Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study
Aim: The aim of the present case — control study was to examine the possible associations between periodontal disease indices and the risk of lung cancer development in a sample of Greek out-patients referred to a medical and a dental private practice. Materials and Methods: A total of 200 individua...
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irk-123456789-1379842018-06-18T03:03:50Z Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study Chrysanthakopoulos, N.A. Original contributions Aim: The aim of the present case — control study was to examine the possible associations between periodontal disease indices and the risk of lung cancer development in a sample of Greek out-patients referred to a medical and a dental private practice. Materials and Methods: A total of 200 individuals were interviewed and underwent an oral clinical examination, and 64 of them were suffered from several histological types of lung cancer. The estimation of the possible associations between lung cancer as a dependent variable and periodontal disease indices as independent ones was carried out by using a multiple regression analysis model. Results: Probing pocket depth (odds ratio (OR) = 2.72, 95% confidence interval (CI) 1.05–7.06), clinical attachment loss (OR = 3.51, 95% CI 1.30–9.47) bleeding on probing (OR = 1.93, 95% CI 0.98–3.81) were significantly associated with the risk of developing lung cancer. Smoking (OR = 2.49, 95% CI 1.20–5.17) was significantly associated with the mentioned risk, whereas it was consisted as a confounder regarding the estimated associations between moderate/severe clinical attachment loss and presence of bleeding on probing with the risk of developing lung cancer. Conclusion: Probing pocket depth as an index for periodontal disease severity was statistically significantly associated with the risk of developing lung cancer. 2016 Article Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study / N.A. Chrysanthakopoulos // Experimental Oncology. — 2016 — Т. 38, № 1. — С. 49–53. — Бібліогр.: 38 назв. — англ. 1812-9269 http://dspace.nbuv.gov.ua/handle/123456789/137984 en Experimental Oncology Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України |
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Original contributions Original contributions |
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Original contributions Original contributions Chrysanthakopoulos, N.A. Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study Experimental Oncology |
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Aim: The aim of the present case — control study was to examine the possible associations between periodontal disease indices and the risk of lung cancer development in a sample of Greek out-patients referred to a medical and a dental private practice. Materials and Methods: A total of 200 individuals were interviewed and underwent an oral clinical examination, and 64 of them were suffered from several histological types of lung cancer. The estimation of the possible associations between lung cancer as a dependent variable and periodontal disease indices as independent ones was carried out by using a multiple regression analysis model. Results: Probing pocket depth (odds ratio (OR) = 2.72, 95% confidence interval (CI) 1.05–7.06), clinical attachment loss (OR = 3.51, 95% CI 1.30–9.47) bleeding on probing (OR = 1.93, 95% CI 0.98–3.81) were significantly associated with the risk of developing lung cancer. Smoking (OR = 2.49, 95% CI 1.20–5.17) was significantly associated with the mentioned risk, whereas it was consisted as a confounder regarding the estimated associations between moderate/severe clinical attachment loss and presence of bleeding on probing with the risk of developing lung cancer. Conclusion: Probing pocket depth as an index for periodontal disease severity was statistically significantly associated with the risk of developing lung cancer. |
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Chrysanthakopoulos, N.A. |
| author_facet |
Chrysanthakopoulos, N.A. |
| author_sort |
Chrysanthakopoulos, N.A. |
| title |
Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study |
| title_short |
Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study |
| title_full |
Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study |
| title_fullStr |
Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study |
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Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study |
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correlation between periodontal disease indices and lung cancer in greek adults: a case — control study |
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Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України |
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2016 |
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Correlation between periodontal disease indices and lung cancer in Greek adults: a case — control study / N.A. Chrysanthakopoulos // Experimental Oncology. — 2016 — Т. 38, № 1. — С. 49–53. — Бібліогр.: 38 назв. — англ. |
| series |
Experimental Oncology |
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AT chrysanthakopoulosna correlationbetweenperiodontaldiseaseindicesandlungcanceringreekadultsacasecontrolstudy |
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2025-07-10T02:42:10Z |
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2025-07-10T02:42:10Z |
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1837226087115915264 |
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Experimental Oncology 38, 49–53, 2016 (March) 49
CORRELATION BETWEEN PERIODONTAL DISEASE INDICES
AND LUNG CANCER IN GREEK ADULTS: A CASE — CONTROL STUDY
N.A. Chrysanthakopoulos
Maxillofacial and Oral Surgery, 401 General Military Hospital of Athens, Athens 11527, Greece
Department of Pathological Anatomy, Medical School, University of Athens, Athens 11528, Greece
Aim: The aim of the present case — control study was to examine the possible associations between periodontal disease indices and
the risk of lung cancer development in a sample of Greek out-patients referred to a medical and a dental private practice. Materi-
als and Methods: A total of 200 individuals were interviewed and underwent an oral clinical examination, and 64 of them were
suffered from several histological types of lung cancer. The estimation of the possible associations between lung cancer as a depen-
dent variable and periodontal disease indices as independent ones was carried out by using a multiple regression analysis model.
Results: Probing pocket depth (odds ratio (OR) = 2.72, 95% confidence interval (CI) 1.05–7.06), clinical attachment loss (OR =
3.51, 95% CI 1.30–9.47) bleeding on probing (OR = 1.93, 95% CI 0.98–3.81) were significantly associated with the risk of de-
veloping lung cancer. Smoking (OR = 2.49, 95% CI 1.20–5.17) was significantly associated with the mentioned risk, whereas
it was consisted as a confounder regarding the estimated associations between moderate/severe clinical attachment loss and pre-
sence of bleeding on probing with the risk of developing lung cancer. Conclusion: Probing pocket depth as an index for periodontal
disease severity was statistically significantly associated with the risk of developing lung cancer.
Key Words: periodontal disease, lung cancer, adults, chronic inflammation, risk factor.
Lung cancer (LC) is one of the most deadly of all
types of cancer, and the 5th cause of mortality nowa-
days in industrialized countries and occurs as a result
of genetic, environmental and behavioral risk factors [1,
2]. Common genetic factors are age, male gender, ge-
netic predisposition, enzymes polymorphism and other
unknown factors. The environmental and behavioral risk
factors include smoking, exhibition in inhaled gases/
polluted air and previous pulmonary diseases such
as chronic obstructive pulmonary disease, tuberculo-
sis (TBC) and lung fibrosis.
The last suggestion led to the hypothesis that
systemic chronic inflammation could play an essen-
tial role in development and/or disease progression.
Chronic inflammation may enhance mutagenesis and
cell proliferation, inhibit apoptosis, reduce the adap-
tation to oxidative stress, promote angiogenesis, and
increase the secretion of inflammatory mediators [2].
Periodontal disease (PD) and especially periodon-
titis is a common and destructive disease of the oral
cavity, leads to tooth loss, its development is a com-
plex process that occurs over a long period of time,
as a result of bacterial infection and inflammation
which spreads in periodontal fibers and alveolar bone,
the supporting structures of teeth [3]. Periodontal
tissues infection leads to systemic effects and an in-
crease in circulating levels of inflammatory biomark-
ers, that correlate directly with the severity of disease,
such as C-reactive protein, interleukin-1 and -6. The
biological mechanisms of those associations remain
unknown although various inflammatory biomarkers,
such as the mentioned may be involved as mediators
of systemic inflammation [4, 5]. To be more specific,
it remains unknown whether systemic inflammation,
invasion of pathogenic bacteria in systemic circula-
tion or immune response to perio dontal infection may
affect the risk for various systemic diseases develop-
ment, including cancer [4].
Recent epidemiologic reports has linked perio-
dontal pathogens to several systemic diseases,
such as cardiovascular disease, diabetes mellitus,
respiratory disease, and systemic infections. Those
associations possibly mediated through biomarkers
of systemic infection and inflammation [6, 7].
A possible correlation between PD and cancer risk
in different locations, most notably in the oral cavity, up-
per gastrointestinal system, lung, pancreas, and other
organs has also been proposed [8–14]. In two of those
prospective studies [9, 10] a correlation between tooth
loss, as another PD indicator, and the risk of cancer was
recorded, however such correlations regarding LC re-
main unclear [10]. Tooth loss is caused by dental caries
and PD, however the distribution of all causes depends
on age and other variables. Chronic periodontitis is re-
sponsible for tooth loss in older individuals, whereas
in younger ages the main cause is dental ca ries. There-
fore, although tooth loss could be an indicator of PD, its
correlation is not always strong [15].
Poor oral health or hygiene, as indicators of PD,
are possible risk factors for cancer in different organs
according to recent epidemiological studies [8, 9, 16,
17]. It has been hypothesized that PD increases the risk
of LC through bacterial load and subsequent chronic
systemic inflammation [9, 10]. However to our knowledge
previous studies have not objectively evaluated the role
of PD in LC or precancerous lesions. Several reasons
Submitted: January 18, 2016.
Correspondence: Fax: 0030–2610–225288;
E-mail: nikolaos_c@hotmail.com; nchrysant@med.uoa.gr
Abbreviations used: AC — adenocarcinoma; BOP — bleeding
on probing; CAL — clinical attachment loss; LC — lung cancer; LCC —
large cell carcinoma; PD — perio dontal disease; PPD — probing
pocket depth; SCC — squamous cell carcinoma; SCLC — small cell
lung carcinoma; TBC — tuberculosis.
Exp Oncol 2016
38, 1, 49–53
50 Experimental Oncology 38, 49–53, 2016 (March)
could explain a possible link between periodontitis and
cancer. Both diseases have several risk factors in com-
mon, while smoking, advanced age and low socio-
economic status have been implicated in cancer and
periodontitis [18].
The present retrospective case — control study was
carried out to examine the possible correlation between
PD indices such as probing pocket depth (PPD), clinical
attachment loss (CAL) and bleeding on probing (BOP)
and the LC risk in a sample of Greek adults.
MATERIALS AND METHODS
Study sample. The material consisted of 200 sub-
jects, 126 males and 74 females. Cases and controls
were selected from a private medical and dental prac-
tice, completed a health questionnaire and underwent
an oral clinical examination.
Patients selection criteria. Patients and controls
was necessary to have a mean of 20 natural teeth,
since large numbers of missing teeth could lead to over-
or underestimate the dental variables and the possible
associations that were under consideration and the
criteria of established periodontitis [19], which referred
to at least 2 teeth with CAL ≥ 6 mm and more that one
site with PPD ≥ 5 mm.
None of the participants had received scaling
and root planning procedures or periodontal treat-
ment during the previous 6 months or prescription
of anti-inflammatory or systemic antibiotics or other
systemic drugs the previous 6 weeks [20]. In order
to avoid as much as possible, potential confounding
influences on the study parameters, individuals with
acute infections, cardiovascular diseases, diabetes
mellitus, rheumatoid arthritis, immuno-suppressed
patients because of haematological malignancy or re-
cent transplantation and those who received treatment
for the mentioned diseases, liver cirrhosis and con-
current medication with general glucocorticoids were
excluded from the study. They also excluded patients
with advanced LC under medical treatment, patients
with lung metastases of a primary focus at a diffe-
rent location, patients diagnosed with mesothelioma
or other focuses in the region of head-neck-thorax
(carcinogenesis field theory [21]). These criteria
were applied because of potential effects on the oral
tissues. Hospital patients did not include or patients
with several location of cancer in which smoking is con-
sidered as a proven risk factor such as larynx cancer,
nasopharyngeal cancer, etc.
The patients’ group was consisted of individuals
in which the diagnosis of LC was set initially by histo-
logical examination during the endoscopic procedure
and they had been given instructions regarding their
oral hygiene after diagnosis and before the applica-
tion of any treatment method, such as surgery, radio-
therapy or chemotherapy.
Controls group selection was carried out by the
friendly and collegial environment of cases group
in an effort to control potential confounders such
as socio-economic level.
Oral clinical examination. One well trained and
calibrated dentist performed the examinations at the
mentioned private practices. The clinical measure-
ments concerned the following variables: For each
tooth, except for the 3rd molars and the remaining
roots PPD, CAL and BOP were measured by a Wil-
liam’s 12 PCP probe (PCP 10-SE, Hu-Friedy Mfg. Co.
Inc., Chicago, IL, USA) at six sites (facial, lingual, disto-
facial, mesio-facial, disto-lingual and mesio-lingual).
The presence of PPD was classified as follows [22]:
score 0: moderate periodontal pockets, 4–6.0 mm,
and score 1: advanced periodontal pockets, > 6.0 mm.
The severity of CAL classified as follows [23]:
score 0: mild,1–2.0 mm of attachment loss, and
score 1: moderate/severe, ≥ 3.0 mm of attachment
loss. The record for PPD and CAL measurements
concerned the immediate full millimeter.
The presence/absence of BOP was classified
as follows: score 0: absence of BOP, and score 1:
presence of BOP and deemed positive if it occurred
within 15 s of probing.
Questionnaire. All participants were filled in a self-
administered questionnaire that included variables
such as age, gender, smoking status (active, former/
no-smokers), socio-economic and educational level
and data regarding their general medical history with
reference to medication, several chronic systemic
disorders and the dental follow-up frequency.
A randomly chosen sample of 40 (20%) individuals was
re-examined clinically by the same dentist after 3 weeks
in order to establish the intra-examiner variance. After con-
sideration of the code numbers of the double examined
individuals no differences were recorded between the 1st
and the 2nd clinical assessment (Cohen’s Kappa = 0.98)
whereas for the mentioned time period no oral hygiene
instructions were given to the participants.
Ethical consideration. The present study was not
an experimental one. In Greece only experimental studies
must be reviewed and approved by authorized commit-
tees (Dental Schools, Greek Dental Associations, Minis-
try of Health, etc). Individuals who agreed to participate
in the present study signed an informed consent form.
Statistical analysis. For each individual, case and
control the worst values of PPD and CAL at the six sites
per tooth and the presence/absence of BOP were re-
corded and coded as dichotomous variables. Current
and former smokers were coded as 1, individuals with
a high socio-economic (income/monthly ≥ 1000 €)
and educational (graduated from University/College)
level were coded as 0, males participants were coded
as 1, individuals that reported genetic predisposition
for LC, history of previous chronic pulmonary disease
and a regular dental follow-up were coded as 1. Age
groups distribution was coded as 0, 1, 2 and 3 for ages
48–49, 50–59, 60–69 and 70+, respectively.
Univariate analysis was carried out to test the rela-
tionship between the independent variables examined
and the LC risk, separately, by using χ2 test. Multivariate
regression analysis was carried out to model the as-
sociations between the dependent variable, LC, and
Experimental Oncology 38, 49–53, 2016 (March) 51
independent ones that were determined by the enter
method. Adjusted odds ratios (OR’s) and 95% con-
fidence interval (CI) were also calculated. Finally, the
independent variables were included to stepwise method
in order to estimate gradually the variables that showed
significant correlations with the dependent one. The sta-
tistical method Cohran’s and Mantel — Haenszel’s was
applied, in an effort to control possible con-founders,
in order to avoid biased secondary associations. Statisti-
cal analysis was performed using the statistical package
of SPSS ver.17.0. A p value less than 5% (p < 0.05) was
considered to be statistically significant.
RESULTS
The mean age of the sample was 61.4 ± 4.2 years.
The most frequent histological type in males was
squamous cell carcinoma (SCC) (47.8%), followed
by small cell lung carcinoma (SCLC) (30.4%), ade-
nocarcinoma (AC) (13.0%) and large cell carcinoma
(LCC) (8.8%), whereas in females AC (44.4%) followed
by SCC (33.3%), SCLC (16.7%) and LCC (5.6%).
Table 1 presents univariate analysis of cases and
controls regarding the examined variables. PPD,
BOP, history of previous chronic pulmonary disease,
smoking and irregular dental follow-up were statisti-
cally significantly associated with LC risk. Table 1 also
presents unadjusted OR’s and 95% CI.
Table 1. Univariate analysis of cases and controls regarding each inde-
pendent variable examined
Variables Cases,
n (%)
Controls,
n (%)
p
value OR 95% CI
Gender:
Males
Females
46 (71.9)
18 (28.1)
80 (58.8)
56 (41.2)
0.075 1.79 0.94–3.40
Age (years):
45–49
50–59
60–69
70+
4 (6.3)
11 (17.2)
41 (64.0)
8 (12.5)
10 (7.4)
32 (23.5)
73 (53.7)
21 (15.4)
0.578 – –
Socio-economic level:
Low
High
38 (59.4)
26 (40.6)
91 (66.9)
45 (33.1)
0.300 1.38 0.75–2.56
Educational level:
Low
High
52 (81.3)
12 (18.7
97 (71.3)
39 (28.7)
0.133 0.57 0.28–1.19
Smoking:
No
Yes
14 (21.9)
50 (78.1)
59 (43.4)
77 (56.6)
0.003* 2.74 1.38–5.42
Cancer family history:
No
Yes
50 (78.1)
14 (21.9)
117 (86.0)
19 (14.0) 0.160 1.72 0.80–3.71
History of previous pul-
monary disease:
No
Yes
33 (51.6)
31 (48.4)
99 (72.8)
37 (27.2)
0.003* 2.51 1.35–4.67
Annual dental follow-up:
< 2 times or no/year
2 times/year
27 (42.2)
37 (57.8)
38 (27.9)
98 (72.1) 0.045* 0.53 0.29–0.99
Periodontal pockets:
Depth 4.0–6.0 mm
Depth > 6.0 mm
46 (71.9)
18 (28.1)
116 (85.3)
20 (14.7) 0.024* 2.27 1.10–4.68
CAL:
Mild 1–2.0 mm
Moderate/severe
≥ 3.0 mm
46 (71.9)
18 (28.1)
107 (78.7)
29 (21.3)
0.290 1.44 0.73–2.86
BOP:
No
Yes
22 (47.8)
42 (52.2)
74 (54.4)
62 (45.6)
0.008* 2.28 1.23–4.22
Note: *p value: statistically significant.
After performance of the first method (step 1a) of the
regression model it was found that all the exa mined
variables except for dental follow-up and age were sig-
nificantly associated with LC risk, according to the OR’s.
Statistically significantly associations were recorded
between moderate/severe CAL, BOP and risk of de-
veloping LC (Table 2). Table 2 also presents adjusted
OR’s with 95% CI. The final method (stepwise/step 7a)
showed that smoking, PPD, CAL and BOP were signifi-
cantly associated with LC risk. PPD was also significantly
associated with LC risk after adjusting for confounders,
such as smoking and dental follow-up (Table 3).
Table 2. Presentation of correlation between independent variables
and LC according to Enter (first step) and Wald method (backward) of mul-
tiple logistic regression analysis model
Step Variables B S.E. Wald df Sig. Exp
(B)
95% CI for
EXP (B)
Lower Upper
1a Gender 0.548 0.373 2.158 1 0.142 1.730 0.833 3.596
Smoking 0.618 0.416 2.201 1 0.138 1.854 0.820 4.193
Socio-eco-
nomic level 0.448 0.400 1.256 1 0.262 1.565 0.715 3.427
Educational
level −0.238 0.486 0.240 1 0.624 0.788 0.304 2.041
Age 0.031 0.025 1.540 1 0.215 1.032 0.982 1.084
Cancer family
history 0.011 0.477 0.001 1 0.981 1.011 0.397 2.576
History of pre-
vious pulmo-
nary disease 0.558 0.384 2.109 1 0.146 1.747 0.823 3.711
Annual dental
follow-up −0.688 0.369 3.474 1 0.062 0.502 0.244 1.036
BOP 0.760 0.366 4.310 1 0.038 2.139 1.043 4.385
Periodontal
pockets 0.817 0.510 2.563 1 0.109 2.264 0.833 6.156
CAL 1.162 0.524 4.912 1 0.027 3.197 1.144 8.937
Constant 5.364 1.754 9.358 1 0.002 0.005
7a Smoking 0.913 0.373 6.008 1 0.014 2.492 1.201 5.173
Annual dental
follow-up −0.588 0.351 2.803 1 0.094 0.555 0.279 1.106
BOP 0.656 0.347 3.575 1 0.059 1.927 0.976 3.805
Periodontal
pockets 1.002 0.486 4.259 1 0.039 2.724 1.052 7.056
CAL 1.256 0.506 6.163 1 0.013 3.513 1.303 9.474
Constant 3.134 0.653 23.001 1 0.000 0.044
Table 3. Application of Cohran’s and Mantel — Haenszel’s, statistical
method for controlling possible confounders
Variables Exp (B) 95% CI
Periodontal pockets
Non-smokers
Smokers
2.279
6.708
0.574–9.047
2.182–20.622
CAL
Non-smokers
Smokers
2.138
2.205
0.652–7.006
1.051–4.627
BOP
Non-smokers
Smokers
2.514
2.416
0.778–8.121
1.143–5.106
Periodontal pockets
Regular dental follow-up annually
Irregular dental follow-up annually
2.745
21.048
1.043–7.227
2.585–171.392
CAL
Regular dental follow-up annually
Irregular dental follow-up annually
3.639
13.520
1.298–10.205
1.644–111.154
BOP
Regular dental follow-up annually
Irregular dental follow-up annually
2.041
4.000
0.921–4.520
1.413–11.327
DISCUSSION
The present case — control research showed
that deep periodontal pockets were associated with
an increased LC risk, after controlling for possible
52 Experimental Oncology 38, 49–53, 2016 (March)
confounders such as smoking and dental follow-up.
Despite the fact that more investigation is required
in order to confirm such findings, the current obser-
vations suggest that improvement of oral hygiene and
smoking cessation could be an effective preventive
measure against LC development.
The possible influence of gender as a cancer risk
factor is known, however it is considered as a con-
founder. The results showed no association between
gender and LC risk, finding that was in accordance
with those from previous reports [9, 10].
Similarly, age is also considered as a confounder,
although older individuals are in a higher risk for
total cancer, LC [24, 25], initiation and progression
of PD [26]. No association was found between age
and LC risk in the present study.
Another crucial confounder is socio-economic
level, however, it has not been proven its possible role
as a LC risk factor. Its role is indirect in cases of previ-
ous pulmonary diseases such as TBC that is associ-
ated with a lower socio-economic level and LC devel-
opment [27, 28]. No association was observed in the
current study between those variables examined.
The possible role of educational level as a risk
factor of developing LC has not been investigated ac-
cording to previous reports. However, it is supposed
that high-educated individuals take care of their own
oral hygiene more than low-educated ones [29, 30].
No association was recorded between educational
level and LC risk in the current study. There is strong
evidence suggesting a genetic predisposition for
LC. Studies of familial aggregation have shown familial
risk on the same order of that reported for breast and
colon cancer [31, 32]. The results of the present study
did not confirm such an association.
Smoking is considered as a causal risk factor of to-
tal cancer and LC [33]. It has been shown that smoking
is associated with SCC and SCLC, mainly, and in less
cases with lung AC. It is still remaining unknown the
reasons why only 15% of smokers develop LC [34]. The
current study confirmed its role as a causal risk factor.
On the other hand smoking is considered as a risk fac-
tor for PD development and progression [35, 36] and
a proven confounder as well. Based on the mentioned
suggestions the statistical method of adjustment —
Cohran’s and Mantel — Haenszel’s was carried out
to assess if possible significant correlations between
both diseases could be attributed to smoking status
or not. It was found that smoking was a confounder
of CAL and BOP.
According to the results PPD was associated with
an increased LC risk after controlling for certain con-
founders such as smoking and socio-economic status.
Similar reports that have investigated the possible
associations between PD indices and LC risk, or total
cancer have not been carried out, whereas the majority
of the available studies are prospective and have based
on questionnaires and self-reported data.
Arora et al. [37] were found that individuals with
PD showed an increased LC risk however after con-
trolling for certain confounders such as gender, age,
socio-economic and educational status the mentioned
association was not found to be statistically significant.
That research was based on a questionnaire and self-
reported information regarding periodontal tissues
condition examined and different PD indices were used.
In another prospective study among health pro-
fessionals in which a self-reported questionnaire was
used for estimation of periodontal tissues status [9],
PD was significantly associated with LC risk after con-
trolling for smoking and several risk factors. The main
finding was that a limited number of remaining teeth
(0–16 vs 32) was associated with an increased LC risk.
Hujoel et al. [8] based on Russel Index for
PD definition were found that individuals with PD had
an increased risk of total cancer and a significantly
increased LC risk, finding that was not confirmed
in never smokers.
A similar research in Japan [38] reported that
a small number of remaining teeth was associated with
an increased LC risk.
An important factor that may be taken into account
during the design process of such studies, is the
epidemiological phenomenon of “confounding”. Both
diseases, PD and cancer share some common risk
factors such as smoking and socio-economic status.
Consequently, a correlation between both diseases
would be expected even if a causal link did not exist.
Confounding may also occur through unknown factors,
for example a genetic predisposition, or mutual risk
factors. However, the question still remains whether
the association between PD and cancer is causal
or is con-founded by unmeasured factors.
Another practical problem is the accuracy defini-
tion of PD which is essential to establish on reliable
and reproductive indices [39]. Data of such studies
have carried out based on prospective or retrospec-
tive methodology in an attempt to control possible
systema tic biases, selection biases mainly, and con-
founding. However, smoking remains a possible inter-
pretation as the correlations that have reported con-
cerned smokers, whereas no correlations have been
reported between PD and cancer in non-smokers.
It is important to highlight that the decision on includ-
ing older individuals who have at least 20 remaining
natural teeth, may lead to an under-estimation of older
individuals with previous PD and who may have had
teeth extracted for periodontal reasons. In addition,
it is essential to be noted that there was not any chance
of benchmarking between the findings of the current
study with those of similar previous studies, whereas
on the other hand the present study was a first attempt
to approach that possible correlation in Greece.
In conclusion, PD parameters such as deep perio-
dontal pockets were associated with an increased risk
of developing LC.
The present study constitutes a part of my MSc
Thesis which was announced on May 2015 at Medical
School, University of Athens.
Experimental Oncology 38, 49–53, 2016 (March) 53
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