Because of its ability to undergo MT, OL poses challenges for both diagnosis and management [11]. It is associated with a high risk of developing cancer either in an area near the lesion, in some other parts of the oral cavity, or head and neck region [12]. In etiological terms, OL is classified as idiopathic OL (with absence of causal factors), and tobacco-associated OL [13, 14]. There is a significant association between tobacco consumption and development of OL. The ingestion of tobacco is thought to expose the oral epithelium to free oxygen and nitrogen radicals which can impair antioxidant mechanisms. Elevated level of these free radicals presents as oral pre-cancerous and cancerous lesions. Additionally, alcohol has been shown to have a synergistic effect on growth of OL, but definitive evidence is still lacking [15].
In India, 4.5% adults consume betel quid with tobacco daily [8]. Recent report highlights that around 24% Indian adults consume areca nuts and a majority (14.2%) of them combine areca nut with tobacco [16]. These findings suggest a reason for high prevalence of OL in India. Individuals residing in MP (Central India) have high prevalence of tobacco and alcohol consumption [9, 10], but the prevalence of OL has not been assessed in large population. A previous study from MP assessed 1241 patients and reported an OL prevalence of 4.02% [17]. We assessed 9954 patients and observed a prevalence of 5.6%. Other studies from Northern (7.1%) and Southern (8.2%) parts of India have reported higher prevalence of OL [18, 19]. However, studies from other parts of India have reported lower prevalence (0.63–2.60%) [20, 21]. This variation in prevalence of OL could be attributed to differences in demographic patterns, cultural beliefs, and patterns of tobacco consumption among different people and different geographic areas.
Tobacco consumption in any form is the principal risk factor of OL. Various studies have reported a clear and significant association between tobacco consumption and OL [5, 22–24]. We observed that the history of smoking tobacco was significantly associated with the presence of OL and those having history of smoking were found be at 1.32 times higher risk of developing OL. Likewise, history of consumption of smokeless tobacco was significantly associated with the risk of developing OL and this risk was 318.6-times higher than those who did not consume smokeless tobacco. The risk of developing OL is related to the age of adverse habit initiation, and the type and amount consumed. While, Western countries report a significant association between OL and consumption of tobacco (both smoked and smokeless) and alcohol [24], Southeast Asian nations associate OL with betel quid consumption [25]. The action of various carcinogens, including tobacco depends on the duration of exposure. This fact highlights the higher prevalence of OL in older populations [23].
Alcohol consumption leads to accumulation of toxic ethanol metabolites, altered DNA repair mechanism, and raised cellular permeability, which results in increased cell entry of various carcinogens including tobacco (smoked/smokeless), thus highlighting the synergistic effect of alcohol and tobacco consumption [26]. An early study from Southern India reported that alcohol consumption was an independent risk factor and history of ever alcohol consumption was significantly associated with the risk of developing OL in non-smokers (2.1-times) and non-chewers (1.8-times) [27]. In another study, alcohol consumption resulted in significantly higher OL risk in both never-users and current users of tobacco. Compared to non-drinkers, drinkers of 0.1 to 14.9 g/d, 15 to 29.9 g/d, and ≥30 g/d had a relative risk of 1.7, 2.9, and 2.5, respectively [28]. While, a study concluded that alcohol is a promoter rather than an initiator, as it was not associated with the development of OL [29]. In our study, though history of alcohol consumption was associated with 1.15-times higher risk of developing OL, it did not achieve significance level. Likewise, a meta-analysis reported that alcohol consumption was associated with 1.54-times higher risk of developing OL; however, this was not significantly associated [5]. These contradictory findings need to be confirmed in prospective studies with large sample size.
The prevalence of OL is higher among males than females and increases with advancing age. It usually affects individuals over 40 years of age [30]. We observed a significant association between the presence of OL and adult age group. Additionally, patients aged ≥50 years had 1.08-times higher risk of developing OL than those aged <50 years. Other studies have reported similar findings [5, 22]. The median age of smokers with OL is reported to be significantly less than in non-smokers [31]. Likewise, we observed that the prevalence of OL increased with increase in age, from 0.7% (in patients aged 18-38 year) to 21.3% (in patients aged >70 year). This could be attributed to the fact that early and chronic exposure to adverse habits (consumption of tobacco and/or alcohol) results in higher prevalence in elderly age group.
Male sex is a risk factor for developing OL [5]. We observed that male sex was significantly associated with the presence of OL and female sex was found to be a protective factor, with 0.77-times less risk of developing OL. This could be attributed to the cultural differences, as males are more commonly involved in practicing adverse habits than females [9]. OL and other potentially oral malignant lesions are predominant among males, particularly in chronic smokers [22]. Additionally, in our study, enrolled patients were predominantly males (1.3:1) and the prevalence of OL was also more in males than females (3.9:1). Thus, higher proportion of males than females could have affected the prevalence of OL.
This was a prospective study involving a large population. However, our study had certain limitations. First, we relied on the presence and absence of adverse habits and thus, could not comment on the effect of type, amount, and duration of adverse habits (both tobacco and alcohol). Second, we confirmed the diagnosis clinically, and histopathological examination of lesion was not performed. Third, we did not follow-up the patients, thus we could not check for MT of OL. Finally, we excluded the patients with known history of oral cancer, so we did not evaluate the effect of adverse habits on development of oral cancer.