Clinical Study: Periodontal Status in Smokers and Nonsmokers: A Clinical, Microbiological, and Histopathological Study

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Hindawi Publishing Corporation

International Journal of Dentistry


Volume 2012, Article ID 571590, 10 pages
doi:10.1155/2012/571590

Clinical Study
Periodontal Status in Smokers and Nonsmokers: A Clinical,
Microbiological, and Histopathological Study

Maddipati Sreedevi,1 Alampalli Ramesh,2 and Chini Dwarakanath2


1 Indira Gandhi Institute of Dental Sciences, Pondicherry 607402, India
2 The Oxford College of Dental Sciences, Bangalore 560068, India

Correspondence should be addressed to Maddipati Sreedevi, sreedevi206@gmail.com

Received 17 September 2011; Accepted 21 October 2011

Academic Editor: Hessam Nowzari

Copyright © 2012 Maddipati Sreedevi et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.

A case-control study was done to assess the influence of smoking on clinical, microbiological, and histopathological parameters.
Methods. Two hundred dentate male patients (100 smokers and 100 nonsmokers) ranging between 25 and 50 years were enrolled
in the study. Periodontal parameters were recorded. Plaque samples were collected for microbial analysis for BANA test. Gingival
biopsies were obtained from selected site for assessing histopathological changes. Results. Both groups showed almost similar
plaque levels (P = 0.258), but smokers had reduced gingival (0.62 ± 0.31) and bleeding indices (28.53 ± 17.52) and an increased
calculus index (1.62 ± 0.36). Smokers had an increased probing depth of 4–7 mm (P = 0.009) and overall increased CAL. No
difference in microbiota was found between the two groups. Histopathologically smokers showed a decreased blood vessel density
(8.84 ± 0.96) and inflammatory cells (52.00 ± 9.79). Conclusions. It is quite possible that many of the pathogenic mechanisms
involved in tissue degradation in periodontitis in smokers could be quite different from those in nonsmokers.

1. Introduction modifiable environmental risk factor responsible for excess


prevalence of periodontal disease in the population and has
Periodontitis is defined as an inflammatory disease of the a direct influence on periodontal variables.
supporting tissues of the teeth caused by specific microor- The 1996 World Workshop in Periodontics reviewed a
ganisms or groups of specific microorganisms, resulting number of studies and confirmed that “smoking entailed
in progressive destruction of the periodontal ligament and an overall increased risk for severe periodontal disease and
alveolar bone with pocket formation, recession, or both [1]. estimated overall odds ratio 2.82” [5].
Periodontal diseases are infections caused by dental Earlier investigators had attributed the increased preva-
plaque, but risk factors can modify the host response to lence and severity of periodontal disease seen in smokers to
microbial aggression [2]. Some of the known risk factors the greater presence of plaque and calculus than compared to
are diabetes, tobacco smoking, pathogenic bacteria, and nonsmokers. However, with the better understanding of the
microbial tooth deposits. host response, evidence suggests that the effect of smoking
Smoking is a known risk factor for many diseases, and on periodontal status is independent from the plaque index
increasing evidence suggests that smoking adversely affects and oral hygiene of individual. So, this clearly suggests that
periodontal health [3]. The concept that smoking tobacco smoking has a direct influence on periodontal tissues.
may be detrimental to periodontal health is not new. In fact, Smokers have been associated with deeper pockets and
Pindborg observed an association between acute necrotizing greater attachment loss, more pronounced radiographic
ulcerative gingivitis and smoking nearly 60 years ago [4]. evidence of furcation involvement, and increased alveolar
Since then, various investigators have attempted to identify bone loss. There is an established biologic rationale for the
the role of tobacco smoking in the etiology of periodontal negative effect of smoking on periodontal tissues. It has an
diseases. These studies suggest that smoking is a single, immunosuppressive effect on the host, adversely affecting
2 International Journal of Dentistry

host-bacterial interactions, and this alteration may be due to (3) Patient should not have been subjected to periodon-
changes in the composition of subgingival plaque. Smoking tal therapy or any antibiotic medication during the
may also provide a conducive environment for some of the last 6 months.
periodontopathic species in the plaque and may be one
reason why smoking is a risk factor in periodontal disease Exclusion criteria for both groups include female patients,
development [6]. former smokers, and aggressive periodontitis patients.
Smoking exerts a strong, chronic, and dose-dependent All the patients were subjected to a detailed case history.
suppressive effect on gingival bleeding on probing. Bleeding The following data was also obtained from subjects belong-
on probing was less evident in smokers than nonsmokers, ing to smokers group:
indicating its effect on gingival blood vessels. The mechanism (1) Number of cigarettes or beedies consumed daily.
by which smoking suppresses gingival bleeding is not
understood exactly [7]. (2) Frequency of smoking.
On the basis of the observation that smokers may present (3) Number of years of smoking.
with a lower level of gingival inflammation, it has been
speculated that the gingival blood flow in smokers may be Informed consent was obtained from all the subjects.
less in comparison to nonsmokers. This would also induce a A thorough periodontal examination was carried out
decreased local host response. So, smoking is thought mainly under good artificial light, and parameters selected for the
to affect the periodontal tissues by way of the vascular and study were carefully recorded. However, the consistency
immunological response of the body. and accuracy of measurement were randomly checked by
While there is overwhelming clinical evidence to asso- another examiner so as to keep interexaminer variation
ciate smoking with destructive periodontal disease, the negligible.
mechanisms that may predispose smokers to periodontitis Plaque index of Silness and Loe [8], gingival index of
remain to be fully elucidated. Loe and Silness [9], bleeding index [10], and NIDR calculus
To explore more into the above facts, this study evaluated index [11] were initially recorded.
the clinical, microbiological and histopathologic changes in
smokers and compared these to the nonsmokers. 2.3. Periodontal Status. Parameters such as pocket depth,
clinical attachment loss, mobility, and furcation were
recorded. The periodontal pocket depth and clinical attach-
2. Materials and Methods ment loss were recorded using a William’s periodontal probe.
2.1. The Study Population. Two hundred dentate male Furcations were assessed using Nabers probe.
patients comprising hundred smokers and hundred non- Periodontal disease has often been described as site
smokers all in the age group ranging between 25–50 years specific. Since the mean scores may not reflect the severity
were selected from among the patients referred to the of the problem clearly, it was decided to classify the probing
Department of Periodontics at The Oxford Dental College depth sites into three groups as follows:
Hospital and Research Centre, Bangalore. The subjects for sites showing <4 mm of probing depth,
the study were selected randomly taking into consideration
only their smoking history. sites showing 4–7 mm of probing depth,
Ethical clearance for the study was obtained from the sites showing >7 mm of probing depth.
Research and Ethical Committee of The Oxford Dental
College Hospital and Research center, Bangalore. Clinical attachment was classified under three groups as
follows:
2.2. Selection of Subjects. The following criteria were applied sites showing attachment loss <4 mm,
while selecting patients under smokers group (test group): sites showing attachment loss between 4–7 mm,
(1) Patient should have been smoking since three years sites showing attachment loss >7 mm.
or more.
Numbers of teeth showing mobility, recession, and teeth
(2) Patient should not have had any known systemic
with furcation were calculated separately.
conditions that could influence periodontal health.
(3) Patient should not have been subjected to periodon-
2.4. Microbiological Examination. BANA test is done to
tal therapy or any antibiotic medication during the
assess the microbiological status.
last 6 months.
One site with the deepest probing depth is chosen for
The criteria for choosing patients under nonsmokers group plaque collection. Supragingival plaque in this site was
(Control group) were as follows: carefully removed, and then, a curette is used to collect
subgingival plaque. The adherent plaque from the curette
(1) Subjects should not have smoked at anytime in their is wiped onto the BANA-impregnated strip found at the
lives. lower edge of the BANA reagent card. An upper reagent
(2) Patient should not have had any known systemic strip containing Evan’s black dye was then activated through
conditions that could influence periodontal health. dampening with distilled water, and the strip was folded at
International Journal of Dentistry 3

the perforation mark so that the lower and upper reagent Table 1: Age distribution.
strips come in direct contact with each other. After folding,
Nonsmokers Smokers
the card was inserted into a slot on top of the BANA Age in years
incubator and incubated for 5 min at 35◦ C. The light would No % No %
operate during incubation and would automatically shut off 25–30 36 36.0 38 38.0
once the heating cycle was completed. A bell sound was heard 31–35 20 20.0 16 16.0
once the heating cycle is complete. Naphthylamide released 36–40 22 22.0 23 23.0
due to the presence of any one of the BANA-hydrolyzing 41–45 11 11.0 15 15.0
bacterial species diffused into the upper reagent strip, where
46–50 11 11.0 8 8.0
it reacted with the Evan’s black dye to form a permanent
blue-black colour. Total 100 100.0 100 100.0
The test was considered positive if blue colour was Mean ± SD 35.10 ± 7.14 35.13 ± 7.05
visible on the upper reagent strip after incubation and was Remarks Samples are age matched with P = 0.976
considered negative if no blue colour was visible.
Table 2: Distribution of pack years.
2.5. Histopathological Examination. After the clinical exami-
nation and microbiological test, preparation was done to take Pack years Number (n = 100) %
biopsy of the interdental papilla between the lateral incisor <1 year 12 12.0
and canine of the left side of the upper arch. Biopsy was 1–5 years 50 50.0
obtained by sharp dissection with a Bard Parker blade no. 5–15 years 24 24.0
15 under local anesthesia. >15 years 14 14.0
The biopsy specimen was immediately transferred to
a bottle containing 50% formo-alcohol (50 mL of 10%
formalin and 50 mL of alcohol) and kept for 24 hours for
fixation.
3. Results
Slides were prepared by standard histological technique The mean age of nonsmokers was 35.10 ± 7.14 and the
using haemotoxylin and eosin stains. mean age of smokers was 35.13 ± 7.05. The age was matched
All the slides were viewed under compound microscope between the two groups (Table 1).
attached with a micrometer scale at 20x (objective) magni-
fication to which a camera was attached. Four views of each 3.1. Distribution of Smokers by Pack Years. 12 subjects had a
slide was then photographed with the scale adjusted for each smoking history of <1 pack year, 50 subjects had a history of
photograph. These photographs were then transferred to a smoking for about 1–5 pack years, 24 of them for about 5–
computer and were assessed. 15 pack years, and 14 of them had a smoking history of >15
Numbers of inflammatory cells and blood vessel density years (Table 2).
(number of blood vessels) were estimated, and then, diam-
eter of each vessel was measured using calipers. Vessels and 3.2. Periodontal Parameters. Smokers had a slightly higher
cells intersecting the grid lines were excluded. plaque index than that of nonsmokers. The mean plaque
The diameter of blood vessels measured was then divided index in smokers was 1.11 ± 0.44, whereas in nonsmokers
into three groups as: it was 1.04 ± 0.44 with P value of 0.258. This difference was
Diameter <4 mm; 4–8 mm and >8 mm. not statistically significant as shown in Table 3.
All the observations made were recorded on tables as per Nonsmokers had a higher gingival index score of 0.86 ±
the criteria laid out and the data thus collected was subjected 0.41 than smokers who had a mean score of 0.62 ± 0.31. The
to extensive statistical analysis. difference was found to be statistically significant (P ≤ 0.001)
(Table 3).
2.6. Statistical Methods [12, 13]. Chi-square and Fisher Smokers demonstrated lower bleeding scores than non-
exact test have been used to test the proportions of study smokers. The mean bleeding index in nonsmokers was
parameters between nonsmokers and smokers. Students t 39.54 ± 23.03 and of smokers was 28.53 ± 17.52. This
test (two tailed, independent) and Mann-Whitney U test difference was statistically significant (P = 0.001) (Table 3).
have been used to find the significance of study parameters Smokers demonstrated consistently higher scores for
between nonsmokers and smokers. Analysis of variance has calculus than nonsmokers. The mean calculus index in
been used to find the significant association of pack years and smokers was 1.62 ± 0.36 as compared to 1.40 ± 0.55 in
the study parameters. Kruskal-Wallis test (a nonparametric) nonsmokers. This difference showed statistical difference
has been used to find the significant association of PD and between the two groups (P = 0.001) (Table 3).
CAL with pack years. Comparison of PD between nonsmokers and smokers
The statistical software, namely, SPSS 11.0 and Systat 8.0 showed that 98.57% of sites in nonsmoker group had
were used for the analysis of the data and Microsoft word and probing depth <4 mm, whereas this was 97.22% in smokers
Excel have been used to generate graphs, tables, and so forth. group. This was statistically significant with P = 0.006.
4 International Journal of Dentistry

Table 3: Comparison of PI, GI, BI, and CI between nonsmokers Table 6: Comparison of mobility between nonsmokers and
and smokers. Results are presented in Mean ± SD (min-max). smokers.

Parameters Nonsmokers Smokers P value Number of teeth


Nonsmokers (n = 100) Smokers (n = 100)
with mobility
1.04 ± 0.44 1.11 ± 0.44
PI 0.258 16% 29%
(0.33–2.20) (0.40–2.31)
0.86 ± 0.41 0.62 ± 0.31
GI <0.001∗∗
(0.16–2.00) (0.12–1.54) Table 7: Comparison of recession between nonsmokers and
39.54 ± 23.03 28.53 ± 17.52 smokers.
∗∗
BI 0.001
(2.23–100) (3.30–100.0) Number of teeth
1.40 ± 0.55 1.62 ± 0.36 Nonsmokers (n = 100) Smokers (n = 100)
CI 0.001∗∗ with recession
(1.40–2.00) (0.63–2.00) 59% 79%

Table 4: Comparison of probing depth between nonsmokers and Table 8: Comparison of furcation between nonsmokers and
smokers. Results are presented in trimean (min-max). smokers.
Number of teeth
Parameters Nonsmokers Smokers P value Nonsmokers (n = 100) Smokers (n = 100)
with Furcation
98.57 97.22
PD <4 mm% 0.006∗∗
Present 16% 32%
(13.33–100) (0–100)
1.29 2.58
PD 4–7 mm% 0.009∗∗ Table 9: Comparison of BANA test positive between nonsmokers
(0–70.56) (0–76.92)
0 0 and smokers.
PD >7 mm % 0.859
(0–16.11) (0–12) Nonsmokers Smokers
BANA test results
(n = 50) (n = 50)
19 18
Table 5: Comparison of clinical attachment loss between nonsmok- Positive
(38.0%) (36.0%)
ers and smokers. Results are presented in trimean (min-max).
31 32
Negative
Parameters Nonsmokers Smokers P value (62.0%) (64.0%)
3.52 6.78
CAL <4 mm% 0.004∗∗ Table 10: Comparison of number of IC and BV density between
(0–49.46) (0–37.10)
nonsmokers and smokers. Results are presented in Mean ± SD
3.29 7.99
CAL 4–7 mm% 0.004∗∗ (min-max).
(0–72.58) (0–83.97)
0.09 3.39 Number of IC Nonsmokers Smokers
CAL >7 mm% 0.030∗ P value
(0–53.3) (0–54.49) and BV density (n = 50) (n = 50)
64.70 ± 12.68 52.00 ± 9.79
Number of IC 0.319
(4–468) (3–297)
The percentage of sites showing PD of 4–7 mm was 1.29 11.12 ± 1.23 8.84 ± 0.96
in nonsmokers and 2.58 in smokers. Again, this was also BV density 0.179
(2–45) (1–27)
statistically significant with P value of 0.009.
In both nonsmokers and smokers, few sites showed PD
>7 mm which was not statistically significant at P = 0.859 Smokers had significantly more teeth with recession
(Table 4). (79.0%) when compared to nonsmokers (59.0%) with P =
The percentage of sites showing CAL <4 mm in non- 0.003 which was significant (Table 7).
smokers was 3.52 and in smokers was 6.78 with P value of Smokers had significantly more teeth with furcation
0.004 which was highly significant. (68.0%) when compared to nonsmokers (84.0%) with P =
3.29% of sites had CAL of 4–7 mm in nonsmokers, and 0.013 (Table 8).
the same was 7.99% in smokers. This showed a statistically
significant result with P = 0.004. 3.3. Microbiological Test (BANA Test). The test was positive
The mean percentage of sites in nonsmokers with CAL in 38% of subjects in nonsmokers and 36% of subjects
>7 mm was 0.09, and this value was higher in smokers of who were smoking. The results showed no difference in
about 3.39%, which was again significant with P = 0.030. microbiota in both the groups with P = 0.836 (Table 9).
The above results indicate that there was an increased
attachment loss in smokers when compared to nonsmokers 3.4. Histopathological Parameters. Number of inflammatory
(Table 5). cells in nonsmokers was 64.70 ± 12.68 and 52.00 ±
Smokers had significantly more teeth with mobility 9.79 in smokers. Even though smokers had less cells than
(29%) when compared to nonsmokers (16.0%) with P = nonsmokers, this was not statistically significant (P = 0.319)
0.030 which was statistically significant (Table 6). (Table 10).
International Journal of Dentistry 5

Table 11: Comparison of BV diameter <4 between nonsmokers and


smokers.
BV diameter <4 mm Nonsmokers (n = 50) Smokers (n = 50)
0 4 (8.0%) 6 (12.0%)
1–10 41 (82.0%) 43 (86.0%)
>10 5 (10.0%) 1 (2.0%)

Table 12: Comparison of BV diameter 4–8 mm between nonsmok-


ers and smokers.
BV 4–8 mm Nonsmokers (n = 50) Smokers (n = 50)
0 4 (8.0%) 11 (22.0%)
Figure 1: Histopathological photograph of gingival tissue in
1–10 37 (74.0%) 35 (70.0%)
smoker showing smaller blood vessels.
>10 9 (18.0%) 4 (8.0%)

Table 13: Comparison of BV diameter >8 mm between nonsmok-


ers and smokers.
BV >8 Nonsmokers (n = 50) Smokers (n = 50)
0 40 (80.0%) 40 (80.0%)
1–10 10 (20.0%) 10 (20.0%)
>10 — —

Blood vessel density in nonsmokers was 11.12 ± 1.23, and


the density reduced in smokers, where it was 8.84 ± 0.96.
This difference was not significant (P = 0.179) (Table 10).
Figure 2: Histopathological photograph of gingival tissue in
nonsmoker showing smaller blood vessels.
3.5. Diameter <4 mm. Nonsmokers had 46 vessels with this
diameter, whereas they were 44 in smokers.
This showed statistically similar results between the two
groups (P > 0.05) (Table 11). Probing depth of 4–8 mm significantly increased as pack
years increased with P value of <0.001 (Table 15).
3.6. Diameter 4–8 mm. Vessels with this diameter were 46 in Clinical attachment loss <4 mm, 4–8 mm and >8 mm
nonsmokers and 39 in smokers. So, blood vessel diameter significantly increased as pack years increased with P =
4–8 mm was significantly less in smokers (P = 0.073) 0.005, <0.001 and <0.001, respectively (Table 15). See Figures
(Table 12). from 1 to 6 for further clarification.

3.7. Diameter >8 mm. Vessels with this diameter were signif- 4. Discussion
icantly similar in both the groups, as both the groups had 10
vessels in this category (P > 0.05) (Table 13). The global rise in the number of people addicted to
The periodontal parameters in smokers were then corre- smoking, and mortality and morbidity associated with it,
lated with the number of pack years to evaluate the effects of has made smoking a major public health hazard. But the
chronic smoking. exact mechanism how smoking increases the severity for
Plaque index increased significantly with the increase in periodontitis is not fully understood. Whether smoking
number of pack years (P = 0.002) (Table 14). causes a local effect on the periodontium or the systemic
Gingival index did show a decrease as pack years effects of smoking that causes periodontal disease is not
increased to 15 years but later increased as pack years known. This study was done to know the effects of smoking
increased to more than 15 years with (P = 0.577) (Table 14). on the periodontium by studying the clinical, microbial, and
Bleeding index decreased up to 5–15 years and then histopathological parameters.
showed an increase when the pack years was >15 years (P = To equate and nullify the effect of all other possible
0.237) (Table 14). contributing factors, patients belonging to same age group
Calculus index showed an increased value as pack years (25–50 yrs) with no other known systemic problems were
increased, which is suggestive of significance (P = 0.058) selected for the study. Although some of the previous studies
(Table 14). [3, 7, 14, 15] included subjects who had quit smoking for a
Probing depth <4 mm significantly decreased as pack period of 2–5 yrs or more under the nonsmokers category, it
years increased with P value of <0.001. was decided in this study to exclude former smokers in order
6 International Journal of Dentistry

Table 14: Mean pattern of clinical parameters with years of smoking.

Pack Years of smoking


Clinical parameters P value
<1 years 1–5 years 5–15 years >15 years
PI 1.05 ± 0.31 0.99 ± 0.35 1.16 ± 0.44 1.47 ± 0.59 0.002∗∗
GI 0.69 ± 0.32 0.60 ± 0.26 0.58 ± 0.31 0.69 ± 0.41 0.577
BI 31.04 ± 15.21 25.75 ± 17.20 28.58 ± 15.33 36.29 ± 22.58 0.237
CI 1.64 ± 0.37 1.54 ± 0.35 1.69 ± 0.39 1.81 ± 0.28 0.058

Table 15: Pattern of clinical parameters with years of smoking.

Years of smoking
Clinical parameters P value
<1 years 1–5 years 5–15 years >15 years
99.38 97.78 96.06 87.21
PD <4 mm% <0.001∗∗
(84.2–100.0) (0–100) (17.31–100.0) (63.33–100)
0.62 1.66 3.81 12.9
PD 4–7 mm% <0.001∗∗
(0–14.58) (0–33.33) (0–76.92) (0–32.67)
0 0 0 0.07
PD > 7 mm% 0.724
(0–0.52) (0–12.00) (0–6.17) (0–4)
4.16 5.67 6.96 15.61
CAL <4 mm% 0.005∗∗
(0–12.50) (0–37.10) (0–36.56) (0.64–26.11)
2.94 3.87 10.98 38.06
CAL 4–7 mm% <0.001∗∗
(0–14.06) (0–71.88) (0–42.98) (2.78–83.97)
0 0 0.23 2.25
CAL >7 mm% <0.001∗∗
(0–0) (0–24) (0–54.49) (0–20.0)

Figure 3: Histopathological photograph of gingival tissue in Figure 5: Histopathological photograph of gingival tissue in
smoker showing larger blood vessels. smoker showing inflammatory cells.

Figure 4: Histopathological photograph of gingival tissue in Figure 6: Histopathological photograph of gingival tissue in
nonsmoker showing larger blood vessels. nonsmoker showing inflammatory cells.
International Journal of Dentistry 7

to eliminate any long-term effect of smoking on periodontal reflection of a reduction of the capacity of the host to mount
tissues. an effective defence through the inflammatory process.
Females were purposely excluded from the study for the Another not necessarily contradictory hypothesis may
main purpose that it would have been difficult to recruit be advanced to explain these findings. It is possible that
females who admit that they smoke. The other reason for substances in tobacco smoke can reduce the capacity of
excluding them was to avoid potential hormone-induced microorganisms in plaque to produce irritants. Conse-
microcirculatory changes [16–18]. quently, the extent to which gingival inflammation occurs,
Since patients with any known systemic problems were and the extent to which it is necessary for the host to
not included, it was considered reasonable that comparisons maintain an inflammatory response, might be less marked,
made between smokers and nonsmokers group accurately yielding a lowered incidence rate [37].
reflected the influence of smoking on periodontium. Decreased inflammatory signs in the present study can
Patients were selected only on the basis of their smoking be attributed to decrease in the number of inflammatory
status and not depending on their periodontal status, as cells as shown histopathologically. Smoking can drastically
some previous studies [2, 19–21] selected patients who were alter the typical presentation of gingivitis and periodontitis
diagnosed with periodontitis. This selection was mainly done by masking the signs of inflammation. Thus, the diagnosis of
as it was decided to study the relationship of smoking to peri- these diseases is made more difficult, yet the disease effects
odontal health. The duration of smoking in the cases ranged are worse.
from 3 to 30 yrs, which was later calculated into pack years. Regarding bleeding on probing, this study is in agree-
The oral hygiene status as depicted by plaque scores ment with other studies [33, 45–47] showing decreased
were almost similar in both the groups even though smokers gingival bleeding in smokers. The mechanisms by which
had slightly higher scores that were not significant and this smoking suppresses gingival bleeding are not understood.
finding is in agreement with the other previous studies Traditionally, the reduced bleeding in smokers has been
[2, 3, 22–24]. Contradicting these studies, others have shown attributed to gingival vasoconstriction induced by the actions
higher plaque levels in smokers [25–31]. Few studies even of nicotine-stimulated adrenaline and noradrenaline on α1 -
showed less plaque levels in smokers [32, 33]. One study adrenergic receptors. There is some evidence to support this
concluded that poorer cleanliness found in smokers both theory in animal models. However, the available evidence
before and after toothbrushing may be explained, in part at support this hypothesis in humans is not concluded, as
least, by their shorter tooth brushing time [34]. smoking can cause vasodilatation in some tissues. Contra-
There was significantly less gingival inflammation in dicting these results, some studies have shown increased
smokers, which is in agreement with the earlier studies gingival bleeding [3, 48, 49].
[22, 32, 35–37]. The results of the present study showed more calculus
Suppression in smokers of the normally developing gin- deposition in smokers agreeing with the results of the other
gival inflammatory reaction associated with plaque provo- studies [29, 41, 48, 50]. It seems likely, therefore, that
cation may be due to tobacco smoke products interfering smoking primarily affects the mineralization rate rather than
with the vascular inflammatory response. It is generally the formation rate of supragingival plaque. The reason why
accepted that smoking causes vasoconstriction of peripheral smoking is associated with an elevated risk for supragingival
vessels. It is therefore conceivable that such a constrictive calculus deposition remains incompletely understood. It may
action on gingival vessels would result in the suppression exert its influence systemically via the saliva or locally via
of vascular properties of inflammation such as bleeding, a conditioning of tooth surfaces to deposition, or both. It
redness, and exudation. Smoking has previously been shown may be speculated that smoking causes a modification of
to affect oral PMN leukocytes, indicating an impairment of the saliva resulting in elevated levels of calcium and possibly
PMN-function [38, 39]. Thus, smoking seems to influence phosphorous. Further, it can be considered that a reduced
both vascular and cellular properties of the inflammatory flow may cause elevation of the calcium and phosphate con-
reaction. The suppression of vascular inflammatory reaction centrations. Thus, paradoxically, smoking might promote
under the influence of smoking might then indicate an the calcification of subgingival plaque notwithstanding its
impairment of the defense mechanisms within the tissues suppressive action on some inflammatory events. This may
and possibly render them more susceptible to plaque infec- have accounted for greater calculus scores in smokers [51,
tion. 52].
These results are not in agreement with other studies Chen et al. have shown no difference in the calculus
[40–42], showing increased inflammation. Some studies deposition in their 10-year longitudinal study [53].
showed no differences in the inflammatory status between There were no significant difference in periopathogens in
smokers and nonsmoker [32, 43]. this study as confirmed by BANA although this contradicts
If, however, it is hypothesized that the inflammatory the study by Kazor et al. [54] who showed a positive relation
response of the gingiva is a clinical manifestation of the between BANA pathogens and smoking. This difference
degree or capacity of the host to respond to irritation (a pos- could be attributed to 4-plaque samples examined by Kazor
tulate which has also been proposed by others (Page) [44], et al., but in the present study, only one plaque sample from
then the present findings may be explained in the following deepest pocket depth irrespective of diseases activity was
manner. In smokers, what has been termed the lowered considered. This is in agreement with the other earlier studies
incidence rate may, perhaps, be better understood as a showing no difference [55–59].
8 International Journal of Dentistry

Few other studies showed difference in the subgingival bundit and Wikesjo [70],Bergström [71], and Calsina et al.
microflora [18, 43, 60, 61], but the microbial analysis varied. [2].
There are problems associated with microbiological The present study showed that smokers have more severe
investigations of the oral flora that may affect the interpre- periodontal disease than non-smokers and that it has a
tation of the results of the studies. Sampling methods vary strong, chronic, dose-dependent effect on periodontium.
widely, and, together with undoubted differences from site Tobacco smoking, mostly in the form of cigarette
to site within the mouth, such variations may affect the smoking, was recognized as the important environmen-
results of studies. Identification of organisms by different tal risk factor in periodontitis. Tobacco smoking affects
methods such as culture-, immunofluorescence-, and DNA- the oral environment and ecology, the gingival tissues
based techniques gives rise to potentially different outcomes. and vasculature, the inflammatory response, the immune
Under these circumstances, it was imperative that studies response, and the homeostasis and healing potential of the
with adequate numbers of subjects were performed in order periodontal connective tissues. While there is overwhelming
to overcome the background of extreme variation, which clinical evidence to associate smoking with destructive
will potentially mask the effects of smoking on the oral periodontal disease, the mechanisms that may predispose
microflora. Of those that appear to satisfy these require- smokers to periodontitis remain to be fully elucidated.
ments, some early studies tended to show no differences. It was also apparent that while smoking may suppress
However, there are now a number of studies that suggest gingival angiogenesis, the mechanisms by which cigarette
a trend for smokers to harbour more or greater numbers smoking dampens periodontal inflammation are not yet fully
of potential periodontalpathogens than nonsmokers without understood.
increasing the amount of plaque. This undoubtedly sup- The findings of the present study emphasizes that
ports the attractive hypothesis that a significantly different periodontal tissue in smokers are affected more than the
subgingival environment in smokers, related to an altered controls with minimal signs of inflammation. The best
immune response, should result in a different microflora. way to prevent periodontitis in smokers is by enrolling the
Further investigation with the latest methods is still required subjects in smoking cessation programmes, and so, it is
to confirm that such differences are directly related to an obvious implication that smoking prevention should be
smoking. included in dental public health education by advocating,
Smokers showed a reduced blood vessel density com- advising, and facilitating smoking cessation programmes
pared to nonsmokers contradicting other studies [62–64] among the patients.
who showed no difference. The suppressive effect on the
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