Congenital Abnormalities

Many congenital abnormalities are important to recognize preoperatively. These include Ehlers-Danlos syndrome, cutis laxa, pseudoxanthoma elasticum, osteogenesis imperfecta, and progeria. A common factor in these disorders appears to be that congenital errors in the metabolism of collagen invariably result in poor wound healing. Elective surgery in patients with these conditions should be avoided.


The emphasis up to this point has been on conditions that downregulate the phases of wound healing, resulting in poor wound repair. An overactivation of the wound |

healing process can also occur, as evidenced by the formation of hypertrophic scars and keloids. These two conditions share an excessive production and deposition of ยง

collagen without the equivalent balance of degradation and remodeling. They also appear to occur more frequently in areas that are under increased skin tension or constant motion; earlobes appear to be an exception to this rule. The major difference between these two conditions is that while hypertrophic scars tend to remain within the original tissue injury site and will eventually regress over time, keloids grow beyond the boundaries of the injured site and do not regress.

Keloids and hypertrophic scars also differ histopathologically. Keloids contain abundant mucin and large, thick bundles of collagen that lie haphazardly within the dermis. They are also quite vascular. The keloid extracellular matrix is composed primarily of glycoproteins and water. In contrast, hypertrophic scars contain well-organized fibrillar collagen, contain no mucin, are less vascular, and contain abundant myofibroblasts (38).

It is unclear whether the pathogenesis of keloids is secondary to the overproduction of collagen or a defect in collagen degradation (39). Various theories propose a deficiency or defect in collagenase, a disproportionate level of collagenase inhibitors, or an abnormal growth regulation of fibroblasts mediated through TGF-p (40,41). It is well documented that the metabolic activity in keloids is much greater than in hypertrophic scars. A variety of cytokines and growth factors have been implicated in the regulation of this metabolic activity (42). TGF-p and IL-1 have been shown to increase collagen gene expression in vitro. Studies have demonstrated that inhibiting TGF-p leads to reduced scar formation.

Two cytokines that appear to be major factors in downregulating collagen production and reducing scar formation are IFN-g and IFN-a. Clinical trials using intra-lesional injections of IFN-g and IFN-a have demonstrated significant decreases in keloid and hypertrophic scar formation. Some authors have suggested that the formation of keloids is the result of a cell-mediated response to sebum released from sebaceous glands following incision. The specific mechanism involved in the development of keloids is still unknown and remains an area of active research.

The treatment of keloids is challenging and controversial. Treatment is aimed at reducing the metabolic activity within the keloid and ultimately suppressing the production of collagen. The goal in the treatment of both hypertrophic scars and keloids is to improve their appearance by decreasing the volume of collagen and extracellular matrix. While intralesional injection of steroids continues to be the mainstay of treatment, there have been a number of clinical trials supporting alternative methods of therapy for keloids (43). These include, but are not limited to, re-excision of the keloid followed by low-dose radiation therapy (1500-2000 cGY), laser excision, interferon injection, treatment with adrenocorticotropic hormone (ACTH), vitamin A, retinoic acid, compressive devices, and the use of silicone sheeting (44,45).

How To Reduce Acne Scarring

How To Reduce Acne Scarring

Acne is a name that is famous in its own right, but for all of the wrong reasons. Most teenagers know, and dread, the very word, as it so prevalently wrecks havoc on their faces throughout their adolescent years.

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