Nicotine & Tobacco Research, 2019, 1600–1608

doi:10.1093/ntr/nty147
Review
Received February 27, 2018; Editorial Decision July 4, 2018; Accepted July 10, 2018

Review

Impact of Smoking Cessation on Periodontitis:

A Systematic Review and Meta-analysis of
Prospective Longitudinal Observational and

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Interventional Studies
Fábio R. M. Leite PhD1, Gustavo G. Nascimento PhD1, Stina Baake BDS1,
Lisa D. Pedersen BDS1, Flemming Scheutz Dr.PH1, Rodrigo López Dr.Odont1
Section of Periodontology, Department of Dentistry and Oral Health, Aarhus University, Aarhus, Denmark
1

Corresponding Author: Gustavo G. Nascimento, PhD, Section of Periodontology, Department of Dentistry and Oral Health
Aarhus University, Vennelyst Boulevard 9, DK-8000 Aarhus C, Denmark. Telephone: +45 8716 8194; E-mail: ggn@dent.au.dk

Abstract
Aims: This systematic review aimed to estimate the effect of tobacco smoking cessation on the risk
for periodontitis compared to the risk among never-smokers and to evaluate the effect of tobacco
smoking cessation on the clinical outcomes of nonsurgical periodontal treatment.
Methods: Electronic searches were performed in PubMed, Scopus, and Embase. Search strat-
egy included MeSH and free terms: periodontitis, periodontal diseases, smoking, tobacco use,
tobacco, tobacco products, cigarette, pipe, and cigar. Only original prospective longitudinal
observational and interventional studies that investigated the association between smoking ces-
sation and periodontitis onset or progression were included. Meta-analyses were conducted to
summarize the evidence.
Results: A total of 2743 articles were identified in electronic searches; out of which only six were
included in the meta-analysis. Pooled estimates showed that the risk of periodontitis incidence
or progression among those who quit smoking was not significantly different from the risk for
never-smokers (risk ratio [RR]  =  0.97; 95% confidence interval [CI]  =  0.87% to 1.08%). Smokers
had approximately 80% higher risk of periodontitis than quitters (RR  =  1.79; 95% CI  =  1.36% to
2.35%) and never-smokers (RR = 1.82; 95% CI = 1.43% to 2.31%). Periodontal therapy resulted in up
to 0.2 mm (95% CI = −0.32% to −0.08%) higher gain in attachment level and extra 0.32 mm (95%
CI = 0.07% to 0.52%) reduction in pocket depth among quitters over nonquitters after short follow-
up (12–24 months).
Conclusions: Few studies on the topic were identified. Smoking cessation reduced the risk for
periodontitis onset and progression, and improved the outcomes of nonsurgical periodontal
therapy.
Implications: This review provides the first quantitative evidence of the impact of smoking cessa-
tion on the risk for periodontitis onset and progression. The findings have demonstrated that the
risk for periodontitis becomes comparable to that of never-smokers and that nonsurgical peri-
odontal treatment outcomes improve after smoking cessation. Dental professionals ought to con-
sider smoking cessation interventions as a relevant component of the periodontal therapy.

© The Author(s) 2018. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. 1600
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Nicotine & Tobacco Research, 2019, Vol. 21, No. 12
Introduction
Tobacco smoking has well-documented harmful effects on physical
health with major economic costs to society. It is the leading avoid-
able cause of disease, including the burden of cardiovascular dis-
eases, cancer, and respiratory diseases, causing impoverishment by
long-term treatments and loss of productivity.1 Health care expend-
iture related to smoking represented 1.8% of the entire world gross
domestic product in 2012.1
Tobacco smoking is also associated with inflammation-driven
oral conditions such as periodontitis and oral cancer.2–4 Concerning
periodontitis, tobacco smoking sustains a chronic inflammatory pro-
cess that results in the destruction of the periodontal ligament and of
the supporting alveolar bone, ultimately resulting in tooth loss.5 In
2010, around 700 million people suffered from severe periodontitis,6
with numbers expected to rise due to increasing life expectancy and
more retained teeth due to less dental caries.
Despite the evidence suggesting the detrimental effects of smok-
ing on periodontitis,7 little is known about the effect of smok-
ing cessation on periodontitis. Two systematic reviews focusing
on the effects of smoking cessation on the results of periodontal
treatment have been published.8,9 Even though one of them also
reported incidence or progression rates of periodontitis after smok-
ing cessation, the search strategy used by the authors restricted the
number of included studies and the lack of a meta-estimate pre-
cluded the authors to quantify the impact of smoking cessation on
periodontitis.9
Given the gap left by the previous systematic reviews and the
lack of conclusive results about the effect of smoking cessation on
periodontitis, we aimed to systematically review prospective longi-
tudinal studies to determine the effect of smoking cessation on the
risk for periodontitis incidence and progression compared to never-
smokers. In addition, we reviewed the longitudinal effect of smok-
ing cessation on the clinical outcomes of nonsurgical periodontal
treatment.
Methods
This review followed the Meta-analysis Of Observational Studies in
Epidemiology (MOOSE) guidelines.10
The review questions followed the PECOS format:
1. “What is the prospective longitudinal impact of tobacco smok-
ing cessation on the risk for periodontitis onset and progression
among adults?”
(P) Population: Adults;
(E) Exposure: Individuals who quit tobacco smoking;
(C) Comparison: Individuals who never smoked tobacco or indi-
viduals continuing tobacco smokers;
(O) Outcome: Periodontitis incidence or progression;
(S) Study design: Prospective longitudinal observational studies.
2. “Does tobacco smoking cessation impact on clinical response to
periodontal therapy?”
(P) Population: Adults;
(E) Exposure: Individuals who quit tobacco smoking;
(C) Comparison: Individuals who never smoked tobacco or indi-
viduals continuing tobacco smokers;
(O) Outcome: Clinical periodontal response to periodontal
therapy;
(S) Study design: Prospective longitudinal interventional studies.
1601
Eligibility Criteria
Longitudinal prospective observational studies and interventional
studies exploring the association between smoking cessation and
periodontitis were the candidates for this review. To be included, the
study should have presented at least two measurements of periodon-
titis over time, and information on smoking cessation in comparison
with either never-smokers or continuing smokers. The definitions of
smoking and of periodontitis, so as the threshold to determine its
incidence or progression, were accepted as described by the authors.
Cross-sectional and retrospective longitudinal studies were not
considered, neither were reviews, case reports, letters, comments,
and conference abstracts.
Search Strategy
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The main biomedical databases PubMed, Embase, and Scopus
were searched up to and including May 2017. The following initial
search was conducted on PubMed: ((“Periodontal diseases”[Mesh])
OR “Periodontitis”[Mesh]) OR “Chronic Periodontitis” [Mesh])
OR “Periodontal diseases”[all]) OR “Periodontitis”[all]) OR
“Chronic Periodontitis” [all])) AND ((“Smoking”[Mesh]) OR
“Tobacco Use”[Mesh]) OR “Tobacco”[Mesh]) OR “Tobacco
Products”[Mesh]) OR “Smoking”[all]) OR “Tobacco Use”[all]) OR
“Tobacco”[all]) OR “Tobacco Products”[all]) OR “Cigarette”[all])
OR “Pipe”[all]) OR “Cigar”[all])). Date and language restrictions
were not applied. To increase literature saturation, the reference
lists of all included studies or relevant reviews were hand searched
for additional studies. The gray literature was checked in a Google
Scholar search by analyzing the first 200 hits.
Studies Selection and Data Extraction
References were entered in Endnote X8.01 (Thomson Reuters, New
York, NY) and duplicates removed. According to the inclusion and
exclusion criteria, titles and abstracts were independently screened
by reviewers (GGN and FS). Studies with potential to be included in
the review were full text accessed independently and the lists subse-
quently compared.
Information regarding authors’ name, year of publication, sam-
ple size, country of data origin, follow-up time, smoking behavior
and periodontal measures were extracted. Information on periodon-
titis incidence or progression was also gathered. Information on
the statistical approach chosen by the authors, crude and adjusted
results, and confounders were also collected for observational stud-
ies. If more than one category of periodontal status was described,
only the most extreme was considered in the meta-analysis. For
those populations with multiple assessments along the years, only
the most recent estimate with longer follow-up was included in the
meta-analysis. All disagreements were resolved through consensus
during all steps of the review process. Authors were contacted if fur-
ther details regarding the study methods or results were necessary.
Critical Appraisal
The quality of the studies was independently assessed by the same
two reviewers using the Newcastle–Ottawa scale for cohort studies
in case of observational studies11 and the modified version of the
Newcastle–Ottawa scale for nonrandomized studies for the inter-
ventional studies.13 The reviewers had consensus meetings on how
to assess the questions previously to the process. The scores for
each dimension were displayed in a graph to enable comparison of
strengths and caveats of each study.
1602
Data Synthesis
Observational Studies
Analyses were carried out in Stata 14.2 (StataCorp, College Station,
TX). Meta-analyses were performed for the following comparisons:
(1) never-smokers versus quitters; (2) quitters versus continuing
smokers; (3) never-smokers versus continuing smokers. In add-
ition, indirect comparisons between never-, former and continuing
smokers were estimated using network meta-analysis. As network
meta-analysis requires the raw data to calculate the indirect com-
parison estimates, only studies with these data available were
pooled. A combined estimate of risk ratios (RRs) was obtained using
both fixed- and random-effect models. The latter was preferred in
case of heterogeneity, for example, I2 > 50% or chi-square p value <
0.05. For estimates described as odds ratio, if data were accessible,
RR was calculated.12
Sensitivity analysis was performed to test the stability of the
results and the influence of each study on the pooled estimate by
removing one study at a time. Additionally, contour-enhanced fun-
nel plots and the Egger test were used to verify small-study report-
ing bias by detailing statistical significance on a funnel-plot in a
meta-analysis.13
Interventional Studies
It was not possible to perform a meta-analysis of interventional stud-
ies due to the heterogeneity of the data.
Results
Initial searches retrieved 2743 studies before the 1153 duplicates
were removed. From the 1590 manuscripts with titles and abstracts
screened, 58 were considered for full-text reading, 10 were included
in the review and 6 presented data for meta-analysis (Supplementary
Table  1) . Main reason for exclusion from meta-analysis was the
lack of data to obtain a relative risk estimate. Figure 1 illustrates the
articles selection along all steps of the process. The critical appraisal
results according to the different domains of the Newcastle–Ottawa
scale for both observational and interventional studies are shown in
Supplementary Figure 1.
Observational Studies
Key features of each study are summarized in Table  1. All reports
were originated from high-income countries and the follow-up time
ranged from 4 to 32 years. Smoking behaviors were assessed using
Figure 1. Flow-chart of the studies selection along the process.
Nicotine & Tobacco Research, 2019, Vol. 21, No. 12
self-reported questionnaires in all included studies, whereas peri-
odontal tissue destruction was determined through full mouth radio-
graphs in four studies and partial mouth clinical examination in the
other four. We found considerable variation in the parameters used
for determining periodontitis incidence or progression (Table 1).
RR estimates could not be calculated from two studies.14,15
According to the pooled estimates of adjusted data, the risk for
periodontitis incidence or progression among those who quit smok-
ing was not significantly different from the risk for never-smokers
(RR  =  0.97; 95% CI  =  0.88% to 1.07%) (Figure  2, A). Low het-
erogeneity was observed between studies (I2 0.0%; chi-square
p = 0.772). Supplementary Figure 2 shows that smoking cessation
had a similar impact on the risk of periodontitis incidence and pro-
gression. In addition, the Egger test and the contour-enhanced funnel
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plot (Supplementary Figure 3) discarded the presence of small-stud-
ies effect (Egger test p = 0.249).
Smokers had approximately 80% higher risk of periodontitis
than quitters (RR = 1.79; 95% CI = 1.36% to 2.35%) and never-
smokers (RR = 1.82; 95% CI = 1.43% to 2.31%) (Figure 2, B and
C respectively). Similar findings were also revealed by the network
meta-analysis (Supplementary Figure 4).
Sensitivity analysis revealed that the omission of any study would
not affect the pooled estimate of any meta-analysis (Supplementary
Figures 5–7).
Interventional Studies
Main findings from the interventional studies are described in
Table 2. The reports originated from a middle-high-income16 and a
high-income country,17 respectively. After the periodontal therapy,
patients were followed for up to 12 months17 and 24 months.16 For
both studies, information on smoking behaviors relied on carbon
monoxide level measurement and periodontal disease status on full
mouth clinical examination.
Periodontal treatment resulted in 0.2  mm higher gain in attach-
ment level among quitters than that among nonquitters in Rosa and
colleagues’ study21 whereas no differences were detected by Preshaw
et  al.17 Pocket depth reduction after periodontal treatment was
0.3 mm21 and 1.1 mm17 higher among quitters than among nonquitters.
Discussion
Even though it has been advocated that patients should quit smok-
ing to reduce the risk for periodontitis,18 this is the first systematic
review to show that after smoking cessation the risk for periodon-
titis incidence and progression can be reversed to the same level as
that of never-smokers. These studies also revealed that smokers had
approximately 80% higher risk of periodontitis than quitters and
never-smokers, corroborating findings from previous meta-analysis.4
Results from observational studies demonstrated that smoking ces-
sation reduces attachment loss progression,19,20 pocket deepening,21,22
and radiographic bone loss.19,20,28,29 Moreover, patients complying
with smoking cessation programs along nonsurgical periodontal
therapy presented more attachment gain21 and less deep pockets16,17
compared to nonquitters.
Even though after smoking cessation tobacco products are quickly
eliminated from the organism, tobacco effects on inducing systemic
inflammation might last for months or years.25 For instance, the det-
rimental effects of smoking on cardiovascular disease and cancer can
be seen even 20 years after smoking cessation.26 Possible causes are
persistent higher levels of proinflammatory proteins, for example,
Table 1. Main Characteristics of the Observational Prospective Longitudinal Studies

Periodontitis
Follow-up Periodontitis incidence or
Study Country Sample time assessment Periodontitis classification progression Crude results Adjusted results Confounders

Jansson et al. Sweden N = 507 20 years Full-mouth Ratio between the Change in bone level — Smokers had higher Plaque index
200215 radiographic distance from apex bone loss than
assessment to alveolar crest and nonsmokers:
from apex to CEJ coefficient 0.028
(SE 0.011)
Paulander Sweden N = 295 (164 10 years Full-mouth The distance between Change in Former smokers: RR 0.7 — —
et al. women) aged radiographic CEJ and the level bone level > (95% CI = 0.3% to
2004*,23 50 years at assessment of the periodontal 0.5 mm 1.7%)
baseline ligament space
Airila- Sweden N = 50 (26 17 years Full-mouth Distance between the Change in bone Smokers had lower bone — —
Månsson women) with radiographic bone margin and the height height proportion
et al. periodontitis, assessment most apical portion of proportion (%) (75.65 ± 14.75)
200514 N = 18 healthy- the defect ≥ 2 mm than former smokers
Nicotine & Tobacco Research, 2019, Vol. 21, No. 12

never-smokers (85.82 ± 3.72)
age-gender and never-smokers
matched (86.63 ± 4.15). Healthy
controls never-smokers controls
had average bone height
proportion of 93.83
(±2.24)
Baljoon et al. Sweden N = 91 10 years Full-mouth Bone loss (resorption of ≥2 increase of Former smokers: RR 1.6 Baseline: age, bone
2005*,24 (24 smokers, radiographic inter-dental marginal vertical defects (95% CI = 0.7% to height, plaque,
24 former assessment bone ≥2mm) 3.6%) number of teeth,
smokers, and 43 vertical defects
never-smokers)
Okamoto Japan N = 1332 men 4 years Partial mouth CPI scores ≥3 CPI score 3 or 4 in ≥ 30–39 years: 30–39 years: Age, alcohol
et al. aged exam (10 teeth/ (individual level) 1 sextant Former smokers: Former smokers: consumption
2006*,21 30–59 years all sextants) OR = 0.7 (95% OR = 0.7 (95%
CI = 0.3% to 1.4%) CI = 0.3% to 1.4%)
RR = 0.7 (95% RR = 0.7 (95%
CI = 0.3% to 1.4%) CI = 0.3% to 1.3%)
1–19 cig.: OR = 1.2 1–19 cig.: OR = 1.2
(95% CI = 0.6% (95% CI = 0.6% to
to 2.2%) 2.5%)
RR = 1.2 (95% RR = 1.2 (95%
CI = 0.6% to 1.3%) CI = 0.6% to 2.2%)
20 cig.: OR = 1.0 20 cig.: OR = 1.0 (95%
(95% CI = 0.6% CI = 0.5% to 1.8%)
to 1.7%) RR = 1.0 (95%
RR = 1.0 (95% CI = 0.5% to 1.7%)
CI = 0.6% to 1.2%)≥21 ≥21 cig.: OR = 2.2
cig.: OR = 2.2 (95% (95% CI = 1.2% to
CI = 1.2% to 4.0%) 4.0%)
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Table 1.  Continued
1604

Periodontitis
Follow-up Periodontitis incidence or
Study Country Sample time assessment Periodontitis classification progression Crude results Adjusted results Confounders

RR = 2.0 (95% RR = 2.0 (95%

CI = 1.2% to 3.2%) CI = 1.2% to 3.2%)
40–49 years: 40–49 years:
Former smokers: Former smokers:
OR = 0.9 (95% OR = 0.9 (95%
CI = 0.6% to 1.4%) CI = 0.6% to 1.4%)
RR = 0.9 (95% RR = 0.9 (95%
CI = 0.6% to 1.3%) CI = 0.6% to 1.3%)
1–19 cig.: OR = 1.3 1–19 cig.: OR = 1.2
(95% CI = 0.6% (95% CI = 0.6% to
to 2.5%) 2.4%)
RR = 1.3 (95% RR = 1.2 (95%
CI = 0.6% to 2.2%) CI = 0.6% to 2.3%)
20 cig.: OR = 1.6 (95% 20 cig.: OR = 1.6 (95%
CI = 1.0% to 2.6%) CI = 1.0% to 2.6%)
RR = 1.5 (95% RR = 1.5 (95%
CI = 1.0% to 2.2%) CI = 1.0% to 2.2%)
≥21 cig.: OR = 2.2 ≥21 cig.: OR = 2.0
(95% CI = 1.3% (95% CI = 1.2%
to 3.6%) to 3.4%)
RR = 2.0 (95% RR = 1.8 (95%
CI = 1.3% to 2.9%) CI = 1.2% to 2.7%)
50–59 years: 50–59 years:
Former smokers: Former smokers:
OR = 1.4 (95% OR = 1.4 (95%
CI = 0.7% to 2.5%) CI = 0.8% to 2.7%)
RR = 1.3 (95% RR = 1.3 (95%
CI = 0.7% to 2.2%) CI = 0.8% to 2.3%)
1–19 cig.: OR = 2.5 1–19 cig.: OR = 2.6
(95% CI = 0.8% to (95% CI = 0.7% to
9.2%) 9.9%)
RR = 2.2 (95% RR = 2.2 (95%
CI = 0.8% to 4.9%) CI = 0.7% to 5.1%)
20 cig.: OR = 3.4 20 cig.: OR = 3.5 (95%
(95% CI = 1.5% CI = 1.5% to 8.0%)
to 7.6%) RR = 2.8 (95%
RR = 2.7 (95% CI = 1.4% to 4.6%)
CI = 1.4% to 4.5%) ≥21 cig.: OR = 15.1
≥21 cig.: OR = 14.3 (95% CI = 4.1% to
(95% CI = 4.0% 54.8%)
to 51.6%) RR = 6.0 (95%
RR = 5.9 (95% CI = 3.1% to 8.2%)
Nicotine & Tobacco Research, 2019, Vol. 21, No. 12

CI = 3.0% to 8.1%)

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Table 1.  Continued

Periodontitis
Follow-up Periodontitis incidence or
Study Country Sample time assessment Periodontitis classification progression Crude results Adjusted results Confounders

Thomson New N = 810 aged 32 years Partial mouth AL ≥1 site with ≥ 3mm — OR = 1.47 (95% Sex, SES, plaque, use
et al. Zealand 32 years exam at age 26 AL CI = 0.62% to of dental services
2007*,19 (02 quadrants, 3.50%)
03 sites/tooth) RR 1.30 (95%
and full-mouth CI = 0.70% to
at age 32 (06 2.05%)
sites/tooth)
Morita et al. Japan N = 7678 aged 5 years Partial mouth PD ≥ 4mm in ≥ 1 sextant PD ≥ 4mm in ≥ 1 — Males: Age, BMI, history of
2011*,22 21–69 years exam (10 teeth (worst condition of the sextant Former smoker: HR diabetes mellitus
of all sextants) sextant was recorded) 0.99 (95% CI = 0.8%
to 1.2%)
Current smoker:
Nicotine & Tobacco Research, 2019, Vol. 21, No. 12

HR = 1.4 (1.2–1.6)
Females:
Former smoker:
HR = 1.05 (95%
CI = 0.6% to 1.8%)
Current smoker:
HR = 1.4 (0.95–2.1)
Gätke et al. Germany N = 2558 aged 5 years Half mouth exam PD and AL ≥2 sites with ≥ 3mm — Former smokers: Age, sex
2012*,20 20–81 years (04 sites/tooth) AL IRR = 0.9 (95%
CI = 0.8% to 1.1%)
Current smokers:
IRR = 1.2 (95%
CI = 1.0% to 1.4%)

*Studies included in meta-analysis. Smoking was self-reported assessed in all cases.

AL = attachment loss; BMI = body mass index; CEJ = cement-enamel junction; CI = confidence interval; cig = cigarettes; CPI = community periodontal index; HR = hazard ratio; IRR = incidence rate ratio; OR = odds
ratio; PD = pocket depth; RR = risk ratio; SES = socioeconomic status.
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1606 Nicotine & Tobacco Research, 2019, Vol. 21, No. 12

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Figure 2. (A) Pooled effect of smoking cessation on the incidence and progression in former smokers compared to never-smokers. (B) Pooled effect of smoking
on the incidence and progression in continuing smokers compared to former smokers. (C) Pooled effect of smoking on the incidence and progression in
continuing smokers compared to never-smokers. Data are presented as relative risk for each study (boxes), 95% confidence intervals (CIs) (horizontal lines) and
summary as relative risk with 95% CI (diamond).

C-reactive protein and fibrinogen which increase plasma viscosity.27
The increase in proinflammatory markers and in some antigens lev-
els are due to slowly reversible damages to blood vessels and lungs,
which keep producing for years after smoking cessation inflammatory
molecules.28 After smoking cessation, C-reactive protein and neutro-
phils levels were still elevated after 10 and 20 years respectively, the
tissue plasminogen activator antigen, an indicator of endothelial dys-
function, persisted high for 5 years with complete normalization after
20  years.25,29,30 A  previous systematic review suggested a possibility
of periodontitis risk reversal within 10 years after smoking cessation,
whereas response to periodontal therapy improved after 1  year.9,17
However, our results suggest that smoking cessation has beneficial
effects on the risk for periodontitis and on the response to periodontal
therapy already in the first 12 months after quitting smoking.
According to Yarnell,27 the initial quick decline in proinflamma-
tory molecules levels after smoking cessation has been associated
with the reversal of local and systemic acute effects of smoking, for
example, hypoxia. In fact, periodontal ligament cells respond in a
few hours to hypoxic conditions, modulating the expression of the
receptor activator of nuclear factor kappa B ligand, a key event to
alveolar bone resorption.5,31,32 Moreover, hypoxic conditions seem
to induce formation of reactive oxygen species and to reduce cata-
lase levels, part of the redox system, which increase the oxidative
stress perpetuating inflammation and bone resorption.33 Sayardoust
et  al.34 showed in a randomized clinical trial that higher levels of
hypoxia-inducible factor 1 alpha in the moment of dental implant
placement resulted in higher marginal bone loss in the future. In
terms of treatment, intermittent hypoxia or oxygen fluctuating levels
reduce the migratory abilities of some oral cells retarding the overall
healing process.35 Thus, the reduction in the inflammatory stimulus
after smoking cessation, including hypoxia, seems to be beneficial to
decrease the connective tissue and bone destruction.
This review is not free of limitations. An important problem of
clinical trials with smoking participants is the loss to follow-up. Both
 Nicotine & Tobacco Research, 2019, Vol. 21, No. 12 1607

interventional studies included in this review reported high losses to

month 12. Mean PD reduction

density changes for all groups.

(95% CI = 0.07% to 0.52%)
over the other two groups at
reduction in PD of 0.32 mm
Mean AL gain after 24 months
follow-up. The main reasons for abandoning the study have been

after 12 months 1.1 mm for

nonquitters and 1.6 mm for
quitters. Nonquitters and
reported to be related to guilt and shame of not being able to quit

results. No AL and bone

oscillators had the same
Quitters had an additional
Mean PD reduction after
smoking, younger age, lower schooling years, and lack of previous
Main results

24 months 0.3 mm.
willingness to quit smoking.36 Another aspect that should be exam-
ined relates to the occurrence of relapse following smoking cessa-
tion. Even though interventions have been conducted to prevent this
0.2 mm.

issue, the proportion of individuals returning to smoking over time

seems to be a major challenge in smoking cessation studies.37 Our
results support a positive effect of quitting smoking on periodontitis
and they would not invalidate the results from interventional studies;
however, the high follow-up losses might have underestimated the
Criteria for response to

AL gain, PD reduction
periodontal therapy

effect of combined nonsurgical periodontal therapy with a smoking

and bone density

cessation program.38 In addition, the high follow-up losses combined

AL gain and PD

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with the short-term follow-up of interventional studies may have
reduction.

changes.

contributed to the small differences in clinical outcomes observed

between quitters and smokers. Probably, with longer follow-up dif-
ferences between both groups shall increase.
The restriction to prospective longitudinal studies and the com-
bination of data from almost 13 500 individuals strengthened the
tooth). Radiographic: bone
Periodontitis assessment

Full-mouth exam (06 sites/

Full-mouth exam (06 sites/

evidence of the reversibility of periodontitis risk with smoking ces-

sation. Results from direct and indirect comparisons estimated with
both conventional and network meta-analyses support the consist-
density changes

ency of our findings. Furthermore, the exclusion of any study from

these included in the review would not nullify the association sup-
porting the robustness of the results. Therefore, the results emphasize
tooth)

the important role of activities promoting and reinforcing smoking

cessation and the influence of smoking policies on periodontal health.
AL = attachment loss; CI = confidence interval; CO = carbon monoxide; PD = pocket depth; ppm = parts per million.
Quitters: CO <10 ppm
Smoking assessment

Quitters: CO <8 ppm

Conclusions
Risk for periodontitis onset and progression after smoking cessa-
tion seems to be comparable to that of never-smokers. In addition,
smoking cessation seems to improve the response to nonsurgical
periodontal therapy. Thus, while there is little evidence on whether
smoking cessation interventions on the chair-side are effective or
not, current evidence indicates that smoking cessation promotion
3, 12, 24 months
Follow-up time

3, 6, 12 months
Table 2. Main Characteristics of the Interventional Included in This Review

and reinforcement ought to be included in the periodontal treatment

strategy of smokers with periodontitis.

Supplementary material
continued smoking,

continued smoking,

Supplementary data are available at Nicotine and Tobacco Research online

11 oscillated)
N = 61 (18 quit

N = 26 (10 quit

smoking, 32

smoking, 10

6 oscillated)
Sample

Funding
The study was self-funded by the authors and their institution.

Declaration of Interests
United Kingdom
Country

The authors state that there are no potential conflicts of interest.

Brazil

Acknowledgments
Fábio R. M. Leite and Gustavo G. Nascimento shared first authorship.
Rosa et al. 201416

Preshaw et al.

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