Tobacco use and its association with oral disease is a major contributor to the global oral disease burden.1,12,13 Tobacco is mainly used either in a smoking form or a smokeless form. Periodontitis is chiefly regarded to be a slowly advancing condition. However, in the presence of environmental and systemic elements like diabetes it enhances the progression of the disease process.1 In India, tobacco is consumed as beedis (34%), snuff (2%), cigarettes (30%), hookah (9%), chewing tobacco (19%), cigars and cheroots (5%).14.
The association between periodontitis and smokeless tobacco has also been the topic of meticulous investigations. The interconnection between oral cancer and tobacco consumption is well-established in the literature. However, very few studies present the relation to periodontal health.
Beedi smoking is a widespread mode of tobacco intake in Southern parts of Asia, considering to nearly one-third of the tobacco yielded in India for smoking.15 Beedis are manufactured by rolling a rectangular, dried piece of tendu leaf with 0.15–0.25 g of sundried, flaked tobacco. These tobacco-filled leaves deliver more tar, carbon monoxide and nicotine and bear an increased potential of oral cancers. (16,17,18)
The other form that is more prevalent is smokeless tobacco which is employed to elucidate tobacco that is taken without heating or burning while being consumed. The smokeless forms of tobacco are predominant in India and include various forms like mishri, betel quid chewing, khaini, paan, gutka, and snuff. 19
A universally utilized biochemical approach to tobacco smoke exposure is cotinine, a proximate metabolite of nicotine. It can be estimated in saliva, blood, or urine, and is regarded as a precise estimate of smoking. Cotinine emerges by cytochrome P450-mediated C-oxidation of nicotine. This product is very stable and has a prolonged half-life of average 16 hours and is perpetually constant as compared to measuring nicotine directly.9
Cotinine is detectable in the body fluids of active and passive smokers. Cotinine can be measured by Gas-Liquid Chromatography (GLC), RadioImmunoAssay (RIA) or Liquid Chromatography (LC) in various body constituents, including urine, blood, hair, saliva, amniotic fluid, and cervical mucus.20 This study uses competitive inhibition of Enzyme-Linked Immunosorbent Assay (ELISA) for estimation of cotinine as it’s the most reliable method. Asha et al in 201521 concluded that estimation of salivary cotinine by immunochromatographic assay is an effective means for observing nicotine addiction in tobacco consumers.
Bernert et al. stated that the serum cotinine levels were very closely associated to unstimulated saliva (> by 4%) than to stimulated saliva (> by 41%). Thus, unstimulated saliva is a more dependable biochemical marker.22
Beedis are an alternate type of cigarette, with more nicotine content.23 Thus the mechanism of periodontal destruction might be same for beedi and cigarette smoking with enhanced effects.
Beedi smoking had a positive impact on gingival health and this condition further declined on long-term use. This finding is in accordance with the description by Newburn et al.24 Gingival health assessed by gingival index has a negative impact on tobacco chewing per day and for number of years chewed. This may be attributed to the report that salivary IgA levels are higher in tobacco chewers compared to smokers in unstimulated whole saliva thus providing a protective effect on gingival tissue.25
Longer duration of smoking (years) showed a significant correlation with plaque index according to Aziz et al26 studies. The present study also demonstrated that plaque index increased over the years as tobacco was chewed accumulating calculus supragingivally and subgingivally on the tooth surface.
Lower gingival bleeding in smokers and tobacco chewers is rationalized as because of the presence of nicotine - a source of peripheral blood vessel vasoconstriction 27 which was also noted in the present study. The present study also found that bleeding is suppressed after long-term use of beedi (mean-0.35, r-0.02). This agreed with the analysis that the extent of smoking in years, concealed the effect on gingival bleeding on slight probing (− 0.200 and 0.997).26
Generally, the rationale behind the increased CAL and PPD in patients subjected to tobacco smoke is double. According to the literature, there is no direct alteration of bacterial flora between non-smokers and smokers.28 Hence, the pernicious outcomes of tobacco on the host arise through dual channels. Firstly, it systemically brings about a variation of the immune response. Secondly, it functions locally by liberating vasoactive substances and cytotoxic metabolites. These are created by tobacco combustion and successively affect the vascular response and fibroblasts.29
Periodontal pocket and clinical attachment level had a negative impact on number of times chewed per day but the negative impact decreases as the number of years chewed increases. This agrees with an older systematic review which stated smokeless tobacco had higher levels of PGE2 and lymphocyte (B and T) and thus may have an initial protective mechanism as the tobacco is chewed.30 The composition of tobacco chewed might also have an impact on periodontium. Tobacco is chewed mostly with areca nut. Studies have stated that betel/areca nut chewing had a shielding effect on tooth loss (TL) and clinical attachment loss (CAL)31 The true effect of nicotine might be reduced.
Another explanation is that slaked lime, areca nut, and ST surge the formation of ROS in the periodontal tissues, which escalates alveolar bone loss and inflammation by reducing endothelial nitric oxide synthase expression and forming pro-inflammatory cytokines as established by Seyedroudbari and Khan, 1998; Haque et al, 2000; Chang et al, 2009.32.
Contrary to periodontal destruction being more in beedi smokers it was found that cotinine level was higher in tobacco chewers which agreed with a study done for urinary cotinine level detection in beedi smokers and tobacco chewers.33 However the cotinine value is found to be higher in both the groups compared to a no the cut of point. According to Jarvis et al9, an optimal salivary or plasma cotinine cut-point of 15ng ml− 1 was decided to differentiate non-smokers from smokers.
The difference between beedi smoking and tobacco chewing can also be accredited to the truth that the nicotine level varies between each beedi smoked and the amount of tobacco chewed. Several factors play a role in the quantity of cotinine being estimated. For Beedi smokers’ consumption of nicotine during smoking relies on puff volume, the extent of dilution with room air, depth of inhalation, intensity, and rate of puffing. In tobacco chewers, the amount of tobacco taken each time, the duration for which it is placed in the mouth, and the extent of dilution with other products like slaked lime or areca nut. In general, the cotinine concentration also depends on the time when the saliva was collected after the last smoke or chewed and on the salivary flow rate. These parameters can also influence the results but couldn’t be taken into consideration as it was not practicable.
Yet tobacco chewers had a greater gingival and plaque index when compared to gingivally healthy subjects. Tobacco chewing also affected the periodontium with eleveated clinical attachment loss and probing pocket depth relative to its lesser sulcus bleeding index. Kumar et al34 concluded that half of the subjects who chewed tobacco had periodontal destruction and 66% had a loss of attachment indicating a deteriorated oral hygiene, gingival status, and periodontal status. This finding is in correlation to the study done by Warad et al35 who concluded that all their study subjects had poor oral hygiene status with increased periodontal destruction.
This study based on the obtained clinic-biochemical parameters can be inferred that both beedi smokers and tobacco chewers has adverse effect on gingival and periodontal health. Beedi has more adverse effect on clinical parameters when compared to tobacco chewers. Salivary cotinine is a reliable biomarker for any kind of tobacco consumption. The obtained salivary cotinine was slightly higher in tobacco chewing. Number of beedi smoked or tobacco chewed per day and number of years it’s been consumed also has effect on the clinico-biochemical parameters. A large-scale study should be carried out to obtain a correlation to the number of beedi smoked or chewed to clinicobiochemical parameters. A detailed study is yet to be done regarding the pathway of destruction of periodontium by beedi smoking and tobacco chewing at a molecular level.