The role of morphofunctional interactions of cellular structures of connective tissue in the pathogenesis of pathological scarring in children
Abstract
Aim. To analyse the connective tissue structures and their interaction in the pathogenesis of pathological scarring in children. Materials and methods. In the period from 2016 to 2019, under our supervision there were 23 children. The average age is 8 ± 0.7 years. Scars formed subsequently in domestic injuries, operations, burns. The average lifetime of scars is 1.7 ± 0.9 years, from the moment of injury to excision. Intraoperatively 72 biopsy samples of scars were selected, of which the distribution of scar tissue was as follows: hypertrophic - 54 (75 %), keloid - 38 (52.8 %), atrophic scars - 16 (22.2 %). The micropreparations were stained with hematoxylin and eosin, picrofuchsin according to Van Gieson fuchselin according to Unna. The IHC study was carried out according to the standard protocol using monoclonal rabbit antibodies to Collagen I, III and IV type (Diagnostic BioSystems, Germany). The IHC study was carried out on a Leica Bond MAX immunohistostainer using the Bond Polymer Refine Detection detection system. Subsequently, using the Morphology 5.0 computer based image analysis program (VideoTest, Russia). Results. With a hypertrophic scar: hyperplastic fibroblasts, pronounced granulation tissue with formed fibrous regions. When IHC reaction is expressed expression of type IV collagen. In the observation of cell structures, multinucleated macrophages connected by intercellular contacts with fibroblasts were revealed. With keloid scars, fibrosed bundles of collagen and fibroblastic polymorphism are visible. With IHC, a decreased expression of type IV collagen is observed than that of type I, which is the predominant type of fiber. Atrophic scar is based on loose connective tissue, the basis of which is granulation tissue. Collagen, elastic and argyrophilic fibers, reduced expression of type I and III collagen are not very pronounced. There are preserved skin appendages in the thickened epidermis. Conclusion. To improve the quality of life of patients, a further deeper study of the pathogenetic mechanisms of scar development is required, which will allow predicting and optimizing adequate methods for correcting skin scars.