Physiology of cutaneous cicatrization

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Germán Alfredo Ramírez Hernández Universidad Surcolombiana.
Abstract

A wound is the result of aggression which produces a continuity solution in tissues. When it is an acute injury, it becomes ulceration; if it goes on for more than three weeks it is called ulcer. Cicatrization is a complex process aims at repairing a damaged tissue which involves a permanent physiological pattern and overlapped stages; however, chronic wounds do not follow this healing pattern. They reach healing when injury cause is eliminated and wound bed is properly treated. Importance of being aware of these processes lies in the intervention capacity in its different stages which facilitates the injury healing and achieving wound bed modification.

 

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Author Biography / See

Germán Alfredo Ramírez Hernández, Universidad Surcolombiana.

Cirujano General, Coordinador Clínica de heridas y ostomias, Hospital Universitario de Neiva, Profesor Asistente,
References

Porter, R. 2004. Breve historia de la medicina. Tercera edición. Barcelona: Ediciones Taurus 6:100-105.

Harvey, G. 1942. Historia de la cirugía. Segunda edición. Barcelona: Editorial Iberia 5:456-470.

Krasner, D., Sibbald, G. 2002. Chronic wound care. Third edition. San Diego: Appleton and Lange 12:120-140.

Rivington, L.G. 2002. Hanging wet-to-dry dressings out to dry, advanced in skin and wound care. Adv Wound Care 15:279-284.

Lazaurus, G.S. 1994. Definitions and guidelines for assessment of wounds and evaluation of healing. Wounds 130:489.

Bradley, U., Cullum, N., Nelson, E.A. 1999. Systematic reviews of wound care management dressings and topical agents used in the healing of chronic wounds. Health Techn Asses 3:1-18.

Hartoch, R.S. 2007. Emergency management of chronic wounds. Emerg Med Clin North Am 25(1):203-221.

Clark, R.A.F., ed. 1996. The molecular and cellular biology of wound repair. 2nd ed. New York: Plenum Press 1996.

Kirsner, R., Eaglstein, W. 1993. El proceso de curación de las heridas. Clínicas Dermatológicas. Ed. Interamericana, Madrid 11:653-662.

Schiro, J.A., Chan, B.M.C., Roswit, W.T. et al. 1991. Integrin a2b1 (VLA-2) mediates reorganization and contraction of collagen matrices by human cells. Cell 67:403-10.11

Montesano, R, Orci, L. 1988. Transforming growth factor-b stimulates collagen- matrix contraction by fibroblasts: implications for wound healing. Proc Natl Acad Sci U S A 85:4894-4897.

Shah, M., Foreman, D.M., Ferguson, M.W.J. 1995. Neutralisation of TGF-b1 and TGF-b2 or exogenous addition of TGF-b3 to cutaneous rat wounds reduces scarring. J Cell Sci 108:985-1002.

Brown, L.F., Yeo, K.T., Berse, B. et al. 1992. Expression of vascular permeability factor (vascular endothelial growth factor) by epidermal keratinocytes during wound healing. J Exp Med 176:1375-1379.

Clark, R.A.F., Quinn, J.H., Winn, H.J., Lanigan, J.M., Dellepelle, P, Colvin, R.B. 1982. Fibronectin is produced by blood vessels in response to injury. J Exp Med 156:646-651.

Leibovich, S.J., Ross, R. 1975. The role of the macrophage in wound repair: a study with hydrocortisone and antimacrophage serum. Am J Pathol 78:71-100.

Riches, D.W.H. 1996. Macrophage involvement in wound repair, remodeling, and fibrosis. In: Clark, R.A.F., ed. The molecular and cellular biology of wound repair. 2nd ed. New York: Plenum Press 95-141.

Paladini, R.D., Takahashi, K., Bravo, N.S., Coulombe, P.A. 1996. Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16. J Cell Biol 132:381-397.

Goliger, J.A., Paul D.L. 1995. Wounding alters epidermal connexin expressionand gap junction-mediated intercellular communication. Mol Biol Cell 6:1491-1501.

Clark, R.A.F. 1990. Fibronectin matrix deposition and fibronectin receptor expression in healing and normal skin. J Invest Dermatol 94:Suppl:128S-134S.

Larjava, H., Salo, T., Haapasalmi, K., Kramer, R.H., Heino, J. 1993. Expression of integrins and basement membrane components by wound keratinoctyes. J Clin Invest 92:1425-1435.

Hunt, TK, ed. 1980. Wound healing and wound infection: theory and surgical practice. New York: Appleton-Century-Crofts.

Gray, A.J., Bishop, J.E., Reeves, J.T., Laurent, G.J. 1993. Aa and Bb chains of fibrinogen stimulate proliferation of human fibroblasts. J Cell Sci 104:409-413.

Xu, J., Clark R.A.F. 1996. Extracellular matrix alters PDGF regulation of fibroblast integrins. J Cell Biol 132:239-249.

Vaalamo, M., Mattila, L., Johansson, N. et al. 1997. Distinct populations of stromal cells express collagenase-3 (MMP-13) and collagenase- 1 (MMP-1) in chronic ulcers but not in normally healing wounds. J Invest Dermatol 109:96-101.

Welch, M.P., Odland, G.F., Clark, R.A.F. 1990. Temporal relationships of F-actin bundle formation, collagen and fibronectin matrix assembly, and fibronectin receptor expression to wound contraction. J Cell Biol 110:133-145.

Detmar, M., Brown, L.F., Berse, B. et al. 1997. Hypoxia regulates the expression of vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) and its receptors in human skin. J Invest Dermatol 108:263-268.

Nissen, N.N., Polverini, P.J., Koch, A.E., Volin, M.V., Gamelli, R.L., DiPietro, L.A. 1998. Vascular endothelial growth factor mediates angiogenic activity during the proliferative phase of wound healing. Am J Pathol 152:1445-1452.

Brooks, P.C., Clark, R.A.F., Cheresh, D.A. 1994. Requirement of vascular integrin avb3 for angiogenesis. Science 264:569-571.

Pintucci, G., Bikfalvi A., Klein S., Rifkin, D.B.1996. Angiogenesis and the fibrinolytic system. Semin Thromb Hemost 22:517-524.

Clark, R.A.F., Folkvord J.M., Hart C.E., Murray M.J., McPherson, J.M. 1989. Platelet isoforms of platelet-derived growth factor stimulate fibroblasts to contract collagen matrices. J Clin Invest 84:1036-1040.

Iruela-Arispe, M.L., Dvorak, H.F. 1997. Angiogenesis: a dynamic balance of stimulators and inhibitors. Thromb Haemost 78:672-677.

Risau, W. 1997. Mechanisms of angiogenesis. Nature 386:671-674.

Babu, M., Diegelmann, R., Oliver, N. 1992. Keloid fibroblasts exhibit an altered response to TGF-beta. J Invest Dermatol 99:650-655.

Desmouliere, A., Redard, M, Darby, I, Gabbiani, G. Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar. Am J Pathol 1995;146:56-66.

Folkman, J., D’Amore, P.A. 1996. Blood vessel formation: what is its molecular basis? Cell ;87:1153-1155.

Madri, J.A., Sankar S., Romanic, A.M. 1996. Angiogenesis. In: Clark, RAF, ed. The molecular and cellular biology of wound repair. 2nd ed. New York: Plenum Press 355-371.

Folkman, J. 1997. Angiogenesis and angiogenesis inhibition: an overview. EXS 79:1-8.

Gabbiani, G., Chaponnier, C., Huttner, I. 1978. Cytoplasmic filaments and gap junctions in epithelial cells and myofibroblasts during wound healing. J Cell Biol 76:561-568.

Clark, R.A.F., Ashcroft, G.S., Spencer, M.J., Larjava, H., Ferguson, M.W.J. 1996. Reepithelialization of normal human excisional wounds is associated with a switch from avb5 to avb6 integrins. Br J Dermatol 135:46-51.

Pilcher, B.K., Dumin, J.A., Sudbeck, B.D., Krane, S.M., Welgus, H.G., Parks, W.C. 1997. The activity of collagenase-1 is required for keratinocyte migration on a type I collagen matrix. J Cell Biol 137:1445-1457.

Werner, S., Smola, H., Liao, X. et al. 1994. The function of KGF in morphogenesis of epithelium and reepithelialization of wounds. Science 266:819-822.

Guo, N., Krutzsch, H.C., Inman, J.K., Roberts, D.D. 1997. Thrombospondin 1 and type I repeat peptides of thrombospondin 1 specifically induce apoptosis of endothelial cells. Cancer Res 57:1735-1742.

Greiling, D., Clark, R.A.F. 1997. Fibronectin provides a conduit for fibroblast transmigration from collagenous stroma into fibrin clot provisional matrix. J Cell Sci 110:861-870.

Toole, BP. 1991. Proteoglycans and hyaluronan in morphogenesis and differentiation. In: Hay ED, ed. Cell biology of extracellular matrix. 2nd ed. New York: Plenum Press 305-341.

Woodley, D.T., Yamauchi, M., Wynn, K.C., Mechanic, G., Briggaman, R.A. 1991. Collagen telopeptides (cross-linking sites) play a role in collagen gel lattice contraction. J Invest Dermatol 97:580-585.

Madlener, M., Parks, W.C., Werner, S. 1998. Matrix metalloproteinases (MMPs) and their physiological inhibitors (TIMPs) are differentially expressed during excisional skin wound repair. Exp Cell Res 242:201-210.

Bailey, A.J., Bazin, S., Sims, T.J., Le Lous, M., Nicholetis, C., Delaunay, A. 1975. Characterization of the collagen of human hypertrophic and normal scars. Biochim Biophys Acta 405:412-421.

Tredget, E.F., Nedelec, B., Scott, P.G., Ghahary, A. 1997. Hypertrophic scars, keloids, and contractures: the cellular and molecular basis for therapy. Surg Clin North Am 77:701-730.

Machesney, M., Tidman, N., Waseem, A., Kirby, L., Leigh, I. 1998. Activated keratinocytes in the epidermis of hypertrophic scars. Am J Pathol 152:1133-1141.

Zhang, K., Garner, W., Cohen, L, Rodriguez., J, Phan, S. 1995. Increased types I and III collagen and transforming growth factor-beta 1 mRNA and protein in hypertrophic burn scar. J Invest Dermatol 104:750-754.

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