The Impact of Cigarette Smoking and Vaping Use on the Development and Progression of Periodontitis: A Systematic Review

ABSTRACT

Background

Periodontitis is a widespread inflammatory disease that impacts the tissues surrounding and supporting teeth. As well as being untreated, it leads to serious dental and overall health issues. While cigarette smoking is widely recognized as a major risk factor for the development and progression of periodontitis, the effects of vaping use on periodontal health remain a subject of growing concern.

Aim

This paper aims to investigate the impact of both traditional smoking and vaping use on periodontal health, as well as determine which method poses a greater risk for periodontal disease.

Methods

The current systematic review adhered to the PRISMA standards for quantitative systematic reviews. A systematic search was conducted across four databases: Medline, CINAHL, Embase, and Cochrane Central Register of Controlled Trials (CENTRAL), yielding 2179 studies. Duplicate studies (n = 585) were identified and removed using RefWorks.

Results

The result of this review revealed that cigarette smokers experience worse periodontal conditions than vape smokers and non‐smokers. Cigarette smokers exhibited higher Gingival Index (GI), poorer Plaque Index (PI), lower Bleeding on Probing (BOP), mean Probing Depth (PD) exceeding 3 mm, and greater Clinical Attachment Loss (CAL). A total of 13 studies were included in this systematic review. Specifically, six studies compared cigarette smokers with vaping smokers and non‐smokers, while another six studies focused on the comparison between cigarette smokers and non‐smokers. Furthermore, one study assessed vaping smokers against non‐smokers.

Conclusion

This review focuses on the substantial differences in periodontal health between cigarette smokers, vape users, and nonsmokers. Cigarette smoking has been linked to more severe periodontal diseases, including a higher Gingival Index, a lower Plaque Index, and worse Clinical Attachment Loss. While vaping seems to have a lower influence on periodontal health, it deserves further examination. Understanding these distinctions is critical for creating targeted therapies and public health measures to reduce the negative impacts of tobacco and vaping on oral health.

1. Introduction

Oral health is an essential component of overall health and well‐being, encompassing not only functional and structural integrity but also psychological and aesthetic dimensions [1]. The concept of Oral Health‐Related Quality of Life (OHRQoL) has emerged as a comprehensive measure of both physical and mental well‐being, reflecting the momentous role oral health plays in daily life [2]. Moreover, periodontal diseases are among the most common oral conditions worldwide, ranging from reversible gingivitis to destructive periodontitis, and in extreme cases, to a life‐threatening condition called “noma” which is a rapidly progressive, often fatal gangrenous infection affecting the oral and facial tissues, typically seen in severely malnourished or immunocompromised individuals. These conditions are primarily infectious, arising from a complex interplay between pathogenic organisms and the host's immune response. While gingivitis is typically nonspecific and manageable, periodontitis involves the pathological loss of periodontal attachment and alveolar bone, often requiring multifaceted intervention. Its onset is linked to a dysbiotic microbial biofilm [2, 3].

Gingivitis results from microbial plaque accumulation on the teeth, leading to localized gingival inflammation. Even minimal plaque levels can trigger immune‐mediated inflammatory infiltration. If plaque is not regularly disrupted, this imbalance may progress, creating a dysbiotic state that initiates gingival disease [3].

Diagnosis of periodontal diseases employs several clinical indices. The Gingival Index (GI), extensively used in periodontal research, assesses gingival inflammation severity. Similarly, the Plaque Index (PI) evaluates supragingival plaque accumulation using a 0–3 scale at four sites per tooth [4]. Gingival bleeding, assessed by the Gingival Bleeding Index, is a well‐established early marker of inflammation. Research indicates that bleeding sites show greater inflammatory infiltration, and inflammation decreases with bleeding cessation [3]. Furthermore, for periodontitis, diagnosis is based on clinical attachment loss (CAL) and pocket depth (PD). CAL readings above 3 mm indicate pathology, with deeper pockets signifying increased severity. PD is measured at multiple sites on each tooth. The Community Periodontal Index for Treatment Needs (CPITN) classifies PD as follows: ≤ 3 mm (none/mild), > 3– < 6 mm (moderate), and ≥ 6 mm (severe) [5]. Radiographs further aid in evaluating the extent and pattern of alveolar bone loss [4].

Periodontal disease affects individuals across all economic and cultural sectors, each bringing unique expectations regarding oral health standards and treatment affordability. Access to care is often limited by financial constraints, making cost a key factor in the utilization of periodontal therapy. To address this, it is essential to minimize the gap between available clinical services and patient affordability, while also enhancing public awareness of the value and effectiveness of contemporary periodontal treatments [5].

In Asia, surveys indicate a 15%–20% prevalence of severe periodontitis and 5%–15% for advanced stages among adults [5]. Periodontitis typically affects specific teeth or surfaces rather than the entire dentition and may progress severely in one area while sparing a nearby tooth. Its pathogenesis cannot be explained by plaque or immune response alone but is attributed to a combined herpesvirus‐bacterial infection [4]. Moreover, studies have also investigated gingivitis prevalence. Albandar and Kingman (1999) reported a 32.2% rate among 9689 American participants using BOP, with both localized and extensive cases [5]. Murray et al. (2015) found gingival inflammation in half of 69,318 UK children aged 5–15 years [6], while Zhang et al. (2010) observed that over 82% of 1143 Chinese adults had a GI above 1 [7].

Periodontitis is categorized as chronic, aggressive (localized or generalized), necrotizing, or linked to systemic diseases [8]. While describing gingivitis severity (mild, moderate, severe) helps in patient communication, no standardized clinical definitions exist. Recent findings also suggest that localized gingivitis may provoke systemic inflammation, though further evidence is needed to distinguish levels of severity [9]. Furthermore, susceptibility to plague‐induced inflammation varies by individual, depending on local and systemic risk factors, referred to as predisposing and modifying variables [9].

In the scope of treatment of periodontitis disease, treatment begins conservatively, with professional cleaning through scaling and root planning to remove plaque and calculus above and below the gum line [10]. Addressing risk factors is central to managing periodontitis [10]. However, outcomes of nonsurgical and surgical therapy are poorer in smokers, who show less improvement in gingival inflammation, pocket depth, and clinical attachment compared to nonsmokers [11].

It is important to note that smoking is a noteworthy behavioral risk factor for periodontitis and has notable effects on gingival tissues. Components of cigarette smoke induce microvascular vasoconstriction and fibrosis both locally and systemically. As a result, typical signs of gingivitis, such as bleeding on probing, may be masked despite the presence of substantial inflammatory cell infiltration [12]. Smoking damages periodontal structures by destroying alveolar bone, blood vessels supplying the pulp, and periodontal ligaments. It also impairs immune response, contributing to tooth mobility and eventual loss [10]. For further explanation, several mechanisms explain smoking's negative impact on periodontal healing: impaired neutrophil function, increased pathogenic colonization, reduced serum and salivary IgG and IgA levels, and inhibited fibroblast activity and proliferation [13]. Emerging studies also link smoking to increased expression of advanced glycation end‐product receptors in periodontal tissues [13].

Due to smoking‐induced vascular constriction, gingival inflammation may go undetected. Since gingivitis diagnosis relies on bleeding on probing, clinicians may underestimate disease severity in smokers. Encouragingly, smoking cessation restores gingival bleeding, crevicular fluid flow, and blood flow to levels seen in non‐smokers, indicating reversibility of vascular effects [12]. Nicotine and carbon monoxide in cigarettes further hinder wound healing. Although research over the past two decades has advanced understanding, the exact mechanisms of smoking‐induced periodontal damage remain unclear [12].

Vaping, a newer form of nicotine use, has gained popularity among youth. Despite growing use, awareness of its risks remains limited, while 74% of smokers acknowledge the dangers of traditional cigarettes, only 24% of vape users recognize vaping's potential harm [10]. Vaping is often perceived as a safer alternative, which contributes to its popularity [11]. Some users promote vaping as a form of nicotine replacement therapy to aid smoking cessation [14].

Recent studies have highlighted the systemic health consequences of vaping. Risks associated with nicotine‐containing vapes include nicotine addiction, disrupted adolescent brain development, and cognitive and behavioral difficulties [10]. Additionally, vaping increases the risk of traumatic injuries, particularly blast injuries from battery explosions, especially in regions lacking specific safety regulations for vape manufacturing [15]. In addition, in vitro studies have demonstrated the biological effects of vaping. Exposure to vaping aerosol has been linked to DNA damage and mitochondrial dysfunction in lung fibroblasts [16]. Similarly, another study found that both cigarette smoke and vape aerosol contribute to the overproduction of reactive oxygen species (ROS) in bone marrow mesenchymal stem cells [17].

However, while cigarette smoking is a well‐established risk factor for periodontal health, increasing the risk of gingivitis and periodontitis, evidence regarding the impact of vaping on gingival tissues is limited. Therefore, it can be hypothesized that vaping may have similar effects on periodontal health as traditional smoking. Thus, this review aims to evaluate and compare the effects of cigarettes and vaping on periodontal health.

2. Methods

A systematic review attempted to address the review question by examining previously published studies on smoking, vaping, and their effects on the periodontium. Systematic reviews aim to prevent bias and create a thorough and comprehensive search plan by discovering, assessing, and summarizing all relevant publications on a specific subject [18]. The systematic review adhered to the PRISMA standards for quantitative systematic reviews [19]. The protocol for the current systematic review has been recorded in the prospective international register of systematic reviews, PROSPERO, with the registration number (CRD12025632158).

2.1. PICO

The study employed the PICO criteria, which were identical to the research's inclusion criteria (P = population, I = intervention, which is not relevant in this systematic review; thus, the phrase “the phenomena of interest” was used instead, C = comparison, O = outcome) [18]. For the group of people sampled who are exclusive cigarette smokers, exclusive vape or e‐cigarette users, participants should not be diabetic or pregnant; the intervention, which is the phenomenon of interest, is vaping and the use of vaping for at least 1 year; the comparison with traditional smokers such as cigarettes and if no study or not enough studies are found the comparison will be with non‐smokers for both smoking types (cigarettes vs. non‐smokers and vape users vs. non‐smokers) then an analysis will be done to reach the results and the effect of both types of smoking on the periodontal status like gingivitis or periodontitis is the outcome of this systematic review and this will be measured by using the indexes like GI, PI, BOP, PD, and CAL to diagnose the disease [1].

2.2. Inclusion Criteria

The inclusion criteria for the systematic review were derived from the research question as follows:

• 1.The population is the cigarette smokers and vape or e‐cigarette users, and due to a lack of studies that compare those two groups together, the reviewer had to include the non‐smokers.
• 2.The intervention was denoted by the term “phenomenon of interest” because vaping cannot be considered as an intervention due to ethical reasons.
• 3.The comparison is between vape or e‐cigarette users and cigarette smokers, but due to a lack of studies, the comparison for both types of smoking was with non‐smokers.
• 4.The outcome was the gingival health status and whether there was any sign of gingivitis or periodontitis.

2.3. Exclusion Criteria

• 1.The study excluded non‐English written studies and qualitative studies.
• 2.The exclusion criteria for the patients: diabetic patients are not included in the study because they tend to have a higher risk of developing periodontal diseases, especially periodontitis; pregnant women are not included because they have high sex steroid hormones, which will increase the risk of developing periodontal diseases, which will affect the results of the study [2].

2.4. Eligibility Criteria

Studies included in the systematic review are all on human patients and written in English. The systematic review will look at studies that investigated the association between periodontal health and risk factors, which are vaping and traditional smoking. The systematic review will compare the effects of each type and investigate which one of them does the most damage to the periodontium. The sample will be either a current smoker or a vape user, and cannot be both. Studies included in this review are case‐control studies. Case‐control studies were selected to detect existing cases and assess the related historical aspects. Case‐control research enables a more workable strategy. Potential relationships and exposures can be found using this study design [3]. Participants are smokers or users of vapes adults male and female adults. No publication date restrictions were imposed. Studies that investigate the gingival parameters such as GI, PI, BOP, PD, and CAL were included to give more accurate numerical results. The outcome of this systematic review is based on those parameters to diagnose the periodontal disease (gingivitis or periodontitis) in association with the risk factors (cigarettes and vapes).

2.5. Search Strategy

A systematic review was conducted to examine the effect of cigarette smoking and vaping on the health of the gingiva. The databases that were searched and reviewed are Medline, CINAHL plus Embase, and Cochrane Trials Library. searching began with each database separately to ensure best practice and effectiveness. The MeSH terms were used 1‐ (“electronic cigarettes” or “vaping”), 2‐ (“tobacco smoking” or “cigarettes” or cigarettes smoking” or “smoking”), 3‐ (“oral health” or “gingival health” or periodontitis or gingivitis) then the MeSH terms 1 and 3 combined in the search with ‘AND’ then the MeSH terms 2 and 3 were combined with “AND”, then all of the 3 MeSH terms were combined with “AND” to get the most systematic search in these databases and have a sufficient number of studies. Then all studies found from all four databases and three searches were moved to RefWorks to remove any duplicate studies.

2.6. Study Selection

After transferring the studies to RefWorks and deleting all duplicates, the screening process occurred. The reviewer individually examined the studies from all sources, vetted them based on their title and abstract to satisfy the inclusion criteria, and then appraised the resources to make a final decision. After deleting any extraneous studies from the RefWorks file, the reviewer eliminated all inaccessible studies, read the complete text of the remaining studies, and determined if they met the inclusion criteria. Selected studies as case‐control studies comparing smokers and nonsmokers. The investigations should produce clear results, the sample should be fit and not diabetic or pregnant, and the participants should be adults. The studies included were quantitative, with indices of GI, PI, BOP, PD, and CAL. Case‐control studies were used to detect existing cases and evaluate the historical context. Case‐control research allows a more practical strategy. This study design allows for the identification of potential correlations and exposures [3].

2.7. Data Extraction

Information extracted from each study was, 1‐ the number of participants, 2‐ the average age of participants, 3‐ the study setting, 4‐ the study design used, 5‐ the country the study was performed in, 6‐ smoking cigarettes inclusion criteria to show the accuracy of the studies selected, 7‐ Nonsmoker inclusion criteria to show the accuracy of the studies selected, 8‐ the daily rate of tobacco consumption, and 9‐ smoking cigarettes duration in years. In studies that compare the vaping effect on non‐smokers, the extracted information was 1‐ the number of participants, 2‐ the average age of participants, 3‐ the study setting, 4‐ the study design used, 5‐ the country the study was performed in, 6‐ vaping smoking inclusion criteria to show the accuracy of the studies selected, 7‐ nonsmoker inclusion criteria to show the accuracy of the studies selected, 8‐ the daily frequency of vaping, and 9‐ vaping smoking duration in years. The extracted results of the studies are demonstrated in Table C1. The table shows all the studies included in this systematic review and the periodontal indices used in each study, with their results against each study and index. The table was added to the results of studies section to make it easier for the readers to see and understand the overall result of the systematic review.

2.8. Risk of Bias

The risk of bias tool assessing the quality of studies used in this systematic review is CASP [4]. CASP is a set of eight checklists for critical appraisal, and it is utilized when reading research. Different types of studies can be appraised using CASP, such as systematic reviews, randomized controlled trials, cohort studies, case‐control studies, economic evaluations, diagnostic studies, qualitative studies, and clinical prediction rules, all have appraisal checklists available from CASP. Each study was appraised according to the CASP checklist, depending on the design of the study that was appraised. The CASP tool was used because the areas required for critical evaluation of evidence are effectively and succinctly covered by the CASP tool, and because it has a variety of questions for every study design [5]. For case‐control studies, CASP provides a checklist to appraise these design studies. The checklist has three sections. Each section assesses a different part of the study. The first section assesses the validity of the results by answering questions in this regard. The second section is to assess the results, and the final section is to appraise whether the results can help locally. Each study included in this systematic review followed the case‐control checklist in CASP to assess its risk of bias. This tool was used to help assess the internal validity of case‐control studies. This tool consisted of twelve criteria in three sections, and the possible answer for each criterion was Y: Yes, N: No, or X: Can't tell. All non‐Yes responses indicated a risk of bias. The reviewer could not answer some questions from the checklist and left the door open for further development in the future. The reviewer used the symbol (‐) in the answer gap for these two questions.

2.9. Data Synthesis

The review intended to explore smoking as a risk factor through its effect on periodontium health and then compare traditional smoking with electronic smoking, such as vapes, and smoking has been studied thus far, as well as to describe the state of the literature in terms of which smoking method causes more damage to periodontium health and can increase the chance of having a periodontal disease and influence one. The researcher presents a method for generating summary distributions by combining information from different summary statistics (mean and standard deviation) reported in multiple studies and accounting for differences in sample sizes. The similarity of the included studies was qualitatively assessed, and the results of the different measures of gingivitis indexes GI, PI, BOP, PD, and CAL were compared between groups of cigarette smokers, vape smokers, and non‐smokers. The consistency between the results of direct and indirect comparisons between groups was also evaluated based on the different readings of the gingivitis indexes. This aims to include all the variations between studies, to obtain a distribution that covers all published studies related to the study variables.

3. Results

3.1. Study Selection

The last search in January 2022 found 2179 studies across four different databases, which are Medline (n = 686), CINAHL (n = 779), plus Embase (254), and Cochrane Central Register of Controlled Trials (CENTRAL) (n = 460). Figure 1 shows the PRISMA flowchart. Five hundred and eighty‐five duplicate studies were found using RefWorks [6] then the duplicate studies were removed. One thousand five hundred and ninety‐four studies were screened by their title and abstracts. One thousand four hundred and forty‐six studies were excluded because they didn't meet the eligibility criteria. Sixty six studies were not accessible, so they were excluded from our final selection. This resulted in 82 full‐text studies being read and screened against the eligibility criteria as mentioned in the methods section. Seventeen studies were investigating an irrelevant population, 8 were measuring the effect of interventions that are not related to our phenomenon of interest, 20 studies were looking for irrelevant outcomes, and 24 studies used an illegible study design. Finally, 13 studies were included in this systematic review.

Figure 1.

PRISMA flowchart.

3.2. Study Characteristics

Thirteen case‐control studies were extracted and included in this systematic review. Six studies compared cigarette smokers with vaping smokers and non‐smokers [7, 8, 9, 10, 12, 13]. Six studies compared cigarette smokers with non‐smokers [11, 14, 15, 16, 17, 18]. One study compared vaping smokers with non‐smokers [17]. All studies were published between 1987 and 2020; seven studies were carried out in Saudi Arabia [7, 8, 9, 10, 12, 13, 17], three studies in Sweden [11, 14, 15], two studies in Spain [16, 19], and one study in Thailand [18]. As for the participants included in the study, the ages of the participants ranged from 20 to 73 years old. The number of participants ranged from 80 to 1311, where the number of nonsmoking participants ranged from 26 to 954, the number of vape smokers from 26 to 47, and the number of cigarette smokers from 28 to 889. Regarding the daily frequency of vaping and cigarette smoking, the average daily consumption of vaping smokers ranged from 6.5 (0.9) to 30.2 (8.5) times per day, and the average daily consumption of cigarette smokers ranged from 9.5 (0.6) to 30 cigarettes per day. In terms of the duration of vaping and cigarette smoking, the average duration of vaping smokers ranged from 2.2 (0.2) to 8.7 (3.8) years, and the average duration of cigarette smokers ranged from 5.4 (1.6) to 22 (10.7) years. Four studies did not report how long the study participants had been smoking [11, 16, 18, 19]. A summary of the participants' demographic characteristics is reported in Table A1 in Appendix A.

3.3. Risk of Bias Within Studies

The CASP checklist tool was used to assess the risk of bias in case‐controlled studies. Each included study was examined independently for risk of bias by two reviewers. Additionally, a third reviewer may be used to resolve conflicts. This contributes to a more thorough and reliable assessment of the risk of bias in the research under consideration. Results were reported in Table C1 (Critical Appraisal Skills Program, 2018). The expert who developed the CASP checklist does not recommend a grading system because these checklists were created to be used as instructional pedagogic tools in a workshop context. See Table B1 in Appendix B.

3.4. Results of Studies

The included research studies looked at differences in periodontal status indexes (GI, PI, BOP, PD, and CAL) between cigarette smokers, vape smokers, and non‐smokers in a clinical setting. Table C1 in Appendix C shows the results of periodontal status indicators in terms of mean and standard deviation (SD). All thirteen studies reported solely the PD as a periodontal parameter. The cigarette group had consistently higher mean PD values than the vape and nonsmoking groups. Two studies found a considerable increase in mean PD in the vape group compared to the Nonsmoker group [20, 21], four indicated a modest increase [22, 23, 24, 25], and one showed no difference [26].

Meanwhile, PI appeared in twelve studies, with mean PI values consistently higher in the cigarette group compared to the vape and nonsmoker groups in nine studies [20, 21, 22, 23, 24, 25, 26, 27, 28], while two studies showed a slight rise [27, 29], and one study found no difference [30]. Nine studies have also documented bleeding on probing (BOP) [20, 21, 22, 23, 24, 25, 26, 29, 30]. Except for one study that showed a decrease in the mean BOP value, all other studies showed an increase in the mean BOP value in the nonsmoker group compared to the cigarette and vape group [15].

CAL was reported in six studies [23, 24, 26, 28, 31], and [30], and CAL mean values were higher in all studies in the cigarette group, showing that people who smoked cigarettes lost more clinical attachment than vape smokers and non‐smokers. Three studies [23, 24, 26] found differences in the mean CAL values of the vape group. Two of them revealed a mild increase [23, 24], whereas one study found no differences compared to the nonsmoker group [26]. The latter index, used as a periodontal parameter, GI, appeared in only two studies [11, 16]. The mean GI values in the first study were higher in the cigarette group compared to the nonsmoker group [16], while the second study did not show any difference in the outcomes between groups [11]. Except for three studies, the overall results of the retrieved studies revealed consistently increasing values in the smoke groups [27, 29, 30]. Interestingly, two investigations found minor variations in all periodontal markers [29, 30]. The results of all reported studies, as indicated in Table C1 in Appendix C, show that cigarette smoking has a deleterious influence on periodontal tissue when compared to vape smoking and nonsmokers. They also discovered that vaping smokers had outcomes more similar to nonsmokers than cigarette smokers.

4. Discussion

This systematic review demonstrates that cigarette smoking exerts a profound detrimental effect on periodontal health compared to both vaping and nonsmoking. Cigarette smokers consistently showed elevated Gingival Index (GI), Plaque Index (PI), deeper Probing Depths (PD) often exceeding 3 mm, and greater Clinical Attachment Loss (CAL), indicating marked progressive periodontal destruction. These clinical findings corroborate existing evidence that tobacco smoke induces oxidative stress within periodontal tissues, suppresses host immune defenses, and accelerates alveolar bone loss, thereby driving periodontitis progression [24, 32, 33, 34].

Conversely, vape users exhibited periodontal outcomes worse than non‐smokers but consistently less severe than those of cigarette smokers. Vape smokers demonstrated elevated mean GI, PI, CAL, and PD values relative to non‐smokers, establishing that electronic nicotine delivery systems, while sometimes promoted as safer alternatives, nonetheless pose a risk for periodontal deterioration [22, 31]. The higher GI and PI in both cigarette and vape users likely reflect not only the direct toxicological effects of nicotine and other substances but also behavioral factors such as inadequate oral hygiene, especially notable among traditional smokers [22, 31].

However, there remains a substantial knowledge gap regarding the long‐term impact of vaping on periodontal health, especially given the relatively recent advent of these devices. Existing studies often lack longitudinal follow‐up, limiting the ability to infer chronic outcomes or cumulative damage. Future research should prioritize well‐powered, prospective cohort studies assessing vaping duration, intensity, and flavoring agent effects to comprehensively characterize periodontal risks.

A notable and consistent observation across studies was that non‐smokers displayed the highest mean levels of bleeding on probing (BOP), while vape users showed lower BOP values than both non‐smokers and cigarette smokers. This paradox aligns with the well‐documented vasoconstrictive properties of nicotine, which suppress gingival blood flow and mask the clinical signs of inflammation despite ongoing periodontal breakdown [35]. Ehsan's recent case‐control study in Afghanistan further substantiates this, reporting a meaningfully reduced BOP in smokers (45%) compared to non‐smokers (78%) despite smokers exhibiting suggestively greater PD and CAL values [34]. Consequently, these data highlight the insidious nature of nicotine's effects, obscuring early inflammatory signs and potentially delaying diagnosis and intervention.

It is important to note that the dose‐dependent nature of this vasoconstriction has been well characterized, with maximum suppression of gingival bleeding typically achieved at 10 to 20 cigarettes per day [36, 37]. In vape users, while the exact mechanisms remain less clear, nicotine content in e‐liquids is believed to contribute similarly to reduced gingival bleeding [38]. This differential impact on clinical inflammatory markers between cigarette and vape users necessitates cautious interpretation of periodontal assessments in these populations.

Recent research dispels any notion that vaping is biologically inert. Evidence links vaping to increased oxidative stress, alterations in lung cellular functions, enhanced inflammatory responses, and DNA damage [22, 39]. In vitro experiments have demonstrated that flavoring chemicals commonly added to vape aerosols exacerbate DNA damage and modulate inflammatory mediators such as prostaglandin E2 and cyclooxygenase within gingival fibroblasts, key factors in periodontal tissue destruction [40, 41]. Moreover, recent studies emphasize vaping's role in disrupting periodontal microbial symbiosis and exacerbating inflammation, highlighting complex biological pathways through which e‐cigarette aerosols may compromise periodontal tissues [34, 42].

The relationship between tobacco exposure and periodontal disease is unequivocally dose‐dependent. Heavier and longer‐duration smokers suffer severe periodontal breakdowns. Vape users with over 5 years of daily use exceeding 15 episodes per day face a notably higher risk than infrequent users, though their risk remains lower than that of cigarette smokers [33]. This gradient of harm underscores the importance of quantifying both intensity and duration in evaluating periodontal risk profiles.

Immunologically, vaping may exert broader suppressive effects on immune gene expression than cigarette smoking. Studies indicate that vape users exhibit extensive downregulation of immune‐related genes, particularly within the nasal mucosa, reflecting profound immune suppression at mucosal surfaces [43]. Kowalski et al. (2025) emphasize that chronic tobacco use, regardless of delivery method, accelerates biofilm accumulation, disrupts normal wound healing, and promotes dysbiotic oral microbiota. They advocate for an integrated clinical approach pairing periodontal therapy with behavioral and pharmacological smoking cessation support to optimize outcomes [42].

Methodological variability across included studies, such as differences in participant demographics, sample sizes, and periodontal measurement techniques, contributes to observed heterogeneity. Older studies may lack rigorous control of confounders or detailed vaping exposure characterization, whereas newer studies employ more refined methodologies, including standardized indices and biochemical validations. Future systematic reviews would benefit from meta‐analyses incorporating subgroup and sensitivity analyses to better elucidate heterogeneity sources and isolate vaping‐specific effects.

While smoking cessation is known to improve oral health in the general population, its benefits in medically complex patients, such as those with type 2 diabetes, are less clear. La Rosa et al. systematically reviewed the effects of cessation in diabetic patients and found only limited improvements in periodontal parameters post‐cessation, primarily due to methodological constraints such as small sample sizes and underpowered subgroup analyses. These findings highlight the urgent need for larger, well‐designed prospective studies and reinforce the importance of multidisciplinary care wherein dental professionals actively promote cessation within comprehensive disease management frameworks [33, 42].

Despite vaping's perception as a potentially reduced‐risk alternative, this review supports a more cautious stance. E‐cigarette use has been associated with oral microbiome dysbiosis, elevated oxidative stress, impaired tissue repair, and persistent inflammation. Additionally, clinical reports have documented traumatic oral injuries linked to device malfunctions, adding to their risk profile [44]. It should be clarified that such injuries predominantly involve noncertified or counterfeit devices, underscoring the need for regulation and patient education regarding device safety.

The observed heterogeneity across studies may be partly attributed to demographic and methodological variability. Most included studies predominantly sampled male participants [20, 21, 22, 23, 25, 26], and two studies featured younger cohorts by approximately a decade [29, 30]. Cultural and regional factors, notably the predominance of studies from Saudi Arabia, may introduce confounders such as dietary habits and living conditions, limiting generalizability [20, 21, 22, 23, 24, 25, 26].

Extensive evidence confirms tobacco smoking as a robust risk factor for periodontitis, with dose‐dependent effects on disease severity and progression [45, 46]. Cigarette smokers consistently exhibit higher rates of periodontal inflammation, tooth loss, and edentulism relative to non‐smokers [47]. The harmful effects are especially pronounced in younger individuals, with approximately 51% of periodontitis cases attributable to cigarette smoking in one study [47]. A dual‐pathogenesis model likely underpins this increased risk, involving impaired host immune responses, heightened susceptibility to infection, and diminished phagocytic activity [48].

Vape users demonstrate marked immunosuppressive effects reflected in diminished expression of numerous immune‐related genes, particularly more so than cigarette smokers [43]. While no momentous differences were found in GI, PI, CAL, and PD mean scores between groups, exposure to vaping is associated with deterioration of periodontal and gingival health, oral microbiome alterations, and documented cases of extensive tooth damage due to device explosions [44]. The cytotoxic, genotoxic, and carcinogenic potential of e‐cigarette vapor components further underscores the need for caution [49].

Notably, many oral and pharyngeal symptoms reported by e‐cigarette users are minor and transient, with some evidence that switching from conventional cigarettes to vaping may alleviate certain symptoms [49]. However, a recent systematic review suggested that vaping may attenuate clinical inflammatory signs of periodontitis and peri‐implantitis compared to traditional cigarettes, though both nicotine‐containing products negatively impact periodontal health, supported by in vitro findings [50]. The effectiveness of vaping in smoking reduction and cessation varies, with reported quit rates between 13.2% and 22.9% [51]. Paradoxically, increased gingival inflammation was observed in individuals switching from cigarettes to vaping in a small clinical study [52].

Several confounding factors influence these findings. Nicotine consumption among cigarette smokers was nearly double that of vape users across studies [21, 22, 23, 24]. Cigarette smokers also had longer smoking durations and were generally older, while vape users tended to be younger. Importantly, the association between periodontal disease and smoking is dependent on both dose and duration, with vape users exhibiting daily use over 15 times and a history exceeding 5 years showing heightened periodontal inflammation risk [24]. It is estimated that smoking cessation could prevent approximately 64% of periodontitis cases, underscoring the critical public health impact of tobacco control [53].

Finally, demographic factors such as sex, age, and socioeconomic status may have influenced the observed periodontal outcomes despite rigorous exclusion criteria to limit confounders such as diabetes, pregnancy, and use of other tobacco products. The regional concentration of studies in Saudi Arabia, where lifestyle and dietary factors differ, may further affect generalizability [20, 21, 22, 23, 24, 25, 26].

In practical terms, dentists and oral healthcare teams should actively promote smoking cessation, facilitate transitions to reduced‐risk nicotine delivery systems when complete cessation is not achievable, and closely monitor periodontal status in smokers and vapers, especially in vulnerable populations such as those with diabetes [42]. While formal grading of recommendations (e.g., GRADE) was beyond the scope of this review, these practical implications underscore the role of multidisciplinary care in tobacco‐related periodontal disease management.

The weight of data indisputably demonstrates that both cigarette and vape smoking have a negative influence on periodontal health, albeit in different ways and magnitudes. Clinical vigilance in diagnosis, treatment, and behavioral risk modification is imperative. Integration of smoking cessation strategies into periodontal care is essential, not optional, to mitigate both oral and systemic health consequences [34, 54]. As emphasized by Kowalski et al. [42] and La Rosa et al. [33, 54], future clinical practice and clinical trials must prioritize evidence‐based interventions and foster cross‐disciplinary collaboration to effectively address the harm of tobacco exposure and maintain oral health.

4.1. Implications for Future Practice, Policy, and Research

This study had important implications for cigarette smokers, vape smokers, and non‐smokers. Perhaps most importantly, future research should examine the effect of cigarette smoking, vape smoking, and nonsmoking on periodontal health. Evidence‐based policies should also be developed to reduce the risk of periodontal disease, depending on the effectiveness of cigarette smoking and vaping on the periodontal status. Although the results of this systematic review come mainly from the strength of extracting direct results from previous studies, that specifically examine the relationship between cigarette smokers, vape, and non‐smokers and their relationship with periodontal disease are few, and the number of participants is still low, in addition to the lack of use all indexes of periodontal status in all studies, so there is a need to conduct more research in this area in the future. The study results may serve as a springboard for new research studies to examine the relationship between cigarette smokers, vaping, and non‐smokers.

4.2. Conclusions

The findings of this study revealed that the indices of periodontal state were similar between vape smokers and non‐smokers, with cigarette smokers having the worst markers. To corroborate the findings of this investigation, a long‐term clinical study including all periodontal parameters is urgently needed. Furthermore, the data indicated that there is a knowledge gap about the impact of cigarette and vape users. Finally, through normal community health awareness activities, the general public should be educated that vaping is not a safe alternative to smoking.

Author Contributions

Muamar O. Aldalaeen: conceptualization, methodology, software, data curation, supervision, writing – review and editing, writing – original draft. Rabia H. Haddad: investigation, validation, writing – review and editing, formal analysis, supervision, writing – original draft. Bushra Kh. Alhusamiah: visualization, data curation, formal analysis, investigation, writing – original draft, writing – review and editing. Ashraf Jehad Abuejheisheh: project administration, resources, supervision, visualization, writing – original draft, software.

Ethics Statement

The authors have nothing to report.

Consent

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Transparency Statement

The lead author Ashraf Jehad Abuejheisheh affirms that this manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

Appendix A.

A.1.

Table A1.

Summary of participants' demographic characteristics.

Study	Country	Study design	Nonsmoker/vaping/cigarettes smoking inclusion criteria	Number of participants	Age of participants	Daily frequency of vaping and cigarette smoking	Duration of vaping and cigarette smoking in years
Bergström, and Ellasson, 1987 [14]	Sweden	Case‐control	Self‐reported non‐smokers (had never smoked). Past smokers were excluded.	166 men and women non‐smokers and 76 men and women smokers	The average age of non‐smokers was 43.7 SD (10.3) years, and the average age of cigarette smokers was 42.3 SD (11.6) years	The mean daily tobacco consumption at the time of the investigation was 13.9 SD (7.0) cigarettes/day	The duration of cigarette smoking was for at least 22 SD (10.7) years of duration
			Self‐reported cigarette smoking for at least 22 years, SD (10.7).
Bergström, 1989 [11]	Sweden	Case‐control	Non‐smokers were selected randomly. Self‐reported non‐smokers (had never smoked).	59 men and women non‐smokers and 75 men and women smokers	The age of participants was 30, 40, and 50 years of age	The mean daily tobacco consumption at the time of the investigation was 15.3 SD (8.0) cigarettes/day	The duration of cigarette smoking is not mentioned
			Participants were asked if they were smokers through clinical history taking.
Martinez‐Canut et al. 1995 [16]	Spain	Case‐control	Self‐reported non‐smokers (had never smoked).	422 men and women non‐smokers and 889 men and women smokers	The average age of participants was 42, SD 10.3 years	The mean daily tobacco consumption at the time of the investigation was more than 20 cigarettes/day	The duration of cigarette smoking is not mentioned
			Self‐reported cigarette smoking.
Bergström et al. 2000 [15]	Sweden	Case‐control	Self‐reported non‐smokers (had never smoked).	133 men and women non‐smokers and 50 men and women smokers	The average age of participants was 20–69 years	The mean daily tobacco consumption at the time of the investigation was 13.3 SD (7.5) cigarettes/day	The duration of cigarette smoking was at least 20.4 SD (12.8) years of duration
			Self‐reported cigarette smoking for at least 20.4 years, SD (12.8).
Gloria Calsina et al. 2002 [19]	Spain	Case‐control	Self‐reported non‐smokers (had never smoked).	31 men and women non‐smokers and 65 men and women smokers	The average age of participants was 20–70 years	The mean daily tobacco consumption at the time of the investigation was more than 30 cigarettes/day	The duration of cigarette smoking is not mentioned
			Self‐reported cigarette smoking (smoking at the time of the study)
Torrungruang et al. 2005 [18]	Thailand	Case‐control	Self‐reported non‐smokers (had never smoked).	954 men and women non‐smokers and 282 men and women smokers	The average age of participants was 50–73 years	The mean daily tobacco consumption at the time of the investigation was more than 15 cigarettes/day	The duration of cigarette smoking is not mentioned.
			Self‐reported cigarette smoking at least 100 cigarettes in their lifetime and smoking at the time of the study.
Javed et al. 2017 [10]	Saudi Arabia	Case‐control	Self‐reported non‐smokers (had never smoked or used any kind of tobacco product).	30 men non‐smokers, 31 men vaping smokers, and 33 men smokers	The average age of non‐smokers was 40.7 SD (1.6) years, the average age of vape smokers was 37.6 SD (2.1) years, and the average age of cigarette smokers was 41.3 SD (2.8) years	The mean daily frequency of vaping at the time of the investigation was 6.8 SD (0.8)/day	The duration of Vaping smoking was 2.2 SD (0.2) years of duration.
			Self‐reported vape smoking for at least 12 months without using tobacco.
			Self‐reported cigarette smoking for at least 5 cigarettes/daily for at least 12 months.			The mean daily tobacco consumption at the time of the investigation was 13.3 SD (2.6) cigarettes/day	The duration of cigarette smoking was 5.4 SD (1.6) years of duration.
Al‐Aali et al. 2018 [17]	Saudi Arabia	Case‐control	Self‐reported non‐smokers (had never smoked or used any kind of tobacco product).
Self‐reported vape smoking for at least 1 year.	45 men non‐smokers and 47 men vaping smokers	The average age of non‐smokers was 42.6 SD (2.7) years, and the average age of vape smokers was 35.8 SD (6.2) years	The mean daily frequency of vaping at the time of the investigation was 6.5 SD (0.9)/day	The duration of Vaping smoking was 4.4 SD (1.8) years of duration.
AlQahtani et al. 2018 [7]	Saudi Arabia	Case‐control	Self‐reported non‐smokers (had never smoked or used any kind of tobacco product).	40 men non‐smokers, 40 men vaping smokers, and 40 men smokers	The average age of non‐smokers was 40.7 SD (1.6) years, the average age of vape smokers was 37.6 SD (2.1) years, and the average age of cigarette smokers was 45.8 SD (6.8) years	The mean daily frequency of vaping at the time of the investigation was 6.5 SD (0.9)/day	The duration of Vaping smoking was 8.7 SD (3.8) years of duration.
			Self‐reported vape smoking for at least current e‐cig users.
			Self‐reported cigarette smoking for at least 10 cigarettes/daily for more than 5 years.			The mean daily tobacco consumption at the time of the investigation was 14.6 SD (3.8) cigarettes/day	The duration of cigarette smoking was 21.3 SD (5.2) years of duration.
Mokeem et al. 2018 [13]	Saudi Arabia	Case‐control	Self‐reported non‐smokers (had never smoked or used any kind of tobacco product).	38 men non‐smokers, 37 men vaping smokers, and 39 men smokers	The average age of non‐smokers was 40.6 SD (4.5) years, the average age of vape smokers was 28.3 SD (3.5) years, and the average age of cigarette smokers was 42.5 SD (5.6) years	The mean daily frequency of vaping at the time of the investigation was 9.2 SD (1.4)/day	The duration of Vaping smoking was 3.1 SD (0.4) years of duration.
			Self‐reported vape smoking for at least 12 months without using tobacco. With no history of tobacco smoking.
			The mean daily tobacco consumption at the time of the investigation was 16.2 SD (2.5) cigarettes/day	The duration of cigarette smoking was 17.2 SD (2.5) years of duration.
			Self‐reported cigarette smoking for at least 5 cigarettes/daily for at least 12 months.
Alqahtani et al. 2019 [8]	Saudi Arabia	Case‐control	Self‐reported non‐smokers (had never smoked or used any kind of tobacco product.).	35 men non‐smokers, 34 men vaping smoker, and 35 men smokers	The average age of non‐smokers was 32.2 SD (0.6) years, the average age of vape smokers was 33.5 SD (0.7) years, and the average age of cigarette smokers was 36.3 SD (1.2) years	The mean daily frequency of vaping at the time of the investigation was 14.3 SD (1.2)/day	The duration of Vaping smoking was 3.5 SD (0.6) years of duration.
			Self‐reported vape smoking at least once daily for at least 1 year.
			Self‐reported cigarette smoking for at least 1 cigarette/daily for at least 1 year.			The mean daily tobacco consumption at the time of the investigation was 9.2 SD (0.6) cigarettes/day	The duration of cigarette smoking was 10.2 SD (4.1) years of duration.
ArRejaie et al. 2019 [9]	Saudi Arabia	Case‐control	Self‐reported non‐smokers (had never smoked or used any kind of tobacco product).	32 men non‐smokers, 32 men vaping smokers, and 32 men smokers	The average age of non‐smokers was 42.6 SD (2.7) years, the average age of vape smokers was 35.8 SD (6.2) years, and the average age of cigarette smokers was 40.4 SD (3.5) years	The mean daily frequency of vaping at the time of the investigation was 6.5 SD (0.9)/day	The duration of Vaping smoking was 4.4 SD (1.8) years of duration.
			Self‐reported vape smoking for at least the past year.
			Self‐reported cigarette smoking for at least the past year.			The mean daily tobacco consumption at the time of the investigation was 11.3 SD (2.5) cigarettes/day	The duration of cigarette smoking was 13.7 SD (7.2) years of duration.
Vohra et al. 2020 [12]	Saudi Arabia	Case‐control	Self‐reported non‐smokers (had never smoked or used any kind of tobacco product).	26 men non‐smokers, 26 men vaping smokers, and 28 men smokers	The average age of non‐smokers was 33.5 SD (1.4) years, the average age of vape smokers was 31.6 SD (2.4) years, and the average age of cigarette smokers was 33.3 SD (2.2) years	The mean daily frequency of vaping at the time of the investigation was 30.2 SD (8.5)/day	The duration of Vaping smoking was 0.9 SD (0.2) years of duration.
			Self‐reported vape smoking for at least once daily without using tobacco.
			The mean daily tobacco consumption at the time of the investigation was 13.5 SD (5.5) cigarettes/day	The duration of cigarette smoking was 6.1 SD (0.5) years of duration
			Self‐reported cigarettes smoking for at least one pack or up to 20 cigarettes/daily

Appendix B.

B.1.

Table B1.

CASP risk of bias tool for case‐control studies.

Author	Q1*	Q2*	Q3*	Q4*	Q5*	Q6(a)*	Q6(b)*	Q7*	Q8*	Q9*	Q10*	Q11*
Bergström, and Ellasson, 1987 [14]	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y
Bergström, 1989 [11]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y
Martinez‐Canut et al. 1995 [16]	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y
Bergström et al. 2000 [15]	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y	Y
Gloria Calsina et al. 2002 [19]	Y	Y	N	Y	N	Y	Y	Y	Y	Y	Y	Y
Torrungruang et al. 2005 [18]	Y	Y	Y	Y	N	Y	Y	Y	N	N	Y	Y
Javed et al. 2017 [10]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y
Al‐Aali et al. 2018 [17]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y
AlQahtani et al. 2018 [7]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y
Mokeem et al. 2018 [13]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y
Alqahtani et al. 2019 [8]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y
ArRejaie et al. 2019 [9]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y
Vohra et al. 2020 [12]	Y	Y	Y	Y	N	Y	Y	Y	Y	N	Y	Y

Q1: Did the study address a clear focus issue?

Q2: Did the authors use an appropriate method to answer their question?

Q3: Were the cases recruited acceptably?

Q4: Were the controls selected acceptably?

Q5: Was the exposure accurately measured to minimize the bias?

Q6: (a) Aside from the experimental intervention, were the groups treated equally?

Q6: (b) Have the authors taken account of potential confounding factors in the design and/or in their

analysis?

Q7: How large was the effect of the phenomenon of interest?

Q8: How precise was the estimate of the effect of the phenomenon of interest?

Q9: Does the reviewer believe in the results?

Q10: Can the results be applied to the local population?

Q11: Do the results of this study fit with other evidence?

Y: Yes. N: No. X: Can't tell.

Appendix C.

C.1.

Table C1.

Outcomes assessment of studies.

	Non‐smokers					Vapers					Smokers
Author	GI mean (SD)	PI mean (SD)	BOP mean (SD)	CAL mm mean (SD)	PD mm mean (SD)	GI mean (SD)	PI mean (SD)	BOP mean (SD)	CAL mm mean (SD)	PD mm mean (SD)	GI mean (SD)	PI mean (SD)	BOP mean (SD)	CAL mm mean (SD)	PD mm mean (SD)
Bergström, and Ellasson, 1987 [14]	NA	35.6 (3.34)	NA	NA	2.36 (0.03)	NA	NA	NA	NA	NA	NA	58.7 (6.23)	NA	NA	2.59 (0.06)
Bergström, 1989 [11]	1.1 (0.1)	1.0 (0.07)	NA	NA	0.9 (0.05)	NA	NA	NA	NA	NA	1.1 (0.08)	1.1 (0.08)	NA	NA	1.4 (0.04)
Martinez‐Canut et al. 1995 [16]	0.48 (0.56)	NA	NA	3.84 (0.84)	3.36 (0.61)	NA	NA	NA	NA	NA	0.81 (0.56)	NA	NA	4.5 (1.04)	3.96 (0.64)
Bergström et al. 2000 [15]	NA	0.72 (0.03)	16.4 (1.38)	NA	5.2 (0.64)	NA	NA	NA	NA	NA	NA	0.83 (0.05)	24.6 (3.77)	NA	16.8 (3.46)
Gloria Calsina et al. 2002 [19]	NA	1.7 (0.4)	40.5 (19.0)	3.9 (0.6)	3.2 (0.4)	NA	NA	NA	NA	NA	NA	1.7 (0.3)	35.6 (16.0)	4.5 (0.9)	3.5 (0.4)
Torrungruang et al. 2005 [18]	NA	58.1 (23.6)	NA	2.8 (0.9)	2.3 (0.9)	NA	NA	NA	NA	NA	NA	66.3 (24.6)	NA	3.7 (1.4)	2.8 (0.8)
Javed et al. 2017 [10]	NA	21.4 (2.8)	27.5 (3.2)	0.8 (0.1)	5.6 (0.8)	NA	23.3 (3.4)	4.6 (2.9)	1.1 (0.3)	5.1 (1.2)	NA	52.1 (6.6)	5.8 (0.8)	2.1 (0.2)	29.3 (1.7)
Al‐Aali et al. 2018 [17]	NA	47.6 (9.6)	39.8 (18.1)	NA	4.5 (0.7)	NA	52.2 (11.9)	24.7 (5.3)	NA	5.9 (1.4)	NA	NA	NA	NA	NA
AlQahtani et al. 2018 [7]	NA	34.1 (14.7)	38.9 (9.6)	NA	4.4 (0.6)	NA	51.9 (10.2)	23.3 (5.1)	NA	5.3 (1.5)	NA	67.4 (7.5)	16.7 (3.9)	NA	7.8 (1.2)
Mokeem et al. 2018 [13]	NA	22 (2.0)	35 (8.0)	0.3 (0.1)	1.4 (0.9)	NA	29 (3.0)	17 (3.0)	0.6 (0.2)	1.9 (0.9)	NA	49 (8.0)	20 (5.0)	3.1 (1.1)	4.6 (1.2)
Alqahtani et al. 2019 [8]	NA	12.6 (1.1)	19.8 (1.3)	NA	0.8 (0.1)	NA	27.3 (2.4)	6.6 (1.3)	NA	3.2 (0.3)	NA	38.6 (3.9)	6.8 (1.2)	NA	4.3 (0.2)
ArRejaie et al. 2019 [9]	NA	29.7 (5.2)	39.3 (14.7)	NA	4.5 (0.7)	NA	43.5 (8.1)	14.7 (5.3)	NA	15.9 (1.4)	NA	56.4 (12.3)	18.4 (4.8)	NA	23.8 (2.7)
Vohra et al. 2020 [12]	NA	16.6 (2.1)	22.1 (3.3)	0.2 (0.02)	1.5 (0.2)	NA	25.6 (6.2)	11.5 (0.8)	0.2 (0.04)	1.5 (0.3)	NA	39.3 (8.2)	12.1 (3.6)	0.3 (0.09)	4.2 (0.5)

Note: Percentage of the gingival index (%). Percentage of plaque index. The percentage of blood when probing. Clinical attachment loss in millimeters. Pocket depth in millimeters.

Abbreviations: BOP, bleeding on probing; CAL, clinical attachment loss; GI, gingival index; mm, millimeters; NA, not available; PD, pocket depth; PI, plaque index; SD, standard deviations.

Aldalaeen M. O., Haddad R. H., Alhusamiah B. K., and Abuejheisheh A. J., “The Impact of Cigarette Smoking and Vaping Use on the Development and Progression of Periodontitis: A Systematic Review,” Health Science Reports 8 (2025): 1‐16. 10.1002/hsr2.71245.

Data Availability Statement

All data generated or analyzed during this study are included in this published article.