Chronic alcohol consumption increases pulpal inflammation and impairs tertiary dentin formation in rats after direct pulp capping

To evaluate the prolonged and excessive effects of alcohol consumption on the inflammatory response and tissue mineralization in rat molars undergoing a direct pulp capping (DPC). Twelve Wistar rats were randomly assigned to Water (water as hydration source) or Alcohol (gradually increasing alcohol solution reaching 20% by day 14 and maintained until day 56) groups. On day 28, the pulp tissue of the left or right first upper molars was exposed and capped with a bioceramic reparative material, followed by sealing with glass ionomer cement. After capping, the following experimental groups were formed ( n = 6): Water-DPC and Alcohol-DPC. Contralateral untreated molars served as controls. Pulp responses were assessed by histology and immunohistochemistry for inflammatory and mineralization markers. Data were analyzed using the Mann–Whitney U- test ( P <.05). Chronic alcohol intake significantly reduced body weight compared to Water-group ( P <.05). The Alcohol-DPC group had intense inflammatory response, increased tissue disorganization, and pulp tissue necrosis compared to the Water-DPC group, which had mild inflammation and mainly partial tissue disorganization ( P <.05). Tertiary dentin formation was significantly greater in the Water-DPC group, with collagen fiber deposition, whereas Alcohol-DPC had minimal or no tertiary dentin formation beneath the exposure site. IL-1β immunolabeling was stronger in Alcohol-DPC than in Water-DPC group ( P <.05). Both experimental groups had an exacerbated DSPP immunolabeling beneath the exposed area ( P >.05). Rats subjected to alcohol exposure exhibited impaired dental pulp repair after capping, leading to increased inflammation, tissue disorganization, pulp necrosis, besides elevated IL-1β immunolabeling. Although chronic alcohol consumption appears to impair tertiary dentin formation, DSPP immunolabeling was not influenced. Alterations in nutritional intake, metabolic status, and stress related to the protocol may also have contributed to these findings.