Despite growing knowledge of the adverse effects of cigarette smoking on general health, smoking is one of the most widely prevalent addictions around the world. Globally, about 1.1 billion smokers and over 8 million people die each year because of cigarette smoking. Smoking acts as a source for a variety of oral and systemic diseases. Various periodontal issues such as increased pocket depth, loss of alveolar bone, tooth mobility, oral lesions, ulcerations, halitosis, and stained teeth are more common among smokers. This systematic review was conducted according to the guidelines from PRISMA, and research articles were retrieved from the Web database sources on 31 May 2021. The quality of research articles was ensured by the type of evidence from combined schema incorporating as schema-13 evidence type description, Cochrane health promotion and public health field (CHPPHF), and the health gains notation framework-14 screening question for quality assessment of qualitative and quantitative studies. Smokers have been found to have bleeding on probing, periodontal pockets, and clinical attachment loss compared to nonsmokers. Oral and respiratory cancers are among the most lethal known diseases caused by cigarette smoking and other commonly occurring sequelae such as stained teeth, periodontal diseases, etc.
Oral diseases appear to be a global problem that should be addressed as a matter of global health concern. Oral health issues include various behavioral and social features such as habits, oral health knowledge, practices, availability, modifiable risk factors, and accessibility to oral health treatments [1]. Health is considered as a significant factor in making life valuable [2]. In general, lifestyles and behavioral patterns are continuously changing, making people more susceptible to oral disorders. Common preventable risk factors for oral diseases include consuming great amounts of sugary food and alcohol and smoking excessively [3]. Back in 2015, untreated oral disorders crippled over half of the world’s population (age-standardized prevalence: 48.0 percent), affecting 3.5 million individuals worldwide [4,5][4][5].
Oral and orofacial problems can affect children and adolescents, affecting physical functioning and psychosocial well-being [6]. One of the scientific theories used to influence human health-related behaviors is the knowledge, attitude, and practices (KAP) theory. According to the KAP theory, healthy knowledge is the foundation for developing an optimistic and healthy lifestyle, attitudes are the motivating factor behind changing behavior, and the goal is to promote oral health [7]. This is why oral health professionals play a critical role in disease prevention and diagnosis through screening and raising awareness [8]. Recently, a shift of focus in health care has been noticed, signaling a transition from biological to a more complete and broader biopsychosocial concept of health [9].
Rationale: The most critical risk factor associated with the onset of various gingival and periodontal diseases is tobacco smoking. It reduces the quality of life of patients and poses a risk to oral health. It has been demonstrated that oral health among smokers is compromised in comparison to nonsmokers. Thus, this study is aimed at reviewing the literature to evaluate the effect of smoking on oral health.
Objectives: In this systematic review, we aim to examine the effects of cigarette smoking on oral health, present the major oral diseases caused by cigarette smoking, and determine if there is any possibility of bacterial or fungal infections among smokers.
Characteristics | Inclusion Criteria | Exclusion Criteria |
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Serial # | Keywords | PubMed | Scopus | WOS | MDPI |
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Study design | Clinical studies including trials and randomized clinical trials, evaluation studies, original research articles | Review articles, narrative reviews, short communication, case report, editorials, letters, unpublished articles, abstracts, systematic reviews, and meta-analyses | |||
Study period | Last 10 years | Articles before 2011. | |||
Publication language | English | Other than English | |||
Interventions | Articles examining the impact of cigarette smoking on oral health initiatives. Individual and community-based studies reported with context, effects, disease outcome of smoking and the process |
Articles that only have the observational data. | |||
Publication status | Published | Not published yet |
1 | Smoking and oral health | 184 | 910 | 777 | 36 |
2 | Smoking effects on oral health | 134 | 223 | 140 | 05 |
3 | Cigarette smoking | 1186 | 460 | 508 | 421 |
4 | Smoking and tobacco use | 2192 | 678 | 397 | 249 |
Total articles retrieved | 3696 | 2271 | 1822 | 711 | |
Removal of duplicate articles | 972 | 657 | 507 | 120 |
Authors | Study Design | Duration of Study | Sample Obtained From | Sample Size | Methodology | Study Outcomes | Author Conclusion |
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Yuki D et al., 2013 [10] | Quasirandomized cross-over | 4 days | Blood, Saliva | 16 | After smoking one cigarette, the analysis of plasma and saliva nicotine and cotinine. | The concentration profiles of saliva cotinine were identical to those of plasma cotinine, and all of the computed cotinine pharmacokinetic characteristics were the same in both plasma and saliva. | Saliva cotinine, which reflects plasma cotinine content and kinetics, might be a suitable and less intrusive cigarette smoke exposure measurement. |
Al-Bayaty et al., 2013 [11] | Comparative cross-sectional | Not mentioned | Blood and teeth | 197 | BOP, PI, and the levels of serum haptoglobin, cotinine, and alpha 1-antitrypsin were tested. | BOP levels were determined to be low, while plaque indices were modest. Smokers had considerably greater levels of serum haptoglobin, cotinine, and alpha 1-antitrypsin than nonsmokers. | A study found that smoking for a longer period, but not for a higher number of cigarettes per day, was linked to less gingival bleeding in smokers. |
Medina Solis CE et al., 2014 [12] | Cross-sectional | Not mentioned | Questionnaire | 22,229 | Questionnaires base study to evaluate risk factors. | The prevalence of oral or dental diseases was 25.7%. | Tobacco users were more likely to report oral and dental issues. |
Haswell et al., 2014 [13] | Cross-sectional | 28 days | Urine, Saliva, Blood | 263 | The levels of biomarkers in 143 smokers, 61 never-smokers, and 61 ex-smokers were compared. A total of 27 potential biomarkers were evaluated. |
14 biomarkers were substantially different between smokers and never-smokers, and 12 of these 14 biomarkers could differentiate between smokers and former smokers, indicating the possibility of reversibility. | Twelve of the twenty-seven BOBE are potentially valuable instruments for future product evaluation. |
Du D et al., 2014 [14] | RCT | Pre-/postintervention data | Teeth | 322 | A 0–100 mm visual analog scale was used to measure baseline cravings. Craving assessments were taken at 50 s, 3, 5, 7, 15, 20, 25, and 30 min after the medication was given. |
Both treatments demonstrated equal maximal effects on desire alleviation and decreased cue-induced craving. At 50 s, 3 min, and 5 min after treatment, the 2.5 mg nicotine film alleviated cue-induced desire to a larger extent than the 2 mg nicotine lozenge. | While both had equal maximal effects, the 2.5 mg nicotine film alleviated cue-provoked cravings substantially faster than the 2 mg nicotine lozenge. For low-dependence smokers, nicotine film might be effective for providing fast desire relief. |
Lee CP et al., 2015 [15] | Case control | 5 year | Blood | 507 | Single-nucleotide polymorphisms (SNPs) in DNA repair genes (CHAF1A and CHAF1B) and a chromosomal segregation gene (AURKA) were discovered using a genotyping assay and gene–environment interaction analysis. | AURKA’s Phe31Ile polymorphism (rs2273535, T91A) was shown a linkage of an increased risk of oral cancer. The 91A allele’s gene dosage was likewise linked to greater risk of mouth cancer. Furthermore, by high usage of cigarettes, the AURKA 91AA homozygote can be modify resulting to a high risk of oral cancer. |
The functional Phe31Ile polymorphism of AURKA gene may be a strong susceptibility gene in the incidence of oral cancer. |
De Carvalho LD et al., 2014 [16] | RCT | One year | Physical check-up | 26 | G1: etch-and-rinse in nonsmokers. G2: selective enamel etching in nonsmokers. G3: etch-and-rinse in smokers. G4: selective enamel etching in smokers. One operator applied a nanofilled resin composite to each group and light-cured it sequentially. |
Only minor discoloration revealed a statistically significant difference between groups 1, 3, and 4 after 12 months when compared to baseline in the evaluations. | The clinical efficacy of resin composite cervical restorations was unaffected by cigarette smoking. |
Abduljabbar T et al., 2017 [17] | RCT | 3 months | Oral BBL swab | 22 | The presence of oral erythematous lesions and the position of the denture in jaws were examined by a clinical oral examination. Exfoliative cytology was used to confirm the appearance of fungal hyphae. | Fungal CFU/mL levels were statistically substantially greater in smokers than nonsmokers at the 3-month follow-up. | In both smokers and nonsmokers, aPDT is effective at inactivating oral fungus colonization. |
Javed F et al., 2017 [18] | RCT | 12 weeks | Questionnaire/Teeth | 54 | At baseline and during a 12-week follow-up, periodontal parameters were measured. Group A: mechanical curettage (MC) with adjunct antimicrobial photodynamic therapy (aPDT) Group B: mechanical curettage (MC) only. |
Patients in groups A and B had significantly lower PI and PD at 12-week follow-up as compared to their baseline levels. At the 12-week follow-up, patients in Group B had substantially greater PI and PD than those in Group A. | When compared to MC alone, MC with aPDT is more successful in treating peri-implant mucositis in cigarette smokers. |
Rodriguez-Rabassa M et al., 2018 [19] | Cross-sectional | Not mentioned | Saliva | 34 | To evaluate the response from the host, cytokine and chemokine expression analyses were performed. | Some bacterial species connected with the smokers group have associations with hormones and cytokines found to be statistically different between smokers and nonsmokers. Inflammation and carcinogenesis in the oral cavity have been linked to these variables. |
The findings might help researchers figure out how the salivary microbiome, host inflammatory responses, and metabolism interacts in smokers. |
Blasi PR et al., 2018 [20] | Secondary analysis | 2015–2017 | Questionnaire | 718 | Between the baseline and the 6-month follow-up survey, professional dental treatment was received. | The findings provide light on variables that may encourage or discourage low-income smokers from seeking professional dental treatment. | This study provides enough material regarding smoking effects on oral health and motivates the public to visit the dental clinics. |
AlAhmari et al., 2019 [21] | RCT | 3 months | Teeth | 83 | The periodontal parameters were examined at baseline, 1 month, and 3 months follow-up. | Probing pocket depth (PD), plaque index (PI), and the clinical AL were all increased in smokers than nonsmokers after 1 and 3 months of follow-up. | For treatment of CP among the cigarette smokers, the results of SRP with and without aPDT are compromised. |
Angst PDM et al., 2019 [22] | RCT | 2 year | Teeth | 62 | PD, BOP and CAL. | The test group’s mean PPD was higher at the start than the control groups, but the two groups were similar after two years. Significant decreases in PPD and BOP, as well as an increase in CAL, were found with time, with no significant differences between groups. |
During the two years of SPT, oral prophylaxis with oral hygiene instructions alone or in conjunction with subgingival instrumentation was able to preserve the previously achieved periodontal state to a comparable level. |
AlDeeb M et al., 2013 [23] | RCT | 12 weeks | Peri-implant sulcular fluid, radiography | 25 | The baseline (before therapy) and the 12-week follow-up (after therapy). The ultrasonic scaler and profuse irrigation were used to provide full-mouth disinfection (FMD). A diode laser was used to perform the photodynamic treatment (PDT). |
All groups showed statistically significant reductions in PI and PD markers at the baseline examination and after 12 weeks of follow-up. At 12 weeks, BOP among smokers had increased significantly. | In cigarette smokers, PDT with additional mechanical debridement decreased plaque index and probing depth while increasing probing bleeding and lowering proinflammatory indicators. |
Julkunen -Iivari A et al., 2020 [24] | Cohort | 1985–2015 | Teeth | 1080 | Associations between tobacco products, periodontal health parameters, education level, and death ages. | Tobacco products, as well as a low level of education, are linked to poor periodontal health. Tobacco users who had a lower level of education had greater PI, calculus, and GI scores than nonusers. When compared to nonusers, missing teeth and a lower education level were associated with a significantly greater frequency of deep periodontal pockets. |
Tobacco products were found to be hazardous to periodontal health. |
Javed F et al., 2020 [25] | Cohort | Not mentioned | Saliva | 46 | Full-mouth PI, BOP, PD and AL, marginal bone loss (MBL), and missing teeth. Levels of IL-17A and IL-23 in saliva were measured. |
Marijuana users, cigarette smokers, and nonsmokers with periodontitis had poorer clinic-radiographic characteristics than periodontally healthy nonsmokers. | The whole salivary immune-inflammatory response may be somewhat poorer in marijuana users compared to heavy cigarette smokers and nonsmokers with periodontitis. |
Nettore IC et al., 2020 [26] | Cross-sectional | Oct 2014-Feb 2019 | Flavor recognition | 348 | Oral administration of aqueous aromatic solutions was used to detect 21 distinct chemicals in the test. The total of the correctly detected tastes was used to determine the flavor score (FS). | Cigarette smoking seemed not to influence flavor recognition. | Smoking was not significantly associated with the flavor identification. |
Varghese J et al., 2020 [27] | RCT | 3 months | Saliva | 40 | Periodontal parameters were assessed. Saliva samples were collected before start and after the end of treatment to determine the levels of salivary 8-hydroxyguanosine (8-OHdG) using the ELISA method. CPs: Chronic periodontitis in smokers. CPns: CP nonsmokers (CPns). CHS: Clinically healthy subjects in smokers. CHns: CH nonsmokers. |
At baseline, the PI, GI, PD, and clinical AL values in the CPs and CPns groups were substantially greater than those in the CHns and CHs groups. The CPs group had considerably greater baseline salivary levels of 8-OHdG than others. CP group showed improvement by the third-month recall interval; however, the CPs still had a greater level of 8-OHdG values than the CPns. |
According to this study for detecting periodontal tissue degradation the salivary 8-OHdG levels might be recognized as an oxidative biomarker, which reveals an ongoing periodontal destructive condition in smokers. |
Wychowanski P et al., 2021 [28] | Case series | 2012–2015 | Bone | 164 | In the maxilla, immediate implants were placed. Implants were placed in the palatal alveolus in the posterior area. Insertion Torque Value (ITV) and two types of equipment were used to assess implant stability: Periotest (PT) and Osstell (ISQ). Cone beam computed tomography images were used to assess minor bone loss. |
Smokers had greater PT values at 6 months post-implantation in an aesthetic region compared to those of nonsmokers. At six months after implantation, smokers’ ISQ scores were considerably lower than nonsmokers’ scores. Smokers had greater PT values in the posterior area than nonsmokers on the day of implantation, 6 months after surgery, and 24 months after surgery. On the day of implantation, as well as 6 months later, smokers had lower ISQ levels than nonsmokers. In the aesthetic and posterior areas, smokers had lower ITV measures than nonsmokers. |
According to this study, smoking has a deleterious impact on the durability of immediate implants in the maxilla. |