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53
Volume 86 Number 1
Gonc
xalves, Feres, Zimmermann, et al.
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
55
Volume 86 Number 1
Figure 1.
Flowchart of the study.
Table 1.
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
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.
Table 2.
With Obesity
(n = 18)
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
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
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
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
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
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).
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
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
Table 4.
Gonc
xalves, Feres, Zimmermann, et al.
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
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
Volume 86 Number 1
27.
28.
29.
30.
Gonc
xalves, Feres, Zimmermann, et al.
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