Abstract

Hypertrophic and keloid scars are two types of raised, abnormal scars. Hypertrophic scars grow within the borders of the original wound and eventually grow smaller, but keloids grow beyond the original wound borders, do not grow smaller on their own, and are difficult to treat. Keloids usually occur in people with darker skin colour. Sometimes it is still difficult to determine if a raised scar is a hypertrophic scar or a keloid. This study from the Netherlands aimed to find out if both these abnormal scars form because they retain characteristics of the young, immature scars, rather than maturing in a normal way. The authors examined the types of cells present in the outer (epidermis) and the inner (dermis) layer of the skin and found that the hypertrophic and keloid scars closely resembled immature scars, rather than normal healthy scars in two important ways: the outer layer cells did not mature properly (increased involucrin expression); the inner layer cells of normal skin express a protein called CD34 and do not have cells that function to contract tissue (α‐SMA), but in the abnormal scars this is reversed ‐ CD34 is missing and the (α‐SMA) contracting cells are present. Unlike abnormal scars, the cells of the inner and outer layer of immature scars showed increased cell growth (Ki67). The outer layer of the abnormal scars was much thicker and the inner layer had many cells (vimentin), but these cells had stopped growing (known as p16). It was difficult to separate the hypertrophic scars from the keloids based on what the inner layer looks like, but hypertrophic scars have more cells that contract and keloids have very thick bands of connective tissue in their inner layer. In conclusion, the results of this study suggest that hypertrophic and keloid scars maintain characteristics of immature scars and do not mature like normal scars do. This is a summary of the study: Hypertrophic and keloid scars fail to progress from the CD34−α‐smooth muscle actin (SMA)+immature scar phenotype and show gradient differences in α‐SMA and p16 expression

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