archives of oral biology 58 (2013) 717–723

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The effects of non-surgical periodontal therapy on oxidant

and anti-oxidant status in smokers with chronic periodontitis

Aysun Akpinar a,*, Hulya Toker a, Hakan Ozdemir a, Vildan Bostanci a, Huseyin Aydin b
a
Department of Periodontology, Cumhuriyet University Faculty of Dentistry, Sivas, Turkey
b
Department of Biochemistry, Cumhuriyet University Faculty of Medicine, Sivas, Turkey

article info abstract

Article history: Aim: The aim of this study was to determine the effect of non-surgical periodontal treat-
Accepted 13 November 2012 ment on gingival crevicular fluid (GCF) and serum oxidant–antioxidant levels in smoking
and non-smoking patients with chronic periodontitis.
Keywords: Methods: Twenty-nine patients with chronic periodontitis (15 smokers (CP-S) and 14 non-
Periodontitis smokers (CP-NS)) and 20 periodontally healthy subjects (10 smokers (H-S) and 10 non-smokers
Smoking (H-NS)) totalling 49 subjects were included in this study. GCF was collected from at least two
Total antioxidant status pre-selected sites (one moderate and one deep pocket) in patients with CP. In the healthy
Total oxidant status group, GCF samples were collected from one site. Probing pocket depth, clinical attachment
Crevicular fluid level (CAL), gingival and plaque indices, and bleeding on probing were measured. To determine
Serum serum total oxidant status (TOS) and total antioxidant status (TAS), venous blood was drawn
from each subject. The GCF, serum sampling, and clinical measurements were recorded at
baseline and 6 weeks after periodontal treatment.
Results: The study showed statistically significant improvement of clinical parameters after
periodontal treatment in both smokers and non-smokers. In the CP-S group, there were no
significant differences in GCF TAS levels at both moderate and deep pocket sites between
baseline and 6 weeks ( p > 0.05). GCF TAS levels in the CP-NS groups were significantly increased
( p < 0.05) at moderate and deep pocket sites between baseline and 6 weeks. GCF TOS levels in the
CP-S groups were significantly decreased ( p < 0.05) at deep pocket sites between baseline and 6
weeks. There was no significant difference in serum TAS levels of the all periodontitis patient
groups between at baseline and 6 weeks ( p > 0.05). Serum TOS levels in the CP-S and CP-NS
groups were significantly decreased ( p < 0.05) after periodontal treatments.
Conclusions: The periodontal treatment improves the clinical parameters in both smokers
and non-smokers. These results confirm that non-surgical periodontal therapy can reduce
oxidative stress.
# 2012 Elsevier Ltd. All rights reserved.

anaerobic or facultative bacteria within the subgingival

1. Introduction
Periodontal diseases result from the complex interaction
between pathogenic bacteria and the host’s immuno-inflam-
matory responses. It is believed that while the primary
etiological agent is specific, predominantly gram-negative
biofilm,1 the majority of periodontal tissue destruction is
caused by an inappropriate host response to those micro-
organisms and their products.1,2
It is widely accepted that the host response to subgingival
bacteria plays a critical role in periodontal pathogenesis3 and
that pathogenic processes are modified by environmental and

* Corresponding author at: Department of Periodontology, Cumhuriyet University Faculty of Dentistry, Sivas 58140, Turkey.
Tel.: +90 346 2191010; fax: +90 346 2191237.
E-mail addresses: aysun@cumhuriyet.edu.tr, aysunakpinar73@hotmail.com (A. Akpinar).
0003–9969/$ – see front matter # 2012 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.archoralbio.2012.11.009
718 archives of oral biology 58 (2013) 717–723
acquired risk factors such as smoking.4 For example, smokers
demonstrate 2.6–6 times increased prevalence of periodontal
diseases compared to non-smokers5 and a reduced response
to periodontal treatment.6,7
Chronic periodontitis (CP) is initiated by the sub-gingival
biofilm,8 but the progression of destructive disease appears to
depend upon an abnormal host response to those organ-
isms.3,9,10 Over the past few years, strong evidence has
emerged to implicate oxidative stress in the pathogenesis of
periodontitis.10,11 Free radicals and reactive oxygen species
(ROS) are essential to many normal biologic processes. Low
levels of certain free radicals and ROS can stimulate the
growth of fibroblasts and epithelial cells in culture, whereas
higher levels may result in tissue injury.12 The deleterious
effects of increased oxidative stress are termed oxidative
damage; generally, they appear after exposure to a relatively
high concentration of ROS and/or a decrease in antioxidant
defense system against ROS.
Normally, there is a balance between ROS and antioxidants
that may be disturbed by a variety of factors, including
smoking. Smoking increases ROS production and is a signifi-
cant source of oxidative stress.13,14 It depletes systemic
endogenous antioxidant capacity, resulting in increased
pro-oxidant burden.15
Periodontal disease is associated with reduced total
antioxidant status (TAS) and increased oxidative damage
within the oral cavity.14,16,17 Recently, it was demonstrated
that smoking increases the levels of free radicals in periodon-
tal tissues.18 Palmer et al.19 reported that cigarette smoke
contains a large amount of oxidative species, and therefore
smoking represents a significant source of oxidative stress. In
addition, decreased antioxidant levels in blood, gingival
tissue, saliva, and GCF have been shown in periodontitis
and gingivitis patients who smoke.15,18,20
The reduction of oxidative stress and increase in antioxi-
dant capacity after the non-surgical periodontal therapy were
reported in literature.9,10,21 Chapple22 indicated that periodon-
titis could be associated with reduced local antioxidant
defense and suggested that systemic and local TAS levels in
CP might reflect increased oxygen radical activity during
periodontal inflammation and can be restored to control
subject levels by successful non-surgical therapy. Further-
more, Kim et al.23 found that the TAS in saliva decreased
directly after SRP. With time, it increased slightly and was
relatively unchanged compared to the baseline. It was
assumed that nonsurgical therapy did not improve the TAS
in severe chronic periodontitis patients with non-smoking.
D’Aiuto et al.24 demonstrated that acute increases in reactive
oxygen metabolites in serum and systemic inflammation
occurred following periodontal therapy in smokers. In
contrast, Guentsch et al. suggested that non-surgical peri-
odontal treatment leads to a reduction of malondialdehyde
and glutathione peroxidase to levels comparable to healthy
controls.
As yet, the relationship between smoking and GCF serum
oxidant–antioxidant status in periodontitis has not been
clarified. Possible alterations in GCF and serum antioxidant
composition may influence clinical periodontal status as well
as the response to non-surgical periodontal treatment in
smokers. Thus, the aim of this study was to determine the
effect of non-surgical periodontal treatment on GCF and
serum antioxidant levels in smoking and non-smoking
patients with chronic periodontitis.
2. Material and methods
2.1. Study population
Twenty-nine otherwise healthy chronic periodontitis patients
(15 smokers (CP-S), 14 non-smokers (CP-NS)), and 20 systemi-
cally and periodontally healthy volunteer subjects (10 smokers
(H-S), 10 non-smokers (H-NS)), were selected at Cumhuriyet
University Faculty of Dentistry, Department of Periodontology
for periodontal problems. Written informed consent was
obtained from all subjects and the study protocol was
approved by the Medical Ethics Committee of Cumhuriyet
University.
All subjects were systemically healthy. Subjects were
excluded from the study if they had a taken course of non-
steroidal, anti-inflammatory drugs or antimicrobial drugs
within a 3 month period before the study began; were
pregnant or lactating; had used mouthwashes or vitamin
supplements within the previous 3 months; had a history of
current drug use; or had special dietary requirements.
The selection of patients was made according to the criteria
approved by the 1999 International Workshop for the
Classification of Periodontal Diseases and Conditions.25
Twenty-nine subjects with generalized chronic periodontitis
characterized by at least 30% teeth with pockets >5 mm were
recruited from new patients of the department. X-rays were
taken from all subjects. Cigarette consumption was deter-
mined by verbal questioning. Smokers were enrolled if they
regularly smoked 20 cigarettes/day, and non-smokers were
characterized as not having smoked cigarettes in their
lifetime. Healthy control groups had no attachment loss with
the teeth having periodontal pockets 3 mm and no bleeding
on probing and they had no radiographic evidence of alveolar
bone loss. These individuals were systemically and periodon-
tally healthy volunteers.
2.2. Clinical measurements and non-surgical periodontal
therapy
Prior to crevicular fluid collection, plaque index (PI),26 gingival
index (GI),26 probing pocket depth (PD), clinical attachment
level (CAL), and presence of bleeding on probing (BOP) were
measured. Based on the initial probing PD measurements, the
study sites were further classified and at least one moderate
(4–6 mm) and at least one deep (>6 mm) pockets of teeth were
selected per subject.27,28 PD and CAL measures were obtained
using a Williams’ periodontal probe. All clinical periodontal
measurements were performed by the same examiner (A.A.).
In all subjects, individual acrylic stents were fabricated with
grooves as reference points for the clinical measurements.
After recording the baseline measurements, non-surgical
therapy, which consists of oral hygiene instructions, scaling,
and root planning (SRP), was performed on subjects with
periodontitis.29 The SRP procedure was performed quadrant
per quadrant under local anaesthesia in four visits using
 archives of oral biology 58 (2013) 717–723
specific curettes (Hu-Friedy, Chicago, USA). Treatment was
completed within at most 14 days. No antibiotics were
prescribed during the treatment. All data and GCF sampling
from the sampling sites were recorded at baseline and 6 weeks
after the periodontal treatment.
2.3. Crevicular fluid sampling
Clinical measurements were made after the GCF sampling in
same session. Only the upper anterior teeth were included in
the study to improve the access and to reduce the risk of
salivary contamination during these processes. GCF was
collected from one moderate and one deep pocket site. Before
GCF samplings, the sample site was carefully isolated using
cotton rolls to avoid saliva contamination. A standard paper
strip (Pro Flow, Amityville, NY, USA) was placed in the pocket
until mild resistance was felt and then left in place for 30 s. The
strip were then placed into an Eppendorf tube and immedi-
ately frozen at 80 8C until the day of analysis. In the case of
visible contamination with blood, the strips were discarded.
2.4. Blood sampling
Venous blood samples were collected from the antecubital
vein in tubes. The anticoagulated blood was separated into
plasma and serum by centrifugation. Venous blood samples
were allowed to stand for 30 min before being centrifuged at
3000  g for 10 min. All samples were kept in 80 8C conditions
until the date of analysis.
2.5. Assays of total oxidant status (TOS), total
antioxidant status (TAS)
All laboratory analyses were performed on the same day. On
the day of the assay, 400 mL of phosphate buffered saline (pH 7)
was added to the tubes containing the paper strip. The tubes
were gently shaken for 1 min and then centrifuged at 2000  g
for 5 min. The supernatants were divided into two aliquots for
the determination of TOS and TAS.
TOS and TAS levels in serum and GCF samples were
measured using a new measurement method developed by
Erel.30 TOS and TAS levels were measured using commercially
available kits (Rel Assay, Mega Tıp, Gaziantep, Turkey) by
Erel’s colorimetric method30,31 at 520 nm absorbance as
previously described for GCF by Canakcı et al.32
In the TOS method, oxidants present in the sample
oxidized the ferrous ion-o-dianisidine complex to ferric ion.
The oxidation reaction was enhanced by glycerol that is
Table 1 – Mean (WSD) demographic for periodontally healthy and chronic periodontitis patients.
CP-S (n = 14) CP-NS (n = 15)
Age (mean  SD) 38.4  5.5 37.7  5.9
Female (n) 5 8
Male (n) 9 7
CP-S: chronic periodontitis smokers patients.
CP-NS: chronic periodontitis non-smokers patients.
H-S: healthy smokers patients.
H-NS: healthy non-smokers patients.
719
abundantly present in the reaction medium. The ferric ion
produced a coloured complex with xylenol orange in an acidic
medium. The colour intensity measured spectrophotometri-
cally was related to the total amount of oxidant molecules
present in the sample. The assay was calibrated with
hydrogen peroxide, and the results were expressed in terms
of micromolar hydrogen peroxide equivalent per litre (mmol -
H2O2 equiv./L).
The TAS method is based on the bleaching of characteristic
colour of a more stable ABTS (2,20 -Azino-bis(3-ethylbenzothia-
zoline-6-sulfonic acid)) radical cation by antioxidants. The
assay has precision values lower than 3%. The results were
expressed as mmol Trolox equiv./L.
2.6. Statistical analysis
Data were expressed as means  SD and percentage where
appropriate. Analysis of normality was conducted, and non-
parametric approaches were used based on the distribution of
the data. Baseline and 6-week PI, GI, PD, and CAL values in
both smokers and non-smokers were analyzed with Wilcoxon
rank test. The ratio of BOP in both smokers and non-smokers
were analyzed with Mc Nemar test. Serum and GCF, TOS, and
TAS levels in all groups were analyzed by Kruskall Wallis test
followed by post hoc Tukey test. Spearman correlation
analyses in all groups were used for TOS and TAS levels. A
p value of <0.05 was considered statistically significant.
3. Results
The demographic data including gender and age in the
periodontitis patients and healthy controls are summarized
in Table 1. In the present study, smokers were matched with
nonsmokers with respect to the baseline characteristics of
clinical parameters.
3.1. Clinical findings
Table 2 presents mean PD, CAL, PI, and GI values at baseline
and 6 weeks after treatment in all study groups.
Mean PD and CAL values were significantly reduced after
periodontal treatment in all periodontitis patients ( p < 0.05).
There were statistically significant differences in PD values
between smokers and non-smokers at 6 weeks.
PI and GI values at 6 weeks of all periodontitis patients were
significantly lower than those at baseline ( p < 0.05). There
were no significant differences in the PI and GI values between
H-S (n = 10) H-NS (n = 10)
38.0  7.2 37.0  7.4
4 5
6 5
720 archives of oral biology 58 (2013) 717–723

Table 2 – Clinical parameters of GCF sampling site at baseline and 6-week in patients with chronic periodontitis patients
and healthy ((min–max) median value and percentage).
H-NS (n = 10) H-S (n = 10) CP-NS (n = 15) CP-S (n = 14)

Moderate pocket Deep pocket sites Moderate pocket Deep pocket sites
sites sites

Baseline 6-week Baseline 6-week Baseline 6-week Baseline 6-week

b,c a,b b,c a,b,c b,c a,b,c b,c
PD (mm) (1–2) 1 (1–3) 2 (3–5) 5 (2–4) 3 (6–8) 7 (2–6) 4 (4–6) 5 (2–4) 2.5 (6–8) 7 (2–7) 4a,b,c
PI (0–1) 0 (0–1) 0 (1–3) 2b,c (0–1) 0a (1–3) 2b,c (0–1) 0a,b (1–3) 2b,c (0–1) 0a,b,c (1–3) 2b,c (0–1) 0a,b,c
GI 0 0 (1–3) 2b,c (0–1) 0a,b (1–3) 2b,c (0–1) 0a,b (1–3) 2b,c (0–1) 0a,b,c (1–3) 2b,c (0–1) 0a,b
CAL (mm) 0 0 (7–10) 8b,c (6–9) 8a,b,c (8–13) 10b,c (6–9) 8a,b,c (6–10) 8b,c (5–9) 7a,b,c (7–12) 10b,c (6–10) 9a,b,c
BOP (%) 0 0 100 0a 100 6.7a,b,c 100 0a,b,c 92.9 7.1a,b,c
CP-S: chronic periodontitis smokers patients.
CP-NS: chronic periodontitis non-smokers patients.
H-S: healthy smokers patients.
H-NS: healthy non-smokers patients.
a
Significantly different from baseline ( p < 0.05).
b
Significantly different from H-NS ( p < 0.05).
c
Significantly different from H-S ( p < 0.05).

smokers and non-smokers at 6 weeks ( p > 0.05). Likewise,
there were no significant differences in % BOP between
smokers and non-smokers ( p > 0.05) while % BOP values
showed significant decreases in response to periodontal
treatment in all patients ( p < 0.05).
3.2. Laboratory findings
TAS and TOS values were determined in serum and GCF. There
was no significant difference in GCF-TAS levels between the
baseline and 6 weeks in the moderate and deep pocket sites of
the CP-S group ( p > 0.05) (Table 3). GCF-TAS levels in the CP-NS
group showed significant increases in moderate and deep
pocket sites after periodontal treatment ( p < 0.05).
In the both CP-S and CP-NS groups, GCF-TOS levels at 6
weeks at deep pocket sites were significantly lower than those
at baseline ( p < 0.05).
GCF-TOS levels at baseline were significantly different
between the H-S group and CP-S group at deep pocket sites
( p < 0.05). Also in the CP-S and CP-NS groups, there were
significantly GCF-TOS levels at the moderate and deep pocket
sites at 6 weeks, which were lower than all healthy groups
( p < 0.05).
Serum TAS levels were significantly higher in the H-NS
group than in the H-S group ( p < 0.05) (Table 4). However, in
the CP-S and the CP-NS groups, serum TOS level at 6 weeks
were significantly lower than those at baseline ( p < 0.05).
3.3. Correlations
In the H-NS group, there was a significant positive correlation
between GCF-TAS and TOS levels at pocket sites at baseline
(r = 0.714, p < 0.05). In the H-S group, a significant negative
correlation was found between GCF-TOS and GI values at
pocket site and serum TAS values at baseline (r = 0.644 and
r = 0.655, respectively, p < 0.05).
In the CP-NS group, a negative correlation was found
between serum and GCF-TAS levels at moderate pocket sites
after treatment (r = 0.786, p < 0.05). Also, negative correla-
tions were found between GCF-TAS levels and PI values at
deep pocket sites (r = 0.578, p < 0.05). Negative correlations
were found between GCF-TOS levels and GI values at deep
pocket sites (r = 0.541, p < 0.05).
In the CP-S group, a positive correlation was found between
GCF-TAS levels at deep pocket site and PD values at baseline
(r = 0.636, p < 0.05). Also, in the CP-S group, a positive
correlation was found between GCF-TOS levels and PD values
at 6 weeks (r = 0.642, p < 0.05).
4. Discussion
This study investigated changes in TOS and TAS levels in GCF
and serum in chronic periodontitis with smokers and non-
smokers undergoing non-surgical periodontal therapy. We
found that there were significant improvements after peri-
odontal treatment, and this improvement was evident at
moderate and deep pocket sites for PD and CAL values. In the
CP-NS group, the GCF-TOS levels were markedly reduced at
moderate and deep pocket sites following periodontal therapy.
Although the GCF-TAS levels were markedly increased at
moderate and deep pocket sites following periodontal therapy,
this difference was not found in CP-S group.
Abundant cross-sectional data support the adverse rela-
tionship between smoking and periodontal diseases.33–35 A
strong dose–response relationship between the amount
smoked and the severity of periodontal destruction has also
been shown, further supporting the role of smoking as a risk
factor for periodontitis.27,36–38 Smokers are almost four times
more likely to have severe periodontitis than non-smokers.39
However, the exact mechanisms by which smoking exerts its
deleterious effect on the periodontium remain unclear. One
potential mechanism is tissue damage mediated by oxidative
species originating in tobacco smoke and tobacco-induced
inflammation, in addition to the direct cigarette smoke-
mediated depletion of antioxidants. To our knowledge, this
is the first study to investigate the possible effects of both
smoking and initial phase of periodontal treatment on GCF
and serum total oxidant capacity and total antioxidant
capacity in periodontitis patients.
 archives of oral biology 58 (2013) 717–723 721

Assays of total oxidant–antioxidant capacity have the

(7.9–10.4)a,b,c 10
advantage that they analyze the combined effectiveness of

6-week
(0–0.2) 0.1
contributing species, which may be greater than the sum of

DEEP pocket sites

the effects of the individual antioxidants.9 The assays are
Table 3 – TOS, TAS levels in GCF sampling site at baseline and 6 weeks in patients with chronic periodontitis patients and healthy. ((min–max) median value).

more efficient, cheaper, and less time-consuming than

performing large numbers of individual assays.40

(8.7–10.6)c 10.1
Numerous studies have evaluated the use of GCF and
Baseline
(0–0.1) 0.1
serum to investigate the local activity of oxidative stress
markers and antioxidants during periodontitis.16,41,42 A
CP-S (n = 14)

study32 that investigated the TAS and antioxidants in the

serum, saliva, and GCF of women with periodontitis and
(9.1–10.7)b,c 10.1

preeclampsia reported that the super oxide dismutase level

Moderate pocket sites

6-week

and the glutathione peroxidase activity in the GCF and

(0–0.1) 0.1

serum, and TAS in the saliva, GCF, and serum of female

patients with preeclampsia and periodontitis were lower
than those of the control group. These findings were
(9.7–10.8) 10.5

confirmed by several studies16,42,43 in which antioxidant

Baseline
(0–0.1) 0.1

concentration was lower in GCF in periodontitis subjects

compared to healthy controls. Also, the results of the
present study showed that the TAS level in GCF was lower in
all periodontitis patients than in the healthy non-smoking
(7.7–10.2)a,b,c 9.9

controls. There was also a significant reduction in levels of

6-week
Deep pocket sites

TAS in the GCF of H-S compared to H-NS.

(0–0.1) 0.1a

Studies demonstrated significantly lower TAS in serum

and plasma samples from periodontitis subjects.16,42,43
However, all studies involved relatively small numbers of
(9.4–10.7) 10

patients in each group and may have been underpowered.

Baseline
(0–0.1) 0.1

Brock et al.16 found that the reduced serum TAS concentra-

CP-NS (n = 15)

tion in periodontitis did not quite reach statistical signifi-

cance, whereas differences in plasma levels did, possibly
reflecting differences in the handling of serum and plasma
(8.8–10.4)a,b,c 10
Moderate pocket sites

before assay. Our data are in agreement with these reports in

(0.1–0.2)a 0.1
6-week

as much we also could not find a statistically significant

decrease in serum TAS.
TOS levels in serum, saliva and GCF, which were all
significantly higher in the CP group compared with controls,
(9.7–10.6) 10
(0.6–1.6) 0.1
Baseline

suggested that not only a local but also a systemic increase

occurred in oxidant status of CP which was supported by a
large, analytical epidemiological study of plasma antioxidant
levels in periodontitis.44 In our study, GCF TOS is higher than
(9.9–11.3) 10.5
H-S (n = 10)

the serum GCF. In this regard, our work the study by Akalin
(0.1–0.1) 0.1

et al.41 and Wei et al.21 compatible.

The reduction of oxidative stress and increase in antiox-
idants capacity after the non-surgical periodontal therapy
CP-NS: chronic periodontitis non-smokers patients.

were reported in the literature.9,17,20,21 While Brock et al.16

H-NS (n = 10)

Significantly different from baseline ( p < 0.05).

(9.7–11.3) 10.6

reported that non-surgical periodontal therapy with improve-

(0.1–0.1) 0.1

Significantly different from H-NS ( p < 0.05).

CP-S: chronic periodontitis smokers patients.

Significantly different from H-S ( p < 0.05).

ments in clinical parameters can increase the antioxidant

defense in GCF and serum in chronic periodontitis patients,
H-NS: healthy non-smokers patients.

Kim et al.23 found that the TAS in saliva decreased directly

after SRP. With time, it increased slightly and was relatively
GCF-TAS (mmol Trolox equiv./L)

H-S: healthy smokers patients.

unchanged compared to the baseline. Chapple.22 indicated

GCF-TOS (mmol H2O2 equiv./L)

that systemic and local TAS levels in CP might reflect

increased oxygen radical activity during periodontal inflam-
mation and can be restored to control subject levels by
successful non-surgical therapy. In another study by the same
investigators, periodontal treatment did not alter plasma TAS,
but GCF-TAS increased to control subject levels.9 However, in
those studies, non-smoking periodontitis patients were
included. In contrast to these studies, Buduneli et al.15
b
a

evaluated the possible effects of smoking and gingival

722 archives of oral biology 58 (2013) 717–723
Table 4 – TOS, TAS levels in serum sampling site at baseline and 6 weeks in patients with chronic periodontitis patients
and healthy ((min–max) median value).
H-NS (n = 10) H-S (n = 10)
Serum TAS (mmol Trolox equiv./L) (0.6–3.3)b 9 (2–2.7) 2.2
Serum TOS (mmol H2O2 equiv./L) (2.8–8.4) 5 (2–7.8) 3.7
CP-S: chronic periodontitis smokers patients.
CP-NS: chronic periodontitis non-smokers patients.
H-S: healthy smokers patients.
H-NS: healthy non-smokers patients.
a
Significantly different from baseline ( p < 0.05).
b
Significantly different from H-S ( p < 0.05).
inflammation on salivary antioxidants in gingivitis patients.
They found no significant difference in any of the antioxi-
dant indices between any of the groups. Recently, possible
effects of smoking on total antioxidant capacity of saliva
and plasma samples have also been investigated by
Charalabopoulos et al.45 in young, healthy males. The
researchers who found no significant differences in salivary
antioxidant defenses of non-smokers and smokers, either
before or after smoking. Furthermore, Guentsch et al.6 found
that total antioxidant activity did not differ between
smokers and non-smokers, and periodontal therapy had
an effect on lipid peroxidation and glutathione peroxidase
levels in saliva. The results of our study reported that non-
surgical periodontal therapy made no significant difference
in GCF-TAS level in CP-S patients. After non-surgical
periodontal treatment, however, GCF-TAS levels significant-
ly increased in CP-NS group.
The results of the present study suggest that significant
oxidative stress may occur in periodontitis. Non-surgical
therapy seems to restore and control the levels of TAS and
TOS. The findings also suggest that significant relationships
are present between oxidant–antioxidant status and peri-
odontal parameters in the pathology of periodontitis.
However, further studies are needed to confirm whether
oxidant status is a cause of periodontitis. Such studies
might lead to targeting oxidant status as a therapy for
periodontitis.
Funding
This work is supported by the Scientific Research Project Fund
of Cumhuriyet University under the project number ‘‘Dis-076’’.
Competing interest
None declared.
Ethical approval
Faculty of Dentistry Ethics Committee at Cumhuriyet Univer-
sity. B.30.2.CUM.0.04.00.00/100.
CP-NS (n = 15) CP-S (n = 14)
Baseline 6-week Baseline 6-week
(2–3.3) 2.5 (2–3.3) 2.6 (2.1–3.1) 2.6 (2.4–3.2) 2.6
(1.3–9) 3.2 (1.2–7.8)a 2.8 (0.5–10) 2.7 (0.5–5.7)a 1.6
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