At present, there is strong evidence that connects several pathologies of the oral cavity with cigarette smoking, whose possible effects on the mouth are manifold, including staining of natural teeth and restorations, black hairy tongue, nicotinic stomatitis, and serious lesions such as oral carcinoma[8, 11]. In particular, the association between cigarette smoking and alcohol causes an increase in the risk of occurrence of oral precancerous lesions and cancer lesions, as alcohol is capable of dissolving some carcinogenic compounds present in tobacco smoke, such as nitrosamines, and produces vasodilation, which facilitates the absorption, by the mucosa, of the toxic substances contained in the smoke.
Additionally, smoking can cause important alterations in saliva because saliva is the first body fluid that comes into contact with the gaseous phase of cigarette smoke. Tobacco use has been shown to cause an immediate stimulation of the salivary fluid. Although there are no documented long-term effects of this stimulation per se, reduced enzyme levels and buffering capacity of the saliva relative to non-smoking patients has been reported for smokers[4, 13].
In this study, we detected decreased levels of IgA, IgG, and IgM in the saliva of smoking subjects; these Igs carry out a protective function against infections. Additionally, despite having similar nutritional and oral hygiene habits, our smoking patients were in worse periodontal condition than control patients, demonstrating high levels of bacterial plaque, gingival inflammation, and deep periodontal pockets.
The high percentage of PD (49.3%), together with the presence of a lower percentage of CAL (29.6%) observed in patients of the test group, is probably due, in part, not only to the apical migration of the periodontal attachment but also to migration, in some pseudopockets, of the gingival margin in the coronal direction.
Cigarette components generate a thicker layer of bacterial plaque, which appears to be less easily removed by patients, and maintain a chronic level of inflammation of gingival tissues[15, 16].
We also recorded a loss of periodontal clinical attachment in our smoking subjects that represents an irreversible process which, if not adequately treated, can lead to dental mobility and, ultimately, tooth loss due to a lack of adequate periodontal support. The gingival inflammation process and periodontal destruction observed in smokers can be connected not only to the presence of bacterial plaque and of periodontal pathogenic species but also to decreases in the host’s defenses vis-à-vis a decrease in saliva Igs[18–20]. In fact, cigarette smoking can alter T-cell immunoregulation and B-cell differentiation, generating a decrease in production of Igs, which protect the oral mucosa against periodontal pathogenic bacteria. A low level of salivary Igs can be regarded as a risk factor for oral diseases, especially periodontal diseases[21, 22].
Wang et al. highlighted the interconnection between periodontal disease and levels of antibodies, and in particular, that the periodontal therapy is able to determine a reduction of antibody titers of the serum against periodontal bacteria, and an increase of the antibody avidity.
Thus, in the presence of periodontitis, the body reacts by producing antibodies against microorganisms that are responsible for the infection; however, in the case of smoking subjects, there is a reduced number of T-helper lymphocytes that are essential for the functioning of B lymphocytes and for the production of antibodies, for which the final result is a decrease in the levels of antibodies.
Decreased IgA levels in saliva are associated with an increased degree of gingival inflammation. The results of our study are aligned with those obtained by Shilpashree, who highlighted a decrease in IgA in cigarette smokers. Cigarette smoking is considered to be a risk factor for the development of periodontal diseases. Among the possible pathogenetic hypotheses, the following have been considered: reduced function of gingival fibroblasts, alteration of neutrophils, and alteration of the serum antibody response against pathogenic microorganisms.
The reduction of immunoglobulin levels could, in some way, bind to the processes of development of periodontal lesions, although there are currently limited evidence that the salivary Igs have a protective action against periodontitis.
Furthermore, among the main limits of the study, there is the small number of examined subjects.
The results and the considerations are to be considered as preliminary findings and further studies should be conducted on a larger number of subjects in order to confirm the details of this pilot study.
The smokers, being at risk of occurrence of various oral diseases, should be monitored smoothly by a dentist.
In particular, a control of the state of periodontal health by a periodontist at regular time intervals should be performed, in order to keep under control the possible sites of periodontal infection, and implement, in the case, the required therapies.
Appropriate protocols of oral hygiene, at home and professionally, appear therefore fundamental in maintaining the health of the periodontium, even in patients who smoke[25, 26].