Hypercholesterolemic diet in periodontal health: effect on oxidative status and alveolar bone

ANTONA, M.E.,; RAMOS C.; ZAGO, V.,; FERREIRA MONTEGO, A.G.,; PEREZ ALCARAZ, I.B.,; GONZÁLEZ, P.M.,; PUNTARULO S.; FRIEDMAN S.M.; STEIMETZ, T.; MACRI E.V.

Mar del Plata

Otro; Reunión Anual de Sociedades de Biociencia 2019; 2019

Hypercholesterolemia(HC) is a risk factorfor CVD. Periodontitis (P) is an inflammatory disease that mightaffect the teeth supporting tissues and induce reactive species(RS) production in periodontal tissue. Cholesterol-rich dietsdecrease bone health. The objective of this study was to assessthe implications of an hypercholesterolemic diet on gingivaloxidative status and the alveolar bone loss in rats with andwithout P. Methods: Wistar rats (24) were assigned into 2groups: control (C) fed pellets, and high-cholesterol diet (HCD).After 3 weeks, 6 rats per group were euthanized (C0, HCD0) and6 animals per group were subjected to ligature-induced P and 72h later these rats (C72, HCD72) were euthanized. Blood wasdrawn for lipid profile. X rays were used for periodontal bonesupport measurements (PBS, %). Mandibles were processed withHematoxiline&Eosine. In interradicular bone, periodontalligament height (hPL) was measured. In gingival tissuehomogenate were determined the oxidation rate of 2?,7?dichlorofluorescein diacetate (DCFH-DA) (spectrofluorimetrycally)and catalase (CAT) content (enzymatic method). Results (mean±SD): HCD0 and HCD72 presented HC (p<0.01). In gingivaltissue, HCD increased DCFH-DA oxidation rate as compared tocontrols (HCD0: 13.9 ± 0.2, C0: 3.3 ± 0.2 u.a./min.mg protrespectively; p<0.001); and P produced increases in the dyeoxidation rate (HCD72: 23.2 ± 0.2, C72: 10.0 ± 0.5 u.a./min.mgprot respectively; p<0.001). CAT content increased by HCD ascompared to control fed rats (p<0.001), but remainedunchanged by P. In alveolar bone, PBS% decreased with bothHCD and P (p<0.01), and hPL was increased in HCD72 rats ascompared to controls (471 ± 56 and 325 ± 91 µm, p<0.003). HCand P are involved in dynamic events associated with RSproduction. The generation of oxidative stress would increasecellular damage and HC influenced gingival and alveolarhomeostasis and may induce the progression of P by increasingalveolar bone resorption.