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Journal Technologies of Living Systems №4 for 2015 г.
Article in number:
Skeletal muscular tissue plasty by spongy allogeneic biomaterial in experimental animals
Authors:
A.I. Lebedeva Ph.D. (Biol.), Senior Research Scientist, FSBI «Russian Eye and Plastic Surgery Centre» of the Russian Federation Ministry of Health, Ufa, Russia. E-mail: jeol02@mail.ru L.A. Musina Dr.Sc. (Biol.), Leading Research Scientist, FSBI «Russian Eye and Plastic Surgery Centre» of the Russian Federation Ministry of Health, Ufa, Russia. E-mail: morphoplant@mail.ru O.R. Shangina Dr.Sc. (Biol.), Leading Research Scientist, FSBI «Russian Eye and Plastic Surgery Centre» of the Russian Federation Ministry of Health, Ufa, Russia. E-mail: alloolga@mail.ru
Abstract:
Scar formation which leads to the organ functioning disorder is an integral healing attribute of muscular tissue deep damages. Automyoplasty and cellular technologies, gene therapy etc. are labour-intensive and traumatic methods which entail complications. One of the most successfully developing direction for muscular tissue regeneration is the use of biodegrade grafts [2]. The aim of the investigation was to determine morphological aspects of skeletal muscular tissue regeneration with the use of allogeneic spongy biomaterial (ASB) following the mechanical damage. Material and methods. In the first experimental group (36 rats) a defect 3-4 mm long was inflicted in mid-third shin muscle of belly region and then ASB of the corresponding size, was placed into the mass between the proximal and distal stumps and fixed by filiform tendinous graft. In the control series (36 rats) a defect 3 -4 mm long was inflicted in the gastrocnemius muscle area. After the procedure in both cases Vicryl 6-0 sutures were placed onto the skin. The fibular nerve was not damaged. ASB was made in that case from rat tendonds and treated by lyophilization methods which allowed to achieve structural modification to spongy form. There were used histological, histochemical, immunohistochemical and electron-microscopic methods. Results of the investigation. Biodegradation with gradual release of collagen, hyaluronic acid, keratin and dermatan sulfate was taking place. The resorption products stimulated massive invasion of CD68+ phagocytic macrophages and cells of an inflammatory orientation (TNF-a, IL1). In the regenerate there was revealed a low number of connective tissue cells expressing profibrogenic cytokines (vimentine, FGF-b1, TGF-b1) as compared with the control group which stipulated full-fledged phagocytosis and inhibition of scar development. Early activation and proliferation of myogenic cell precursors (MyoD+) with further differentiation into myosymplastis was revealed. During the process of ASB replacement, the formation of muscular connective tissue regenerate was taking place with prevailing organotypic vascularized loose connective tissue the share of which, with time, reduced and was replaced by the muscular tissue. Parallel oriented bundles of muscular fibers grew into the channels of the preceding spongy graft, hypertrophied and gradually displaced stromal elements to the periphery of the muscular bundle. That was the way endomysium and perimysium were formed. Biomaterial spongy modification plays an essential part which reconstructs a connective tissue framework. It allows to compensate an extensive muscle defect and in so doing it acts as a muscular framework. In the control group there was observed a substantial deficit of glycosaminoglycanes. Low content of CD68+ and MyoD+ cells was determined. A pronounced expression of profibrogenic cytokins (TGF-b1) and expression suppression of anti-inflammatory factors could contribute to incomplete phagocytosis of wound detritus and immune tension in the tissue [1]. Active proliferation of fibroblastic, vimentin and TGF-b1+ cells have also contributed to rapid synthesis of collagen fibres and defect replacement by the scar with its further transformation to fat tissue. Thus, ASB stimulates adequate regeneration of skeletal muscular tissue following the defect inflict.
Pages: 61-63
References

 

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