Detrimental effects of chronic sugar‐sweetened carbonated soft drink consumption on inflammatory response and the size of apical periodontitis: An animal‐based study

This study aimed to evaluate the effects of chronic consumption of two sugar-sweetened carbonated soft drinks - one containing caffeine (Coca-Cola®) and one without (Sprite®) - on the progression of periapical lesions and the levels of pro-inflammatory cytokines in rats. Twelve Wistar rats were divided into three groups (n = 4): Control group, Coca-Cola group and Sprite group. The rats in Coca-Cola and Sprite groups were given ad libitum access to their respective soft drinks for 3 months, while the Control group received filtered water. After 2 months of consumption, the pulps of the lower left first molars were exposed for 28 days to induce periapical lesions. Following euthanasia, the jaws were removed, and the periapical lesions were assessed using micro-computed tomography imaging. Blood samples were collected to analyse the pro-inflammatory cytokines IL-1β, IL-6, IL-2, IL-17 and TNF-α via Luminex assay. Non-parametric data were analysed using the Kruskal-Wallis test followed by Dunn's test, while parametric data were analysed using one-way ANOVA followed by Tukey's test (p < 0.05). Both the Coca-Cola and Sprite groups exhibited periapical lesions with significantly greater volume and diameter compared to the Control group (p < 0.05). Additionally, both soft drink groups had significantly higher levels of IL-1β, IL-6 and IL-2 compared to the Control group (p < 0.05). The Sprite group displayed significantly higher levels of IL-1β than the Coca-Cola group (p < 0.05), while the Coca-Cola group showed significantly elevated TNF-α levels compared to both the Control and Sprite groups (p < 0.05). No significant differences in IL-17 levels were observed among the groups (p > 0.05). The chronic consumption of sugar-sweetened carbonated soft drinks, regardless of caffeine content, has detrimental effects on the inflammatory response and progression of apical periodontitis in rats.