This is the first systematic examination of the combined exposure to depression, smoking, and alcohol, as well as their interaction with periodontitis. On gender and age stratification, significant multiplicative interactions were identified for smoking-depression, drinking-depression, and smoking-drinking. Results showed that moderate drinking reduced the risk of periodontitis and significantly interacted with depression, whereas heavy drinking significantly increased the risk of periodontitis.
Our study found that cigarette smoking served as a risk factor for periodontal diseases [9]. Results showed that both former (OR: 1.16, 95% CI: 1.02 to 1.32) and current smokers (OR: 1.67, 95% CI: 1.37 to 2.03) were more likely to develop periodontitis than non-smokers in the general population (PHQ-9 score < 10). This result was inconsistent with previous studies, which indicated no significant difference between never-smokers and ex-smokers regarding periodontitis risk [24, 25]. The proposed explanation was that smoking effects on inducing systemic inflammation can continue for months or years despite the fact that cigarette smoke extracts have been removed from the body after smoking cessation [9]. It has been further reported that until approximately 6 years after quitting smoking, the smoking-related risk for periodontitis will diminish and approach to that of never-smokers [26]. Importantly, our results futher found that smoking interacted with drinking on the prevalence of periodontitis. In line with previous studies, these results indicated the relationship between cigarette smoking and periodontitis risk varied with alcohol assumption increment [17].
Extensive studies have reported the effect of smoking-depression interaction on cardiovascular health [27, 28]. To our knowledge, this is the first time that the interaction between smoking and depression has been indicated in periodontitis. Previous evidence have demonstrated that psychological stress and smoking may serve as mediators for the prevalence of periodontal diseases [29]. Both biological mechanisms,such as inflammatory responses [9] and behavioral theories have been proposed to explain how smoking and depression independently influenced periodontitis. The mechanisms underlying the correlations between smoking and periodontitis shared similarities with those linking depression to periodontitis [9]. One proposed explanation for this synergistic effect is that smokers with a history of depression can have a prolonged and/or augmented inflammatory response since the anti-inflammatory response capability may be downregulated by depression condition. Then, a hyper-inflammatory response can be reinforced by smoking status, thereby accelerating the progression of periodontitis [9].
Further results showed that the smoking-depression interaction differed by age and gender. This interaction was only significant in males not females due to the exceptionally low smoking rates among women in this study, particularly in older women. Additionally, depressed men frequently failed to maintain healthy behaviors, such as smoking cessation [30]. Similarly, this association was more pronounced in aged populations. The aging effect, which increased susceptibility to periodontitis, may be attributed to the declining immunity ability brought on by aging, as well as increased cumulative exposure to smoking and depression over time [31]. Considering our findings, more attention should be paid to the screening and prevention of periodontitis in depression subjects and depression in periodontitis patients by collecting comprehensive information regarding the smoking history and depressive symptoms.
This is the first work to reveal a J-shaped relationship between drinking and periodontitis. It is well-acknowledged that drinking could either exacerbate or protect against oral diseases. This depended on the quantity, frequency, timing and pattern of alcohol consumption [32]. Here, we explored the role of the dose and frequency of alcohol consumption in periodontitis risk. Our results demonstrated that heavy drinking increased the risk but low drinking reduced the risk of periodontitis. A similar J-shaped relationship, indicating an inverse relation at lower intake levels (≤ 12.5 g/day) and a positive association at high exposure levels (≥ 50 g/day), was also observed in all cancer mortality and other diseases [33]. Light to moderate alcohol consumption may help to enhance the individual immune system defences against periodontitis by lowering systemic inflammation [32]. However, the cumulative average intake should be constrained since the function of immune cells, such as T-cells and neutrophils may be affected by alcohol consumption when alcohol intake exceeded a certain threshold [34]. Subsequently, the risk for infectious complications including periodontitis can be elevated due to the excessive alcohol intake [11]. Overall, these may explain our results and help us understand the complicated relationship between alcohol consumption and the periodontitis progression and its concurrent prevention.
Notably, populations with depression also showed the J-shaped association between drinking and periodontitis. It has been shown that low drinkers (< 14 g/d) reduced the risk by 45%, whereas heavy drinkers (> 56 g/d) increased the risk by 94% in the depression population. These results may be explained by the negative additive interaction. It has been speculated that drinking and depression may have antagonistic effects on each other. Previous research has demonstrated the complicated interaction between depression and drinking. It is reported that drinking can both exacerbate and relieve the stress related to depression [10]. Another potential hypothesis is that depressed individuals who do not drink have more tendency to select smoking as a coping behaviour [28]. As with many diseases, smoking is a stronger risk factor for periodontitis than drinking [9] as the the former effect can be strengthened by the complex mixture of tobacco smoke and subdivided into primary and passive second-hand effects. In line with these findings,we confirmed the J-shaped correlation between drinking-depression interaction and periodontitis risk. These evidence further strengthen and validate the dose-response relationship between drinking exposure and periodontitis risk, indicating once more caution is needed with regard to any level of drinking during depression condition.
Our study has some strengths. First, we analyzed a large-scale population and examined the complicated interactive relationship between different influencing factors rather than fouse on only one single factor. Second, data from the NHANES were selected using a complex, multi-stage probability sampling design fully representative of the general population across the United States. Third, multiple confounding factors were considered in this study, including sociodemographic characteristics and history of diabetes. There are some limitations to this study. First, no causality can be inferred from the data due to the cross-sectional nature of the study. Therefore, further study is needed to solve geographic restrictions from a large multinational population.