A clinical study by Emanuele Verga MD
Keloid, so named for the frequent similarity of the lesion with the claw of a crab, is a benign fibrocitic skin tumor, or an abnormal wound healing process, the result of an altered response of the skin to a trauma of various kinds: chemical (as burns, chemical peelings), physical (such as piercing, tattoos, abrasions, not absorbable fillers), surgery, infectious (such as acne, chicken pox). Keloids can occur in all healing processes, thus also in first intention process and sometime, are formed in patients that do not report any physical trauma.
The evolution of a skin lesion scar is regulated by two factors normally in balance between them: TGF-b (cytochine transforming growth factor b) and NO (nitric oxide), both able to stimulate the production of collagen. TGF-b stimulates the transformation of fibroblasts into myofibroblasts and its redundant deflects the normal healing to hypertrophic scar, an elastic scar which by definition does not overflow from the primary lesion, characterized by the production of elastin, high level of collagen production (greater than normal but lower than keloid scar and by a high number of fibroblasts (which become myofiboblasts, determining retractable capacity to the scar that can be defined as “cellular”).
The increase of nitric oxide, however, inhibits the transformation of fibroblasts into myofibroblasts, deflecting the normal healing to the keloid and indirectly influences also on the biosynthesis of melanin by the melanocyte, activating the tyrosinase enzyme, in order to produce protective mechanisms against ROS induced damages. Basically, the occurrence of more keloids in high phototypes would be due to oxidative stress in skin cells that have a genetic mutation, mainly by ultraviolet radiation.
Keloid scars occur mainly in higher phototypes, while they are much less frequent in lower phototypes. Moreover, keloids more frequently occur in young than elderly patients, in part because younger dermis has greater collagen synthesis and contains more elastic fibers, causing more skin tension. Keloid has hard texture and is characterized by the overflow than the primary lesion and is considered “acellular”, compared to hypertrophic scars.
Inside Keloids, indeed, are found fibroblasts, which show altered anabolic activity but also a high production of collagen, due to the increase of collagenase inhibitors and an increase of new microvessels. Upstream of these conditions there is the expression of a genome with a gene mutation, although still not well identified but supported by expression of familiarity, which alters both the equilibrium proliferation / apoptosis of cells involved in the wound healing process in favor proliferation, and the balance anabolism / catabolism of the cells themselves, in favor of anabolism or, practically, there is more collagen formed of what is catabolized.
The most affected skin areas are the chest, above the sternum and the ear. Once developed, keloids are difficult to treat, and have a high rate of recurrence regardless of treatment adopted. Intralesional infiltrative therapies using official pharmacopoeia drugs are currently the therapeutic approach of choice, as the safest and most effective.
Here is reported a clinical case of keloid scar of the sternal region, in which is tested the effectiveness of some drugs introduced more recently as protocols infiltrative of keloids (verapamil, netilmicin, and 10% glucose solution), compared to what used more usually and for a long time, such as triamcinolon acetonid.