Inflammatory diseases of periodontal tissues: rationale for the use of the drug «Omega 3» by NSP


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An important role in the dynamics of inflammation is played by a group of substances formed in blood cells (leukocytes, platelets) and in endotheliocytes. The source of their formation is the phospholipids of cell membranes. Violation of the strictly ordered structure of phospholipids in the cell membrane makes them available to the action of phospholipase A2. As a result, hydrolytic cleavage of an unsaturated fatty acid (arachidonic, pentanoic) occurs — one of the two hydrophobic tails of the phospholipid molecule. With arachidonic acid, a cascade of chemical reactions begins, which go in two directions. Under the action of pro-inflammatory inducible cyclooxygenase 2 (COX-2), which is encoded by a separate gene that does not function normally, it produces acid arachidonides — pro-inflammatory type II prostaglandins (PGE2, PGF2). The expression of this gene occurs in vascular endotheliocytes, macrophages, fibroblasts, osteoclasts under the influence of microbial mucopolysaccharides and tissue breakdown products. Further conversion of prostaglandins occurs under the action of thromboxane synthetase, resulting in the formation of thromboxane A2 (TxA2). Under its action, vasoconstriction, platelet aggregation, thrombosis, edema, and pain occur. Endotheliocytes also contain the enzyme prostacyclin synthetase, which converts PGE2 to prostacyclin (PGI2). The action of PGI2 is directly opposite to thromboxane A2 (platelet disaggregation, vasodilatation). But with damaged endothelium, prostacyclin synthetase is lacking and part of PGE2 is converted into thromboxane A2. If lipoxygenase shows its activity, then pro-inflammatory type IV leukotrienes (LTV4, LTS4) are formed in neutrophils, macrophages and osteoclasts, which increase the permeability of the vascular wall, causing edema, have a chemotactic and chemokinetic effect (non-targeted action). Also, along with pro-inflammatory prostaglandins and leukotrienes, anti-inflammatory prostaglandins (PGEs TxAz, etc.) and type V leukotrienes are synthesized in the body. The substrate for their synthesis is eicosapentaenoic and docosahexaenoic acids, which accumulate in the phospholipids of the membranes of neutrophils, macrophages, fibroblasts, and osteoclasts and, moreover, are competitive inhibitors of arachidonic acid. As a result of studies of the effect of EPA and DHA, leukotrienes B4 and Bs on the content of osteoclasts in the alveolar process of the bone, it was noted that the introduction of LTV4 into the submucosa of the gums leads to an increase in the emigration of macrophage monocytes from the blood to the bone, followed by their transformation into osteoclasts, while how the preliminary introduction of EPA and DHA into the body significantly reduces the number of osteoclasts in the alveolar process, even with the introduction of LTV4. LTV5 does not significantly change the content of osteoclasts in the alveolar process. Also, the results of the study of the effect of EPA and DHA on the content of cyclooxygenase and lipoxygenase products of arachidonic acid in gingival blood and mixed saliva show a significant decrease in pro-inflammatory PGE2 and LTV4 even below normal. When taking drugs containing EPA and DHA, side effects were not observed, in contrast to the action of drugs from the group of non-steroidal anti-inflammatory drugs, which also inhibit the synthesis of prostaglandins that protect the gastrointestinal tract, which leads to gastrointestinal intolerance, and also have an irritant effect on mucous membrane of the stomach and duodenum. Nature’s Sunshine Products is bringing Omega 3 (EPA) to market. This unique product, which contains fish oil obtained from fish living in cold waters, including salmon and mackerel, contains polyunsaturated fatty acids: eicosapentaenoic and docosahexaenoic acids in a dosage of 180 mg and 120 mg, respectively. The pronounced anti-inflammatory effect of the drug, due to a decrease in the synthesis of pro-inflammatory substrates, a decrease in the number of osteoclasts in the alveolar process even with the introduction of LTV4, as well as participation in the synthesis of anti-inflammatory substrates, justifies the need to include the drug in the complex therapy of inflammatory diseases of periodontal tissues.

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