Similarly, healing time in the collagenase-treated wounds was shorter when compared to the silver sulfadiazine treated wounds (p < 0.001).

  Despite both of these studies showing more rapid debridement as well as a shorter time to wound closure with the use of collagenase, neither of these articles reported anything regarding the final scar result. The present study addressed the scar outcome and found that the scar incidence was lower with the use of collagenase. Indeed, this was a retrospective review, which limited the validity of the conclusion. However, the observation made in this review should serve to prompt a prospective study.

  It is currently accepted that earlier wound closure results in less scarring. Though this is a generally accepted fact, the mechanism of early wound closure that decreases scar formation is unclear. The question remains as to whether the decreased hypertrophic scar is related to an earlier wound closure secondary to a more rapid debridement of the eschar or if it is related to the increased level of collagenase that decreases the rate of collagen production.

  Garner³ hypothesized the lack of an overlying epidermis resulted in excess fibroblast collagen synthesis. To test this hypothesis, human keratinocytes were added to a human fibroblast culture. A significant decrease in fibroblast collagen synthesis was demonstrated. Furthermore, this suppression of collagen synthesis was dose dependent, that is, the greater the percentage of keratinocyte conditioned medium, the greater the suppression of collagen synthesis. The addition of an unconditioned medium did not have any effect. A question remains: was this result simply related to the mere presence of the keratinocytes or were the keratinocytes releasing something, such as collagenase, which in turn decreased the collagen synthesis?

  Laboratory studies by Ghahary et al.⁴ involved establishing cultures of fibroblasts from both normal skin and hypertrophic tissue. Separate collagenase assays were then performed using both of these fibroblast cultures. Their findings revealed that the amount of mRNA for collagenase was lower in the hypertrophic fibroblasts than in the normal control fibroblasts. This study indicated that the reduced collagenase production and activity contributed to the excessive collagen deposition seen in hypertrophic scar.

  Arakawa et al.⁵ performed a similar study. Dermal fibroblasts were cultured from hypertrophic scar as well as normal skin. Collagenase assays of the fibroblasts were performed. Their results indicated reduced collagenase gene expression in the hypertrophic scar fibroblasts. These findings were consistent with those of Ghahary et al.⁴

  The tissue inhibitor of metalloproteinase (TIMP) is known to naturally regulate the action of collagenase and, thus, raises the question as to whether the increased collagen production is related to an increase in TIMP rather than a decrease in actual production of collagenase. Ghahary et al.⁴ and Arakawa et al.⁵ discovered similar levels of TIMP mRNA in hypertrophic scar and normal cells. Thus, one would conclude that the increased hypertrophic scar is related to a decrease in the production of collagenase and not an increased inhibition on the existing collagenase.

Conclusion

  Scar formation as a result of burn injury remains a challenge to the burn care professional. Scar in functional areas can result in decreased function and even lead to an inability to perform one’s usual work tasks. Also, hypertrophic scar can leave unacceptable cosmetic results, especially when dealing with the face. The mechanism of scar is not well understood.