The closure of open wounds resulting from trauma involves the depositing of new connective tissue matrix. The amount required is dictated by the severity of injury in terms of depth and area. This new connective tissue matrix is immature, and in some cases, can undergo modifications, a reduction in size. This reduction is called wound contraction and forces generated by resident fibroblasts are responsible for it. The mechanics for wound contraction require the organization of surrounding connective tissue matrix. This proposed mechanism involves a cooperation between cell generated cytoplasmic muscular forces and collagen fibers. Experimental work shows that resident fibroblasts function as individual units in this reorganization process. Evidence is lacking to support the idea that a specialized cell, the myofibroblast acting as a multicellular contractile unit could be accountable for producing wound contraction. The morphological appearance of stress fibers in resident fibroblasts in healing wounds may in fact signify the termination of that cell’s involvement in the process of wound contraction. Experimental evidence argues for fibroblast locomotion being the mechanism attributed for organization of the connective tissue matrix. Further the control of this cellular force appears linked to the composition of the newly deposited collagen matrix. A matrix rich in type III collagen contracts faster and to a greater degree than one made from type I collagen. It is suggested that granulation tissue that has a type III rich collagen matrix will contract more readily than one with less type III collagen. Evidence presented from in vitro models suggests that fibroblasts generate the forces of contraction, and collagen controls those forces in wound closure by the wound contraction process.


Collagen Fibril Hypertrophic Scar Lattice Contraction Wound Contraction Cell Locomotion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Dunphy, JE, Udupa KN. Chemical and histological sequence in the normal healing of wounds. New Engl J Med 253: 847–851, 1955.CrossRefGoogle Scholar
  2. 2.
    (NOT QUOTED IN TEXT!) Gabbiani, G, Hirschel BJ, Ryan GB, Statkov PK, Majno G. Granulation tissue as a contractile organ. A study of structure and function. J Exp Med 135: 719–734, 1972.CrossRefGoogle Scholar
  3. 3.
    Ehrlich, HP. Wound closure: Evidence of cooperation between fibroblasts and collagen matrix. Eye 2: 149–157, 1988.CrossRefGoogle Scholar
  4. 4.
    Ehrlich, HP, Borland KM, Muffly KE, Hall PF. Contraction of collagen lattice by peritubular cells from rat testis. J Cell Sci 82: 281–294, 1986.Google Scholar
  5. 5.
    Bell, E, Ivarsson B, Merrill C. Production of a tissue like structure by contraction of collagen lattices by human fibroblasts of different proliferative potential in vitro. Proc Natl Acad Sci (USA) 76: 1274–1278, 1979.CrossRefGoogle Scholar
  6. 6.
    Green, MC, Sweet HO, Bunker LE. Tight Skin, a new mutation of the mouse causing excessive growth of connective tissue skeleton. Am J Pathol 82: 493–512, 1976.Google Scholar
  7. 7.
    Hirschel, BJ, Gabbiani G, Ryan GB, Majno G. Fibroblasts of granulation tissue: Immunofluorescent staining with antismooth muscle serum. Proc Soc Exp Biol Med 138: 466–469, 1971.Google Scholar
  8. 8.
    Barak, LS, Yocum RR, Nothnagel EA, Webb WW. Fluorescence staining of the actin cytoskeleton in living cells with 7nitrobenz2oxa1, 3diazole Phallacidin. Proc Natl Acad Sci (USA) 77: 980–984, 1980.Google Scholar

Copyright information

© Springer-Verlag London Limited 1990

Authors and Affiliations

  • H. Paul Ehrlich

There are no affiliations available

Personalised recommendations