:1-5.
  28. Clark RAF, et al., J Inves. Derm. 1982:79:264-269.
  29. .Doillon CJ, et al., Scan. Elect. Micro. 1985;2:897-903.
  30. .Sudbeck BD, et al., J Biol. Chem. 1994;269(47):30022-30029.
  31. Parks WC, WOUNDS 1995;7(5):23A-37A.
  32. Saarialho-Kere UK, et al., J. Clin. Inves. 1993;92:2858 2866.
  33. Albritton JS, Clin. Pod. Med. & Surg. 1991;8(4):773-785.
  34. Kollenberg LO, Pod. Today 1995;12:49-62.
  35. Kollenberg, LO, Pod. Today 1996;1:51-54.
  36. Kleinman HK, et al., J Cell Bio. 1981;88:473-485.
  37. Palmieri B, Int’I J Tissue Reaction 1992;14:21-25.38. Mian M, et al., Int’I J Tissue
  38. Reaction 1991;12(5):275-269.