Abstract
This study evaluated the effects of the chronic consumption of different concentrations of alcohol on the experimental periodontitis (EP). 160 rats were divided into 4 groups: (EP-NT) rats with EP and no alcohol exposure; (EP-A14) rats with EP exposed to 14% alcohol; (EP-A25) rats with EP exposed to 25% alcohol; (EP-A36) rats with EP exposed to 36% alcohol. The animals from the EP-A14, EP-A25 and EP-A36 groups were subjected to different concentrations of alcohol 30 days before EP induction. The histological characteristics, percentage of bone in the furcation (PBF) and bone metabolism in the furcation region were evaluated. The PBF and tartrate-resistant acid phosphatase (TRAP) data were subjected to statistical analysis. The EP-A14, EP-A25 and EP-A36 groups had lower PBFs compared with the EP-NT group. A more severe inflammatory process and a greater number of TRAP+ cells were also observed. In the EP-A14, EP-A25 and EP-A36 groups, the inflammatory process became more severe as the ingested alcoholic concentration increased. An increase in RANKL immunolabeling and a significantly higher number of TRAP+ cells were also observed. We conclude that chronic alcohol consumption increases the severity of experimental periodontitis in a dose-dependent manner by increasing the magnitude of local inflammatory responses and stimulating alveolar bone resorption.
Highlights
Periodontitis is a multifactorial infectious-inflammatory disease [1], and its progression may be affected by local and systemic risk factors, including social and behavioral factors such as smoking and alcohol abuse [2, 3]
According to a table generated by a computer program, the animals were divided into the following groups: an experimental periodontitis (EP)-NT group (n = 40), normal rats with EP; an EP-A14 group (n = 40), rats with EP that were exposed to alcohol at a concentration of 14% (v/v); an EP-A25 group (n = 40), rats with EP that were exposed to alcohol at a concentration of 25% (v/v); and an EP-A36 group (n = 40), rats with EP that were exposed to alcohol at a concentration of 36% (v/v)
The EP-A14, EP-A25 and EP-A36 groups showed higher levels of AST at day 0 compared to baseline (p 0.05)
Summary
Periodontitis is a multifactorial infectious-inflammatory disease [1], and its progression may be affected by local and systemic risk factors, including social and behavioral factors such as smoking and alcohol abuse [2, 3]. The assessment of risk factors associated with periodontitis is of great importance when determining treatment and prognosis. Many clinical studies have evaluated the relationship between alcohol abuse and the risk of periodontal disease and have reported some evidence of an association [4,5,6,7,8,9].
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