Influence of a High-fat Diet in the Progression of Apical Periodontitis.

INTRODUCTION: This study evaluated the effects of a high-fat diet (HFD) on the progression of apical periodontitis (AP) in rats. METHODS: Eight-week old Wistar rats (N = 24) were included in this study. Half of the animals received an HFD and the other half a control diet (CD). AP lesions were induced 8 weeks later by creating pulp exposure of the mandibular left first molars. The animal's body mass was verified on a weekly basis. After 21 and 40 days, the animals were sacrificed. Blood was collected for biochemical tests, and the liver was removed for hepatic triglycerides analysis. The left hemimandibles were removed, radiographed, and then prepared for histologic evaluation. The right hemimandibles (region near molars) were removed for bone mineral density analysis by dual-energy X-ray absorptiometry. RESULTS: Radiographs showed that AP lesions were significantly larger in the HFD group compared with the CD group (P < .05). Histologic analysis confirmed that the AP lesions were larger and revealed a more severe inflammatory infiltrate in the HFD group. Bone mineral density was reduced in the HFD group compared with the CD groups (P < .05). The HFD resulted in a significant increase in body mass (P < .05), liver mass (P < .05), relative liver mass (P < .05), and hepatic triglycerides (P < .05). The levels of triglycerides and very-low-density lipoprotein were significantly higher in the 40-day HFD group compared with the 21-day HFD and 21- and 40-day CD groups (P < .05). CONCLUSIONS: Findings suggest that an HFD can influence the progression and severity of AP.

Cigarette smoke impairs granulosa cell proliferation and oocyte growth after exposure cessation in young Swiss mice: an experimental study.

BACKGROUND: Cigarette smoke is associated with decreased female fertility, causing damage to ovarian function and disturbing follicle development. However, the effects of cigarette toxicants on ovarian function depend on duration and intensity of exposure. The aim of this study was to assess the effects of brief, intense exposure to tobacco smoke on granulosa cell number, oocyte growth, and follicle size during puberty in female Swiss mice. METHODS: Ten female Swiss mice aged 35 days were exposed to tobacco smoke from 3R4F reference research cigarettes. They were exposed to an automatic smoking machine 8 h/day, 7 days/week for 15 days. Ten age-matched controls were kept in a different room and exposed to ambient air. At the end of 15 days, five mice in each group were euthanized and the ovaries were analyzed for follicular morphometry and granulosa cell count. The remaining animals were kept for an additional 30 days for further analysis as an ex-smoker group and control group. Comparison between the two groups was evaluated by the Student's t-test or a two-way ANOVA followed by Bonferroni post-test was applied for multiple comparisons. RESULTS: We found that cigarette smoke impaired antral follicular growth even after exposure cessation (p < 0.001). Both smoking and ex-smoking groups exhibited similar follicle diameter. However, at the same follicular stage, the number of granulosa cells was smaller in the ex-smoking group compared to smoking animals (p < 0.001). This was associated with increased oocyte diameter in ex-smoking animals compared to smoking animals (p < 0.01). CONCLUSIONS: The negative effects of cigarette smoking seem to last even after exposure has been interrupted. Moreover, brief exposure during puberty may induce silent oocyte disruption, which could in turn lead to decreased fecundity rates.