Involvement of upper torso stress amplification, tissue compression and distortion in the pathogenesis of keloids.

Keloids are benign tumours composed of fibrous tissue produced during excessive tissue repair triggered by minor injury, trauma or surgical incision. Although it is recognized that keloids have a propensity to form in the upper torso of the body, the predisposing factors responsible for this have not been investigated. It is crucial that the aetiopathoical factors implicated in keloid formation be established to provide guidelines for well-informed more successful treatment. We compared keloid-prone and keloid-protected skin, identified pertinent morphological differences and explored how inherent structural characteristics and intrinsic factors may promote keloid formation. It was determined that keloid prone areas were covered with high tension skin that had low stretch and a low elastic modulus when compared with skin in keloid protected areas where the skin was lax with a high elastic modulus and low pre-stress level. Factors contributing to elevated internal stress in keloid susceptible skin were the protrusion of hard connective tissue such as bony prominences or cartilage into the dermis of skin as well as inherent skin characteristics such as the bundled arrangement of collagen in the reticular dermis, the existent high tension, the low elastic modulus, low stretch ability, contractile forces exerted by wound healing fibroblastic cells and external forces. Stress promotes keloid formation by causing dermal distortion and compression which subsequently stimulate proliferation and enhanced protein synthesis in wound healing fibroblastic cells. The strain caused by stress also compresses and occludes microvessels causing ischaemic effects and reperfusion injury which stimulate growth when blood rich in growth factors returns to the tissue. The growth promoting effects of increased internal stress, primarily, and growth factors released by reperfusing blood, manifest in keloid formation. Other inherent skin characteristics promoting keloid growth during the late stages of wound healing in the upper torso are the thinner epidermis, the presence of vellus hairs, the absence of protective immunoglobulin A (IgA), and the thick fragile quality of upper torso skin. As it is not known why there is a predilection for keloids to form in the upper torso of the body, this hypothesis implicating and associating inherent morphological characteristics and elevated stress in the aetiopathogenesis of keloids is of potential value in terms of prevention, management and treatment of these enigmatic tumours.

Keloids show regional distribution of proliferative and degenerate connective tissue elements.

Keloids, formed by the deposition of excessive scar tissue, are characterised by the presence of thick hyalinised collagen bundles. Contradictory reports about keloid morphology include: hyperproliferation of dermal fibroblasts versus few fibroblasts; rich as opposed to poor vascularisation; dilated against occluded microvessels; distinct collagen nodules versus their absence, and elevated levels of types I and III collagen as opposed to no change when compared with normal dermis. This study attempted to clarify the controversies concerning keloid morphology by examining entire keloids and establishing baseline histological characteristics. Keloidal specimens from 32 patients were processed and comprehensively examined using light microscopy. The results of the study showed that keloids comprise many distinct regions, categorized as the zone of hyalinising collagen bundles, fine fibrous areas, area of inflammation, zone of dense regular connective tissue, nodular fibrous area and area of angiogenesis. The microvascular supply to each of these regions was impaired and features of degeneration and necrosis of keloid fibroblastic cells and microvessels were ubiquitous. Impairment of the healing stage of chronic inflammation, inefficient healing by fibrosis, multiple and exaggerated phases of vascular and fibrous granulation and remodelling stages manifest in keloid formation. The uneven distribution of cells may be due to the generation of traction forces by keloid cells. These forces also modify DNA and protein synthesis, leading to an overproduction of extracellular matrix components. This study provides a structured basis for future ultrastructural and immunocytochemical research of keloids and other fibroproliferative disorders.