In-Vitro Wound Contraction in the Horse: Differences Between Body and Limb Wounds

Christine A. Cochrane, PhD; Rachel Pain; Derek C.Knottenbelt, DVM

This usually leads to the formation of exuberant granulation tissue even though these cells express a-smooth muscle actin (SMA).[6,7]

Cell viability remained high throughout the experiment, and there was no significant difference between the three cell types at 96 hours. Although there was no significant difference in the viability between the cell types, a reduction was observed in the NF and GT cells. This was probably due to contact inhibition as the gels contracted, causing some of the cells to die. At 96 hours, the contracted gels containing NF and GT cells were very densely populated.

There are anatomical and physiological differences seen in the horse when wound healing occurs.[5] The problems with the distal limb may be attributed to poor blood supply, which in turn could lead to a deficit in nutrients and other cell mediators, which are needed for normal wound healing.


It is concluded from these studies that during second-intention wound healing in the horse, the differences in wound contraction between wounds on the limbs and the body are caused by differences in the contractile capacity of fibroblasts. The extracellular environment plays a role in the behavior of fibroblast cells. However, local environmental factors, such as the response to inflammation, may play a role in determining the rate of contraction during wound healing. The value of this work has been to show that the contractile variation of fibroblasts from different tissues is highest in the limb. The results do not match the observed wound contraction of in-vivo limb injuries, and, therefore, further research should be considered to determine those factors within the in-vivo limb environment that would allow the limb fibroblasts to contract to their observed full in-vitro potential.



1. Briton JW. Wound management in horses. J Am Vet Med Assoc 1970;157:1585–9.
2. Jacobs KA, Leach DH, Fretz PB, et al. Comparative aspects of the healing of excisional wounds on the leg and body of horses. Vet Surg 1984;13:83–5.
3. Bertone AL. Management of exuberant granulation tissue. Vet Clin N Am Equine Prac 1989;5:551–62.
4. Bertone AL. Principles of wound healing. Vet Clin N Am Equine Prac 1989;5:449–63.
5. Knottenbelt DC. Equine wound management: Are there significant differences in healing at different sites on the body? Vet Dermatol 1997;8:273–90.
6. Wilmink JM, Stolk PWT, van Weeren PR, Barneveld A. Differences in second intention wound healing between horses and ponies: Macroscopical aspects. Equine Vet J 1999a;31:53–60.
7. Wilmink JM, van Weeren PR, Stolk PWT, Barneveld A. Differences in second-intention wound healing between horses and ponies: Histological aspects. Equine Vet J 1999b;31:61–7.
8. Desmonliere A. Factors influencing myofibroblast differentiation during wound healing and fibrosis. Cell BioL Intl 1995;19:471–6.
9. Bertone AL, Sullens KE, Stashak TS, Norridin RW. Effect of wound location and the use of topical collagen gel on exuberant granulation tissue formation and wound healing in the horse and pony. Am J Vet Res 1985;46:1438–44.
10. Lees, MlJ, Fretx PB, Bailey JV, Jacobs KA. Second-intention wound healing. Comp Cont Educ Pract Vet 1989;11:857–64.
11. Stashak TS. Equine wound management. Philadelphia, PA: Lea and Febiger, 1991;1–18.
12. Lorena D, Uchio K, Monte Alto Costa A, Desmouliere A. Normal scarring: Importance of myofibroblasts. Wound Rep Reg 2002;10:86–92.
13. Cochrane CA. Models in vivo of wound healing in the horse and the role of growth factors. Vet Dermatol 1997;8:259–72.
14. Moulin V, Tam BY, Catilloux G, et al. Fetal and human skin fibroblasts display intrinsic differences in contractile ability. J Cell Physiol 2001;188:211–12.
15. Germain L, Jean A, Auger FA, et al. Human wound healing fibroblasts have greater contractile properties than dermal fibroblasts. J Surg Res 1994;57:268–73.
16. Moulin V, Auger FA, Garrel D, et al. Role of wound healing myofibroblasts on re-epithelialisation of human skin. Burns 2000;26:3–12.
17. Cochrane CA, Freeman KL, Knottenbelt DC. Effect of growth factors on the characteristics of cells associated with equine wound healing and sarcoid formation. Wound Rep Reg 1996;4:58–65.
18. Cochrane CA, Rippon MG, Rogers A, et al. Application of an in-vitro model to evaluate bioadhesion of fibroblasts and epithelial cells to two different dressings. Biomaterials 1999;20:1237–44.
19. Moulin V, Castilloux G, Jean A, et al. In-vitro models to study wound healing fibroblasts. Burns 1996;22:359–62.
20. Gabbiani G, Ryan GB, Majno G. Presence of modified fibroblasts in granulation tissue and their possible role in wound contraction. Experientia 1971;27:549–50.
21. Nishiyama T, Tominaga N, Nakajima K, Hayashi T. Quantitative evaluation of the factors affecting the process of fibroblast-mediated collagen gel contraction by separating the process into three phases. Collagen Rel Res 1988;8:259–73.
22. Ehlich HP. The modulation of contraction of fibroblast populated collagen lattices by type I, II, and III collagen. Tissue Cell 1988;20:47–50.
23. Anderson SN, Ruben Z, Fuller GC. Cell-mediated contraction of collagen lattices in serum-free medium: Effect of serum and nonserum factors. In-vitro Cell Dev Biol 1990;26:61–6.
24. Tingström A, Heldin CH, Rubin K. Regulation of fibroblast-mediated collagen gel contraction by platelet-derived growth factor, inteleukin-1a and transforming growth factor-b1. J Cell Science 1992;102:315–22.

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