Aim. To determine the activity of superoxide dismutase and catalase, the content of SH groups in the blood serum of patients with generalized periodontitis in patients with diabetes mellitus 2 type and in their combination. Materials and methods. The study involved 68 people with a clinically established diagnosis of type 2 diabetes mellitus, as well as 32 patients with confirmed generalized periodontitis, divided into 4 groups. The concentration of superoxide dismutase and catalase and the content of SH groups in the blood serum of patients were determined using a biochemical method. Statistical processing of data was carried out using the Shapiro-Wilk criterion. The level of statistical significance of differences between samples was assessed using the nonparametric Mann-Whitney test. Results. The highest levels of catalase activity and the lowest levels of superoxide dismutase activity were found in patients of group 4 with generalized periodontitis against the background of type 2 diabetes mellitus. The indicator of catalase activity in the subjects of the 4th group exceeded by 45.2% the results of the 2nd group and by 28.1% – of the 3rd group. At the same time, the SOD activity of the 4th group was not only lower than the control data, but also 26.8% of the results of the 2nd group (p<0.01) and practically did not differ from the indicators of the 3rd group. It should be noted that the combination of generalized periodontitis and type 2 diabetes causes a decrease in the content of SH groups by 12.7% relative to group 3. This indicates that against the background of type 2 diabetes, the development of combined pathology is accompanied by inhibition of the functional capabilities of antioxidant defense. Conclusions. In the comorbid course of generalized periodontitis and type 2 diabetes mellitus, the intensity of free radical oxidation processes in the blood serum increases with an increase in the concentration of catalase and superoxide dismutase, which indicates the strain of enzyme antioxidant processes with inhibition of functional glutate reserves.
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