Study of the patterns of periodontal destruction in smokers with chronic periodontitis
Sukumaran Anil
Division of Periodontics, College of Dentistry, King Saud University, Post Box 60169, Riyadh 11545,
Saudi Arabia
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Date of Submission
10-May-2007
Date of Decision
22-Oct-2007
Date of Acceptance
22-Oct-2007
Abstract
Cigarette smoking is a well-established risk factor for periodontitis and carries an increased risk for loss
of periodontal attachment as well as for bone loss.
Aims: The purpose of the study was to investigate the pattern of the intraoral distribution of periodontal
destruction among cigarette smokers with periodontitis by assessing the periodontal probing depth (PPD)
and clinical attachment level (CAL).
Materials and Methods: Thirty smokers with chronic periodontitis were enrolled in the study. PPD,
CAL, plaque index (PI), and bleeding on probing (BOP) were measured. The data was pooled for the
anterior sextant and the posterior sextant as well as for the facial and lingual surfaces. The degree of
periodontal destruction was compared in these sextants.
Statistical Analysis: Comparisons were made between maxillary anterior, maxillary posterior,
mandibular anterior, and mandibular posterior using the one-way analysis of variance (ANOVA) test.
When the overall ANOVA showed statistical significance, post hoc testing (Tukey-Kramer multiple
comparisons test) was performed to explore the differences between any two groups. P -values <0.05
were considered significant.
Results: The maxillary anterior sextant showed significantly higher PPD and CAL loss than the other
sextants. Similarly, the maxillary palatal area showed higher probing depth and clinical attachment loss
than the facial sites and the mandibular regions.
Conclusions: From the results it can be concluded that there is variation in the periodontal tissue
destruction in different areas of the oral cavity, with the maximum periodontal destruction in the
maxillary palatal region. These observations emphasize the deleterious effects of smoking on the
periodontal tissues.
Keywords: Attachment loss, bone loss, periodontitis, smoking
How to cite this article:
Anil S. Study of the patterns of periodontal destruction in smokers with chronic periodontitis. Indian J
Dent Res 2008;19:124-8
How to cite this URL:
Anil S. Study of the patterns of periodontal destruction in smokers with chronic periodontitis. Indian J
Dent Res [serial online] 2008 [cited 2010 Nov 3];19:124-8. Available
from: http://www.ijdr.in/text.asp?2008/19/2/124/40466
There is considerable evidence demonstrating the association of periodontal destruction with cigarette
smoking. Cigarette smoking is an important risk factor for periodontal disease. [1],[2],[3] Cigarette smokers
are five times more likely to develop severe periodontitis than nonsmokers. [4],[5] A meta-analysis of the
effects of smoking on periodontal tissue confirmed smoking as a risk factor for periodontal disease with
an odds ratio of 2.82. [6] Epidemiological data indicate that smokers have a greater incidence of tooth loss
than nonsmokers. [7],[8] Furcation involvement in the molar teeth is also more frequent in smokers than in
nonsmokers. [9],[10] These studies suggest that cigarette smoking increases the susceptibility to periodontal
pathogens and to tissue destruction. [5],[6]
Cigarette smoking influences periodontal disease through a variety of systemic effects, for example, there
is impaired chemotaxis, decreased phagocytosis by both oral and peripheral neutrophils, and reduced
antibody production. [11],[12] A substantial body of evidence is available to demonstrate the local
detrimental effects of smoking on periodontal health. These local effects include vasoconstriction caused
by nicotine as well as decreased oxygen tension, which may create a favorable subgingival environment
for colonization by anaerobic bacteria. [13] Although it is possible that the heat from cigarette smoking
could have a local effect on the periodontium, there is hardly any scientific evidence to support such an
effect. Some studies have reported differences in the pattern of periodontal destruction among smokers,
which may imply a localized effect of smoking on maxillary palatal surfaces, especially in the anterior
region. [4],[10],[14]
Smokers tend to have greater numbers of deeper periodontal pockets and greater mean periodontal
probing depth (PPD). [15],[16],[17] Studies have also shown greater mean clinical attachment level (CAL)
loss in smokers compared to nonsmokers. [10],[18] Haffajee and Socransky [19] 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. Baharin et al ., [20]
in a retrospective comparative study showed that the proportion of sites with bone loss of 4.5 mm or
greater was higher in smokers, with the greatest difference being observed in the upper anterior sites.
Even though a few studies have reported that the periodontal destruction pattern may vary in different
areas of the oral cavity among smokers, further studies were recommended to prove the relationship.
Hence, the present study was undertaken to investigate the intraoral distribution of periodontal destruction
pattern among cigarette smokers with periodontitis by studying the PPD and CAL.
Materials and Methods
Study population
A total of 30 systemically healthy smokers aged 25-55 years old were enrolled in the study. They were
selected from among the patients who were referred to the periodontology clinic between September 2005
to February 2006 for diagnosis and treatment of periodontitis. Approval of the ethics committee was
obtained from the College of Dentistry Research Center (CDRC), King Saud University. Periodontal
status of the patients were assessed according the classification of the American Academy of
Periodontology. [21] Smoking status was determined based on the daily consumption of cigarettes. [22]
Subjects with a PPD of ≥4 mm in at least 30% of the teeth, and who had smoked a minimum of 20
cigarettes per day for not less than five years, were included in the present study. The following criteria
were also used to exclude subjects from the study: (1) age less than 25 or more than 55 years; (2) persons
suffering from any chronic medical condition, including diabetes and viral, fungal, or bacterial infections;
(3) persons suffering from aggressive periodontitis, periodontal abscess, or necrotizing ulcerative
gingivitis or periodontitis; (4) persons who had received periodontal treatment or antibiotics within the
preceding three months.
Clinical periodontal examination
An extensive medical history was taken with the help of a printed questionnaire and by interview of 20 to
30 min duration. All clinical measurements were performed by the same examiner. Calibration exercises
for probing measurements were performed in five patients before the actual study. The patients' details
were masked so that the examiner was blind to the patients' information.
PPD and CAL were measured with a calibrated probe (Williams markings) at the mesio-buccal, midbuccal, disto-buccal, mesio-lingual, mid-lingual, and disto-lingual aspect of each tooth. The data was
pooled for the anterior sextants and posterior sextants for comparison. Further comparison of the PPD and
CAL of the facial and lingual surfaces of these sextants were also done. The smoking history was
assessed through a standardized interview and a questionnaire. The smoking exposure was expressed in
terms of consumption (number of cigarette per day) and duration (in years).
Statistical analysis
Mean PPD and CAL were calculated for the entire mouth, for the upper jaw, the lower jaw, the buccal
aspect, the lingual aspect, the anterior teeth, and the posterior teeth. Comparisons were made between
upper anterior, upper posterior, lower anterior, and lower posterior using the one-way analysis of variance
(ANOVA) test. When the overall ANOVA showed statistical significance, post hoc testing (TukeyKramer multiple comparisons test) was performed to explore the differences between any two groups. P-
values <0.05 were considered as significant.
Results
[Table - 1] presents the mean percentage of teeth remaining in each region of the mouth. [Table - 2]
shows the mean plaque index (PI) and bleeding on probing (BOP) for the four sextants studied. The PI
and BOP did not show any statistically significant variations between the maxillary and mandibular
anterior and posterior areas of the mouth.
The mean PPD and clinical attachment loss for all regions are presented in [Table - 3] [Figure - 1]. The
maxillary anterior teeth had significantly deeper pockets than the posterior teeth and the mandibular
region ( P < 0.05) [Figure - 2].
The differences between the lingual and facial sites are presented in [Table - 4]. It was only statistically
significant for the palatal sites in the maxilla, with upper anterior palatal sites showing greater probing
depth difference ( P < 0.001) than the maxillary anterior facial sites, maxillary posterior buccal sites,
palatal sites, lower anterior facial and lingual sites, and lower posterior buccal and lingual sites.
The maxillary anterior palatal sites showed greater mean attachment loss ( P < 0.05) than the maxillary
anterior facial sites, the maxillary posterior palatal sites, and the maxillary posterior buccal sites.
However, the mandibular sites showed lower mean attachment level loss than the maxillary sites ( P <
0.001).
Discussion
Clinical studies have shown clear associations between smoking and alveolar bone loss, loss of
periodontal attachment, and tooth loss. [2],[3],[7],[19] The increased risk of tooth loss may be attributable to
the direct effect of tobacco smoking on periodontal tissues. [15] In other words, smokers are assumed to
have more periodontal destruction than nonsmokers. Mahuca and colleagues [23] evaluated the degree of
periodontal disease and its relationship to smoking habits. They reported higher probing depths and
attachment loss in smokers. Smokers diagnosed with severe forms of periodontitis were shown to have
more affected teeth and a higher mean loss of periodontal attachment than nonsmokers with these
conditions. [18],[24] A number of clinical investigations have reported that cigarette smokers with
periodontitis have more extensive periodontal destruction in the maxillary region. However, in this study,
significant effects were mainly seen in the palatal anterior region. [25]
The difference in patterns of periodontal destruction in smokers as studied by Haber and Kent [26] was
suggestive of a local effect of smoking. Preber and Bergstrom [27] suggested that higher local exposure to
cigarette smoke of the palatal maxillary surfaces, as compared to the other areas, could lead to a
significant increase in probing depth. Van der Weijden et al . [14] reported that the palatal surfaces of the
maxillary anterior teeth showed the highest probing depth and they attributed it to a possible local effect
of smoking. Haffajee and Socransky [19] have also reported a difference in pocket depth and attachment
level profiles at the palatal maxillary sites. Smokers showed the greatest numerical difference in the mean
proportion of sites probing 4 mm and above on the upper anterior palatal surfaces. [20] However, it must be
stressed that probing depth proportion cannot be equated with attachment loss, and CAL measurements
should also be taken into account for a reliable assessment of periodontal destruction.
The results of the present study were different, in that the mean of periodontal probing depth and
attachment loss differ in almost all regions. Data were pooled by maxillary and mandibular regions and
facial and lingual surfaces. In the maxilla, the anterior palatal region showed the highest variation from
the other segments. These findings were in agreement with previous reports showing maximum
periodontal destruction in the maxillary palatal region. [20],[24]
The evidence for the systemic effects of smoking on the periodontium is overwhelming and has been
proposed as the most important factor. [12],[28] However, the possibility of an additional local effect of
tobacco use cannot be ruled out. The present data suggest that there might be a local effect of cigarette
smoking in addition to a systemic effect. Cigarette smoke is more likely to come in contact with the
lingual surface of the maxilla, the area where the differences in attachment level and pocket depth values
were the greatest. Clearly, there is little controversy regarding the effect of cigarette smoking on the
clinical parameters of periodontal disease. What is less clear is the mechanism by which cigarette
smoking causes its harmful effects. One of the mechanisms might be an alteration of the subgingival
microbiota due to smoking. [22] The reduced gingival crevicular fluid flow reported in smokers means that
antibodies and other protective substances derived from the serum will be reduced in quantity. These
factors may influence the host defense, increasing the vulnerability to subgingival microbiota at these
sites. [29] In addition, smoking may affect the vasculature, the humoral immune system, and the cellular
and soluble inflammatory system and may also have effects throughout the cytokine and adhesion
molecule network. [30],[31] The importance of these smoking-related alterations and their precise mode of
action in increasing the risk of periodontal disease remain to be elucidated.
There is considerable evidence for the role of smoking in the etiology of periodontal disease as well as for
its adverse influence on the treatment of periodontitis. In the treatment of periodontal disease in smokers,
caution should be exercised in planning advanced periodontal treatment procedures such as regenerative
surgery. Smoking influences healing; therefore, the capacity for regeneration, particularly of bone
regeneration, may be impeded. [32],[33] The effects of smoking on the outcome of non-surgical periodontal
therapy may manifest as less gingivitis resolution, less probing depth reduction, and less attachment gain
in smokers. [34] The longer-term effects are evidenced by the fact that 80-90% of periodontal treatment
failures occur in smokers. [29],[35]
Acknowledgment
The author wishes to acknowledge Dr. Hamdan Al-Ghamdi for the technical assistance in the compilation
of the data.
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