ANALYSIS OF THE EFFICIENCY OF COMPLEX TREATMENT OF PATIENTS WITH GENERALIZED PERIODONTITIS ACCORDING TO THE CHANGES IN THE ACTIVITY OF BLOOD SERUM ENZYMES
Introduction. The mechanisms of generalized periodontitis (GP) development and methods of its treatment remain obscure, so it is important to study changes in the activity of enzymes responsible for maintaining homeostasis, as well as the inclusion of medicines that regulate them into the complex treatment.
Aim of research is to study the influence of comprehensive treatment in patients with GP on the dynamics of the activity of indicator blood serum enzymes in different observation periods.
Methods. There were examined 29 people with a healthy periodontium and 143 patients with GP aged 19-45 years, somatically healthy, before, immediately after the treatment, after 6 and 12 months. Patients were divided into subgroups with chronic (A) and acute (B) course: IA and IB – the initial degree; IIA and IIB – the I degree; IIIA and IIIB – the II degree. The activity of lactate-dehydrogenase (LDG), arginase and sorbitol dehydrogenase (SDG) in blood serum has been studied. In addition to the basic periodontal therapy, the microalgal medicine Spirulina platensis was prescribed endogenously, and the paste with the same amount of spirulina powder and enterosorbent and 0.05% chlorhexidine bigluconate solution was exogenously prescribed.
Results. In patients with IA and IB subgroups, LDG activity has increased in 1.37- and 1.48-times (p1 <0.01; p1 = 0.001). Under the influence of treatment, it has decreased in all patients, especially after 6 months – in 1.33- and 1.50-times (p2<0.001), but after 12 months it has been increased more (p2> 0.05; p2 <0.05). Arginase activity in IA and IB subgroups has reduced in 1.23- and 1.31-times (p1<0.05; p1=0.005). Due to the therapy, it has increased immediately, after 6 and 12 months, respectively in 1.23- and 1.26-times; in 1.21- and 1.25-times, and in 1.20-1.23-times (p2<0.05; p2> 0.05; p1> 0.05). In subgroups IA and IB, SDG activity has increased in 1.15- and 1.17-times (p1> 0.05), and after the treatment it has decreased immediately in 1.14- and 1.16-times (p2 <0.05); later it increased, but differed slightly from the norm (p1> 0.05).
LDG activity in subgroups IIA and IIB has increased in 1.38- and 1.54-times (p1 <0.01; p1=0.001). After the treatment in subgroup IIA, it has decreased in 1.21-times immediately and after 6 months (p2<0.005), and a year later it has increased (p2>0.05; p1>0.05); in subgroup IIB it has decreased in 1.33-, 1.39- and 1.24-times (p2<0.05; p2<0.01; p2 <0.05 and p1> 0.05). In subgroups IIA and IIB, arginase activity has reduced in 1.32-times (p1=0.001). Immediately after the treatment in subgroup IIA, it has increased in 1.21-times (p2=0.005), and subsequently decreased (p2> 0.05). In the IIB subgroup, its increasing was 1.31-, 1.27- and 1.25-times (p2 <0.05), and the difference with the norm was insignificant. SDG activity in subgroups IIA and IIB has increased in 1.18- and 1.24-times (p1 <0.05; p1=0.01). After the treatment, it has decreased at all terms in both subgroups similarly: 1.13- and 1.16-times; 1.17- and 1.17-times; 1.12- and 1.10-times (p2 <0.05; p2 <0.05; p2> 0.05) and it differed slightly from normal one.
The largest increase in LDG activity was found in subgroups IIIA and IIIB – 1.45- and 1.62-times (p1≤0.001). As a result of therapy immediately, after 6 and 12 months it has decreased in 1.18- and 1.20-times; 1.26- and 1.23-times; 1.13- and 1.15-times (p2 <0.05; p2 <0.05; p2> 0.05; p1> 0.05). In subgroups IIIA and IIIB, arginase activity has reduced in 1.32- and 1.37-times (p1≤0.005). Treatment has increased the indices in group IIIA in 1.22-, 1.22- and 1.18-times (p2<0.05), and in group IIIB it immediately increased in 1.25-times and then decreased (p2 <0.05; p2> 0.05). The activity of SDG in IIIA and IIIB subgroups has increased in 1.31-times (p1=0.001). Under the influence of therapy in subgroup IIIA, it has decreased immediately, after 6 and 12 months in 1.17-, 1.22- and 1.13-times (p2 <0.05; p1> 0.05), and in subgroup IIIB it initially decreased, but after a year it has increased (p2>0.05) and the difference with healthy people became significant.
The altered indices of activity of enzymes studied in patients with GP did not exceed the reference values, but showed a violation of the enzyme system, which was regulated by the treatment. Prior to therapy, reliable (p<0.05-0.005) strong correlations were found between these parameters: LDG with SDG (r> 0.71) and arginase with SDG (r> -0.90). After the treatment, they were not found, six months later one correlation has restored, and a year later – both have restored, which indicates the necessity for the maintenance of endogenous therapy after six months.
Conclusion. GP is accompanied by significant (p1<0.05-0.001) changes in the enzymes activity in the blood: in LDG and SDG, it is increased, and in arginase – it is reduced. Comprehensive treatment has regulated these disorders, especially immediately and after 6 months (p2<0.05-0.001). The activity of LDG and SDG of the initial and the I degree immediately and after 6 months and arginase at the initial degree after 6 and 12 months became the closest to norm. In the GP of the II degree, the data of healthy people were not achieved, but the difference with them was insignificant (p1> 0.05).
2. Dmytryeva LA, Hurevych KH, Tebloeva L.M. Ymmuno-vospalytelnыi otvet pry parodontyte (obzor lyteraturы). Stomatolohyia dlia vsekh. 2010;4: 4-5. (Russian).
3. Volf HF, Rateitskhak ЭM, Rateitskhak K. Parodontolohyia / pod red. prof. H.M. Barera. M.: MEDpress-ynform. 2008: 548. (Russian).
4. Horbachёva YA, Orekhova L.Iu, Shestakova LA. Sviaz zabolevanyi vnutrennykh orhanov s vospalytelnыmy porazhenyiamy polosty rta. Parodontolohyia. 2009;3(52): 3-7. (Russian).
5. Borysenko AV. Vplyv zakhvoriuvan parodontu na zahalnyi stan orhanizmu. Zdorovia suspilstva. 2013; 1: 32-7. (Ukrainian).
6. Hajishengallis G. The inflammophilic character of the periodontitis-associated microbiota . Mol. Oral Microbiol. 2014;29 (6): 248-57.
7. Borysenko AV. Biokhimichni obgruntuvannia kompleksnoho likuvannia heneralizovanoho parodontytu. Suchasni medychni tekhnolohii. 2009;2:69-73. (Ukrainian).
8. Melnychuk HM, Rozhko MM, Zaverbna LV. Hinhivit, parodontyt, parodontoz: osoblyvosti likuvannia: navchalnyi posibnyk 5-te vyd., pererob. i dopovn. 2011: 328. (Ukrainian).
9. Khramova VA, Lystopad HH. Modyfykatsyia metoda opredelenyia po Cninaro y eё yspolzovanye dlia kolychestvennoho opredelenyia sыvorotochnoi arhynazы. Laboratornoe delo. 1973; 10:591-92. (Russian).
10. Bergmeytr HU. Methodos of Enzymatic Analysis. Acad Press. 1965.
11. Biokhimichnyi sklad ridyn orhanizmu ta yikh kliniko-diahnostychne znachennia / za red. O.Ia. Skliarova. 2004: 192. (Ukrainian).
12. Chorna IV, Vysotskyi IIu Klinichna enzymolohiia. Enzymodiahnostyka: navch. posib. Sumy: Sumskyi derzhavnyi universytet; 2013: 242. (Ukrainian).
13. Pavlotska LF. Biolohichna khimiia. Sumy: Universytetska knyha; 2009:379. (Ukrainian).
14. Pyndus TO. Patohenetychne obgruntuvannia kompleksnoho likuvannia ta profilaktyky uskladnen zakhvoriuvan parodonta pry metabolichnomu syndromi [avtoreferat]. Odesa; 2018:36. (Ukrainian).
15. Melnychuk HM, Kimak HB. Vplyv kompleksnoho likuvannia na pokaznyky vuhlevodnoho obminu u khvorykh na heneralizovanyi parodontyt osib molodoho viku. Klinichna ta eksperymentalna patolohiia. 2018. XVII;1(63): 56-60. (Ukrainian).
16. Luchak MV. Markery rannikh stadii ushkodzhennia hepatobiliarnoi systemy u ditei, yaki prozhyvaiut v rehionakh z riznym kharakterom zabrudnennia dovkillia [dysertatsiia]. Lviv; 2016:176. (Ukrainian).
17. Luchak MV. Markery rannoi diahnostyky hepatobiliarnykh rozladiv u ditei, yaki prozhyvaiut v ekolohichno nespryiatlyvykh rehionakh. Bukovynskyi medychnyi visnyk. 2019. 23; 4(92):67-72. (Ukrainian).
18. Ozer J, Rater M, Shaw M. The current state of serum biomarkers of hepatotoxicity. Toxicology. 2008. 245; 3:194-205.
19. Usharani G, Srinivasan G, Sivasakthi S, Saranraj P. Antimicrobial activity of spirulina platensis solvent extracts against pathogenic bacteria and fungi. Advan Biol Res. 2015; 9:292-8.
20. Sudha SS, Karthic R, Rengaramunjan J Athulya. Antimicrobial activity of spirulina platensis and aphanothece sp. on selected clinical bacterial isolates and its antioxidant activity. South As J Biol Sci. 2011; 1:87-98.
21. Berestov VA. Spyrulyna – nashe zdorove y dolholetye. 2002: 47. (Russian).
22. Kuprash LP., Chekman YS., Horchakova NA. Spyrulyna y zdorove. 2000: 76. (Russian).
This work is licensed under a Creative Commons Attribution 4.0 International License.