Smoking effects on the periodontium

Smoking effects on
Periodontium
Copyright ©2021 Periowiki.com
1

Contents
 History
 Classification
 Contents of the tobacco smoke
 Systemic and oral effects
 Smoking effect on the periodontium :-
I. Effect on the plaque & calculus formation
II. Effect on the microflora
III. Effect on immunology
1) Neutrophils
2) Lymphocytes
3) Natural killer cells
4) Cytokines
Effect on physiology
I. Gingival blood flow
II. Oxygen tension in the gingival tissues
III. Gingival inflammation and bleeding
IV. Gingival vasculature
V. Subgingival temperature
Copyright ©2021 Periowiki.com 2

Contents
Effect on the periodontal tissues cells
I. Fibroblasts
II. Cementoblasts
III. Alveolar bone cells
Effect of smoking on response to periodontal therapy
I. Non- surgical therapy
II. Surgical therapy
III. Maintenance therapy
IV. Refractory therapy
 Role of antibiotics in tobacco associated periodontal diseases
 Effects of smoking cessation
Smoking and dental implants
References

Tobacco is a plant within the genus Nicotiana of the Solanaceae
(nightshade) family.
The 1st commercial plantation of tobacco was in Virginia (USA) 1612.
Carl Linnaeus in 1753, named the genus of tobacco plant as
“Nicotiana” after the French ambassador to Portugal, Jean Nicot.
Introduction

History
1. It was first introduced in India in the Kingdom of AdilShahi during 1600 A.D
2. 1604 King James I of England issued the 1st official condemnation of
tobacco, “A counterblast to tobacco”
3. 1848 John Burdell an American dentist, in his book “Tobacco: its use and
abuse”, contains a reference to gingival recession in tobacco users and the
subsequent loosening of teeth.
4. Few references to the relationship between smoking and periodontal
disease appeared in the dental literature until almost a century later when
Pindborg (1949) described the association necrotizing ulcerative gingivitis
and tobacco consumption in Danish military recruits.

Types of tobacco products are: -
Type Nicotine content
Bidi 21.2 to 37.7 mg/gm
Cigarette 10mg to 15mg/gm
Filtered – 14.5mg/gm
Unfiltered – 15.6mg/gm
Cigar 100-200mg
Chewing tobacco 2.6 to 4.1 mg/gm
Electronic cigarette Compared to smoking one tobacco cigarette, the EC
devices and liquid used, delivered one-third to one-
fourth the amount of nicotine after 5 minutes of use.
Pipe tobacco
Hookah Exposed to 100 to 200 times the volume of smoke
inhaled by a single cigarette
Dissolvable tobacco May contain upto 3 times the amount found in 1
cigarette
Chutta 34.5mg/gm

CLASSIFICATION OF SMOKERS
According to CDC criteria, smokers are classified as current smokers, former and
nonsmokers.
•Current smokers: Those who had smoked 100 or more cigarettes over their life
times and smoked at the time of interview.
•Former smokers: Had smoked 100 or more cigarettes in their life time and but
were not currently smoking.
•Non smokers: Who had not smoked 100 or more cigarettes in their life time.
Depending on the number of cigarettes smoked per day as heavy and light
smokers.
•Heavy smokers : Those who smoke ≥ 20 cigarettes/ day
• Light smokers: Those who smoke ≤ 19 cigarettes /day
Pack years is defined as the number of cigarettes (packs) smoked per day
multiplied by the number of years that an individual smoked.

Contents of tobacco smoke
Particulate phase Effects
Tar Carcinogen
Polynuclear aromatic
hydrocarbons
Carcinogen
Nicotine Neuro-endocrine stimulant and
depressant
Phenol, Catecol Co- Carcinogen
Cresol Carcinogen
B-Naphtalamine Carcinogen
N-Nitrosono nicotine Carcinogen
Benzopyrine Carcinogen
Trace metals Carcinogen
Indole, carbazole Tumor accelerator
Gas phase Effects
Carbon monoxide Impairs oxygen transport
Hydrocyanic acid Ciliotoxin and irritant
Acetaldehyde and acrolein Ciliotoxin and irritant
Formaldehyde Ciliotoxin and irritant
Nitrosamines Carcinogen
Hydrazine Carcinogen
Vinyl chloride Carcinogen

Effects of smoking on systemic health

The common oral conditions seen in smokers are leukoplakia, smokeless tobacco
keratosis, smoker's melanosis, submucous fibrosis, leukoedema, hairy tongue, smoker’s
palate.
 Cleft lip and cleft palate twice as common among children born to mothers who
smoked during pregnancy.
Smoking and chewing tobacco stains and discolours teeth, dentures and restorations
 Increased risk for dental caries with smokeless tobacco as compared to smokers
 Tobacco associated bad breath is related to the strength of tobacco smoked. Pipes
and cigars contain a higher concentration of sulphur that produces stronger bad
breath.
Pipe smokers and smokeless tobacco users are prone to excessive wear of the teeth.
The eventual exposure of the dentine can lead to deep tobacco staining.
An estimated 90 percent of oral cancer patients use tobacco. A smoker is six times
more likely to develop oral cancer than a non-smoker. Smokeless tobacco users are at
50 times the risk of oral cancers of the cheek, gums and inner surface of the lips.
Smoking and oral conditions

Effect of smoking on the periodontium

Smoking – oral hygiene status - dental plaque:
associated link
Smoking encourages more dental plaque accumulation:
Kristoffersen (1970), Preber et al(1980), Macgregor (1984), Savage KO
(1999), Nwhator SO (2009 ;2010), Olagundoye O (2009) , yanbadejo P
(2010), Arowojolu MO (2013).
Plaque formation similar in smokers and non-smokers:
Alexander AG (1970), Baastian RJ & Waite IM (1978), Bergstorm and
Preber (1986), Lie et al (1998)
Less plaque levels in smokers:
Feldman RS, Bravacos JS, Rose CL (1983); Machuca G (2000)

Effect of smoking on periopathogens
-No statistically significant difference
between the distribution of periodontal
pathogens :
Studies showing differences in
subgingival microflora
-Preber et al (1992)
- J.L. Stoltenberg & C Krazor et al (1999)
- I.B. Darby (2000)
- L. Bostrom (2001)
-Vander Veldon et al (2003)
- Sreedevi Maddipatti (2012)
- J.J. Zambon (1996)
- M. Umeda (1998)
-A.D. Haffajee and S.S Socransky (2001)
-Kumar PS (2011)

Potential mechanisms contributing to the negative impact of smoking on
subgingival microflora
Yaling Jiang, Xuedong Zhou, Lei Cheng, Mingyun Li. The Impact of Smoking on Subgingival Microflora:
From Periodontal Health to Disease. January 2020 | Volume 11 | Article 66 pgs 1-13.

Yaling Jiang, Xuedong Zhou, Lei Cheng, Mingyun Li. The Impact of Smoking on Subgingival Microflora: From Periodontal
Health to Disease. January 2020 | Volume 11 | Article 66 pgs 1-13.

Shah, S. A., Ganesan, S. M., Varadharaj, S., Dabdoub, S. M., Walters, J. D.,Kumar,P. S. (2017).
The making of a miscreant: tobacco smoke and the creation of pathogen-rich biofilms. NPJ
BiofilmsMicrobiomes 3:26.
Smoke effect on Commensal biofilm Smoke effect on pathogen-rich
biofilm
1) significantly downregulates essential metabolic
functions.
2) significantly increasing expression of virulence
genes, notably lipopolysaccharide (LPS), flagella
and capsule synthesis.
3) epithelial cells mounted an early and amplified
pro-inflammatory and oxidative stress response to
these virulence-enhanced commensal biofilms.
4) early and widespread cell death.
5) smoke-induced transcriptional shifts in
commensal biofilms triggers a florid pro-
inflammatory response, leading to early
commensal death, which may preclude niche
saturation by these beneficial organisms.
1) several metabolic pathways
were over-expressed.
2) muted early response by
epithelial cells.
3) The cytokine-rich, pro-
oxidant, anaerobic
environment sustains
inflammophilic bacteria, and,
in the absence of commensal
antagonism, may promote the
creation of pathogen-rich
biofilms in smokers.

Effect of smoking on calculus formation
There is increased amount of calculus found in smoker -
(i) Increased salivary flow rate
(ii) Increase in the proportion of saliva from parotid gland due to stimulation
by nicotine
(iii) Increased calcium and phosphorus concentrations in the saliva of smokers
Bergstorm J (1999) were in he examined 258 dentally aware individuals with
comparably low levels of periodontal morbidity. He observed that prevalence of
supragingival calculus for current, former & non smokers were -86%, 66% ,
65% respectively indicating a strong association between smoking and
supragingival calculus deposition.

Albander JM (2000) - reported that significantly more pipe smokers than
cigarette smokers had supragingival calculus. This might be because the
pH of pipe smoke is higher than that of cigarette smoke, and because
pipe smokers circulate the smoke around the mouth, whereas cigarette
smoke tends to be inhaled . Moreover, the smoking cycle is much longer in
pipe smokers than in cigarette smokers, causing pipe smokers to salivate more.
Bergstrom et al (2005) - A radiographic investigation into the relationship
between tobacco smoking and subgingival dental calculus was conducted in an
adult population, including 48 current smokers, 57 former smokers, and 125
non-smokers. Results- the subgingival calculus load increased with increasing
smoking exposure, suggesting a dose–response relationship.

Authors observed :
Analysis of individual characteristics (sex, age, smoking) did not reveal any
significant differences between the slow and fast calculus formers.
A statistically significant association (p = 0.002) was found between the rate of
calculus formation and the diagnosis of periodontal disease.
Carla Fons-Badal, Antonio Fons-Font, Carlos Labaig-Rueda, M. Fernanda Solá-Ruiz,
Eduardo Selva-Otaolaurruchi, Rubén Agustín-Panadero. Analysis of Predisposing Factors
for Rapid Dental Calculus Formation. J. Clin. Med. 2020, 9, 858; doi:10.3390/jcm9030858

Effect of smoking on immunology
Neutrophils Lymphocytes
Natural killer
cells
Cytokines

Neutrophils –
-Phagocytic activity reduced (Lindhe J 2003)
-Transmigration across the periodontal microvasculature is impeded (Plamer RM 2005)
-The number of nicotine receptors expressed by human neutrophils for nicotine, cotinine is
increased in smokers and decreases on cessation (Plamer RM 2005).
-Compromised respiratory burst (Palmer RM 2005; Grover Harpreet S et al 2013)
-Higher blood PMN counts than non-smokers (Mac Farlane GD 1992)
- Lower salivary PMN counts (Alavi AL 1995)
- No major differences in the neutrophil numbers in periodontal pocket ( Petopolas G 2004)
- Increased circulatory burden of neutrophil elastase and MMPs (Grover Harpreet S et al 2013)
- Inhibited neutrophil apoptosis resulting in lingering of neutrophils for a longer period of
time, leading to an increase in the cytokine level and causing breakdown of tissue
(Shivanaikar SS, Mohamad Faizzudin 2013)

Chitra Agarwal, Tarun Kumar Baron,Dhoom Singh Mehta. Hidden truth of circulating
neutrophils (polymorphonuclear neutrophil) function in periodontally healthy smoker
subjects. J Indian Soc Periodontol. 2016 Mar-Apr; 20(2): 157–160.
In the nonsmokers, 92% of PMNs were vital cells, but by contrast, in all the
smoking subgroups, the percentage viability of PMNs were significantly
reduced (67–83%) compared to the controls (P < 0.01).
It is also notable that there was a trend for percentage viability to decrease
progressively as smoking consumption increased and this difference was
statistically significant (P < 0.01).
Thus, it was suggested that impaired PMN function may contribute to an
increased risk for periodontitis in later life. The study further supports the
importance of smoking as a risk factor for periodontitis, and smoking
cessation counseling should be a part of dental therapy.

Lymphocytes –
-Increased numbers of T cells (CD3+, CD+4 , CD+8 ) and increased T-cell
proliferation into the periodontal tissues with no effect on B cell count in blood
(LOOS B.G. 2004).
-IgG2 levels reduced in periodontitis patients who are smokers (Gunsolley JC
1997; Califano JV 1999; Quinn SM 1998)
- In smokers there are reduced number of T helper cells essential for functioning
of B lymphocytes and antibody production, with the final result being reduction
in antibodies in saliva (Guica et al 2014).

Mehrdad Radvar, Hooman Shafaee, Nooshin Mohtasham, Farid Shiezadeh, Mona Zamanpour. The effect
of smoking on inflammatory cell infiltrate subtypes in gingival tissue of patients with chronic
periodontitis. August 2017;9(8):4961-4967.
The increase in the proportion of memory T-cells observed in this study, may be
explained as an effort of the host system to compensate the impaired mechanisms of
antibody production.
Nonsmoker subjects showed significantly greater numbers of CD20+, CD68+, CD3+
cells compared to smoker subjects, both at healthy and periodontitis tissue biopsies.
Whereas there was no significant difference in terms of CD45RO.
The amount of inflammatory cells including T-cells, macrophages and B-cells in
inflamed periodontium was greater than healthy periodontium which proved the role
of host defense response to pathogens.
Results of this study, show a reduction of inflammatory mononuclear cells in both
healthy and inflamed periodontium in smokers compared to non-smokers indicating
the immunosuppressive effects of cigarette smoking

Natural killer cells –
- Low natural killer cell activity (Pearson M et al 1979, Riccsrdi 1980)
- Reduction in the regulator of NK cells (Gautam DK 2011)
- Reduction in number of circulating NK cells (Ferson et al 1979)
Cytokines –
-Higher levels of TNF alpha in GCF (palmer et al 2005)
-Levels of IL-1 significantly lower in GCF (Palmer et al 2005)
-PGEg levels elevated in GCF (Bergstrom J et al 1989)
-IL-6 and IL-8 increased in GCF (Bostrom et al 2000)
-IL-4 decreased in GCF (Giannopoulou et al 2003)

IL-1β gene expression in gingival tissue of non-smoker group with chronic
periodontitis was significantly higher than non-smoker healthy group (p=0.011).
Smoker-chronic periodontitis group showed lower IL-1β gene expression than non-
smoker-chronic periodontitis group (p=0.003).
Authors concluded that reduced levels of IL1 and in some extent IL12 in smoking
patients are responsible for higher tissue and bone degenerations and less
treatment responses in smokers.
Amir Moeintaghavi et al. The Effects of Smoking on Expression of IL-12 and IL-1β in
Gingival Tissues of Patients with Chronic Periodontitis. Open Dent J. 2017; 11: 595–602.

Effect on physiology

Smoking effect on gingival blood flow
Clarke and colleagues (1981)- demonstrated an initial increase in gingival blood flow
associated with nicotine consumption using a rabbit model. This was followed by a
reduction to below baseline levels.
Using Doppler Flowmetry, Baab and Öberg (1987)- observed a significant, immediate
increase in gingival circulation in a group of college students during smoking. Gingival
blood flow returned toward baseline within 10 minutes. His study group consisted of 12
young smokers with a daily consumption of 5–15 cigarettes who had been smokers for 2–8
years.
However, Palmer and colleagues ( 1999) measured gingival blood flow, also using a laser
Doppler technique, and their data did not support the view that smoking compromised
blood flow in the periodontal tissues.
Mavropoulus et al (2003) & Meekin et al(2000) – stated smoking did not compromise
blood flow in periodontal tissues.
However as the authors concede the technique of laser Doppler flowmetry is only
applicable in the measurement of acute changes in blood flow and there is still the
possibility that chronic exposure to tobacco smoke might affect blood flow in the
periodontal tissues. Copyright ©2021 Periowiki.com 29

Results: The mean blood vessel density for smokers was 12.388±6.472
and for non smokers was 14.800±4.91. The mean lumen area of the vessels
among smokers and non smokers was 19.290±8.775 µm2 and 20.044±7.896
µm2, respectively.
The mean epithelial thickness among smokers was 150.551±32.994 µ and
134.941±30.63 µ for non smokers.
Conclusion: Based on the present histomorphometric study, it could be
concluded that smokers have less vascular density and reduced lumen area
and increased epithelial thickness than non smokers.
However, these changes were not statistically significant.
Kumar V, Faizuddin M. Effect of smoking on gingival microvasculature: A histological
study. J Indian Soc Periodontol 2011;15:344-8

Effect of smoking on oxygen tension in gingival tissues
- Smokers exhibited lower function of oxygen sufficiency in healthy gingiva
(Hanioka et al 2000; Palmer RM 2005)
- Pocket oxygen tension was significantly lower in smokers possibly due to
impaired microcirculatory function (Hanioka et al)
- Correlation of pocket oxygen tension to gingival oxygen saturation of
hemoglobin was significant in non-smokers, but this association was absent
in smokers.

Effect of smoking on gingival inflammation
-Smoking masks overt signs of inflammation the possible reasons may be that tobacco
smoke may : (Scott DA et al 2004)
(i) Cause acute periodontal vasoconstriction,
(ii) Inhibit periodontal angiogenesis in response to inflammatory stimuli,
(iii) Suppress the production of pro-inflammatory mediators
-Markkanen H et al (1984) – stated reduction in the clinical signs of gingivitis reported is
independent of plaque levels.
- Bergstrom J , Preber H (1986) – conclude that, inflammatory gingival response could be
suppressed in smokers.
- B. Danielsen et al (1990) – stated the less gingival inflammation exhibited in smokers is
due to the reduced capacity to mount and maintain an effective defence reaction given
plaque challenge.

-Feldman RS, Bravacos JS, Rose CL. (1983) – Found that gingival
inflammation did not differ between smokers and non-smokers.
- However, MA lie (1998); R. J. Bastiaan & I.M. Waite (1978) ;
R.S. Feldman ( 1983) – study results should less gingival
inflammation in smokers.

Effect of smoking on gingival bleeding
-Dietrich T , Bernimoulin JP, Glynn RJ (2004) – Results stated that smoking has strong,
chronic, dose dependent suppressive effect on gingival bleeding on probing.
- Fouad H. Al-Bayaty (2013) - demonstrated that the duration of smoking in years, but not
the number of cigarettes smoked per day, was associated with reduced gingival
bleeding in smokers.
-Bergstrom J , Preber H :
(i) 1985- The results showed that, although they had a significantly greater plaque index,
smokers displayed a significantly lower bleeding occurrence than non-smokers, the
average being 27% and 40%, respectively.
(ii) 1986 - gingival bleeding and by GI were less pronounced in patients who smoke.
Only 25% of smokers reported bleeding gingiva as compared to 51% of non-smokers
- Muller HP (2002) - Multiple logistic regression analyses adjusted for periodontal probing
depth, plaque and calculus identified smoking status to significantly increase the risk for
the first transition of non-bleeding to bleeding upon probing by 86%.

Effect of smoking on gingival vasculature
-Mirbod SM, Ahing SI, Pruthi VK (2001); Palmer RM (2005) – Higher proportions of small
blood vessels and lower proportions of large blood vessels, with no significant difference
in the density.
- Vijaya Kumar, Mohamed Faizuddin (2011) - Increased vascular density and lumen size
was found in non smokers group than in smokers group. Also a negative correlation
between pack years and the number of blood vessels.
-Rezavandi K et al (2002) – Larger number of blood vessels in inflammed tissues of
non-smokers than smokers.
-Scardina et al (2009) - A significant correlation was found between cumulative smoking
habit and tortuousness of capillary loops in labial mucosa

Effect of smoking on subgingival temperature
- Cristopher R.J. Dinsdale (2005) – results of the study stated that, healthy subgingival
sites represented in smokers represented warmer sites, whereas diseased subgingival
sites represented cooler sites.
-Trikilis N , Rawlinson A, Walsh TF (1999) - Smokers were found to have significantly lower
subgingival temperatures compared to non-smokers, at probing depths of 2, 3, 4,
and 5 mm.
-Smoker’s exhibit decreased sub gingival temperature as compared to nonsmokers which
coincides with the decreased vascularity in smokers. They also take long time to recover
from local anesthetic agent administered.

Effect of smoking on Gingival crevicular fluid
GCF flow rate –
-Persson et al (1999) – Smoking produce transient increases in GCF
flow rate as a result of vasodilatation due to heat produced during smoking
however, chronic Smoking may result in lower resting GCF flow rate
-Kemal Ustan et al (2007) - Study was conducted on 26 age and gender matched
periodontally healthy males. Results showed that, smoking significantly increased
GCF volume compared to non-smoking subjects.
- Luthra Kushal et al (2012) - The study comprised age- and gender-matched
20 male subjects. Results showed a transitional decrease immediately after
smoking is followed by a marked increase in GCF volume 10 min after smoking.

Noushin Jalayer Naderi, Hassan Semyari,Zahra Elahinia. The Impact of Smoking on
Gingiva: a Histopathological Study. Iranian Journal of Pathology 2015;10(3):214-220.
Results:
Smokers had lower GI (1.35 ± 0.48) and higher PI (2.87±0.68) than nonsmokers (2.72
±0.31 and 1.87±0.25, respectively).
The mean count of blood vessels with ≤ 0.5µ diameter was 18.78±10.06 and
5.90±2.93 in smokers, nonsmokers, respectively.
The mean inflammatory cells infiltration in smokers, and nonsmokers were 0.89±1.03
and 70±0.46 that showed significant difference between two groups (P= 0.001,
SD=1.21).
The difference of epithelial hyperkeratosis, atrophy and acanthosis was not different
in smokers and nonsmokers. Loss of normal epithelium pattern comprising of bulbous
rete ridges, loss of polarity and increased parabasal cells was seen in 23(82.14%) of
smokers and 2(6.25%) of nonsmokers.
Conclusion: Despite the normal appearance of gingiva in smokers, smoking increasing
the epithelial changes resemble to early phases of dysplasia and decreasing
inflammatory reaction.

The research by Kaushal Luthra et (2012) revealed an overall low GCF volume
in smokers than in non-smokers. More interestingly, a transitional decrease
immediately after smoking is followed by a marked increase in GCF volume 10
min after smoking.
Aishwarya A.S., Jaiganesh. Effect of Gingival Crevicular Fluid Volume in
Smokers. IJCRR - Vol 09 Issue 17, September, 2017.
The Gingival crevicular fluid volume is known to increase with the degree of
inflammation. The increased Gingival crevicular fluid volume shows the
presence of masked inflammation in smokers. Smoking alters the gingival blood
flow which concomitantly relates to the Gingival crevicular fluid volume. This
review concludes that the result may vary according to the pattern of smoking,
methods of collection of Gingival crevicular fluid and sample size.

Effect of smoking on periodontal tissue cells
Gingival fibroblasts –
-Reduced cell viability
- Disruption of microtubules, vimentin intermediate filaments and actin
- Inhibition in cell adhesion
- Reduced growth
- Increased vacuolisation
- Degeneration of nucleus
- Oxidative damage (GSH depletion) - Colombo G (2012)
- Antiapoptotic effect, contributing to tumor growth – Argentin G (2004)
- Reduced production of type I collagen and fibronectin - Tipton and Dabbous (1995)
-Dose dependent effects-
(i) 10-75mg/ml : - significant inhibition of proliferation (Tanur et al 2000)
(ii) 20-100 ng/ml :- orientation affected
(iii) 5 to 25mMol – cytotoxic effects (Chang et al 2002)

Abdelhabib Semlali,Jamila Chakir &Mahmoud Rouabhia. Effects of Whole Cigarette Smoke on Human
Gingival Fibroblast Adhesion, Growth, and Migration. Journal of Toxicology and Environmental Health,
Part A Volume 74, 2011 - Issue 13.
Authors showed that,
when gingival fibroblasts were exposed once to whole cigarette smoke, this resulted in a
significant inhibition of cell adhesion, a decrease in the number of β1-integrin-positive cells,
increased LDH activity in the target cells, and reduced growth.
The smoke-exposed fibroblasts were also not able to contract collagen gel matrix and
migrate following insult.
Overall results demonstrate that a single exposure to whole cigarette smoke produced
significant morphological and functional deregulation in gingival fibroblasts. This may
explain the higher predisposition of tobacco users to oral infections and diseases such as
cancer.
Michael E. Dinos, MSC USA, James L. Borke, PhD, Gary D. Swiec, DC USA, James C. McPherson, III, PhD,
Jeremy L. Goodin, MSC USA, Augustine H. Chuang, PhD, In Vitro Study of the Adverse Effect of Nicotine
and Physical Strain on Human Gingival Fibroblasts as a Model of the Healing of Wounds Commonly
Found in the Military, Military Medicine, Volume 180, Issue suppl_3, March 2015, Pages 86–91.
Conclusions:
Initial treatment of HGF wounds with cyclical mechanical strain (CMS) resulted in faster
wound repopulation regardless of nicotine presence.
By day 6, wound healing of HGF exposed to both nicotine and CMS is delayed.
These findings suggest that CMS and nicotine may affect fibroblasts and delay wound
healing at other sites in the body as well.

Effect of smoking on periodontal tissue cells
Gingival fibroblasts –
-Anand N (2011) – Acrolein produced a dose dependent cytotoxic effect on human
gingival fibroblasts with complete inhibition of attachment and proliferation at higher
concentrations an in vitro study.
-Similar results observed by Rota et al (2001), Cattaneo et al and Poggi et al.
W. Zhang, F. Song, L.J. Windsor, L.J. Wind. Effects of Tobacco and P. gingivalis on
Gingival Fibroblasts 2010;89(5):527-531.
HGFs were exposed to CSC, P. gingivalis supernatant, and CSC plus P.
gingivalis supernatant. The combined treatment increased collagen degradation,
protein levels of active forms of MMP-1, MMP-2, MMP-3, and MMP-14 in conditioned
media, and the low-molecular-weight fragment of MMP-14 in membrane extracts, as
well as mRNA levels of MMP-1, MMP-2, and MMP-14.
In conclusion, the combined effects of CSC and P. gingivalis increased HGF-mediated
collagen degradation by destroying the balance between MMPs and TIMPs at multiple
levels.

Periodontal fibroblasts –
-Gamal AY (2002) – Results : (i) compromised PDL cell adhesion to root
planed surface (ii) PDL cells round in smoker group while were flat in
control group.
-PDL fibroblast growth and attachment to tissue culture plates
was inhibited by nicotine at high concentrations (over 1 mg/ml).
Vacuolation of PDL fibroblasts exposed to high concentrations of
nicotine were observed by Giannopoulou et al. (1999).
Significant inhibition of proliferation at concentrations of 100 ng/ml
to 2 μg/ml.

Willershausen, I., Wolf, T., Weyer, V. et al. Influence of E-smoking liquids on human periodontal
ligament fibroblasts. Head Face Med 10, 39 (2014).
This in vitro study demonstrated that menthol additives of e-smoking have a
harmful effect on human periodontal ligament fibroblasts. This might indicate that
menthol additives should be avoided for e-cigarettes.
Servet Kesim, Duygu Kılıc, Saim Ozdamar & Narin Liman (2012) Effect of Smoking on Attachment of
Human Periodontal Ligament Cells to Periodontally Involved Root Surfaces Following Enamel Matrix
Derivative Application, Biotechnology & Biotechnological Equipment, 26:5, 3215-3219.
Teeth both from a patient smoking more than 20 cigarettes daily and from another
non-smoking patient were extracted and PDL tissue biopsies were taken from these
teeth. Fibroblasts were cultured.
 Each root surface was divided into six equal parts. Samples were treated with
citric acid and EMD, embedded into cell culture flasks, and kept in the culture for 1
h, 3 h, 5 h and 3 days. Then, electron microscopy analysis was performed.
In the smoking group, collagen fibers were spread parallel to the surface as in the
nonsmoking group, but in one single direction rather than in different directions.
It was observed that EMD application on smoking and non-smoking periodontally-
diseased patients could affect the function of PDL cells and the potential of collagen
production.

Cementoblasts –
Chun Chan Sen et al (2014) –
Concentrations of nicotine > 1.5mM demonstrated cytotoxicity to cementoblasts.
Nicotine attenuated cell migration in a dose-dependent manner.
In addition, nicotine augmented the production of IL-6 and TNF-α in a dose-
dependent manner.
The concentration of 1mM nicotine enhanced the generation of intracellular ROS
in a time-dependent manner.

Alveolar bone cells -
-Angela R. Kamer (2006) : increased production of IL-6 and TNF- alpha
-Beom Suki et al (2011) : effects of nicotine on the proliferation and osteoblast
differentiation of human alveolar bone marrow-derived mesenchymal stem cells
(hABMMSCs): - Calcium accumulation; ALP activity; and mRNA levels of ALP,
bone sialoprotein (BSP), collagen type I α 1 (Col1αI), and runt-related
transcription factor 2 (Runx2) were significantly decreased by treatment
with 2mM of nicotine, while osteocalcin transcripts decreased by treatment
with 1 to 2 mM of nicotine.
-Nicotine :
(i) Induces increased expression of MMPs (1, 2, 3, 13) in osteoblasts
(ii) Suppresses the mineralized nodule formation by osteoblasts
(iii) Enhances osteoclast differentiation through macrophage colony
stimulating and PGE2 production induced by nicotine treated osteoblasts

Effect of smoking on alveolar bone
Bergstorm,SorenEliasson (1991) - included 210 subjects of 24-60 yrs who were
categorized as current Smokers, former smokers and nonsmokers bite wing
radiographs were taken to determine the distance between CEJ and IS. It was observed
that distance between the CEJ and IS was significantly greater in smokers compared
to other groups .
Baljoon M, Natto S, Bergstrom J (2005) population was examined on two occasions with
a 10-year interval, including 91 individuals, 24 smokers, 24-former smokers, and 43 non-
smokers.Assessment of vertical bone loss was based on full sets of intra-oral radiographs
from both time points. The 10-year increase in the proportion of vertical defects was
statistically significant between smokers and non-smokers.
Tang TH, Fitzsimmons TR, Bartold PM (2009) done to determine the GCF Levels of
sRANFKL, OPG in chronic periodontitis pts with varying smoking history were in study
included 149pts, 58-never smokers, 39 former smokers,52- current smokers it was
observed that Ratio of sRANKL and OPG not significant between 3 groups. In current
smokers RANK: OPG was increased and statistically significant .

Smoking as a risk factor for increased prevalence and severity of
vertical bone loss
Baljoon M (2004, 2005) -Risk of vertical defects increased with
increased exposure in cigarette smokers as well as water pipe
smokers .Compared to non-smokers the 10-year relative risk was
2.4-fold increased in light exposure smokers and 5.8-fold
increased in heavy exposure smokers.
(similar results showed by Haghighati et al 2010).

2017
2017
2010
2007
2018
2013
2001
2016
2015
Yixin Zhang, Jinxiu He, Bing He, Ruijie Huang, Mingyun Li. Effect of tobacco on periodontal disease and oral
cancer. Tob. Induc. Dis. 2019;17(May):40.

2016
2013
2018
2013
2006
2017
Yixin Zhang, Jinxiu He, Bing He, Ruijie Huang, Mingyun Li. Effect of tobacco on periodontal disease and oral
cancer. Tob. Induc. Dis. 2019;17(May):40.

Effect of smoking on pathogenesis of periodontitis

Effect of smoking on pocket depths and clinical attachment levels
Smokers tend to have greater numbers of deeper periodontal pockets and greater mean
periodontal probing depth (PPD) (Bergstrom J, Eliasson S 1987, 1989 ; Haber J, Wattles J
1993)Studies have also shown greater mean clinical attachment level (CAL) loss in
smokers compared to nonsmokers. (Axelsson P, Paulander J, Lindhe J. 1998; Schenkein
HA 1995)
Tomar SL, Asma S. (2000) –current smokers were about 4 times as likely as persons who
had never smoked to have periodontitis. 41.9% of periodontitis cases (6.4 million cases)
in the U.S. adult population were attributable to current cigarette smoking and 10.9%
(1.7 million cases) to former smoking. Among current smokers, 74.8% of their
periodontitis was attributable to smoking.
Ogawa H et (2002) – 394 subjects (208 males and 186 females) were surveyed aged 70
years. Approximately 75% of subjects exhibited additional attachment loss over a 2-
year period. Significant associations were found between additional attachment loss
and smoking, and attachment level of 6 mm or more at baseline. Smoking habit and
baseline attachment level of 6 mm or more may be considered risk factors for further
attachment loss among healthy elderly people.

Haffajee AD, Socransky SS. Relationship of cigarette smoking to attachment level profiles. J
Clin Periodontol. 2001 Apr;28(4):283-95.
Conclusion:
Smokers had evidence of more severe periodontal disease than
past or never smokers.
At all levels of mean attachment loss, smokers exhibited more
disease than never smokers.
Difference in mean attachment level between smokers and never
smokers at individual sites was not uniform.
Significantly more loss was observed at maxillary lingual sites and
lower anterior teeth suggesting the possibility of a local effect of
cigarette smoking.

Alaa Omarn, Hadeel Mazin Akram & Azza Wala Aldeen Khairi. THE EFFECT OF SMOKING ON
CLINICAL ATTACHMENT LOSS IN CHRONIC PERIODONTITIS. IJABR 2018;8(1):74-76.
Authors studied the differences of clinical attachment loss between
smoker and non smoker.
50 adult subjects aged between (40 -70) years, were divided into two
groups: 25 smokers and 25 controlled (non-smoker).
The plaque index, gingival index and clinical attachment loss were
measured.
There was a significant difference in clinical attachment loss and plaque
index in smoker group than the control group while gingival index show
no significant difference (the gingival index is higher in non-smoker than
in smoker). Smoking has a great effect on the clinical attachment loss.

Smoking and tooth loss

Meta-analysis of cross-sectional studies did not show any differences
between former and current smokers in the chance of losing 1 or more
teeth (OR = 1.00; 95% CI = 0.80 to 1.24, I2 = 80%), losing more than 8 teeth
(OR = 1.02; 95% CI = 0.78 to 1.32, I2 = 0%) or being edentulous (OR = 1.37;
95% CI = 0.94 to 1.99, I2 = 98%).
Meta-analysis from longitudinal studies showed that, when compared
to never smokers, former smokers presented no increased risk of tooth
loss (RR = 1.15; 95% CI = 0.98 to 1.35, I2 = 76%), while current smokers
presented an increased risk of tooth loss (RR = 2.60; 95% CI = 2.29 to 2.96,
I2 = 61%).
Meta-regression showed that, among former smokers, the time of
cessation was the variable that better explained heterogeneity
(approximately 60%).
Souto, M.L.S., Rovai, E.S., Villar, C.C. et al. Effect of smoking cessation on tooth
loss: a systematic review with meta-analysis. BMC Oral Health 19, 245 (2019).

Study on patterns of periodontal destruction in smokers
-Haffajee and Socransky(2001)- found that the patterns of attachment loss
in smokers and nonsmokers were different.
- Smokers had more clinical attachment loss and greater probing depth in
all areas, with the highest values being in the palatal area
Haber and Kent (1992)
Baharin et al (2006)
Preber and Bergstrom (1986)
Van der Weijden et al (2001)
Sukumaran Anil (2008)

Mullally and Linden
(1996)
had reported that cigarette smokers
were significantly at risk for furcation
involvement in smokers than non smokers.
The study showed a significantly increased
number of molar teeth furcation defects
Kaleem M (2009) furcation involvement was also significantly
increased in smokers as compared to
non smokers. Class II furcation cases were
seen only in smokers.
Effect of smoking on furcation involvement

Effect of smoking on genetic polymorphism
-A positive genotype for IL-1 increases a risk for tooth loss by 2.7 times and smoking
increases the risk of tooth loss by 2.9 times. The combined risk for tooth loss is
estimated to be 7.7 times. There was significant attachment loss in genotype positive
patients who were smokers. (Mc Guire MK 1999)
-Interaction between aryl amines produced in tobacco smoke and N- acetylaminetransferase
2 was determined. In patients with periodontal disease- NAT-2 polymorphism affects
individuals making them as slow or rapid acetylators. Results indicated that patients with
the most severe periodontal condition were the slow acetylators. (Miesel P et al 2000)
- K tanaka et al (2013) - investigated associations between four VDR single-nucleotide
polymorphisms (SNPs) including rs731236 (TaqI), rs7975232 (ApaI), rs1544410 (BsmI) and
rs2228570 (FokI), and the risk of periodontal disease among 131 young Japanese women.
Results showed that, biological interaction between VDR SNP rs7975232 and smoking that
affects periodontal disease.

Effect of passive smoking on periodontal health
Arbus SJ et al (2001) - data derived from the NHANES III, reported that the odds of
having periodontitis was 1.6 higher among individuals exposed to passive smoking
after adjusting for sociodemographic factors, diabetes and dental care.
Yamamoto et al. (2005) - showed that after adjustment for other lifestyle factors,
passive and active smoking increased the likelihood of having periodontitis by 2.9-
fold and 4.9-fold respectively.
Nishida N (2006) - Exposure to passive smoke was associated with elevation of
interleukin-1b, albumin and aspartate aminotransferase levels in saliva. No
increased proportion of periodontal pathogens (A. actinomycetemcomitans, P.
gingivalis, T. denticola, P. intermedia and P. nigrescens) in saliva in passive
smokers, despite periodontal destruction.

Nishida N et al (2008) - A 2-year follow-up of this sample showed a similarly
higher risk for clinical attachment loss in passive and active smokers compared
with nonsmokers.
Johannsen A (2014)- The concentrations of salivary proteins such as albumin,
aspartate aminotransferase and lactoferrin, were significantly elevated in passive
smokers relative to nonsmokers. Regarding periodontal pathogens there were no
significant differences between groups, except for P. nigrescens, which was
present at lower levels in passive smokers.

Passive smoking
Hajifattahi F, Azarshab M, Haghgoo R, Lesan S (2010) Evaluation of the Relationship between
Passive Smoking and Oral Pigmentation in Children. J Dent (Tehran) 7(3): 119-123.
Study evaluated the role of parental smoking on pigmentation of their children’s
oral mucosa. The passive smoker group included 200 children who at least one
member in their family was a smoker.
The control group included 200 children who did not have a smoker in their
family. Furthermore, two groups were matched in the point of view of skin color.
Pigmentation was seen in 150 children (75%) in the experimental group and 122
children (61%) in the control group (P<0.005).
Relative risk of oral pigmentation for children who were exposed to passive
smoking was 1.23.
Melanin pigmentation could be induced by the stimulation of melanocytes by
stimuli present in tobacco smoke such as nicotine and benzopyrene (Ali Hassan Al
Waked. The Impacts of Smoking on Periodontal Health. Biomed J Sci & Tech Res 15(5)- 2019).

Effect of smoking on response to periodontal
therapy
Non- surgical
therapy
Surgical
therapy
Recurrent
therapy
Maintenance
therapy
Implants

Healing response in smokers
Reasons-
Smoking increases platelet adhesiveness, raising the risk of thrombotic micro vascular
occlusion and tissue ischemia.
Carbon monoxide diminishes oxygen transport, and hydrogen cyanide inhibits the
enzyme systems operative in oxidative metabolism and oxygen transport at the
cellular level.
Because of the direct contact of smoke constituents on open wounds, or reduced blood flow,
or impaired leukocyte function, or diminished fibroblast activity, or the drying effect of
mouth-breathing, or the clot-disrupting effect of the negative intraoral pressure produced
during tobacco smoking.
Cytotoxic effect of nicotine and cigarette smoke extract on fibroblasts which in turn may
affect the rate of proliferation, differentiation of these cells. Decreased collagen synthesis
which is an essential component of wound repair.
Smoking is associated with catecholamines release, resulting in vasoconstriction and
decreased tissue perfusion. Copyright ©2021 Periowiki.com 64

Smoking has been shown to impair revascularization during
soft and hard tissue wound healing, which is critical for
periodontal plastic, regenerative, and implant procedures.

Effect of smoking on non- surgical therapy
Response to scaling and root planing
Reduction in pocket depth
Gain in clinical attachment loss

Probing depth reductions in smokers Vs non-smokers
1.At all sites :

2. Only sites with an initial probing depth of 5mm and greater :
Probing depth reductions in smokers Vs non-smokers

Clinical attachment level gains in smokers Vs non- smokers
1. At all sites :
Grossi et al (1997)
Hafajee et al (1997)
Machtei et al (1998)
Winkel et al ( 2001)
No statistically significant differences were
found between the two groups assessed.

2. Only sites with an initial probing depth of 5mm and greater :
Clinical attachment level gains in smokers Vs non- smokers
No statistically significant differences were
found between the two groups assessed.

A meta-analysis Labriola et al (2005) evaluated the impact of smoking on nonsurgical therapy and
found that probing depth reduction in sites where probing
depth was initially ≥5 mm was significantly greater (0.433
mm) in non- smokers than in smokers.
Apatzidou, D.A (2005) Nonsmokers had 0.9 mm more probing depth reduction and
0.6 mm more clinical attachment gain at periodontitis sites
(probing depth ≥5 mm, clinical attachment level ≥3 mm)
compared to smokers at 6 months.
Darby et al (2005) Darby reported 0.7 mm less improvement in
probing depth and 0.4 mm less attachment gain in smokers
compared to nonsmokers at the 6- to 8-week reevaluation
following scaling and root planing.
Kanmaz B, Lappin DF, Nile CJ, Buduneli N.
Effects of smoking on non-surgical
periodontal therapy in patients with
periodontitis Stage III or IV, and Grade C. J
Periodontol. 2020 Apr;91(4):442-453.
14 smoker and 13 non-smoker patients completed the study
protocol and revealed similar clinical findings except for the
higher plaque scores in the non-smokers at 6 months (P
<0.01). Significant differences were found between the study
groups in biofluid cytokine levels at 1 and 3 months (P
<0.01). Gram-negative bacteria were more abundant in the
smokers at baseline and so were Gram-positive bacteria in
the non-smokers (P <0.01). Gram-negative bacteria
repopulated in the smokers faster than in the non-smokers (P
<0.01).
Effect of smoking on Pocket depth and clinical attachment levels after
non- surgical therapy

Effect of smoking on Surgical therapy
Pocket depth reduction after surgery
Deterioration of furcations after surgery
Gain in clinical attachment levels, bone fill,
Recession
Increased membrane exposure after GTR

Preber and Bergstrom et al (1990)- determine the effect of smoking on
periodontal healing in 54 patients . With moderate to severe periodontitis,
24 smokers with persistent pockets after surgery Re-examination at 12
months showed reduction of probing depth in smokers was less as compared
to nonsmokers and it was statistically significant .
Scabbia A, Cho KS, Sigurdsson TJ, Kim CK, Trombelli L (2001) – 57 subjects
were included in the study. In smokers, 16% of deep sites healed to
postsurgery PD values < or = 3 mm as compared to 47% in non-smokers ; 58%
of deep sites in smokers showed a CAL gain > or = 2 mm, as compared to 82%
in non-smokers .
Effects of smoking on flap surgery

Qualitative assessment of the articles consistently showed an improved treatment
effect among non-smokers versus smokers.
The reduction in PD in smokers and non-smokers ranged from 0.76 to 2.05 mm and 1.27
to 2.40 mm, respectively. For CAL, the gain in non-smokers versus smokers ranged from
0.29 to 1.6 mm and 0.09 to 1.2 mm, respectively.
Meta-analysis on eight studies reporting on 363 study participants demonstrated an
increased reduction in mean (95% confidence interval) PD of 0.39 (0.33 to 0.45) mm.
Similar results were found for mean gain in CAL (0.35 [0.30 to 0.40] mm, n = 4 studies).
Conclusions: Considering the relatively homogenous information available, the authors
conclude that active smokers could be candidates for periodontal flap surgical
procedures. However, the magnitude of the therapeutic effect is compromised in
smokers compared with non-smokers. Therefore, cigarette smokers should be: 1)
encouraged to abstain from smoking; and 2) thoroughly informed preoperatively of
substantial reduction in clinical outcomes compared with non-smokers.
Kotsakis GA, Javed F, Hinrichs JE, Karoussis IK, Romanos GE. Impact of cigarette smoking on
clinical outcomes of periodontal flap surgical procedures: a systematic review and meta-analysis.
J Periodontol. 2015 Feb;86(2):254-63.

Scientific rationale for the study: Smoking has been identified as a major risk
factor for periodontitis. However, there is no systematic review and meta-
analysis comparing the
changes of PD and CAL following non-surgical periodontal therapy in smokers
and non-smokers.
Principal findings: Smokers with periodontitis had significantly less PD
reduction and CAL gain than non-smokers with periodontitis within one year
following non-surgical
periodontal therapy (both p < .01).
Practical implications: Clinicians should expect inferior clinical outcomes of
non-surgical periodontal therapy in smokers compared to non-smokers.
Chang J, Meng HW, Lalla E, Lee CT. The impact of smoking on non-surgical periodontal therapy:
A systematic review and meta-analysis. J Clin Periodontol. 2021;48:61–76.

Proportion of plaque was reduced by 20% in non‐smokers and by 18% in
smokers, and BoP by 46% and 37%, respectively.
In the adjusted mixed model, the mean reduction of PPD > 4 mm among
smokers undergoing surgery was 14.4 versus 9.7 in non‐smokers (p < .001).
The odds ratio for being a poor responder was 2.40 (95% CI 1.99–
2.91, p < .001) for smokers.
Conclusion
Although surgical treatment reduced PPD >4 mm in smokers more effectively
than in non‐smokers, significantly more non‐smokers were good responders
after periodontal therapy.
Aorra Naji, Kristina Edman, Anders Holmlund. Influence of smoking on periodontal healing one
year after active treatment. J Clin Periodontol 2020;47(3):343-350.

Effect of smoking on furcations after periodontal surgery
Trombelli L et al (2003) - 31 systemically healthy subjects with moderate to
advanced periodontitis, who presented at least one Class I or II molar
furcation defect, were selected.
Study indicated that (1) FDS produced clinically and statistically significant
PPD reduction, v-CAL gain, and h-CAL gain in Class I/II molar furcation
defects, and (2) cigarette smokers exhibited a less favorable healing
outcome following surgery in terms of both v-CAL and h-CAL gain.
Dannewitz D et al (2006) – 505 molars in 71 patients were evaluated. At
baseline 200 of 505 molars exhibited no FI, 116 degree I, 122 degree II, and
67 degree III FI. A multi-level proportional hazard model revealed smoking,
baseline bone loss, number of molars left, and degree III FI as risk factors
influencing the retention time of molars.

Effect of smoking on regenerative procedures
Smoking effect on Guided tissue regeneration : -
- Prevents tissue maturation and mineralization indicating that the effect of
smoking is crucial at the tissue maturation phase. (Tonetti et al 1995 ; Machtei
et al 2003)
Bowers et al.(2003) found significantly more residual class II defects among
smokers than nonsmokers (62.5% vs. 14.3%) in furcations treated with a
combination of demineralized freeze-dried bone allograft and a
polytetrafluoroethylene membrane.
Cortellini & co-workers (2004) - longer term study of 175 patient followed for an
average of 8 years after guided tissue regeneration therapy; smoking increased
the probability of losing ≥2 mm attachment, whereas compliance with
periodontal maintenance decreased the risk.

Stavropoulous et al (2004) - Forty-seven intrabony defects in 32 patients were
treated by means of polylactic acid/citric acid ester copolymer bioresorbable
membranes. Smokers gained approximately 1 mm less in PAL than non-smokers.
PPD reduction was less pronounced in smokers than in non-smokers, resulting in
somewhat deeper residual PPD in smokers than in non-smokers .
Patel et al (2012) - A meta-analysis of a subgroup of three studies demonstrated
that smoking resulted in significantly less bone gain as measured by a change in
the probing bone level after the treatment of intrabony defects with guided
tissue regeneration. The meta-analysis showed a standardized mean difference
of -2.05 using the random-effects model.
Stramazzotti et al (2015)- Use of PLGA/HA with a rubber dam significantly
improved the periodontal parameters in both smoking and non-smoking subjects.
This improvement was nevertheless lower in smokers than the non-smokers,
confirming the negative impact of smoking on periodontal regeneration.

Reasons for compromised root coverage outcome procedures:
Combination of small blood
vessel numbers in grafts and
flaps, vasoconstriction and
reduced gingival blood flow
Inhibits revascularization
Therefore, reduce graft stability
&
Hence, low predictability

Effect of smoking on root coverage procedures
Leandro Chambrone (2009) - From a total of 632 references, the authors considered
seven studies to be relevant. The meta-analysis indicated a statistically significant
greater reduction in gingival recession and gain in clinical attachment level for
nonsmokers when compared with smokers whose gingival recession was treated with
subepithelial connective-tissue grafts. Additionally, nonsmokers exhibited significantly
more sites with complete root coverage than did smokers . For coronally advanced
flaps, differences between the groups were not significant. (Meta- analysis)
Silva et al.(2007) - evaluated the technique of Coronally Positioned Flap (CPF) with
vertical incision and reported percentages of 69.3% and 91.3% for smokers and non-
smokers, respectively. (similar results shown by Bhaumik Nanavati 2013)
Andia DC et al ( 2008) - Twenty-two defects were treated by CTG in canine and premolar
Miller Class I and II gingival recessions (11 smokers and 11 non-smokers). Individuals
smoking > or =20 cigarettes/day for > or =5 years were considered smokers. At 24
months postoperatively, statistical analysis showed that smokers presented poorer
outcomes with regard to PD, GR, and CAL.

Effect of smoking on root coverage procedures
Cléverson O. Silva et
al (2010)
Twelve non-smokers and 10 smokers treatment planned for FGG At 90 days
postoperatively, FGG width, length, and area were respectively reduced by 31%,
22%, and 44% in non-smokers and by 44%, 25%, and 58% in smokers (no
significant differences between groups; P >0.05). Significant KT increases were
observed in both non-smokers and smokers (5.4 and 4.8 mm, respectively).
Donor-site immediate bleeding was significantly more prevalent in non-smokers
(75%) compared to smokers (30%).At 15 days postoperatively, donor-site
complete epithelialization was much more prevalent in non-smokers (92%) than
in smokers.
Danilo M. Reino et al
(2012)
Twenty heavy smokers (10 males and 10 females) with two bilateral Miller class I
gingival recessions received coronally positioned flaps in one side (Control
group) and extended flap technique in the other side (Test group). Both
techniques promoted low root coverage (Control group: 43.18% and Test group:
44.52%). In conclusion, no difference was found in root coverage between the
techniques.
Nanavati B, Bhavsar
N V, Mali J. (2013)
Ten current smokers (≥10 cigarettes daily for at least 5 years) and 10 non-
smokers (never smokers), each with one 3 to 4-mm Miller Class I recession
defect in an upper canine or bicuspid, were treated with Coronally positioned
flap(CPF). Intra-group analysis showed that CPF was able to reduce Recession
Depth(RD)and improve CAL in both groups (P <0.05). Intergroup analysis
demonstrated that smokers presented greater residual RD at 6 months and
lower percentage of root coverage (60.09% versus 76.05%; P <0.05).

Effect of smoking on maintenance therapy
Periodontal maintenance patients who smoke are reported to be twice as likely
to loose teeth over a period of 5yrs as compared with the nonsmokers on
maintenance therapy (McGuire M, Nunn M.1996).
The detrimental effects of smoking on treatment outcomes appear to be long
lasting, and independent of the frequency of maintenance therapy. After four
different modalities of therapy including scaling, scaling and root planing,
modified Widman flap surgery, and osseous surgery, maintenance therapy was
performed by a hygienist every 3 months for 7 years .
Christoph Reider (2004) – 87 patients who completed active periodontal
treatment followed an SPT programme for atleast 5 years. The results state that,
more than compliance it is the smoking which influenced the treatment
outcomes of SPT, regarding the incidence of new residual pockets during 7.3
years of SPT.

smokers had deeper and more residual
pockets than
nonsmokers, even though no significant
differences in plaque or bleeding on probing
scores were found. These
data suggest that the effects of smoking on
the quality of subgingival plaque, the host
response, and the healing
characteristics of the periodontal tissues may
have a long-term effect on pocket resolution
in smokers that may
not be managed by conventional periodontal
therapy.
Smokers consistently had deeper pockets than nonsmokers and less gain in
attachment when evaluated each year for the 7-year period. Heavy smokers
(>20 cigarettes/day) had more plaque than light smokers, former smokers,
and nonsmokers. Even with more intensive maintenance therapy given every
month for 6 months after flap surgery (Scabbia A et al 2001), smokers had
deeper and more residual pockets than nonsmokers, even though no
significant differences in plaque or bleeding on probing scores were found.
These data suggest that the effects of smoking on the quality of subgingival
plaque, the host response, and the healing characteristics of the periodontal
tissues may have a long-term effect on pocket resolution in smokers that may
not be managed by conventional periodontal therapy.

pockets than
in smokers that may
therapy.
Eleven papers were included in the systematic review: four case-control and
seven cohort studies.
Ten out of the 11 studies concluded that smoking was an important risk factor
for the occurrence of Tooth Loss(TL).
Meta-analysis of four of the cohort studies found that smokers had 3.24 times
the chance of occurrence of TL than nonsmokers undergoing Periodontal
Maintenance Therapy(PMT) (95%CI: 1.33-7.90).
Overall, studies' risk of bias was low.
The quality of the scientific evidence moderately supports that smokers
undergoing PMT have a greater chance of TL than nonsmokers.
Vieira TR, Martins CC, Cyrino RM, Azevedo AMO, Cota LOM, Costa FO. Effects of smoking on tooth
loss among individuals under periodontal maintenance therapy: a systematic review and meta-
analysis. Cad Saude Publica. 2018 Sep 21;34(9):e00024918.

pockets than
in smokers that may
therapy.
Fernando Oliveira Costa, Luís Otávio Miranda Cota. Cumulative smoking exposure and cessation
associated with the recurrence of periodontitis in periodontal maintenance therapy: A 6‐year
follow‐up. J Periodontol 2019;90(8):856-865.
This study followed individuals in periodontal maintenance therapy (PMT) over
6 years and longitudinally evaluated the effects of cumulative smoking
exposure and duration of smoking cessation on the recurrence of
periodontitis(RP).
Recurrence of periodontitis in Non-smokers, Former Smokers, and Current
Smokers groups was 44.2%, 68.2%, and 80.0%, respectively.
After adjusting for confounders, odds ratios (95% confidence interval) for the
Recurrence of Periodontitis in T2(second time, 6years) was 2.80 (2.11 to 5.14)
for Former Smokers and 5.97 (3.58 to 9.88) for Current Smokers.
There was a significant dose‐response relationship between pack‐years of
smoking and the RP, as well as a significant decrease in the risk for the RP as
the years of smoking cessation increased.

Cigarette smoking and refractory periodontitis
Study conducted to learn if refractory periodontitis may be associated with
defects in peripheral blood polymorphonuclear leukocyte (PMN) function,
phagocytosis and chemotaxis were analyzed in 31 otherwise healthy patients and
12 unaffected controls.
Data suggest that there is a strong association between a peripheral blood PMN
defect and refractory periodontitis. Furthermore, these studies suggest that
tobacco use may contribute to this association.
MacFarlane GD, Herzberg MC, Wolff LF, Hardie NA. Refractory periodontitis associated with
abnormal polymorphonuclear leukocyte phagocytosis and cigarette smoking. J Periodontol.
1992 Nov;63(11):908-13.
1) Tobacco smoking probably plays a significant role in the development of
refractory periodontitis (Adams DF 1992; MacFarlane GD, Herzberg MC, Wolff
LF, Hardie NA1992; Magnusson I, Walker CB 1996).
1) An unusually high percentage of refractory patients are smokers (>90%)
MacFarlane GD, Herzberg MC, Wolff LF, Hardie NA 1992; Magnusson I, Walker
CB 1996 when compared to the percentage of smokers in the general
population (~25%) MacFarlane GD, Herzberg MC, Wolff LF, Hardie NA 1992.

Role of antibiotics in tobacco associated periodontal diseases

Paquette, D., Oringer, R.,
Lessem, J., Offenbacher,
S., Genco, R., Persson,
G.R., Santucci, E.A. and
Williams, R.C. (2003)
Tomasi, C. and
Wennstrom, J.L. (2004)
When scaling and root planing were combined with
adjunctive doxycycline gel or minocycline
microspheres, the response in smokers was similar to
that seen for nonsmokers receiving scaling and root
planing alone.
Winkel, E.G., Van
Winkelhoff, A.J.,
Timmerman, M.F., Van
der Velden, U. and Van
der Weijden, G.A. (2001)
In another study comparing adjunctive systemic
antibiotic therapy to scaling and root planing alone,
smokers receiving amoxicillin and metronidazole
showed significantly more improvement in bleeding
scores, probing depth and attachment levels than
smokers receiving only scaling and root planing.
These studies indirectly support the concept that the locally applied antibiotics of the
tetracycline family may not only have an antimicrobial effect, but may also exert a
local host modulating effect by protecting against some of the effects of smoke on the
destructive/inflammatory arm of the host response.

The potential benefit of smoking cessation on the periodontium is
likely to be mediated through a number of different pathways
such as a shift towards a less pathogenic subgingival microflora,
recovery of the gingival microcirculation, and improvements in
aspects of the immune-inflammatory responses.
In general terms, periodontal status and response to treatment in
former smokers is intermediate to that seen in never smokers and
current smokers, and is usually closer to that seen in never
smokers.
From the small number of studies to date, it appears that the
periodontal status of former smokers approximates that of never
smokers after around 10 years since quitting smoking.
Effect of Smoking cessation on periodontal therapy

Effect of Smoking cessation on periodontal therapy
Fiorini t et al (2014) - One study reported that the progression of clinical attachment
loss (AL) ≥3 mm during a 6-year period was approximately three times higher
among smokers than quitters. Two studies (10 and 20 years of follow-up)
observed a decrease in radiographic bone loss of ≈ 30% among quitters when
compared with smokers. Among individuals receiving non-surgical periodontal
treatment, quitters were more likely to have periodontal probing depth reductions
than non-quitters/oscillators. No differences in AL were observed.
Preshaw PM et al (2005) - Patients after 12 months when assessed showed, there
were no differences between the groups following treatment with respect to mean
clinical or radiographic parameters. Analysis of probing depth reductions between
baseline and month 12, however, and comparing quitters with the other two groups
combined, demonstrated a significant difference in favour of quitters .
Furthermore, quitters were significantly more likely to demonstrate probing depth
reductions > or =2 and > or =3 mm than non-quitters and oscillators.

Chambrone L (2013) - Of 2455 potentially eligible articles, two studies were included.
The two studies found that SC seems to promote additional beneficial effects in reducing
probing depths (PD) and improving attachment level following non-surgical periodontal
treatment.
Tooth loss
Ahlqwist et al. (1989) - the mean number of teeth lost in the 12 year period of follow-up
was similar between never smokers and former smokers who had quit any time
before baseline.
Krall et al. (2006) - demonstrated an association between time since cessation
of cigarette smoking and tooth loss risk, suggesting that it may take up to 13 years after
smoking cessation for the risk of tooth loss to drop to that of never smokers.
Dietrich et al. (2007) - for the male USA health professionals, where the risk of tooth loss
declined exponentially soon after smoking cessation but remained significantly
elevated by about 20% even after 10+ years of smoking cessation.

Mechanisms by which smoking affects dental implants
- Compromised PMN function
- The junctional peri-implant epithelium – more permeable to exogenous materials like
nicotine allowing larger amounts of nicotine at the
implant- bone interface
- Interfere with the osteoblastic activity
-At the bone –implant interface –
(i) Larger amount of nicotine available through GCF and saliva
(ii)Inhibit expression of bone matrix related genes and
(iii) fibroblast activity , reduced alkaline phosphate production by PDL fibroblast
-Exposure to nicotine 2.4 mmol/L with acrolein (0.06 mmol/L), acetaldehyde (0.3 mmol/L),
or both caused cumulative cytotoxic responses
-Vasoconstrictive effect of nicotine – causing alterations in the oxygen saturation and
blood flow during healing after implant surgery

Effect of smoking on dental implant therapy
Anatomic location A large systemic review that found a statistically significant two-
fold increased failure rate in maxillary implants in smokers
compared with non-smokers, but no significant difference in
mandibular implant failure rates.
Implant loading Cavalcanti R (2011) in the retrospective cohort study of 1727
patients found that, five years after loading, smokers experienced
almost twice as many implant failures compared with non-smokers.
Non-statistically significant trends in favour of non-smokers were
observed for early implant failures and prosthesis failures.

Effect of smoking on dental implant therapy
Placement of dental implants
in augmented sites (i.e
maxillary sinuses or
ridges):
A large systematic review concluded that smoking has a
particularly strong negative effect on the survival of
implants in either augmented maxillary sinuses or alveolar
ridges. Compared with an overall 2.1 fold increased risk of
implant failure in smokers versus non-smokers, when
implants were placed in augmented sites in smokers the
failure rate was 3.6 fold higher than for implants placed in
augmented sites in non-smokers
Nature of implant surface in
smokers
D’Avila et al.(2010) observed that the sandblasted acid-
etched surface presented better results than the machined
surface after a short healing time in smokers.
Blashi AA et al (2008), Grunder et al (1999)
Lindquist et al (1997) 10 year follow up in mandibular implant prostheses found
that, marginal bone loss was greater in smokers.
Also larger amount of marginal bone loss correlated with
poor oral hygiene in smokers

Dental implants
A protocol was developed in which the smoking patients stopped
smoking 1 week before dental implant placement, followed by 8
more weeks without smoking to allow initial healing.
A prospective evaluation of this protocol in a pilot trial with 78
patients having over 200 implants showed an implant failure rate
of 12% in the patients who followed the smoking cessation
protocol compared with 38% in those who continued to smoke.
(Bain CA 1996).

Dental implants
A critical summary of
Chrcanovic BR,
Albrektsson T,
Wennerberg A. Smoking
and dental implants: a
systematic review and
meta-analysis. J Dent.
2015;43(5):487-498.
A total of 107 studies were included—4 randomized
clinical trials, 16 controlled clinical trials, 16 prospective
studies, and 71 retrospective analyses.
Conclusion: Within the limitations of the available
evidence, patients who smoke may be at twice the risk of
experiencing dental implant failure and postoperative
infections than are patients who do not smoke. Smokers
had more statistically significant marginal bone loss than
did nonsmokers.
Júlia Pereira de Carvalho
and Vanessa Rossi. “Effect
of Smoking in Peri-Implant
Diseases: Literature
Review”. EC Dental
Science 18.8 (2019): 1720-
1724
Main finding was that smoking is considered a risk factor
for failure of dental implants and for the development of
peri-implant. In the comparison of smokers with
nonsmokers, failure in the treatment of the implant is
higher in smokers, as well as in the presence of peri-
implant diseases. The failure rates of implants placed in
grafted maxillary sinuses are observed twice as much in
smokers as in nonsmokers, in addition to the greater of
marginal bone loss.

Dental implants
• Sara A. Alfadda. Current Evidence on Dental Implants Outcomes in
Smokers and Nonsmokers: A Systematic Review and Meta-Analysis. J Oral
Implantol (2018) 44 (5): 390–399.
Three randomized controlled trials and 7 prospective studies were included.
The odds ratio for implant failure among smokers was 2.92 (95% CI, 1.76–
4.83) (P < .001). First-year marginal bone loss in smokers ranged from 0.02
to 0.45 mm.
In the nonsmokers, bone loss ranged from −0.08 to 0.42 mm. Nonsmokers
lost significantly less bone during the first year (WMD = 0.11 mm, 95% CI.
0.03–0.19) and subsequent years (WMD = 0.11 mm, 95% CI, 0.03–0.19, P =
.009).
The available scientific evidence suggests that smoking is associated with
significantly increased rates of implant failure and marginal bone loss.

Dental implants
Wychowa ński, P.; Starzy ńska, A.; Jereczek-Fossa, B.A.; IwanickaGrzegorek, E.; Kosewski, P.;
Adamska, P.; Woli ński, J. The Effects of Smoking Cigarettes on Immediate Dental Implant
Stability—A Prospective Case Series Study. Appl. Sci. 2021, 11, 27.
• The study was conducted on 164 patients between the ages of 27–71 years old. 67 individuals
smoked more than 20 cigarettes daily and 97 were non-smokers.
• 190 immediate implants were inserted in the maxilla. Immediate implantations were performed
with simultaneous augmentation of the socket with xenogenic bone grafting material. In the
posterior region, implants were inserted into the palatal alveolus.
• Primary stability of immediate implants may be lower in the posterior area of the maxilla in
smokers when compared to non-smokers, which may eliminate smokers from immediate implants
in this region.
• Secondary stability of immediate implants may be lower in both the aesthetic and posterior areas
in smokers compared to non-smokers, which may encourage the postponement of final crowns
delivery at 6 months post op and the extension of the occlusal temporary crowns use in some
smoker cases.

References
M. John. Novak and Karen . F. Novak. Chapter 14 – Smoking and Periodontal
Disease. Carranza’s Clinical periodontology 10th edition.
Crawford A. Bain. Implant instillation in the smoking patient. Periodontology
2000 vol 33, 2003, 185-193.
Antonella labriola, Ian needleman & David R. Moles. Systematic review of the
effect of smoking on non-surgical therapy. Periodontology 2000 vol 37, 2005,
124-137.
Mark I. Ryder . The influence of smoking on host responses in periodontal
infections. Periodontology 2000 Vol. 43, 2007, 267–277.
 Annsofi Iohannsen, Cristiano Susin & Anders Gustafsson. Smoking and
inflammation: evidence for a synergistic role in chronic disease. Periodontology
2000, Vol. 64, 2014, 111–126.
Francisco Rivera- Hidalgo. Smoking and periodontal disease. Periodontology
2000, vol. 32, 2003, 50-58.
João Batista César Neto, Ecinele Francisca Rosa, Cláudio Mendes Pannuti,
Giuseppe Alexandre Romito.Smoking and periodontal tissues: a review . Braz Oral
Res., (São Paulo) 2012;26(Spec Iss 1):25-31.

References
Sujatha S Reddy, Shaik Hyder Ali KH. Estimation of nicotine content in popular
Indian brands of smoking and chewing tobacco products.Indian J Dent Res,
19(2),2008.
 Grover Harpreet Singh, Bhardwaj Amit, Singh Yasmin.Smoking and periodontal
disease : Review article . JPSI 2(2) , Mar- Apr 2013 , 7-13.
Ana Pejčić, Radmila Obradović, Ljiljana Kesić, Draginja Kojović. Smoking and
periodontal disease: a review. Medicine and Biology Vol.14, No 2, 2007, pp. 53 –
59.
Maddipati Sreedevi, Alampalli Ramesh, and Chini Dwarakanath. Periodontal
Status in Smokers and Nonsmokers: A Clinical, Microbiological, and
Histopathological Study International Journal of Dentistry volume 2012.
Mahmoud Abu-Ta’a. The effects of smoking on periodontal disease: An
evidence-based comprehensive literature review. Open Journal of Stomatology,
2014, 4, 33-41.
Causal assessment of smoking and tooth loss: A systematic review of
observational studies. Takashi Hanioka, Miki Ojima, Keiko Tanaka, Keitaro
Matsuo, Fumihito Sato and Hideo Tanaka. Public Health 2011.

References
 Sachin S Shivanaikar, Mohamed Faizuddin , Kishore Bhat . Effect of smoking on
neutrophil apoptosis in chronic periodontitis: An immunohistochemical study.
Indian Journal of Dental Research, 24(1), 2013.
Tobacco and Oral Health. January 2012. ASH Briefing: Tobacco and Oral Health.
 D Stramazzotti, C Coiana, A Zizzi, L Spazzafumo, S Sauro, AB D’Angelo, C Rubini
and SD Aspriello. Impact of smoking on guided tissue regeneration using a
biocomposite poly (lactic-co-glycolic) acid/sub-micron size hydroxyapatite with a
rubber dam as an alternative barrier. International Journal of Immunopathology
and Pharmacology 2015;8(1):21–28.
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