Journal of Bone Research
Open Access

Relation between Chronic Consumption of Alcohol and Periodontitis Risk Factors

Jian Zhang^{* *}Correspondence: Jian Zhang, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Maryland, USA, Email:

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Description

A complex infectious-inflammatory disease, including social and behavioral factors like smoking and alcohol misuse, as well as local and systemic risk factors, might have an impact on the evolution of periodontitis. When deciding on a course of treatment and outlook, it is crucial to evaluate periodontitis risk factors. There is some evidence that alcohol abuse increases the risk of periodontal disease, according to numerous clinical studies that have assessed this link. Based on those findings, a meta-analysis came to the conclusion that drinking alcohol was a behavioral risk factor for periodontal disease because it was linked to a higher chance of developing the condition.

The majority of people's lifestyles include drinking alcohol, which is a behaviour that is socially acceptable. The World Health Organization (WHO, 2014) rates alcohol misuse as the third biggest cause of mortality globally, trailing only cancer and cardiovascular disease. Systemic health is negatively impacted by alcohol consumption, with liver cirrhosis being the most prevalent chronic disease caused by alcohol hepatotoxicity. Additionally, alcohol has a direct impact on the immune system, raising the danger of serious infections and changing the metabolic processes that maintain bone homeostasis. Together with the pathology of periodontitis, these effects have the potential to hasten the process of alveolar bone resorption, which will have an impact on the inflammatory response mechanism of periodontitis.

It has been proposed that the harmful effects of long-term alcohol use are dose-dependent. Clinical Attachment Loss (CAL) and weekly alcohol use (5, 10, 15, or 20) are significantly correlated. The frequency of alcohol use was correlated with a higher incidence of periodontitis. According to this, the prevalence of periodontitis was 53% in alcohol-dependent people, and it was respectively 17.2%, 24.0%, and 29.6% in occasional, moderate, and heavy alcoholics. A new study using information from the National Health and Nutrition Examination Survey (NHANES, 2009–2012) found that drinking alcohol was linked to a higher risk of developing periodontitis. However, when compared to people who did not drink alcohol, those who drank one drink per week had the same risk of developing periodontitis. Uncertainty still exists regarding the precise dosage needed to impact the pathophysiology of periodontitis.

Further research is needed to determine how persistent alcohol use impacts the development of periodontal disease. Studies have revealed that persistent alcohol use can have an impact on bone tissue's calcium and phosphorus levels as well as hinder bone healing. Chronic alcohol use increased osteoclastogenesis and the inflammatory response, which had a major impact on how severe apical periodontitis was. As a result, such occurrences brought on by prolonged alcohol use may jeopardize the stability of periodontal tissue. Furthermore, a study using animal models discovered that alcohol consumption at low concentrations (5%) had no effect on alveolar bone loss in the context of causing periodontal disease, indicating that alcohol's negative effects are concentration-dependent. To better understand how persistent alcohol use can affect the development of periodontal disease, more experimental investigations are required.

Depending on when it is consumed, alcohol can affect immunological responses. The anti-inflammatory effects of acute consumption result from a decrease in pro-inflammatory cytokines and a rise in anti-inflammatory cytokines, which raises the possibility of a protective impact. Alcohol has the reverse effect with chronic usage, causing levels of pro-inflammatory cytokines such as Tumour Necrosis Factor (TNF), Interleukin 1 (IL-1), and Interleukin 6 (IL-6) to rise and anti-inflammatory cytokines to fall. In a dose-dependent manner, alcohol enhanced the inflammatory response in PE. Chronic alcohol use at various concentrations, regardless of concentration, worsens EP by amplifying the local inflammatory response and promoting alveolar bone resorption.