Naslov (srp)

Uticaj sojnih razlika na patogenezu periapikalnih lezija zuba u dva soja pacova Dark Agouti i Albino Oxford

Autor

Živanović, Suzana, 1991-

Doprinosi

Ljujić, Biljana, 1974-
Lukić, Miodrag L., 1941-
Čolić, Snježana, 1963-
Popović, Milica, 1965-
Gazdić Janković, Marina, 1987-
Miletić-Kovačević, Marina, 1984-

Opis (srp)

Uvod Periapikalne lezije nastaju kao posledica dejstva mikroorganizama i njihovihprodukata iz inficiranog kanala na periapikalno tkivo. Ova inflamacija možestimulisati destrukciju periapikalnih tkiva i uzrokovati resorpciju alveolarnekosti pri čemu nastaje periapikalna lezija. Periapikalne lezije nemaju uvek istekarakteristike. Ćelije i medijatori inflamacije koje su povezani sa razvojem iveličinom periapikalnih lezija nisu u potpunosti razjašnjeni. Genetska podlogaeksperimentalnih životinja može uticati na patogenezu bolesti. Dark Agouti i AlbinoOxford pacovi se razlikuju u osetljivosti na inflamatorne stimuluse i na indukcijueksperimentalnih autoimunih bolesti.Cilj Cilj ove studije je bio da ispita efekte razlika u imunološkoj reaktivnosti naindukciju periapikalnih lezija.Materijal i metode Periapikalne lezije su indukovane kod DA i AO pacovaizlaganjem pulpe desnih mandibularnih molara oralnoj sredini. Žrtvovanje životinjaje urađeno 21 dan nakon indukcije periapikalnih lezija, mandibule su izolovane ipripremljene za radiografsku i patohistološku analizu. Na ćelije periapikalnihlezija primenjen je PCR u realnom vremenu i protočna citometrija. Nivo citokina iparametra okisidativnog stresa su mereni iz prikupljenih uzoraka krvi i supernatantahomogenata periapikalnih lezija. Dobijeni rezultati analizirani su u softverskomprogramu za statističku analizu podataka Statistical Package for Social Sciences v23.0.Statistička analiza je urađena parametarskim One-Way ANOVA i T- testom nezavisnihuzoraka i neparametarskim testovima Kruskal-Wallis H i Mann-Whitney U zavisno odnormalne raspodele podataka. Statistički značajna razlika u dobijenim vrednostimaizmeđu grupa je smatrana kad je r<.05.Rezultati Radiografskom i patohistološkom analizom je pokazano da su DA pacovirazvili veće periapikalne lezije u odnosu na AO pacove. Infiltracija neutrofilimai makrofagima je bila značajno izraženija u periapikalnim lezijama DA pacova.Protočnom citometrijom je pokazan veći procenat T ćelija, kao i INF-γ CD3+CD4+, IL17 CD3+CD4+, i IL-10 CD3+CD4+ ćelija u periapikalnim lezijama DA pacova.Ekspresija gena koji kodiraju citokine IL-1β, INF-γ, i IL-17 je bila veća kod DA pacova.Ekspresija RANKL je bila značajno veća kod DA pacova, dok je ekspresija OPG bilaveća kod AO pacova. RANKL/OPG odnos je značajno veći u DA pacova. Patološkiproces u periapikalnim lezijama se reflektuje i na sistemski nivo proinflamatornihcitokina: TNF-α i IL-6 je veći kod DA pacova. Markeri oksidativnog stresa usistemskoj cirkulaciji i supernatantu homogenata periapikalnih su izraženiji u DApacovima.Zaključak DA pacovi su razvili veće periapikalne lezije u odnosu na AO pacove.Genetski uslovljena razlika u imunološkoj reaktivnosti snažno utiče na patogenezueksperimentalnih periapikalnih. Poznavanje genetski zasnovanih razlika možedoprineti razumevanju mehanizmima koji povećavaju inflamaciju i progresijuperiapikalnih lezija.

Opis (srp)

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Opis (eng)

Introduction Periapical lesions develop as a consequence of microorganisms and theirproducts from the infected canal on the periapical tissue. This inflammation can stimulate thedestruction of periapical tissues and cause resorption of the alveolar bone, developing periapicallesion. Periapical lesions do not always have the same characteristics. Inflammatory cells andmediators associated with the development and size of periapical lesions have not been fullyelucidated. The genetic background of experimental animals may influence the pathogenesis ofthe disease. Dark Agouti and Albino Oxford rats differ in their sensitivity to inflammatorystimuli and in the induction of experimental autoimmune diseases.Aim The aim of this study was to determine the effects of differences in immune reactivity onthe induction of periapical lesions.Material and methods Periapical lesions were induced in DA and AO rats by exposing thepulp of the right mandibular molars to the oral environment. Animal sacrifice was performed21 days after induction of periapical lesions, mandibles were dissected and prepared forradiographic and pathohistological analysis, as well as for the real-time PCR and flowcytometry. Cytokine levels and oxidative stress parameters were measured from collected bloodsamples and supernatant of homogenous periapical lesions. The obtained results were analyzedin the software program for statistical data analysis Statistical Package for Social Sciencesv23.0. Statistical analysis was performed by parametric One-Way ANOVA and T-test ofindependent samples and nonparametric tests Kruskal-Wallis H and Mann - Whitney Udepending on the normal data distribution. A statistically significant difference in the obtainedvalues between the groups was considered when p<.05.Results Radiographic and pathohistological analysis showed that DA rats developed largerperiapical lesions compared to AO rats. Infiltration by neutrophils and macrophages wassignificantly more pronounced in periapical lesions of DA rats. Flow cytometry showed ahigher percentage of CD3 + cells, as well as INF-γ CD3 + CD4 +, IL-17 CD3 + CD4 +, andIL-10 CD3 + CD4 + in periapical DA lesions. Expression of genes encoding the cytokines IL1β, INF-γ, and IL-17 was higher in DA rats. RANKL expression was significantly higher inDA rats, while OPG expression was higher in AO rats. The RANKL/OPG ratio was shown tobe higher in the periapical lesions of DA rats. The pathological process in periapical lesions isalso reflected on the systemic level of proinflammatory cytokines: TNF-α and IL-6 are higherin DA rats. Markers of oxidative stress in the systemic circulation and periapical homogenatesupernatant are more pronounced in DA rats.Conclusion DA rats developed larger periapical lesions compared to AO rats. The geneticallydetermined difference in immune reactivity strongly influences the pathogenesis ofexperimental periapical lesions. Knowledge of genetically based differences may contribute tounderstanding the mechanisms that increase inflammation and progression of periapical lesions.

Jezik

srpski

Datum

2021

Licenca

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Creative Commons CC BY 3.0 AT - Creative Commons Autorstvo 3.0 Austria License.

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Identifikatori