Effect of Salivary pH and Nicotine Dependence on Dental Caries and Erosion in Smokers and Non-smokers of Dakshina Kannada Population

Introduction

Dental caries is the most prevalent disease which affects human population. Although the prevalence of dental caries has significantly reduced, it is yet considered a major problem. The etiology and pathogenesis of dental caries are considered multifactorial.¹ Saliva has the function of moistening the oral cavity.² Saliva is a complex body fluid and is essential for maintaining the oral health.³ Nicotine, the chief ingredient present in tobacco acts on the cholinergic receptors of central nervous system and some other organs resulting in neural activation which leads to an altered salivary secretion.⁴ Alterations in the pH exerts definitive effects on oral and dental health of a person which seem to have a role in diagnosing wide range of diseases.⁵ Salivary pH is said to be a significant factor that plays an important role in the maintenance of oral health.⁶

During smoking, oral cavity is exposed to hot smoke, mainly by tobacco combustion. The heat or temperature of tobacco pyrolysis and cigarette combustion ranges between 300°C–1000ºC.^7,8 The hot smoke formed can increase temperature of enamel, altering the arrangement and topographical features of apatite crystals in the dental enamel.^7,9 In addition, the constituents or tar of cigarette smoke accumulates on the hard tissues and restorations/ rough prostheses.^7,10 There is no evidence that says cigarette smoking may influence enamel erosion.⁷

As salivary pH level is the most potential cause of dental caries in the smoking population,¹¹ evaluating the causative factors in saliva of individual’s at risk to dental caries can pave the way to make recommendations that will cater specific to individual needs.¹² Thus this study aimed to compare the pH, nicotine dependence and its association in developing dental caries and erosion in smokers and non-smokers in Dakshina Kannada.

Materials and Methods

In this study, a total of 60 males were included. This included 30 smokers and 30 healthy non-smokers (control group), who were selected from referees to the Oral medicine department. The participants included in the study group were male smokers with a habit of smoking for more than one year, and smoking at least one cigarette a day. Compromised patients with diseases, Gastroesophageal reflux disease (GERD), young smokers less than 20 years of age and smokers over 60 years, patients on medications affecting the salivary rate, were excluded from the study. After providing information about the study to the participants and obtaining informed consent from them, 2 mL of non-stimulated saliva was collected using standard methods. Subjects included were asked to avoid eating and drinking for at least two hours before the sample collection. Non-stimulated saliva was collected using spitting method, so that each patient evacuated all the gathered saliva in their mouth into a sterile test tube for ten minutes and 1-2 times per minute and the collected samples were sent to laboratory. Equiptronics (model- 610) pH meter was utilized for salivary pH measurement. After calibration, the electrode device washed with distilled water was placed in the test tube containing patient's saliva. The oral health assessment was done using WHO proforma (2013) and nicotine dependence index using Fagerstorm index. In order to avoid any errors in the pH of saliva, it was asked from all of the participants to avoid eating, drinking and smoking two hours before collecting saliva samples.^13-15

Statistical analysis

Unpaired t test, Chi square test were applied to assess between group differences. p value of less than 0.05 was considered as statistically significant.

Results

The subjects (n=60, males) were equally divided into two groups: healthy non-smokers and smoking individuals (Table 1).

The mean pH in smokers was 5.36±0.30 and non-smokers was 6.13±0.14, showing lower salivary pH values in the smoking subjects (Table 2).

The evaluation of oral health status of the participants showed an increase in the decayed permanent teeth and decrease in the number of sound teeth among smoking subjects compared to non-smoking subjects (Table 3).

The incidence of erosion in smoking individuals was found to be significant. Enamel lesions were found among 50% of smokers, whereas involvement of dentine was found among 26%. No signs of erosion were observed in 23% of the smokers (Table 4).

Fagerstorm nicotine dependence scale assessment showed that more than 50 percent preferred smoking within five minutes after waking in the morning (Figure 1). About 50% of subjects smoked 11-20 cigarettes per day, while 10% of the participants smoked around 30 or more cigarettes (Figure 2). The scores for daily smokers showed that 26 (86.67%) subjects smoked frequently in the morning (Table 5).

Around 50% of the smokers had high nicotine dependence levels while 40% showed a moderate dependence (Figure 3). 

As the nicotine dependency increased, the salivary pH also increased. As depicted in Table 6, the smokers having high nicotine dependency had a pH of 5.17±0.27 while smokers having low nicotine dependency had a salivary pH of 5.80±0 (p <0.05, statistically significant).

Discussion

Smokers who consumed 10-15 cigarettes per day for over six months had acidic salivary pH of 6.3.¹⁶ In chronic smokers, the salivary pH was reduced in the whole stimulated saliva which can be attributed to the reduced buffering capacity of saliva.^15,17-21 The results of the current study showed pH in smokers (5.36±0.30) to be lower than the non-smokers (6.13±0.14), which is similar to the findings of Parvinen.¹³ In a study conducted by Avsar comparing the relationship between passive smoking and dental caries, substantial counts of Streptococcus mutans and Lactobacillus bacteria were observed.¹⁴

Kelbauskas reported that smoking did not have much influence on the occurrence and intensity of dental caries, nevertheless had a great influence on the factors that enhance intensity of dental caries.²² The results of their study showed higher number of decayed permanent teeth (9.8±6.14) compared to that of the non-smoking individuals (2.37±1.42). The smoke from tobacco produces a caries promoting effect due to the alterations in salivary properties.^7,23 Smokers had significantly more decayed dental surfaces than those of the participants who did not smoke.²² In the present study, it can be noted that the number of caries free teeth in smokers (16.17±5.61) was less compared to that of non-smokers (27.7 ± 2.11).

According to the results of present study, a direct relation can be observed between nicotine dependence and salivary pH, which is in concurrence with a study conducted by Saputri.¹⁹ The high nicotine dependent subjects had decreased pH (5.17 ± 0.27) compared to the subjects with low dependency level (5.80±0) and most of the subjects (50% of smokers) smoked 11-20 cigarettes per day. Salivary acidity or pH depends on its flow rate; a research conducted by Dyasanoor showed that increased cigarette consumption decreased the salivary flow.^16,24

From the results, it can be noted that dentition of smokers had more carious teeth than that of non-smokers, which could be attributed to the changes in the salivary properties induced by nicotine.²³ In contrary, Bertoldo in his study rendered that increased nicotine dependence did not directly play a role in the development of dental caries, but could on the periodontium attributing to increased missing teeth.²³

During smoking, tooth surfaces are exposed to hot smoke from tobacco combustion wherein the temperature ranges from 300°C–1000ºC. The increased temperature due to combustion can have a negative impact on the topographical features and arrangement of apatite crystals.⁷ Ibrahim outlined that cigarette smoking promoted changes in dental enamel after exposure to 20 cigarettes per day for five days.⁷ Direct contact with smoke from cigarette resulted in greater enamel loss, which may lead to erosion of the tooth structure. In the present study, 50% of smokers have erosion confined to enamel and 26% subjects had dentin involvement.^7,25 The alterations in the hydroxyapatite crystal morphology may have decreased its resistance to low pH,⁷ which can be ascribed to erosion. In smoking subjects, large and deep depressions revealed areas of exposed enamel rods with their specific hexagonal structure along with other areas of disintegrated enamel rods.²⁶ The ultra-microstructure of enamel can be disarranged due to smoking according to a SEM study.²⁶ 

Conclusion

According to the findings of this study, the salivary pH and nicotine dependence have a major role in the development of caries and erosion of the tooth structure in smoking individuals. The nicotine dependence has a vital role in determining the salivary pH, as seen in smokers. The salivary pH could also be attributed to the occurrence of erosive lesions in smokers which was not observed in non-smokers.

Conflict of Interest

None

Acknowledgements

None