Aim: The purpose of the study was to identify the role of SATB2 in healing of the experimental mandible bone tissue defect filling with a synthetic bone graft material and electrical stimulation impact. Materials and Methods: An experiment was carried out on 48 mature male rats of the WAG population, which were divided into 4 groups. Each group included 12 experimental animals. Group 1 included rats that were modeled with a perforated defect of the lower jaw body. Group 2 included animals that were modeled with a perforated defect similar to group 1. In animals, a microdevice for electrical action was implanted subcutaneously in the neck area on the side of the simulated bone defect. The negative electrode connected to the negative pole of the battery was in contact with the bone defect. The battery and electrode were insulated with plastic heat shrink material. Group 3 included rats that were modeled with a perforated defect similar to previous groups, the cavity of which was filled with synthetic bone graft "Biomin GT" (RAPID, Ukraine). Group 4 included animals that were modeled with a perforated defect similar to groups 1-3, the cavity of which was filled with synthetic bone graft "Biomin GT" (RAPID, Ukraine). The simulation of electrical stimulation was the same as in group 2. The material for the morphological study was a fragment of the body of the lower jaw from the zone of the perforated defect. Immunohistochemical study was performed using rabbit anti-human SATB2 monoclonal antibody. Results: In the regenerate filling the defect in the bone tissue of the lower jaw of rats, there was an increase in SATB2 expression under conditions of electrical stimulation; filling the defect with a synthetic bone graft material; simultaneous filling the defect with a synthetic bone graft material and electrical stimulation. The most pronounced expression of SATB2 was observed under conditions of simultaneous filling the defect with a synthetic bone graft material and electrical stimulation; minimally expressed - in conditions of filling the defect with a synthetic bone graft material; moderately expressed - under conditions of electrical stimulation. In the regenerate, in cases of all treatment methods, SATB2 was expressed by immune cells, fibroblastic differon cells, osteoblasts, and in case of electrical stimulation, also by adipocytes, vascular pericytes and endothelial cells, epidermis. Conclusions: The activation of SATB2 expression identified by the authors is one of the mechanisms for stimulating reparative osteogenesis under the conditions of electrical stimulation; filling the defect with a synthetic bone graft material; simultaneous filling the defect with a synthetic bone graft material and electrical stimulation.
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