Abstract and keywords
Abstract (English):
Subject. Despite the constant efforts of practicing physicians and scientists, the prevalence proportion of inflammatory and destructive periodontal diseases in the world is not subsiding. Previously scientists have examined several different theories on the development of pathological conditions in periodontal tissues, ranging problems from the neurotrophic theory of occurrence to the effect of occlusion injury on periodontal tissues. Theories dealing with the influence of specific and non-specific bacterial plaque have also been studied. None of the theories has become reasonable and single valued. It is believed that the mechanism of the development of the disease is complex, autoimmune, damaging primarily collagen, elastic fibers of the capillary endothelium, gingival ligament and bone tissue. Over the past decade, it has been proven that inflammation in periodontal tissues is initiated and proceeds in response to the introduction of pathogenic bacteria. However, it can be said that not all patients develop an inflammatory response to bacterial invasion. The second important factor in the development and progression of the inflammatory-destructive process is the immune response of a particular individual. Scientists have noted the influence of the non-microbial factor and have come to the conclusion that in the surrounding tissues of the inflamed area there are not only enzymes secreted by bacteria, but also leukocyte proteinases, which in turn are mediators of the tissue destruction. Purpose ― to examine the role of leukocyte proteinases in the pathogenesis of inflammatory periodontal diseases. Methodology. The number of indigenous and foreign literature sources dealing with the study of the role of leukocyte proteinases in the development and maintenance of a destructive inflammatory process has been reviewed by us. Conclusion. The role of the aggressive destructive effect of leukocyte proteinases on periodontal tissues has been analyzed. Leukocyte proteinases are mediators of progressive destruction of connective tissue and can be used as markers to assess the severity of the course and predict the development of the inflammatory process in periodontal tissues.

periodontitis, polymorphonuclear leukocytes, leukocyte proteinases, pathogenesis, inflammatory diseases

1. Bezrukov, V. M., Grigiryants, L. A., Rabukhina, N. A, Baldalyan, V. A. (2003). Ambulatornaya khirurgicheskaya stomatologiya. Sovremennye metody [Outpatient surgical dentistry. Modern method]. Moscow, 90. (In Russ.)

2. Bezrukova, I. V., Grudyanov, A. I. (2002). Agressivnye formy parodontita [Aggressive forms of periodontitis]. Moscow, 127. (In Russ.)

3. Vishnyak, G. N. (1999). Generalizovannye zabolevaniya parodonta [Generalized periodontal diseases]. Kiev, 216. (In Russ.)

4. Golitsyna, A. A., Yugai, U. V., Chagina, E. A., Pervov, Y. Y., Romanchuk, A. L. (2018). Sravnitelny analiz sistemy metalloproteinaz I ih tkanevyh ingibitorov pri parodonte u patsientov s sakharnym diabetom II tipa [Comparative analysis of the system of metalloproteinases and their tissue inhibitors in periodontitis in patients with type II diabetes mellitus]. Rossiisky immunologichesky zhurnal [Russian immunological journal], 12 (21), 3, 247–254. (In Russ.)

5. Grechishnikov, V. V. (2005). Etiologicheskiye factory, vliyaushchie na razvitiye vospalitelno-destruktivnykh izmenenii v tkanyah parodonta [Etiological factors affecting the development of inflammatory and destructive changes in periodontal tissues]. Parodontologiya [Periodontology], 4 (37), 28–32. (In Russ.)

6. Grigoryan, A. S. (1999). Rol I mesto fenomena povrezhdeniya v patogeneze zabolevaniya parodonta [Role and place of the damage phenomenon in the pathogenesis of periodontal disease]. Stomatologiya [Dentistry], 1, 16–20. (In Russ.)

7. Grudyanov, A. I. (1997). Parodontologiya (etiologia, patogenez, lechenie, profilaktika) [Periodontics (etiology, pathogenesis, treatment, prevention) selected lectures]. Moscow : Stomatologii Open Society, 32. (In Russ.)

8. Grudyanov, A. I., Dmitrieva, L. A., Maksimovsky, Y. M. (1999). Parodontologiya. Sovremennoye sostoyanie voprosa I napravleniya nauchnyck razrabotok [Periodontics. Current state of the issue and directions of scientific research]. Stomatologiya [Dentistry], 1, 31–33. (In Russ.)

9. Zazulevskaya, L. Y. (2006). Prakticheskaya parodontologiya [Practical periodontics]. Almaty : Vverena, 348. (In Russ.)

10. Ilyichev, A. V., Belkov, A. P., Maldov, D. G. et al. (2009). Sekretsiya granyl neitrofilov cheloveka pod deistviem formilpeptida I preparata Stimforte [Secretion of human neutrophil granules under the action of formylpeptide and Stimforte]. Immunologia [Immunology], 30, 3, 159–161. (In Russ.)

11. Isachkova, L. M., Plekhova, N. G. (2002). K razvitiyu predstavlenii ob antiinfektsionnoi rezistentnosti [On the development of ideas about anti-infective resistance]. Epidemiologia I infektsionnye bolezni [Epidemiology and Infectious Diseases], 1, 11–15. (In Russ.)

12. Kravtsova, G. A. (2010). Rol' leykotsitarnykh proteinaz i nemikrobnykh faktorov v patogeneze vospalitel'nykh zabolevaniy parodonta (obzor literatury) [Role of leukocytic proteases and non-microbial factors in pathogenesis of inflammatory diseases of parodentium (the review of literature)]. Acta Biomedica Scientifica [Acta Biomedica Scientifica], 6-1.

13. Rumyantsev, V. A., Zhigulina, V. V. (2014). Matriksnyye metalloproteinazy, ikh rol' v razvitii parodontita [Matrix metalloproteinases in periodontal disease]. Aktual'nyye problemy gumanitarnykh i yestestvennykh nauk [Actual problems of the humanities and natural sciences], 8-1, 321-327. (In Russ.)

14. Rumyantsev, V. A., Shimansky, Sh. L., Gasparyan, M. G., Asayan, A. G., Ryabikov, M. D., Moiseyev, D. A., Yusupova, Y. I. (2019). Vliyanie biotekhnologii reprogrammirovaniya makrofagov na initsiirovannuyu vospalitelnuyu reaktsiyu v parodonte myshei (eksperimentalnoye issledovaniye) [Effect of macrophage reprogramming biotechnology on the initiated inflammatory response in the periodontal region of mice (experimental study)]. Vyatskii meditsinsky vestnik [Vyatka Medical Bulletin], 2 (62). (issue date: 12.12.2019). (In Russ.)

15. Shmelkova, T. P. (2008). Vzaimodeistvie chumnogo mikroba I ego antigenov s kletkami krovi cheloveka in vitro [Interaction of the plague microbe and its antigens with human blood cells in vitro: autoref.of thesis Dr Biol Science]. Saratov, 26. (In Russ.)

16. Birkedal-Hansen, H. (1993). Role of matrix metalloproteinases in human periodontal disease. J. Periodontol, 64, 5, 474–484.

17. Buchmann, R., Hasilik, A., Nunn, M. E., Van, T. E. et al. (2002). Dyke PMN responses in chronic periodontal disease: evaluation by gingival crevicular fluid enzymes and elastase-alpha-1-proteinase inhibitor complex. J. Clin. Periodontol, 29, 6, 563–572.

18. Buchmann, R., Ocmus Media, A. G. (2001). Risikofaktoren in der Parodontologie. Sistematische Therapic bei parodontalen Risikofactoren. Dentalhygiene J, 2, 24–31.

19. Campbell, E. J., Owen, C. A. (2007). The sulfate groups of chondroitin sulfate¬ and heparan sulfate-containing proteoglycans in neutrophil plasma membranes are novel binding sites for human leukocyte elastase and cathepsin G. J. Biol. Chem, 282, 14645–14654.

20. Casey, H. R. D. H. (2004). MBA PerioPathways etiology fast-forwarded: The host-bacterial interaction theory and the risk continuum. Contemporary Oral Hygiene, 16–20.

21. Fuchs, T. A., Abed, U., Goosmann, C. et al. (2007). Novel cell death program leads to neutrophil extracellular traps. J. Cell Biology, 176 (2), 231–241.

22. Jancar, S., Sanchez, C. M. (2005). Immune complex-mediated tissue injury: a multistep paradigm. Trends Immunology, 26, 48–55.

23. Kantarci, A., Van Dyke, T. E. (2002). Neutrophilmediated host response to Porphyromonas gingivalis. J. Int. Acad. Periodontol, 4, 4, 119–125.

24. Kessenbrock, K., Frohlich, L., Sixt, M. (2008). Proteinase 3 and neutrophil elastase enhance inflammation in mice by inactivating antiinflammatory progranulin. J. Clin. Invest, 118, 2438–2447.

25. Loeschel, W. J., Grossman, N. S. (2001). Periodontal disease as a specific, albeit chronic infection: Diagnosis and treatment. Clin. Microbiol. Rev, 14, 4, 727–752.

26. Logan, M. R., Odemuyima, S. O., Moqbel, R. (2003). Understanding exocytosis in immune and inflammatory cells: the molecular basis of mediator secretion. J. Allergy Clin. Immunology, 111 (5), 923–932.

27. Nagase, H., Woessner, J. F. (1999). Matrix metalloproteinases. J. Biol. Chem, 274, 31, 21491–21494.

28. Nathan, C. (2006). Neutrophils and immunity: challenges and opportunities. Nat. Rev. Immunol, 6, 173–182.

29. Pham, C. T. (2008). Neutrophil serine proteases fine-tune the inflammatory response. Int. J. Biochem. Cell Biol, 40 (6, 7), 1317–1333.

30. Von Kockritz-Blickwede, M., Nizet, V. (2009). Innate immunity turned inside-out: antimicrobial defense by phagocyte extracellular traps. J. Mol. Med., 87 (8), 775–783.

Login or Create
* Forgot password?