Before considering scar revision, the treating physician must have an understanding of wound healing and how scar tissue forms. Wound healing progresses in 3 phases: an inflammatory phase, a granulation phase, and the final, remodeling phase.
Inflammation is an immediate physiologic response to any injury to the body. In the skin, it serves the additional role of helping to contain and repel any organisms or foreign materials introduced into the tissues by a variety of traumas, including surgical incisions. The various mediators of inflammation are the first materials released in the wound, including activated complement, transforming growth factor-beta, circulating monocytes, tissue macrophages, neutrophils, platelets, clotting factors, and serum proteins, among others. Damaged collagen fibers promote platelet aggregation in the wound. Later, collagen provides the scaffold for wound healing as the major constituent of the extracellular matrix. This primary phase of wound healing typically lasts for 1-2 days.
The granulation or proliferative phase involves fibroblast proliferation within the wound bed. These cells are responsible for the production of the collagen extracellular matrix. Cytokines present in the wound bed at this time also promote the process of angiogenesis and the appearance of granulation tissue, a characteristic of the healing wound. Once collagen is laid down as an extracellular matrix and cells have grown on this scaffold, the wound enters the remodeling phase of wound healing.
The remodeling phase involves the reassortment of collagen fibers laid down in the preceding proliferative phase. Remodeling is the longest period of the wound healing process; it may continue for up to a year. However, 2-3 weeks is a more common interval for this final phase of wound healing. During this time, the net amount of collagen does not increase, but the formation of a more orderly arrangement of fibers helps to greatly increase the wound's tensile strength. When healed properly, the final wound strength reaches 70-80% of prewound strength.
The ideal scar is narrow and fills but does not eclipse the original volume of the wound bed. In fact, the wound often decreases in size upon healing due to contractile forces involved in scar formation. Occasionally, scar formation may be exuberant, as in the cases of hypertrophic scarring or keloid formation. Although discussed in detail in Keloid and Hypertrophic Scar, a brief mention of these unwelcome sequelae of wound healing is warranted.
Hypertrophic scars do not extend beyond the original boundaries of the wound laterally, but scar tissue may rise above the level of the surrounding skin. This commonly results in a very noticeable, irregularly contoured scar. A more extreme example of exuberant growth of scar tissue is the keloid. Keloid scars extend beyond the original borders of the wound, resulting in a raised and expanded scar relative to the original defect. These are often very noticeable, and they occur with increased frequency in persons with dark complexions. In both hypertrophic scars and keloids, components of the extracellular matrix are increased. Thus, while the number of fibroblasts present is normal, the cells present are apparently overactive in their wound healing response.
Kamis, 11 Maret 2010
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Considering Scar Revision
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