Pogorila A. Iatrogenic compression-toxic lesion of the inferior alveolar nerve with filling materials: diagnosis of neuromarker titer activity (NSE, S100 protein) and neuroprotective therapy (experiental-clinical research)

The dissertation is devoted to solving of actual scientific problem, which is to increase the effectiveness of therapeutic measures in patients during the acute period of iatrogenic compression-toxic damage of the inferior alveolar nerve with filling materials due to experimental and clinical substantiation of new additional diagnostic methods based on the study of nerve fiber damage markers (NSE and protein titer S100) and combination therapy using neuroprotectors. Based on a series of experimental and clinical studies, the specific features of the mechanism and course of the ICTD IAN by various filling materials, in-depth study of changes in the trigeminal node at the cellular level are determined. It was established that the earliest diagnostic marker of damage to IAN on serum markers of blood is NSE and S100 protein titer, where the first marker should not exceed the indices of 0.422-0.428 ng / ml, and the S 100 protein - 0.496-0.514 ng / ml. The research results showed that under the conditions of the ICTD IAN with filling materials, the critical period is 14 days, where the maximum escalation of neuromarkers is noted: NSE, relative to the initial level, increases 53.75 times (15.213 ± 0.263 ng/ml p <0.05) using a filling material based on R-F, and 35.95 times (10.460 ± 0.154 ng/ml p <0.05) - ES. 30 days is characterized by the activation of neuroglia, in favor of which is indicated by an increase in S100 protein titers (against the background of the material R-F, 30.18 times (16.571 ± 0.169 ng/ml p <0.05), against the background of ES - 26.3 times (11.860 ± 0.324 ng/ml p<0.05). It was found that when amantadine hydrochloride-based drugs are used to treat neuroprotective drugs based on amantadine hydrochloride during the entire treatment period, the laboratory and clinical indicators significantly improve, which was experimentally confirmed by a decrease in the number of Gasser node cells in the SubG0G1 phase (to 0.766 ± 0.03% versus 10.904 ± 0.27%) and S-cycle (up to 0.19 ± 0.008% versus 0.55 ± 0.018%). The method of laser Doppler sonography confirmed the restoration of the microcirculation of IAN vessels due to active neuroprotective therapy to almost normal levels. The proposed method for the diagnosis and treatment of patients with ICTD IAN, makes it possible to carry out rapid diagnosis of pathology and eliminate early pathobiochemical processes in the complex IAN/trigeminal node, which significantly reduces the number of complications.