Department of Physiology, Faculty of Health Sciences, Nelson R. Mandela School of Medicine, University of Kwazulu-Natal, Durban, South Africa.
Med Hypotheses. 2012 Mar;78(3):356-63. doi: 10.1016/j.mehy.2011.12.008. Epub 2012 Jan 9.
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.
瘢痕疙瘩是一种良性肿瘤,由纤维组织组成,是由轻微损伤、创伤或手术切口引起的过度组织修复产生的。虽然人们已经认识到瘢痕疙瘩有在上半身形成的倾向,但导致这种倾向的诱发因素尚未得到研究。确定与瘢痕疙瘩形成相关的病因病理学因素至关重要,这为更成功的治疗提供了依据。我们比较了瘢痕疙瘩易发区和瘢痕疙瘩保护区的皮肤,确定了相关的形态差异,并探讨了内在结构特征和内在因素如何促进瘢痕疙瘩的形成。结果表明,与瘢痕疙瘩保护区的皮肤相比,瘢痕疙瘩易发区的皮肤覆盖着高张力皮肤,其拉伸性低,弹性模量低;而瘢痕疙瘩保护区的皮肤松弛,弹性模量大,预应水平低。导致瘢痕疙瘩易感皮肤内部应力升高的因素包括骨性突起或软骨等硬性结缔组织向皮肤真皮的突起,以及固有皮肤特征,如网状真皮中胶原的束状排列、固有张力、低弹性模量、低拉伸能力、愈合的成纤维细胞产生的收缩力和外部力。应激通过引起真皮变形和压缩,从而刺激愈合的成纤维细胞增殖和增强蛋白合成,促进瘢痕疙瘩的形成。应激引起的应变还会压缩和阻塞微血管,导致缺血效应和再灌注损伤,当富含生长因子的血液回流到组织时,会刺激生长。增加的内部应力主要是由内部应力引起的生长促进作用,以及再灌注血液释放的生长因子,在瘢痕疙瘩形成中表现出来。在上半身伤口愈合的晚期,促进瘢痕疙瘩生长的其他固有皮肤特征包括更薄的表皮、毫毛的存在、缺乏保护性免疫球蛋白 A(IgA)以及上半身皮肤的厚而脆弱的特性。由于尚不清楚为什么上半身容易形成瘢痕疙瘩,因此,这种将固有形态特征和升高的应激与瘢痕疙瘩发病机制相关联的假说具有潜在价值,可用于预防、管理和治疗这些神秘的肿瘤。
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