J Periodontol January 2015

Effects of Scaling and Root Planing on

Clinical Response and Serum Levels of
Adipocytokines in Patients With Obesity
and Chronic Periodontitis
Tiago Eduardo Dias Gonc
xalves,* Magda Feres,* Glaucia Santos Zimmermann,* Marcelo Faveri,*
Luciene Cristina Figueiredo,* Paloma Gralha Braga,* and Poliana Mendes Duarte*

Background: Despite several investigations suggesting that

obesity is a risk indicator for periodontitis, little is known
about the effect of obesity on periodontal treatment response. The aim of this study is to evaluate the effects of
scaling and root planing (SRP) on clinical parameters and
circulating levels of leptin and adiponectin in patients with
obesity with chronic periodontitis (CP).
Methods: Twenty-four patients with obesity and CP and
24 patients without obesity with CP were submitted to SRP.
Clinical parameters were assessed at baseline and 3 and
6 months after therapy. Serum levels of leptin and adiponectin were evaluated at all time points, using enzyme-linked
immunosorbent assay.
Results: SRP improved the clinical parameters of both
groups at 3 and 6 months (P <0.05). Nonetheless, the patients without obesity presented a lower mean probing depth
(PD) at 6 months after therapy and a greater reduction in
PD from baseline to 6 months in the full-mouth analysis
(primary outcome variable) and in initially deep sites (P <0.05).
Leptin serum levels were higher in patients with obesity
than in patients without obesity at all time points (P <0.05).
No changes in the serum levels of leptin and adiponectin
were observed in groups with and without obesity after
therapy (P >0.05).
Conclusions: Patients with obesity and CP presented
lower reductions in PD than patients without obesity with
CP at 6 months after SRP. Furthermore, the treatment did
not affect the circulating levels of leptin and adiponectin
in any group. J Periodontol 2015;86:53-61.
KEY WORDS
Adipokines; adiponectin; chronic periodontitis; Leptin;
obesity; root planing.
* Department of Periodontology, Dental Research Division, Guarulhos University,
Guarulhos, Sao Paulo, Sao Paulo, Brazil.
Department of Dentistry, Federal University of Santa Catarina, Florianopolis, Santa
Catarina, Brazil.

pidemiologic studies in different

populations and systematic reviews
have demonstrated an association between obesity and periodontal
diseases.1-5 Evidence indicates a positive correlation between obesity and its
anthropometric measurements (e.g., body
mass index [BMI] and waist circumference) with periodontitis and clinical periodontal parameters (e.g., probing depth
[PD], gingival inflammation, and clinical attachment loss).1,2
The white adipose tissue, especially
the visceral one, secretes several adipocytokines, including resistin, tumor necrosis factor-a, interleukin-6, leptin, and
adiponectin.6,7 Leptin and adiponectin
are important adipocytokines that generally produce opposing molecular effects.
Besides its role on energy homeostasis, as
a cytokine, leptin presents proinflammatory
biologic activities, stimulating secretion
of several proinflammatory mediators related to the innate and T-helper-1 responses.8,9 Instead, adiponectin provides
multiple anti-inflammatory actions, including inhibition of proinflammatory
cytokines, induction of anti-inflammatory
mediators, downregulation of adhesion
molecule expression, and antagonism of
toll-like receptors and their ligands.10,11
It is supposed that the imbalance in the
production of proinflammatory and antiinflammatory adipocytokines may be a
doi: 10.1902/jop.2014.140266

53

Response of Patients With Obesity to Periodontal Therapy

possible link between obesity and periodontitis as a

result of altered inflammatory and immune responses
at systemic and/or periodontal levels. The obesity
induces a chronic systemic inflammatory state that
may negatively affect the onset and progression of
periodontal disease, whereas periodontitis may adversely influence the systemic levels of adipocytokines in favor of proinflammation.12-15
Despite numerous studies showing an association
between obesity and periodontal diseases, few investigations to date have assessed the affect of obesity
on periodontal treatment response.16-20 Some reports have shown that obesity does not have a negative effect on the clinical response to periodontal
treatment in the short term.16,17,19 Conversely, Suvan
et al.20 showed that BMI and obesity are predictors
of unfavorable responses to non-surgical periodontal
treatment after 2 months. Furthermore, patients
with obesity who had significant weight loss after
bariatric surgery presented a short-term better clinical response to non-surgical periodontal therapy
than those who did not have bariatric surgery.18
Because the results of the few studies assessing
obesity as a possible modifying factor in the response to periodontal therapy are contradictory,
additional studies on this topic are still necessary.
Therefore, the aim of this study is to evaluate the
effects of scaling and root planing (SRP) on clinical
response and circulating levels of leptin and adiponectin in patients with obesity and chronic periodontitis (CP) up to 6 months after therapy.
MATERIAL AND METHODS
Sample Size Calculation
The ideal sample size to ensure adequate power in
this study was calculated considering differences of
0.5 mm between groups for full-mouth mean PD
change from baseline to 6 months and a standard
deviation of 0.5 mm.20 Based on these data, it was
determined that 18 patients per group would be necessary to provide an 85% power with an a of 0.05.
However, based on an anticipated attrition rate of 25%,
24 patients per group were included in this study.
Population
Patients with and without obesity with CP (26 males
and 22 females, aged 33 to 70 years; mean age: 48.7
years) were selected from the population referred
to the Dental Clinic of Guarulhos University, Sao
Paulo, Brazil. All eligible patients were invited to
participate in the study, and detailed medical and
dental records were obtained. Patients were informed of the nature, potential risks, and benefits of
their participation in the study and signed an informed consent. The Guarulhos University Ethics
Committee in Clinical Research had previously
approved the study protocol.
54

Volume 86 Number 1

Inclusion and Exclusion Criteria

Inclusion criteria included: 1) aged >30 years; 2) 15
teeth excluding third molars and teeth with advanced
decay indicated for exodontia; 3) diagnosis of
generalized CP21 (>30% of the sites with concomitant PD and clinical attachment level [CAL] 4 mm
and a minimum of six teeth distributed in the different quadrants presenting at least one site with
PD and CAL 5 mm and bleeding on probing [BOP]
at baseline); 4) glycated hemoglobin A1c (HbA1c)
<6.5%; 5) fasting plasma glucose (FPG) of 70 to 99
mg/dL; and 6) C-reactive protein (CRP) <6 mg/L.
The levels of HbA1c (high-performance liquid chromatography method), FPG (glucose oxidase method),
and CRP (latexagglutination test) were all assessed by the Guarulhos University Clinical Analysis Laboratory during patient screening.
Exclusion criteria included: 1) pregnancy; 2) lactation; 3) current smoking and smoking within the
past 10 years; 4) any medical condition requiring
prophylactic antibiotic coverage before dental
treatment; 5) subgingival periodontal therapy in the
previous 12 months; 6) antimicrobial, anti-inflammatory,
immunosuppressive, and lipid-lowering (e.g., statins)
therapies during the previous 6 months; 7) regular
use of mouthrinses containing antimicrobials; and
8) use of orthodontic appliances. Patients reporting
the presence of systemic conditions that could affect the progression of periodontitis and/or gain/
loss of weight (e.g., diabetes mellitus, immunologic
disorders, osteoporosis, hypothyroidism, or hyperthyroidism) were also excluded.
Anthropometric Measurements and
Experimental Groups
One trained examiner (PGB) performed all anthropometric measurements, including weight (kilograms),
height (meters), waist (centimeters), and hip circumferences (centimeters). BMI was calculated as
the weight divided by the square of height (kilograms/
square meters). The waist-to-hip ratio (WHR) was
calculated as the ratio of waist-to-hip circumference.
Patients with obesity were defined as having BMI 30
and <40 kg/m2 and concomitant WHR 0.85 for
females and WHR 0.90 for males. Patients without
obesity were defined as having BMI ranging from 20
to 29.9 kg/m2 and WHR below that determined for
obesity (i.e., WHR <0.85 for women and WHR <0.90
for men).22 The anthropometric measurements were
reassessed at all follow-up visits to verify whether
the patients did not change their obese or non-obese
status during the study.
Non-Surgical Periodontal Therapy
Initially, all patients received supragingival plaque
and calculus removal, exodontia, provisional restoration, and filling overhang removal, as necessary.

Gonc
xalves, Feres, Zimmermann, et al.

J Periodontol January 2015

They were also instructed regarding brushing technique and use of dental floss. A trained periodontist
(GSZ) performed SRP in four to six appointments
lasting 1 hour each, using manual curets and an
ultrasonic device under local anesthesia. Periodontal therapy was completed in 14 days. The
endpoint for each SRP appointment was smoothness of the scaled roots. Local and systemic antimicrobials were not used. All patients received
periodontal maintenance at 3 and 6 months after
therapy, including: 1) professional plaque control
with abrasive sodium carbonate air-powder system;
2) reinstruction of oral hygiene; and 3) subgingival
debridement of deep sites presenting BOP.
Clinical Monitoring
Patients received clinical monitoring at baseline and
3 and 6 months after therapy. One calibrated examiner (TEDG) performed all the clinical examinations. After a calibration exercise, the standard error
of measurement was calculated. Intraexaminer variability was 0.22 mm for PD and 0.24 mm for CAL.
The agreement for categorical variables (e.g., BOP)
was >85%, as calculated by the k-light test. The
following parameters were assessed at six sites
(mesio-buccal, mid-buccal, disto-buccal, mesio-lingual,
mid-lingual, and disto-lingual) per tooth, excluding
third molars, using a manual periodontal probei: 1)
visible plaque accumulation (presence or absence);
2) marginal bleeding (MB) (presence or absence);
3) BOP (presence or absence); 4) suppuration (SUP)
(presence or absence); 5) PD (distance between the
gingival margin and the bottom of the sulcus/pocket
[millimeters]); and 6) CAL (distance between the
cemento-enamel junction and the bottom of the
sulcus/pocket [millimeters]).
Leptin and Adiponectin Monitoring
Fasting peripheral blood was sampled on the days
of the clinical examinations into appropriate tubes.
Immediately after blood collection, the serum was
separated from blood by centrifugation (10 min at
1,300 rpm) and stored in aliquots at -80C.
Aliquots of serum were analyzed by enzyme-linked
immunosorbent assay (ELISA) at baseline and 3
and 6 months using commercially available kits
for detecting adiponectin# and leptin**. ELISA procedures were performed according to the recommendations of the manufacturer using human
recombinant standards. According to the manufacturer, the minimum detectable dose for adiponectin is 0.246 ng/mL and for leptin is <7.8 pg/mL.
The optical density was measured at 450 nm. The
adipocytokine results were reported in concentration per milliliter of serum (picograms or nanograms
per milliliter). A masked operator (PMD) performed
all assays.

Statistical Analyses
The primary outcome variable was the difference
between groups for full-mouth PD change between
baseline and 6 months. Non-parametric statistical
tests were used to evaluate the data that did not
achieve normal distribution by Shapiro-Wilk test.
The following were computed for each patient: 1)
percentages of sites with plaque accumulation
MB; BOP; SUP; PD 5 mm and PD 7 mm; 2) the
mean number of sites with PD 5 mm and PD
7 mm; 3) the full-mouth mean PD and CAL; 4)
BMI; 5) WHR; 6) the glycemic parameters; and
7) adipocytokines. Subsequently, all data were
averaged between groups. Changes in PD and CAL
in the full-mouth and at initially moderate and deep
sites were averaged per patient and then across
patients within each group. The significance of differences between groups for age, anthropometric,
and glycemic parameters at baseline were compared
by unpaired Student t test. The significance of differences between groups for clinical parameters and
adipocytokine levels at each time point were compared
using the Mann-Whitney U test. The Friedman test
was used to detect differences within each group over
time for the clinical parameters and the serum levels
of adipocytokines. Analysis of covariance (ANCOVA)
with adjustments for baseline values was used to detect
differences between groups in the mean changes of
PD and CAL. The x2 test was used to compare the
frequency of sex and the number of patients with low
(no more than four sites with PD 5 mm), moderate
(five to eight sites with PD 5 mm), or high (at least
nine sites with PD 5 mm) risk for disease progression.23 The level of significance was set at 5%.
RESULTS
Retention
This study was conducted from March 2012 to July
2013. Figure 1 presents the flowchart of the study.
Of the 480 individuals screened, 432 were excluded
for not meeting the inclusion criteria, and 48 entered the study (24 with and 24 without obesity).
Three patients from the group without obesity and
six from the group with obesity did not return for the
3-month follow-up visit and were excluded from the
statistical analysis.
Demographic, Anthropometric, and Glycemic
Results
There were no significant differences between groups
for sex, age, and glycemic parameters at baseline

Hu-Friedy, Chicago, IL.

Cavitron Select SPC, DENTSPLY, York, PA.
UNC15, Hu-Friedy.
Serum BD Vacutainer Plus plastic serum tubes, BD Biosciences,
Franklin Lakes, NJ.
# Quantikine, R&D Systems, Minneapolis, MN.
** Quantikine, R&D Systems.

55

Response of Patients With Obesity to Periodontal Therapy

Volume 86 Number 1

Figure 1.
Flowchart of the study.

Table 1.

Demographic Characteristics and Anthropometric and

Glycemic Parameters of the Study Population at
Baseline (mean 6 SD)
Groups
Without Obesity
(n = 21)

With Obesity
(n = 18)

61.9

72.2

0.89

Age (years)

48.4 9.5

48.8 5.9

0.86

BMI (kg/m2)

24.4 1.9

33.2 2.9

<0.001

Variable
Sex (% male)

WHR

0.8 0.06

1.0 0.07

<0.001

The group without obesity also

presented a lower full-mouth
mean PD than the group with
obesity at 6 months after treatment (P <0.05) (Table 2).
Table 3 presents the mean
PD reduction and CAL gain
from baseline to 3 months and
to 6 months. Patients without
obesity had a statistically significantly greater reduction in
mean PD than the patients with
obesity from baseline to the
6-month time point, considering
the full-mouth and the initially
deep site evaluations (P <0.05).
Table 4 presents data for residual sites at the patient level.
Patients presenting at most four,
from five to eight, or at least
nine sites with PD 5 mm after
treatment were categorized as
being at low, moderate, or high
risk, respectively, for future disease progression.23 Nine (42.8%)
patients in the group without
obesity and 13 patients (72.2%)
in the group with obesity were
at high risk for disease progression at 6 months after therapy (P >0.05). In addition, seven
(33.3%) and five (23.8%) patients without obesity and four
(22.2%) and one (5.5%) patients with obesity were at low
and moderate risk for disease
progression, respectively, at 6
months after therapy (P >0.05).

Serum Adipocytokines
Table 5 presents the serum
FPG (mg/dL)
84.3 10.2
84.7 8.5
0.90
levels of leptin and adiponectin
for both groups at baseline and
P <0.05 indicates differences between groups by the unpaired Student t test. There were no differences
between groups for sex (x2 test, P >0.05).
3 and 6 months after therapy.
Leptin serum levels were higher
(P >0.05) (Table 1). As expected, BMI and WHR were
in patients with obesity than in patients without obesity
at all time points (P <0.05). Adiponectin levels did
higher in the obese than in the non-obese group
not differ between groups at any time point (P >0.05).
(P <0.001) (Table 1).
In addition, there were no changes in the serum
Clinical Parameters
levels of leptin and adiponectin for either group
SRP yielded statistically significant improvements in
after SRP (P >0.05).
all clinical parameters of both groups at 3 and 6
DISCUSSION
months compared with baseline (P <0.05) (Table 2).
However, patients without obesity presented addiDespite several investigations suggesting that obesity
tional improvements in mean PD and CAL and in
is a risk indicator for periodontitis,1,2 little is known
the mean number and percentage of sites with PD
about the effect of obesity on periodontal treatment
5 mm between 3 and 6 months (P <0.05) (Table 2).
response. Therefore, this study evaluates the clinical
HbA1c (%)

56

4.9 0.8

5.0 0.9

0.88

Gonc
xalves, Feres, Zimmermann, et al.

J Periodontol January 2015

Table 2.

Mean 6 SDs of Full-Mouth Clinical Parameters for

Both Groups at Baseline and at Follow-Up Visits
Groups
Without
Obesity (n = 21)

With Obesity
(n = 18)

% of sites with plaque accumulation

Baseline
3 months
6 months

84.6 9.7a
37.2 17.2b
32.4 13.3b

83.3 22.1a
35.2 18.4b
39.4 16.5b

0.76
0.48
0.38

% of sites with MB
Baseline
3 months
6 months

23.6 14.6a
7.2 8.5b
6.5 5.5b

17.3 23.0a
7.7 8.0b
3.7 5.4b

0.77
0.80
0.13

% of sites with BOP

Baseline
3 months
6 months

51.6 17.7a
30.4 17.5b
21.8 8.2b

53.2 24.9a
29.7 13.4b
20.3 8.8b

0.81
0.76
0.55

% of sites with SUP

Baseline
3 months
6 months

4.6 6.5a
1.7 3.5b
1.0 2.4b

4.3 8.1a
2.0 2.8b
1.6 3.0b

0.95
0.21
0.40

Mean PD (mm)
Baseline
3 months
6 months

3.4 0.6a
3.0 0.5b
2.7 0.6c

3.6 0.6a
3.3 0.6b
3.0 0.5b

0.24
0.12
0.04

Mean CAL (mm)

Baseline
3 months
6 months

4.4 0.8a
4.2 0.8b
3.9 0.8c

4.9 1.1a
4.7 1.1b
4.4 1.0b

0.18
0.13
0.08

Number of sites with PD 5 mm

Baseline
3 months
6 months

30.3 15.1a
19.2 15.0b
13.5 13.7c

34.9 17.9a
24.6 15.5b
15.9 11.8b

0.40
0.25
0.34

% of sites with PD 5 mm
Baseline
3 months
6 months

22.3 10.4a
14.2 10.3b
9.9 9.4c

25.4 11.8a
18.0 10.7b
11.6 8.2b

0.34
0.24
0.35

Number of sites with PD 7 mm

Baseline
3 months
6 months

11.2 10.0a
6.7 8.1b
4.5 6.4b

11.5 7.8a
9.7 8.2b
5.1 6.3b

0.71
0.15
0.37

8.3 7.0a
5.0 5.5b
3.3 4.5b

8.3 5.2a
7.0 5.7b
3.7 4.5b

0.68
0.15
0.34

Time Point

% of sites with PD 7 mm
Baseline
3 months
6 months

Superscript letters indicate significant differences over time within the same group (Friedman test,
P <0.05). P <0.05 indicates differences between groups at each time point (Mann-Whitney U test,
P <0.05).

response of patients with obesity

and CP to non-surgical periodontal
therapy up to 6 months when compared with age- and sex-matched
patients without obesity. Furthermore, the possible effects of nonsurgical periodontal therapy on
serum levels of leptin and adiponectin were also assessed at 3 and
6 months in both groups. Overall,
the results demonstrated that SRP
was effective in improving clinical
parameters in patients with and
without obesity. However, patients
with obesity exhibited lower reductions in PD at 6 months after therapy, indicating that obesity may, to
some extent, negatively affect the
clinical response to non-surgical periodontal therapy. In addition, periodontal treatment did not yield any
changes in adiponectin and leptin
levels in any group, suggesting that
SRP was not able to modulate these
adipocytokines at the systemic level.
Patients with obesity exhibited
significantly greater mean PD (Table
2) and lower reduction in PD in the
full-mouth analysis and at initially
deep sites compared with patients
without obesity at 6 months after
treatment (Table 3). Patients without
obesity, but not those with obesity,
presented statistically significant gradual improvements from baseline to
3 and 6 months in mean PD and CAL
and in the number and percentage
of sites with PD 5 mm (Table 2).
To date, few studies16-20 have evaluated the response of patients with
obesity to periodontal therapy. Some
investigations 16,17,19 have shown
that patients with and without obesity did not differ in their clinical response to non-surgical periodontal
therapy. Conversely, a previous
study18 showed an improved clinical response to SRP in patients with
obesity that lost weight after bariatric surgery when compared with
obese controls not submitted to bariatric surgery. Furthermore, a recent
study20 reported that BMI and obesity were associated with mean
PD and mean percentage of sites
with PD >4 mm at 2 months after
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Response of Patients With Obesity to Periodontal Therapy

Volume 86 Number 1

Table 3.

Mean 6 SEM PD Reduction and CAL Gain From Baseline to 3 and 6 Months for Full-Mouth
and Initially Moderate and Deep Sites
Groups
PD Category
Reduction in PD (mm)
Full-mouth sites
0 to 3 months
0 to 6 months
Initially moderate sites (PD of 4 to 6 mm)
0 to 3 months
0 to 6 months
Initially deep sites (PD 7 mm)
0 to 3 months
0 to 6 months
Gain in CAL (mm)
Full-mouth sites
0 to 3 months
0 to 6 months
Initially moderate sites (PD of 4 to 6 mm)
0 to 3 months
0 to 6 months
Initially deep sites (PD 7 mm)
0 to 3 months
0 to 6 months

Without Obesity (n = 21)

With Obesity (n = 18)

0.44 0.06
0.73 0.07

0.30 0.06
0.54 0.07

0.08
0.04

0.87 0.12
1.38 0.14

0.70 0.13
1.10 0.15

0.31
0.16

1.86 0.25
3.00 0.23

1.22 0.26
2.30 0.24

0.07
0.04

0.29 0.05
0.54 0.07

0.19 0.06
0.38 0.06

0.21
0.13

0.66 0.11
1.06 0.12

0.53 0.12
0.81 0.13

0.41
0.15

1.14 0.24
2.10 0.23

0.70 0.26
1.56 0.24

0.20
0.07

P <0.05 indicates differences between groups at each time point by ANCOVA.

Table 4.

regarding the non-surgical periodontal therapy protocol used (i.e.,

Number and Percentage of Patients Presenting Low,
quadrant-wise SRP or SRP within 24
Moderate, or High Risk for Disease Progression23 at
hours with or without local antimi6 Months Post-therapy
crobials), the parameter used to define obesity (i.e., BMI and/or waist
Groups
circumference), the inclusion/exclusion
criteria used (e.g., smokers and paWithout
With Obesity
tients with diabetes), and the severity
Risk for Disease Progression
Obesity (n = 21)
(n = 18)
P
of obesity (e.g., inclusion or excluLow risk (4 sites with PD 5 mm)
7 (33.3%)
4 (22.2%)
0.49
sion of Class III obesity). One could
argue that the worse mean PD obModerate risk (5 to 8 sites with PD 5 mm)
5 (23.8%)
1 (5.5%)
0.19
served in the patients with obesity
High risk (9 sites with PD 5 mm)
9 (42.8%)
13 (72.2%)
0.25
after therapy could be attributed to
their poorer compliance with oral
hygiene and/or greater degree of
gingival inflammation. However, it is important to
non-surgical periodontal therapy. In that study20,
observe that patients with and without obesity did
patients with obesity had 3.2% more sites with
not differ in terms of plaque accumulation, MB, and
PD >4 mm and 0.14 mm greater mean PD at 2
BOP at any time point (Table 2).
months after therapy than patients with normal BMI.
Studies in the medical field have proposed that
Unfortunately, significant methodologic differences
patients with obesity present altered immune
among the studies hamper a more direct comparinflammatory responses and adipocytokine signaling,
ison with the results of the present study. First, all of
which may increase the susceptibility to infection and
the abovementioned investigations16-20 have limited
impair would healing.24,25 However, at this stage,
their clinical monitoring period to a maximum of
the mechanisms that could explain the worse clinical
3 months. In addition, studies differed considerably
58

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xalves, Feres, Zimmermann, et al.

J Periodontol January 2015

Table 5.

Serum Levels of Adipocytokines (mean 6 SD) for Both Groups at Baseline and at
Follow-Up Visits
Groups
Adipocytokines (102)
Leptin (pg/mL)
Baseline
3 months
6 months
Adiponectin (ng/mL)
Baseline
3 months
6 months

Without Obesity (n = 21)

With Obesity (n = 18)

292.7 199.1
307.7 194.8
297.4 232.1

441.8 213.7
475.7 194.8
421.8 266.7

0.04
0.02
0.03

44.2 37.1
41.2 23.3
48.2 22.1

52.5 36.0
49.1 25.6
47.4 34.3

0.54
0.75
0.72

There were no significant differences over time within each group by the Friedman test. P <0.05 indicates differences between groups at each time point by
the Mann-Whitney U test.

response of patients with obesity to periodontal therapy are still unknown. Additional evaluations performing local immunologic and microbiologic analyses
and longer follow-up periods are still needed to
clarify this issue.
Adipose tissue acts as an endocrine organ by secreting several proinflammatory and anti-inflammatory
factors, called adipocytokines, that are able to stimulate molecular events in inflammatory and/or autoimmune conditions.6,7 Leptin is an adipocytokine
with proinflammatory properties that has a fundamental role in regulating appetite and energy expenditure but also in controlling immunity and
inflammation.8,9,11 Recent evidence has suggested
that leptin may play a role in the metabolism, defense,
and regeneration of the dental and periodontal
tissues.26 In addition, dental and periodontal tissues
seem to be important sources of leptin not only locally
but also systemically.26 Adiponectin is an adipocytokine with anti-inflammatory properties that is
related to the improvement of insulin sensitivity,
antiatherogenic actions, and regulation of metabolic
homeostasis.10,11 In the present study, serum levels
of leptin are increased in patients with obesity at all
time points, corroborating previous evidence that
leptin concentrations are mostly higher in patients
with obesity compared with normal-weight patients,
with or without periodontitis.12,27-29 Because previous
studies have linked periodontitis with high serum
levels of leptin and lower levels of adiponectin,12-15
changes in the circulating levels of these adipocytokines would be expected after periodontal treatment. However, in this study, although SRP yielded
clinical improvements, it did not affect the circulatory levels of leptin and adiponectin in either group.
Some studies have demonstrated a decrease in serum
levels of leptin in patients with19 or without obesity14

after SRP. Conversely, in agreement with the present

results, other investigations29,30 have also failed to
show changes in the serum levels of leptin and
adiponectin in patients with periodontitis after nonsurgical periodontal therapy.
Although the patients of the present study were
engaged in a maintenance therapy at 3-month intervals, the majority of them still retained several
residual pockets (PD 5 mm) after the proposed nonsurgical periodontal therapy (Tables 2 and 4), which
reflects the failure of this therapy in promoting
a periodontal condition comparable with that of the
periodontally healthy patients. Possibly these residual infected/inflamed sites could be enough to
maintain a systemic load able to sustain the leptin
and adiponectin levels unchanged despite periodontal treatment. Furthermore, a pre-existing
susceptibility for systemic inflammation, possibly
unrelated to periodontal infection, may be another
explanation for the unchanged levels of adipocytokines after therapy, because previous evidence has
identified groups of patients that are resistant to
systemic anti-inflammatory effects after periodontal
therapy.30
The main strength of this study is to be the first
investigation, to the best of the authors knowledge,
to follow the response of patients with obesity to
SRP up to 6 months after therapy. In addition, some
aspects related to participant selection could also
be considered strengths of the present investigation.
Patients with and without obesity were classified
considering both WHR and BMI, which take into
consideration body fat distribution and abdominal
obesity. To avoid interference of other risk factors
for periodontitis, patients with diabetes and smokers
were not included in this study, and all patients
presented low levels of CRP (<6 mg/L). Previous
59

Response of Patients With Obesity to Periodontal Therapy

evidence has demonstrated that CRP directly binds

leptin in extracellular settings, impairing its biologic
actions.31 Therefore, the chronic elevation of CRP,
commonly observed in patients with obesity, may
worsen leptin resistance.31 Finally, anthropometric
measurements were revised at all follow-up visits to
ensure that patients maintained their obese or nonobese status over the course of the study. Conversely, this study has some limitations that should
be taken into consideration. First, four patients fell
into the BMI classification of overweight (BMI from
26.7 to 27.8 Kg/m2), although their WHRs were below
those determined for obesity. Second, there was
a pronounced dropout in the group with obesity,
which ended up with 18 patients. Fortunately, the
sample size calculation estimated that 18 patients
per group would be enough to provide an 85%
statistical power. Furthermore, based on the periodontitis and obesity profiles of the present study
population, these results cannot be extrapolated to
patients with milder periodontitis and Class III
obesity (i.e., BMI 40 kg/m2). Finally, this study is
not considered masked. Because obesity is an
obvious characteristic, both the operator and examiner could certainly deduce the patient group,
which may be a possible bias.
CONCLUSIONS
Patients with obesity presented a worse response to
SRP than patients without obesity at 6 months after
therapy. In addition, this treatment did not affect the
circulating levels of leptin and adiponectin in patients with or without obesity and CP.
ACKNOWLEDGMENTS
This study was supported by Sao Paulo State Research Foundation Grant 2011/14875-3. The authors
report no conflicts of interest related to this study.
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Correspondence: Dr. Poliana Mendes Duarte, Universidade
Guarulhos, Centro de Pos-Graduacxao e Pesquisa, Pracxa
Teresa Cristina, 229, Centro, Guarulhos, Sa
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07.023-070. Fax: 55-11-24641758; e-mail: pduarte@
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Submitted May 5, 2014; accepted for publication July 31,
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