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Research Article
Gender-Specific Associations of Serum Antibody to
Porphyromonas gingivalis and Inflammatory Markers
Michiko Furuta,1Yoshihiro Shimazaki,1,2 Shunichi Tanaka,3Kenji Takeuchi,1
Yukie Shibata,1Toru Takeshita,1Fusanori Nishimura,4and Yoshihisa Yamashita1
1Section of Preventive and Public Health Dentistry, Division of Oral Health, Growth and Development,
Kyushu University Faculty of Dental Science, Fukuoka 812-8582, Japan
2Department of Preventive Dentistry and Dental Public Health, School of Dentistry, Aichi-Gakuin University, Nagoya 464-8650, Japan
3Japanese Red Cross Kumamoto Healthcare Center, Kumamoto 861-8528, Japan
4Section of Periodontology, Division of Oral Rehabilitation, Kyushu University Faculty of Dental Science, Fukuoka 812-8582, Japan
Correspondence should be addressed to Yoshihisa Yamashita; yoshi@dent.kyushu-u.ac.jp
Received October ; Revised December ; Accepted December
Academic Editor: Kazuhiko Nakano
Copyright © Michiko Furuta et al. is 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.
It remains unclear whether serum antibody titer against Porphyromonas gingivalis (Pg) and inammatory components lead to
periodontal deterioration in each gender, as periodontal and systemic status is inuenced by gender. e present study investigates
the gender-specic probable eects of titer against Pg and inammatory markers on periodontal health status in a longitudinal
study. A retrospective study design was used. At two time points over an -year period (in and ), individuals (
males with a mean age of . ±. years and females with a mean age of . ±. years) were surveyed. Periodontal status,
serum antibody titer against Pg, and high-sensitive C-reactive protein (hsCRP) were evaluated. Poisson regression analyses revealed
that the elevated titer against Pg and hsCRP signicantly predicted the persistence of periodontal disease years later in females
with periodontal disease in . Elevated hsCRP was signicantly associated with the incidence of periodontal disease years later
in females who were periodontally healthy in . Males had a weaker association among titer against Pg, inammatory markers,
and periodontal disease. ese ndings suggest that immune response to Pg infection in addition to inammatory components
aects periodontal deterioration in females.
1. Introduction
Oral diseases limit an individual’s capacity in biting, chewing,
smiling, speaking, and psychosocial wellbeing []. e most
common oral diseases are dental caries and periodontal
disease. Periodontal disease, that is, inammatory disorder of
the gingiva, is highly prevalent around the world, and nearly
% of adults have periodontal disease [].
As with many chronic diseases, periodontal disease has
multiple risk factors, and it is important to treat both the local
and systemic factors []. Among local factors for periodontal
disease, it has been recognized that periodontal disease is
caused by specic bacteria in the periodontal pocket [].
Porphyromonas gingivalis (Pg) plays a major role in the path-
ogenesis of periodontal disease and is considered to induce
elevated systemic and local immune responses in periodontal
patients [,]. Elevated serum IgG antibody levels of Pg
have previously been reported to be closely connected to
thepresenceofPg in periodontal pockets [,], reecting
the notion that serum antibody titers against Pg are higher
in periodontal patients than in healthy individuals [–].
Most previous studies have been cross-sectional or short-
term longitudinal in design and such designs do not provide
information or are decient in information on the long-term
association between serum antibody titers against Pg and
periodontal status.
Periodontal disease is a local inammatory condition
and is linked to systemic inammation via host responses.
Several cross-sectional studies have reported that levels of
inammatory markers are higher in patients with periodontal
Hindawi Publishing Corporation
BioMed Research International
Volume 2015, Article ID 897971, 9 pages
http://dx.doi.org/10.1155/2015/897971
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2,470 individuals who visited the Japanese Red Cross Kumamoto Healthcare Center for
medical check-ups in 2011 and had the earliest check-ups between 2003 and 2006.
Group 1:468 visited in 2003 and 2011. Serum samples collected in 2003 were preserved.
Group 2:945 visited in 2004 and 2011.
Group 3:832 visited in 2005 and 2011.
Group 4:225 visited in 2006 and 2011.
e design of this study was explained to group 1in 2011.
447 were obtained informed consent for the use of preserved serum samples.
Participation rate: 96%
Exclusion
19 with insucient serum
sample volume.
14 with fewer than ten teeth.
3with missing value.
Analysis: 411 participants (296 males, 118 females).
Exclusion
Groups 2,3, and 4
F : Flow diagram of study participant selection.
diseasethaninhealthyindividuals[,]. Systemic inam-
mation accompanies chronic inammatory diseases such as
cardiovascular disease, diabetes, and metabolic syndrome
[], and thus systemic inammation is suggested to be an
underlying risk factor in periodontal disease as a localized
inammatory disease.
As another risk factor for periodontal disease, gender is
an important consideration, because periodontal disease is
oen reported to be more prevalent or severe in males than
in females [,,] and associations between periodontal
disease and metabolic syndrome have been conrmed in
females but not in males []. us, the association between
periodontal disease and local and systemic risk factors may
also be expected to have gender dierences. However, most
studies have not considered this hypothesis and did not
use stratied analysis, which would allow determination of
whether the relationship is unique to one gender, or even
opposite in males and females. In this study, we investigated
the gender-specic probable eects of titer against Pg and
inammatory markers on periodontal status in a longitudinal
study, as it remains unclear whether these factors lead to
gender-specic periodontal deterioration.
2. Materials and Methods
2.1. Study Participants. We performed a retrospective study.
Participants were recruited from among , individuals
who visited the Japanese Red Cross Kumamoto Healthcare
Center, Kumamoto, Japan, for periodic medical check-ups
including dental examination in and had the earliest
check-ups between and . e , individuals
were categorized into four groups: visited in and
(group ), visited in and (group ),
visited in and (group ), and visited in
and (group ). In group , serum samples collected in
for another study had been preserved. e design of
this study using preserved serum samples for measurement
of titers against Pg and high-sensitive C-reactive protein
(hsCRP) was explained to individuals (group ) and
written informed consent was obtained from individuals
(participation rate, %). Nineteen participants with insu-
cient serum sample volume were excluded. We also excluded
participants with missing value and fewer than teeth due
to diculties in assessing their current periodontal health
properly []. erefore, participants ( males with a
mean age of 57.6 ±11.2 years and females with a mean age
of 59.2 ± 10.3 years) were analyzed in this study. Participant
ow diagram is presented in Figure .
e study was approved by Kyushu University Institu-
tional Review Board for Clinical Research (-).
2.2. Oral and General Examinations and Questionnaire. One
dentist (ST) assessed the oral health status of participants
in both and . e number of teeth present was
determined. According to the World Health Organization
Community Periodontal Index (CPI) criteria []withmod-
ication, periodontal condition was assessed in all present
teeth to monitor the periodontal health. e highest CPI
codes were recorded in each sextant. Periodontal disease
was dened as at least one sextant with the presence of
periodontal pocket depth ≥mm(CPIcode≥) [].
Overweight was dened as body mass index (BMI) of .
or greater. A venous blood sample was drawn and analyzed
BioMed Research International
for fasting glucose, triglycerides, high density lipoprotein
(HDL) cholesterol, leukocyte count, and dierential leuko-
cyte count (i.e., neutrophils, acidocytes, and monocytes).
Elevated levels of fasting glucose, triglycerides, HDL, and
blood pressure were dened by the Joint Interim Societies
[]. Elevated leukocytes were dened as white blood cell
of ≥. ×9/L []. In the present study, we measured
hsCRP in preserved serum samples in . HsCRP levels of
≥. mg/L were dened as elevated hsCRP []. CRP levels
tend to increase with acute bacterial and viral infections,
age, smoking, myocardial infarction, rheumatoid arthritis,
obesity, type diabetes, hypertension, and cancer []. We
considered the eect of these factors on hsCRP in analysis.
Information on smoking habit, alcohol consumption, and
toothbrushing frequency was obtained by a self-administered
questionnaire. Smokers were categorized as never smokers,
who had never smoked regularly; past smokers, who had
smoked regularly but had stopped smoking more than one
year ago; and current smokers, who had smoked regularly.
Alcohol drinkers were categorized as either current drinker,
who had drunk at least one time per week, or not current
drinkers. Toothbrushing frequency was categorized as either
more than three times daily toothbrushing or not.
2.3. Measurement of Titers against Pg. e immunological
assays used in this study were as described previously [,].
Serum IgG antibody titers against Pg (FDC) were deter-
mined by Leisure Inc. (Tokyo, Japan) using enzyme-linked
immunosorbent assay (ELISA) from serum samples stored
at –∘C. e absorbance of each sample was evaluated and
assigned ELISA unit (EU) values relative to the absorbance
of a pool of sera collected from periodontally healthy control
individuals []. Pg antibody levels are expressed as standard-
ized values calculated as follows: (EU for study serum samples
– EU for control samples)/ ×(SD of control samples) [].
An elevated serum antibody titer against Pg was dened as
having a value greater than median value [].
2.4. Statistical Analysis. Chi-squared test for categorical data
and Mann-Whitney Utest for continuous data were used
to determine signicant dierences (𝑃 < 0.05, two sided)
between males and females or to elevate the associations
between periodontal disease, titer against Pg,andinam-
matory markers. e multivariate associations among them
were examined in Poisson regression models as follows: ()
model with periodontal disease in as a dependent
variable, using cross-sectional data in and () model
with periodontal disease at follow-up as a dependent variable,
using longitudinal data. In the second model, titer against Pg
and inammatory markers were entered as independent vari-
ables. HsCRP, leukocytes, and BMI were treated as inam-
matory markers, because obesity may be linked to chronic
inammation. As potential confounders, age, toothbrushing
frequency, and smoking were included in the model because
they are known to increase the risk of periodontal disease
[]. Fasting glucose, triglycerides, HDL, and blood pressure
were also included in the model, because they are possible to
be associated with inammatory markers. Prevalence ratios
(PRs) and % condence intervals (CIs) were calculated.
SPSS soware (version . for Windows; IBM SPSS Japan,
Tokyo, J a p a n ) w a s u sed for d at a a n a l y s es.
3. Results
e percentage of participants having periodontal disease
was .% in . Oral and systemic health status in
and is shown in Ta b l e . ere were gender dierences in
the number of the present teeth, smoking habit, toothbrush-
ing frequency, and alcohol consumption. Serum antibody
titer against Pg and hsCRP did not show a gender dierence.
Among the data, the associations of periodontal disease
with titer against Pg andwithsystemichealthareshown
in Table .WhenthePoissonregressionmodelincluded
covariates with a signicance level for retention of 𝑃 < 0.2
on bivariate analysis, high titer against Pg was signicantly
associated with the periodontal disease in both males and
females. In females, overweight was signicantly associated
with periodontal disease.
Among longitudinal data, periodontal disease persisted
years later in .% of males with periodontal disease
in and .% of females with periodontal disease in
had persistent periodontal disease years later (Tabl e ).
Among periodontally healthy males in , .% devel-
oped periodontal disease years later, while, for females,
.% developed periodontal disease years later. When we
evaluated the association between hsCRP and possible related
factors, such as fasting glucose, triglycerides, HDL, blood
pressure, and leukocytes, these factors were signicantly
associated with hsCRP. Acute bacterial and viral infections
(𝑛=0), myocardial infarction (𝑛=1), rheumatoid arthritis
(𝑛=1), and cancer (𝑛=21)werenotassociatedwithhsCRP.
PoissonregressionanalysesshowedthatlevelsofhsCRPwere
signicantly related to development of periodontal disease
yearslaterinperiodontallyhealthyfemalesin(PR.;
% CI: .–.; 𝑃value .), even when age, smoking,
toothbrushing frequency, and possible hsCRP-related factors
were included in the model (Model in Tab l e ). Leukocytes
count was not associated with periodontal disease. Persis-
tence of periodontal disease years later in females was
signicantly associated with antibody titer against Pg (PR
.; % CI: .–.; 𝑃value .) and hsCRP (PR .;
% CI: .–.; 𝑃value .). e interaction between Pg
and hsCRP was not statistically signicant. To conrm the
consistency of the results, we treated antibody titer against
Pg as a categorical variable (Model in Tab l e ). ese
associations were not signicant in males.
When the association between titer against Pg in and
systemic health such as lower HDL, elevated triglycerides,
and blood pressure years later was examined, the associa-
tion was not signicant.
4. Discussion
is study showed gender-specic associations of periodon-
tal status with serum titer against Pg and with inammatory
markers in a long-term longitudinal study. Serum titer against
BioMed Research International
T : Characteristics of study subjects in and .
Variabl e s
Males
(𝑛=)
Females
(𝑛=) All 𝑃value Males
(𝑛=)
Females
(𝑛=) All 𝑃value
e number of the present
teeth (median [%, %]) (, ) (, ) (, ) . (, ) (, ) (, ) .
Periodontal dis ease (PD ≥
mm) (%) . . . . . . . .
Serum antibody titer against
𝑃𝑔∗. (., .) . (., .) . (., .) .
Age (median [%, %]) (, ) (, ) (, ) . (, ) (, ) (, ) .
More than times daily
toothbrushing . . . <.
Current/past smoking (%) . . . <. . . . <.
Current alcohol consumption
(%)†. . . <. . . . <.
Overweight (%) . . . . . . . .
Elevated hsCRP (≥mg/L)
(%)∗. . . .
Elevated fasting glucose
(≥ mg/dL) (%) . . . . . . . .
Reduced HDL (males <,
females < mg/dL) (%)‡. . . . . . . .
Elevated triglycerides
(≥ mg/dL) (%)§. . . . . . . .
Elevated blood pressure
(≥/≥ mmHg) (%)‖. . . . . . . .
Elevated leukocytes (≥. ×
cells/L) (%) . . . . . .
Leukocytes (median [%,
%])(
cells/L) . (., .) . (., .) . (., .) . . (., .) . (., .) . (., .) .
Neutrophils (median [%,
%])(
cells/L) . (., .) . (., .) . (., .) . . (., .) . (., .) . (., .) .
Acidocytes (median [%,
%])(
cells/L)
. (.,
.)
. (.,
.)
. (.,
.) . . (.,
.)
. (.,
.)
. (.,
.) <.
Monocytes (median [%,
%])(
cells/L)
. (.,
.)
. (.,
.)
. (.,
.) <. . (.,
.)
. (.,
.)
. (.,
.) <.
∗Serum antibody titer against 𝑃𝑔 and hsCRP were measured in preserved serum samples in .
†Males, 𝑛= ; females, 𝑛= , in .
‡HDL < mg/dL in males and < mg/dL in females for reduced HDL.
§Triglycerides ≥mg/dL or drug treatment for dyslipidemia.
‖Systolic blood pressure ≥ mmHg or diastolic blood pressure ≥ mmHg or antihype rtensive d rug treat ment.
PD, periodontal pocket depth; hsCRP, high-sensitive C-reactive protein; HDL, high-density lipoprotein cholesterol.
Pg and inammatory markers showed a stronger association
with periodontal status in females than in males. To the best
ofourknowledge,thisistherststudytoshowsuchgender
dierences in a longitudinal study.
In this study, we found that serum titer against Pg was
high in participants with periodontal disease at a single time
point, based on cross-sectional data in . is nding
is consistent with several studies [–]. Ebersole et al. []
noted that elevated systemic antibodies against periodon-
tal bacteria were reective of subgingival colonization and
existed as a response to bacterial infection at disease-active
sites. ese results suggest that elevated antibody levels
against Pg areassociatedwithpriordestructiveperiodontal
disease [].
In addition, high titer against Pg inuenced the persis-
tence of periodontal disease over the -year period in females
with periodontal disease at baseline, based on longitudinal
data analyses. is nding is similar to the data of Craig
et al. [], who reported that individuals with progressed
periodontaldiseasehadheightenedserumantibodyresponse
to Pg at baseline. Anderson et al. []observedthatthe
IgG antibody against Pg produced in response to progressing
periodontal disease appeared to lack functional properties
such as direct cytolysis and opsonization in nonhuman
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T : Prevalence ratios for periodontal disease (presence of periodontal pocket depth ≥mm) in in males and females.
Covariates from data of
Males Females
Number of those
having periodontal
disease
(𝑛=)
Crude PR
(% CI)
Adjusted PR†
(% CI)
Number of
those having
periodontal
disease
(𝑛=)
Crude PR
(% CI)
Adjusted PR†
(% CI)
Serum antibody titer against
Pg (%)
Low (.) (.)
High (.) . (.–.)∗∗∗ . (.–.)∗∗∗ (.) . (.–.)∗∗∗ . (.–.)∗∗
Overweight
No (.) (.)
Yes (.) . (.–.) (.) . (.–.)∗∗∗ . (.–.)∗
hsCRP
Normal (.) (.)
Elevated hsCRP (.) . (.–.) (.) . (.–.) . (.–.)
Leukocytes . (.–.) . (.–.)
Fasting glucose
Normal (.) (.)
Elevated fasting glucose (.) . (.–.) (.) . (.–.)
HDL
Normal (.) (.)
Reduced (.) . (.–.) (.)‡
Triglycerides
Normal (.) (.)
Elevated triglycerides (.) . (.–.) (.) . (.–.)
Blood pressure
Normal (.) (.)
Elevated blood pressure (.) . (.–.) (.) . (.–.)
Age
< yrs (.) (.)
≥ yrs (.) . (.–.)∗∗ . (.–.)∗∗ (.) . (.–.)
Toothbrushing frequency
< times/day (.) (.)
≥ times/day (.) . (.–.) (.) . (.–.)
Smoking
Never (.) (.)
Current/Past (.) . (.–.) . (.–.) (.) . (.–.)
Alcohol consumption
No (.) (.)
Current (.) . (.–.) (.) . (.–.)
Poisson regression analysis with periodontal disease (periodontal pocket depth ≥ mm) in as the dependent variable and serum antibody titer against Pg,
overweight, hsCRP, leukocytes fasting glucose, HDL, triglycerides, blood pressure, age, smoking, and drinking in as the independent variables.
∗𝑃<., ∗∗𝑃<., and ∗∗∗𝑃<..
†Adjusted prevalence ratios in the nal multivariable model aer including covariates with a signicance level for retention of 𝑃<..
‡PR was not calculated because of complete separation (the number of females with periodontally healthy and reduced HDL was ).
HsCRP, high-sensitive C-reactive protein; HDL, high-density lipoprotein cholesterol; PR, prevalence ratio; CI, condence interval.
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T : Changes in periodontal disease between and .
Variabl e s
from data of
Periodontally healthy in Periodontal disease in
Males Females Males Females
In In In In
Healthy Periodontal
disease Healthy Periodontal
disease Healthy Periodontal
disease Healthy Periodontal
disease
𝑛= 𝑛= 𝑛= 𝑛= 𝑛= 𝑛= 𝑛= 𝑛=
Serum antibody titer
against 𝑃𝑔†‡ .
(., .)
.
(., .)
.
(., .)
.
(., .)
.
(., .)
.
(., .)
.
(., .)
.
(., .)∗
High serum antibody
level (≥.) to Pg (%)‡. . . . . . . .∗
Overweight (%)‡. . . . . .∗. .
Elevated hsCRP
(≥.) (%)‡. . . .5∗∗ . . . .5∗∗
Leukocytes (
cells/L)†§. (., .) . (., .) . (., .) . (., .) . (., .) . (., .) . (., .) . (., .)
∗𝑃<., ∗∗𝑃<..
†Median (%, %).
‡Comparison between participants with or without periodontal disease in by bivariate analysis.
§Continuous variable of leukocytes was used, because of small number of elevated leukocytes (≥. ×cells/L).
HsCRP, high-sensitive C-reactive protein.
T : Prevalence ratios for periodontal disease in .
Periodontally healthy in Periodontal disease in
Males Females Males Females
PR (% CI)†PR (% CI)†PR (% CI)†PR (% CI)†
Model 1
Serum antibody titer against Pg . (.–.) . (.–.) . (.–.) . (.–.)∗∗
Overweight
No
Yes . (.–.) . (.–.) . (.–.) . (.–.)
hsCRP
Normal
Elevated hsCRP . (.–.) . (.–.)∗∗ . (.–.) . (.–.)∗
Leukocytes‡. (.–.) . (.–.) . (.–.) . (.–.)
Model 2
Serum antibody titer against Pg
Low
High . (.–.) . (.–.) . (.–.) . (.–.)∗
Overweight
No
Yes . (.–.) . (.–.) . (.–.) . (.–.)
hsCRP
Normal
Elevated hsCRP . (.–.) . (.–.)∗∗ . (.–.) . (.–.)∗
Leukocytes‡. (.–.) . (.–.) . (.–.) . (.–.)
Dependent variable, : periodontal disease in , : periodontally healthy in .
Model : continuous variable of serum antibody titer against Pg was included.
Model : categorical variable of serum antibody titer against Pg was included.
∗𝑃<., ∗∗𝑃<..
†Adjusted by age, smoking, toothbrushing frequency, triglycerides, HDL, fasting glucose, and systolic blood pressure in .
‡Continuous variable of leukocytes was used, because of small number of elevated leukocytes.
HsCRP, high-sensitive C-reactive protein; PR, prevalence ratio; CI, condence interval.
BioMed Research International
primates. ey speculated that the antibody response does
not protect against periodontal disease in many patients.
On the other hand, antibody levels to periodontal bacteria
have been reported to remain elevated over a -month
period, despite periodontal therapy []. Although it is
possible that antibody levels against Pg are retained for long
periods, our results suggest that high titers against Pg do not
provide protection against periodontal disease in females, as
compared with males. Generally, antibody plays an important
role in defense against pathogenic bacteria. With regard to
antibody responses against Pg, it has been suggested that
elevated antibody levels are in response to pathogens, but
have little eect on infections []. To determine more about
the exact relationship between antibody level and periodontal
disease in each gender, it will be necessary to repeat the study
in larger numbers of subjects and to assess Pg colonization.
Gender dierences in the longitudinal association
between antibody titer against Pg and periodontal disease
might be explained by disparities in immune responses.
Although sex dierences in immune response remain
incompletely understood, presumably, sex-specic genetic
architecture accounts for dimorphisms in immune response
and host susceptibility, exerting profound eects on
multiple immunologic parameters []. e X-chromosome
encodes approximately , genes, related to immunity
[]. Females have two X-chromosomes, which provides
the added biological advantage of the cellular mosaicism
that is associated with X-inactivation, whereas males are
more vulnerable to X-linked diseases as they have a single
X-chromosome []. Sex dierences in immunity would
be associated with cellular functions dependent on genes
located on the X-chromosome []. We speculate that
protection from periodontal disease by antibody against Pg
diers between males and females, probably due to sexual
dimorphisms in immunoinammatory response that is
inuenced by sex-specic genetic architecture.
When we investigated the association between inamma-
tory markers and progression of periodontal disease, higher
levels of hsCRP were signicantly associated with devel-
opment and persistence of periodontal disease in females,
but not in males. While Paraskevas et al. []reported
strong evidence by meta-analyses of cross-sectional studies
that CRP in periodontal disease was elevated as compared
with healthy individuals, our longitudinal study indicated
gender-specic eects of CRP levels on the progression
of periodontal disease. e dierence in the inammatory
response in females compared to males has long been
noted []. ese dierences by gender may be due to sex
hormone, estrogen. However, this does not provide sucient
evidence because estrogen production seems to diminish in
our female subjects with menopause. Conversely, a lot of
evidences suggest that the declining function of the ovaries in
femalesisassociatedwithspontaneousincreasesinsystemic
proinammatory cytokines [,]. Inammation is known
to cause periodontal disease [,,]. e present results
suggest that the relationship between periodontal disease and
systemic inammation presumably diers by gender because
of the dierences in the inammatory response by gender in
regard to proinammatory cytokine. e exac t mechanism by
which estrogen modulates proinammatory cytokine activity
hasnotyetbeenconclusivelyclaried[,], and further
analyses are needed to fully understand the details of the
mechanism of the interference by estrogen.
ere were several limitations to the current study. We
usedthesamemethodtomeasuretitersagainstPg as reported
by Kudo et al. [], and the percentage of participants with
≥. titers in our study and the study by Kudo et al.
was % and %, respectively. In addition, when we ana-
lyzed receiver operating characteristics (ROC) curves for
periodontal disease (presenting of PD ≥ mm), the optimal
cut-o point of titers against Pg was . (. in Kudo et al.)
and sensitivity, specicity, and the areas under the ROC curve
were ., ., and .. Hence, our participants may
have had higher titers against Pg,ascomparedtothoseinthe
study by Kudo et al. Second, we did not have any information
on oral health behavior such as regular dental visits and
receipt of dental treatment. ese would aect periodontal
status, and thus our ndings could reect confounding by
omitting these variables. ird, we did not measure the sign
of periodontal disease such as clinical attachment loss. It
has been suggested that the elevated antibody levels are in
responsetopathogensandareexpectedtobeinuencedby
the size of the area of infection rather than by the history of
tissue destruction []. At baseline, periodontal pocket depth
would be acceptable in investigating the association between
titers against Pg and periodontal condition. It is not beyond
the realm of possibility that titers against Pg are related to
attachment loss years later. Finally, socioeconomic status
was not included as a factor in this analysis. Future studies
should include this, because it is possible that socioeconomic
status is connected with periodontal and systemic health
status.
Even considering the above limitations, the present study
illustrates that females with high titer against Pg and high
level of inammatory marker are more likely to have peri-
odontal disease some years later, while males have a relatively
weak relationship among the titer against Pg,inammatory
markers, and periodontal disease.
Conflict of Interests
e authors declare that there is no conict of interests
regarding the publication of this paper.
Acknowledgment
is study was supported by Grants-in-Aid for Scientic
Research (, , and ) from the
Ministry of Education, Science, Sports, and Culture of Japan,
Tokyo, J a p a n .
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