The mechanisms underlying the pathogenesis of keloids have not been fully characterized despite extensive past and present research. Results of past and present studies have shown that the immune system is actively involved in the development of these lesions. Future investigations into the biochemistry and immunologic factors of keloids are anticipated and expected to produce additional insight. The inability to identify cellular (fibroblast) abnormalities has led most investigators to focus on the humoral regulators of wound healing, that is, biochemical substances, immunologic mediators and growth factors. Future studies are needed to confirm or refute the presence of AFA. AFA, if they exist, may prove to be useful as immunologic markers of keloids and may help distinguish keloids from hypertrophic scar in the early stages of wound healing. The influence of immunologic mediators may be more impressive early in the development of scars. 'Young' or 'early' is defined as less than two years of age, whereas 'old' or 'late' keloids are more than two years of age. We suggest that future studies stratify keloids into early versus late and also measure the rates of collagen synthesis of fibroblasts derived from the normal and abnormal specimens from the same patient. Analysis of the leukocyte factors will clarify the role the immune system has in the regulation of collagen synthesis. Preliminary investigations have shown that immunotherapy may be of value in the treatment of keloids. The role of fibroblast heterogeneity needs to be investigated. It is not known which aspects of fibroblast heterogeneity are responsible for the localized and accelerated rates of collagen synthesis of keloid fibroblasts.
|Original language||English (US)|
|Number of pages||9|
|Journal||Surgery Gynecology and Obstetrics|
|State||Published - Jan 1 1992|
ASJC Scopus subject areas
- Obstetrics and Gynecology