ANALYTICAL AND QUANTITATIVE CYTOPATHOLOGY AND HISTOPATHOLOGY

1. 180
Analytical and Quantitative Cytopathology and Histopathology®
0884-6812/20/4206-0180/$18.00/0 © Science Printers and Publishers, Inc.
Analytical and Quantitative Cytopathology and Histopathology®
OBJECTIVE: To evaluate the outcome of initial peri­
odontal therapy and additional diode laser decontamina­
tion therapy on clinical parameters and the amount of
tumor necrosis factor alpha (TNF-α) in gingival crevic­
ular fluid (GCF) in patients with chronic periodontitis.
STUDY DESIGN: The study included 22 patients who
were diagnosed with chronic periodontitis and who had
at least 1 (≥5 mm) periodontal pocket in the posterior
region of each upper left hemi-arcade. The study was
designed as a split-mouth study involving mechanical
therapy on the right side and nonsurgical periodontal
therapy plus diode laser decontamination therapy on the
left side.
RESULTS: A statistically significant decrease was ob­
served in clinical parameters at 3 months when com­
pared to the values at baseline in both treatment areas.
The change in clinical parameters at 3 months after
therapy was not significantly different between the
groups (p>0.05). The comparison of GCF TNF-α levels
at baseline and at 3 months in the 2 treatment areas
identified significant changes in the TNF-α levels in
the hemi-arcade treated with laser diode contamination
therapy, whereas the changes in the hemi-arcade treated
with nonsurgical periodontal therapy were not signif­
icant (p>0.05). A between-group comparison revealed
no statistically significant difference at 3 months post-
therapy, while the difference at 1 month was found to be
statistically significant.
Comparison of the Effect of Periodontal
Therapy and Diode Decontamination and
Periodontal Therapy Alone on the Amount of
TNF-α in Systemically Healthy Chronic
Periodontitis Patients
A Non-Randomized Clinical Trial
Arzum Güler Doğru, Ph.D., Ömer Toprak, Ph.D., Devrim Deniz Üner, Ph.D.,
Bozan Serhat I
·
zol, Ph.D., I
·
brahim Kaplan, Ph.D., Mehmet Doğru, Ph.D., and
Fikret I
∙
pek, Ph.D.
From the Departments of Periodontology and of Orthodontics, Faculty of Dentistry, Dicle University, Diyarbakır; the Department of
Periodontology, Faculty of Dentistry, Harran University, Şanlıurfa; the Department of Periodontology, Faculty of Dentistry, Bingöl Uni-
versity, Bingöl; and the Department of Biochemistry, Faculty of Medicine, Dicle University, Diyarbakır, Turkey.
Arzum Güler Doğru is Associate Professor, Department of Periodontology, Faculty of Dentistry, Dicle University.
Ömer Toprak is Specialist Dentist, Department of Periodontology, Faculty of Dentistry, Dicle University.
Devrim Deniz Üner is Assistant Professor, Department of Periodontology, Faculty of Dentistry, Harran University.
Bozan Serhat I
·
zol is Assistant Professor, Department of Periodontology, Faculty of Dentistry, Bingöl University.
I
·
brahim Kaplan is Associate Professor, Department of Biochemistry, Faculty of Medicine, Dicle University.
Mehmet Doğru is Assistant Professor, Department of Orthodontics, Faculty of Dentistry, Dicle University.
Fikret I
∙
pek is Associate Professor, Department of Periodontology, Faculty of Dentistry, Dicle University.
Address correspondence to: Arzum Güler Doğru, Ph.D., Department of Periodontology, Faculty of Dentistry, Dicle University, Diyar-
bakır 21280, Turkey (arzugulerdogru@gmail.com).
Financial Disclosure: The authors have no connection to any companies or products mentioned in this article.

2. Volume 42, Number 6/December 2020 181
Periodontal Therapy and Diode Decontamination
CONCLUSION: The study found that laser therapy
in addition to nonsurgical periodontal therapy has a
positive effect on the clinical parameters and proinflam­
matory TNF-α levels in the early period but makes no
contribution in the long term. (Anal Quant Cytopathol
Histpathol 2020;42:180–188)
Keywords: chronic periodontitis, dental plaque,
dental scaling, dental surgery, diode laser, gingi­
val crevicular fluid, lasers, nonsurgical periodontal
therapy, periodontal attachment loss, periodontal
diseases, periodontal pocket, periodontitis, TNF-α,
tumor necrosis factor alpha.
Periodontitis is the most common type of periodon-
tal disease.1 It presents initially as an inflamma-
tion of the tissue supporting the teeth, mediated
by microbial dental plaque, and is characterized
by loss of attachment and bone loss with disease
progression if left untreated.2 The prevalence of
chronic periodontitis was demonstrated to be high
(>90%) in different studies.3-5
The irreversible destruction of the periodontal
tissue in periodontal disease occurs through host-
mediated mechanisms. Bacterial virulence factors
can cause the direct destruction of the periodon-
tium but can also induce the release of biological
mediators from the host tissue that in turn result
in the destruction of periodontium. The mediators
that are produced as part of the host response that
contribute to tissue destruction include protein-
ases, cytokines, and prostaglandins.6-8 Cytokines
are key mediators that play a fundamental role in
inflammation and periodontal disease.9-11
Tumor necrosis factor alpha (TNF-α) is one of
the mediators that play a role in periodontal dis-
ease. TNF-α is the main mediator of the immune
response involved in tissue and cell remodeling in
the presence of increased neutrophil activity and
matrix metalloproteinase (MMP) release, stimu-
lating the production of osteoclasts and provid-
ing limited tissue repair through the induction of
apoptosis. TNF-α is released particularly from the
macrophages that are activated in response to bac-
terial lipopolysaccharides.
It has been emphasized that mechanical therapy
involving the improvement of oral hygiene, tooth
surface cleaning, and root surface planning can
play an essential role in achieving clinical success
in the treatment of periodontal disease. That said,
mechanical therapy alone cannot guarantee suc-
cess, as it may fail to eliminate pathogenic bacterial
species in the periodontal tissue, and periodontal
instruments may not access all aspects of the tooth
and root surfaces in closed scaling.12 These limita-
tions are defined as the factors that limit the long-
term outcomes of nonsurgical periodontal therapy,
and antibiotics, antiseptics, and nonchemical meth-
ods underpin supportive therapies.13
Among the supportive therapies, dental laser has
come into use in diagnosis, treatment, and preven­
tive medicine.14 Lasers may affect oral microbial
species and disinfect the periodontal environ-
ment15-17 and can also regulate the oral inflamma-
tory response.18-20
The present study investigates the effects of non-
surgical periodontal therapy in addition to laser
therapy on (1) clinical parameters and (2) TNF-α
levels in the gingival crevicular fluid in patients
with chronic periodontitis.
Materials and Methods
The study included a total of 30 subjects who pre-
sented to the Periodontology Clinics of the Dicle
University Faculty of Dentistry and who were di-
agnosed with chronic periodontitis based on clin-
ical and radiological examination findings. As per
the study protocol, the study group comprised pa-
tients with at least 1 (≥5 mm) periodontal pocket
in the posterior region of each upper left hemi-
arcade. Detailed information was provided to the
participating patients about the objectives of the
study, the treatment to be performed, and the
methods of gingival crevicular fluid sampling.
Subsequently, 8 of the 30 patients with chronic
periodontitis were excluded from the study for
the following reasons: 6 did not attend the treat-
ment sessions, 1 became pregnant, and 1 under-
went a tooth extraction. The study group was
formed according to the following criteria: (1) age
above 25 years, (2) non-smoker and not using
drugs, (3) lack of systemic disease, (4) diagnosed
with chronic periodontitis and the presence of
at least 1 periodontal pocket in the right and left
upper jaw (≥5 mm), (5) not having received peri-
odontal therapy in the last 6 months, (6) lack of
endodontic lesions, inadequate canal treatment,
untreated caries, and acute pain.
The plaque index proposed by Silness and Löe
and the gingival index of Löe and Silness were
used to determine the periodontal status of the
respondents. In addition, the clinical attachment
level and probing pocket depth (PPD) were mea-
sured. All measurements were recorded on pre-

3. 182 Analytical and Quantitative Cytopathology and Histopathology®
Doğru et al
prepared index forms. The values obtained from
4 surfaces of each tooth were summed, and the
average values for each tooth were recorded. These
values were then summed, and the average plaque
index, gingival index, clinical attachment level, and
PPD values were determined for each patient.
The study group was organized as follows:
1. Right posterior region (control group): non­
surgical periodontal therapy.
2. Left posterior region (test group): nonsurgi-
cal periodontal therapy+diode laser decon­
tamination.
Treatment Plan
The relationship between microbial dental plaque
and chronic periodontitis was explained to the
participating patients with chronic periodontitis
at the outset of the study. The patients were then
informed of the planned nonsurgical periodontal
therapies, the gingival crevicular fluid sampling
method, and the periodontal pocket decontamina-
tion procedure, after which written consent was
obtained from all the participants. The Modified
Bass tooth brushing technique was explained to
the patients, and they were trained in interdental
brushing and flossing. An appointment was made
for an appropriate date to initiate treatment.
Deep pockets (≥5 mm) were predetermined and
recorded for gingival crevicular fluid sampling. On
the day of treatment, the Silness and Löe plaque
index was obtained in order to avoid any effect
of dental plaque on the gingival crevicular fluid
(GCF) samples. Supragingival plaque and visible
calculi were carefully removed using Gracey Cu-
rettes (Hu-Friedy, Chicago, Illinois, USA) without
causing bleeding, after which gingival crevicular
fluid samples were taken and clinical measure-
ments were made.
All patients underwent tooth scaling and root
planing under local anesthesia using ultrasonic
devices, Gracey Curettes (Hu-Friedy), and a scaler
(Hu-Friedy). The nonsurgical periodontal therapy
was completed in a single session lasting 75 min-
utes on average, and a periodontal intra-pocket
decontamination was then performed to the peri-
odontal pocket in the left upper posterior region
using a GaAlAs diode laser with a wavelength of
940 nm (Ezlase, Germany).
The irradiation parameters were selected based
on the results of previous scientific studies and in
accordance with the safety range recommended by
the manufacturer. Accordingly, a pocket decontam-
ination procedure using a surgical handpiece (400
nm, 4 mm) was performed, starting from the base
of the pocket and dragging the handpiece along
the pocket once in a diagonal motion for 30 sec-
onds (delivering 1 J/s and 1 W/cm2 in continuous
mode).
During the 3-month follow-up period all par-
ticipating patients underwent GCF sampling and
clinical measurements 1 week, 1 month, and 3
months after the initial treatment. The patients
were reassessed for flap surgery and regenerative
therapies at the end of the study and were includ-
ed in the routine patient protocol of our clinic.
Gingival Crevicular Fluid Sampling
The interproximal area, which is the deepest
point of the pathological periodontal pocket, was
selected for sampling so as not to complicate the
sampling in patients with chronic periodontitis.
The sampling area on each tooth was dried with
air spray without causing irritation, and the area
was carefully isolated with cotton pads. An absor-
bent material was used to avoid contamination of
the samples by saliva. A paper strip (Periopaper)
manufactured for GCF sampling was placed into
the pocket using the superficial intracrevicular
technique. After leaving the paper strip in the
sulcus for 30 seconds, the strip was transferred
immediately to a Periotron 8000 that had been
calibrated with distilled water in order to calcu­
late the volume of the GCF collected. A total of 4
samples were collected from each patient, 2 from
the right side and 2 from the left side. The sam-
ples were placed in 2 2-mL Eppendorf tubes that
had been previously enumerated for each patient
and then stored at −30°C until analysis.
Analysis of TNF-α Levels
The samples were centrifuged (1000 G, +4°C for
5 minutes) using special solutions (0.05% PBS) on
the day of analysis to allow the passage of the sam-
ples into the fluid.
A 50 μL standard buffer and a 50 μL sample were
added to the wells in the ELISA kits. Next, 100 μL
of biotin conjugate was added to each well, with
the exception of the chromogen blank well, and
the samples were incubated at room temperature
for 2 hours. The samples were washed with an
irrigation solution 4 times after the incubation,
after which 100 μL of a streptavidin horseradish
peroxidase solution was added to each well, aside
from the chromogen blank well, and the plate was

4. Volume 42, Number 6/December 2020 183
Periodontal Therapy and Diode Decontamination
covered and incubated at room temperature for
30 minutes. Then, 100 μL of stabilized chromogen
was added to each well, and the solution was
observed to turn a blue color. The plate was left
at room temperature for incubation for 25 min-
utes, after which 100 μL of a stop solution was
added to the wells after incubation, and a conver-
sion of the color to yellow was observed. Readings
were taken by the ELISA optic reading device at
450 nm wavelength.
The values expressed as picogram/mL were cal-
culated using the concentration and total amount
as per the following formula:
pg/µL=(concentration×500/GCFamount)/1,000.
Total amount=(pg/µL×GCF amount)/2.
Statistical Analysis of the Data
An analysis of variance and a Student’s t test were
used for the comparison of independent variables
between the control and test groups. Pearson’s
correlation coefficient was used to analyze the re-
lationship between the cytokine levels and clinical
parameters.
Results
The study included a total of 30 subjects who had
been diagnosed with chronic periodontitis follow­
ing a clinical and radiological examination. Of the
total 30 patients with chronic periodontitis, 8 were
excluded from the study (6 did not attend the
treatment sessions, 1 became pregnant, and 1 un­
derwent a tooth extraction). We included 22 sub-
jects (8 female and 14 male patients) in the study.
The average age of the patients included in the
study was determined as 41.8 (Table I).
Clinical and Biochemical Findings in the Control
Group
The control group comprised patients who under-
went nonsurgical periodontal therapy to the right
posterior side. PPD, gingival index, plaque index,
and clinical attachment level were evaluated at
baseline and at 1 week, 1 month, and 3 months
(Table II).
Evaluation of the Gingival Index in the Control Group.
The differences between gingival index values at
1 week, 1 month, and 3 months from baseline were
found to be statistically significant (p<0.05). The
difference in the values at 1 month and at 1 week
was not significant (p>0.05), but the difference
at 3 months was found to be statistically signifi­
cant (p<0.05). The difference in the values at 1
month and at 3 months was statistically significant
(p<0.05).
Evaluation of the Plaque Index in the Control Group.
The differences in plaque index values at 1 week,
1 month, and 3 months from baseline were found
to be statistically significant (p<0.05). The differ­
ences in the values at 1 week and at 1 month,
and at 1 month and at 3 months were found to be
statistically significant (p<0.05). The difference in
the values at 1 month and at 3 months was statis­
tically significant (p<0.005).
Evaluation of the Probing Pocket Depth in the Con­
trol Group. The mean probing pocket depth was
6.49±1.34 mm at baseline, 6.13±1.08 mm at 1 week,
4.09±1.05 mm at 1 month, and 3.36±1.26 mm at
3 months. The change in the PPD values at 1 week
from baseline was not statistically significant (p<
0.05); however, the difference in values at 1 month
and at 3 months was found to be statistically sig-
nificant (p<0.05). The differences in the values
at 1 week and at 1 month, and at 1 month and at
3 months, were found to be statistically signifi-
cant (p<0.05). The difference in the values at 1
month and at 3 months was statistically significant
(p<0.005).
Evaluation of the Clinical Attachment Level in the
Control Group. The mean clinical attachment level
Table I Gender Distribution and Mean Age
Total Gender
no. of Mean distribution,
patients age female/male
Study group 22 41.8 8/14
Table II Clinical Measurements in the Control Group at
Baseline, 1 Week, 1 Month, and 3 Months
Control
group
(right side) Baseline 1 Week 1 Month 3 Months
GI 2.77±0.23 1.95±0.24 1.27±0.45 2.04±0.87
PI 2.54±0.12 0.68±0.19 0.36±0.12 1.18±0.58
PPD 6.49±1.34 6.13±1.08 4.09±1.05 3.36±1.26
CAL 6.63±1.36 6.18±1.54 5.04±0.92 3.59±1.12
CAL = clinical attachment level, GI = gingival index, PI = plaque index,
PPD = probing pocket depth.

5. 184 Analytical and Quantitative Cytopathology and Histopathology®
Doğru et al
was 6.63±1.36 mm at baseline, 6.18±1.54 mm at
1 week, 5.04±0.92 mm at 1 month, and 3.59±1.12
mm at 3 months. The change in the clinical attach-
ment level values at 1 week from baseline was
found to be statistically insignificant (p>0.05), but
the difference at 1 month and at 3 months was
statistically significant (p<0.05).
The changes in the TNF-α concentrations at 1
week and at 1 month from baseline were found
to be statistically significant (p<0.05), but the dif-
ference at 3 months was not significant (p>0.05).
The difference at 1 month and at 1 week was found
to be insignificant (p>0.05), but the difference at
3 months was found to be statistically significant
(p<0.05). The difference in the values at 1 month
and at 3 months was statistically insignificant (p>
0.05).
The difference in the total amount of TNF-α at
1 week and at 1 month was found to be statisti-
cally significant (p<0.05), but the difference at 3
months was not statistically significant (p>0.05).
The difference in the values at 1 month and at 1
week was not statistically significant (p>0.05), but
the difference at 3 months was statistically signifi-
cant (p<0.05). The difference at 1 month and at 3
months was found to be statistically insignificant
(p>0.05) (Table III).
Clinical and Biochemical Findings in the Test Group
The test group comprised patients who under-
went nonsurgical periodontal therapy to the left
posterior side. PPD, gingival index, plaque index,
and clinical attachment level were evaluated at
baseline and at 1 week, 1 month, and 3 months
(Table IV).
Evaluation of the Gingival Index in the Test Group.
The differences in gingival index values at 1 week,
1 month, and 3 months from baseline were found
to be statistically significant (p<0.05). The differ-
ence in the values at 1 month and at 1 week was
found to be significant (p<0.05), but the differ-
ence at 3 months was not found to be statistically
significant (p>0.05). The difference in the values
between 1 month and 3 months was statistically
significant (p<0.005).
Evaluation of the Plaque Index in the Test Group. The
differences in plaque index values at 1 week, 1
month, and 3 months from baseline were found
to be statistically significant (p<0.05). The differ­
ence in the values at 1 month and at 1 week
was not significant (p>0.05), but the difference at
3 months was found to be statistically significant
(p<0.05).
Evaluation of the Probing Pocket Depth in the Test
Group. The mean probing pocket depth was 6.04±
0.45 mm at baseline, 5.40±0.90 mm at 1 week,
3.63±0.82 mm at 1 month, and 3.09±1.14 mm at
3 months. The differences in PPD values at 1
week, 1 month, and 3 months from baseline were
found to be statistically significant (p<0.05). The
differences in the values at 1 week and at 1 month,
and at 1 month and at 3 months, were found to be
statistically significant (p<0.05). The difference in
the values at 1 month and at 3 months was statisti-
cally significant (p<0.005).
The differences in clinical attachment level val­
ues at 1 week, 1 month, and 3 months from base-
line were found to be statistically significant (p<
0.05). The differences in the values at 1 week and
at 1 month, and at 1 month and at 3 months, were
Table III Total Amount and Mean TNF-α Concentrations in the Control Group
Control group
(right side) Baseline 1 Week 1 Month 3 Months
TNF-α concentration (pg/µL) 0.253±0.067 0.155±0.014 0.183±0.052 0.148±0.042
TNF-α total amount (pg/unit) 0.198±0.78 0.065±0.01 0.079±0.012 0.074±0.054
Values are given as mean±SD.
Table IV Clinical Measurements in the Test Group at Baseline,
1 Week, 1 Month, and 3 Months
Test group
(left side) Baseline 1 Week 1 Month 3 Months
GI 2.56±0.34 1.77±0.27 0.81±0.43 1.81±0.97
PI 2.63±0.22 0.59±0.16 0.31±0.23 1.31±0.85
PPD 6.04±0.45 5.40±0.90 3.63±0.82 3.09±1.14
CAL 5.77±0.69 5.45±0.21 3.81±0.39 3.22±1.73
CAL = clinical attachment level, GI = gingival index, PI = plaque index,
PPD = probing pocket depth.

6. Volume 42, Number 6/December 2020 185
Periodontal Therapy and Diode Decontamination
found to be statistically significant (p<0.05). The
difference in the values at 1 month and at 3 months
was statistically significant (p<0.005).
The differences in TNF-α concentrations at 1
week and 1 month from baseline were statistical-
ly significant (p<0.05), but the difference in the
values at 3 months was not statistically significant
(p>0.05). The differences in the values at 1 week
and at 1 month, and at 1 week and at 3 months,
were found to be statistically significant (p>0.05).
The difference in the values at 1 month and at 3
months was statistically significant (p<0.005).
The differences in the total amount of TNF-α
at 1 week, 1 month, and 3 months from baseline
were found to be statistically significant (p<0.05).
The difference at 1 month and at 1 week was
found to be insignificant (p>0.05), but the differ­
ence at 3 months was found to be statistically
significant (p<0.05). The difference in the values
at 1 month and at 3 months was statistically sig­
nificant (p<0.005) (Table V).
Discussion
Inflammatory response emerges in the presence
of pathogenic microorganisms in the mouth in
chronic inflammation. Various studies assessing
this inflammatory response have reported that
cytokines released from the periodontal tissue,
together with bacteria and bacterial products, lead
either directly or indirectly to the destruction of
periodontal tissue.21,22
Previous studies investigating the interaction
between the host and microbial dental plaque in
periodontal disease have examined the cytokines
that are involved in the regulation of the host-
derived immune response and their relationship
with clinical parameters.11
It has been determined that a need exists for
further studies to explore new approaches to
the diagnosis of chronic periodontitis, which is
caused by the complex interactions between the
host re­
sponse and microorganisms, as well as
environmental factors. It has been found also that
changes in the enzymes and cytokines derived from
the bacteria in the gingival crevicular fluid deter-
mine the activity, progression, recovery after treat-
ment, and response to therapy in periodontal dis-
ease.23
Cytokines bind to specific receptors on the tar-
get cells and induce the signaling pathway, result-
ing in phenotypic changes related to the regula-
tion of genes in the target cells.24,25 These play a key
role in all stages of immune response in periodon-
tal disease.10,11,26 Proinflammatory cytokine TNF-α
is the most widely studied, and perhaps the most
important, cytokine in the pathogenesis of peri-
odontal disease, and both of these cytokines play a
role in the induction, regulation, and maintenance
of innate immune response.27
The activity of periodontal disease can be eval-
uated through examinations of saliva, bacterial
plaque, blood, gingival tissue, and gingival cre­
vicular fluid. Previous studies have reported that
gingival crevicular fluid caused by microvascular
leakage as a result of inflammatory dynamics of
the host against bacterial plaque is a better indi-
cator of local tissue destruction due to the tissue
breakdown products found in its content, as well
as its molecular structure and quantity.28
In the present study diode laser therapy was
used to accelerate wound healing following non­
surgical periodontal therapy, to promote the res-
olution of inflammation, and to provide bacterial
disinfection. Diode lasers use a semi-conductive
solid active material that contains a combination
of elements such as gallium (Ga), arsenide (Ar),
aluminum (Al), and indium (In) to convert elec-
trical energy to luminous energy, with a wave-
length of approximately 800–980 nm. Diode lasers
do not interact with the hard tissues of tooth,
which makes them suitable for soft tissue oper-
ations, and they can thereby be used for various
procedures, such as incisions in the surrounding
tissues, excision, tissue elevation and vaporiza-
tion, coagulation of vascular lesions, soft tissue
curettage, periodontal pocket cleaning, and bac-
Table V Total Amount and Mean TNF-α Concentrations in the Test Group
Test group
(left side) Baseline 1 Week 1 Month 3 Months
TNF-α concentration (pg/µL) 0.295±0.105 0.149±0.78 0.091±0.033 0.245±0.123
TNF-α total amount (pg/unit) 0.219±0.41 0.074±0.016 0.020±0.002 0.116±0.085
Values are given as mean±SD.

7. 186 Analytical and Quantitative Cytopathology and Histopathology®
Doğru et al
terial elimination in contaminated dental implant
surfaces.29 Fenol et al reported a significant de-
crease in the amount of bacteria and inflamma-
tion using nonsurgical periodontal therapy when
combined with diode laser at a wavelength of
980 nm.15
Gingival index, plaque index, PPD, and clinical
attachment level are the most commonly used
clinical parameters for evaluating the efficacy of
nonsurgical periodontal therapy in the treatment
of chronic periodontitis. A large number of stud-
ies have noted a significant decrease in gingival
index, plaque index, PPD, and clinical attachment
level scores following nonsurgical periodontal ther-
apy.20,30
In the present study, PPD, clinical attachment
level, gingival index, and plaque index decreased
in both groups that underwent nonsurgical peri-
odontal therapy, and the values at 3 months were
statistically significant when compared to the base-
line values.
Previous studies have shown the clinical benefit
of laser applications in addition to nonsurgical
periodontal therapy,16,31,32 although there are also
studies showing no additional benefit of laser ther-
apy.33 The previous studies in the literature have
reported no difference between laser types and
laser parameters.34,35
The present study found that the gingival index
scores used to evaluate gingival inflammation de-
creased on both sides, but with a more prominent
decrease on the side treated with laser therapy
in addition to nonsurgical periodontal therapy.
This decrease, however, witnessed no statistical
significance between the groups at 1 month and 3
months. That said, the gingival index scores were
lower on the test side at 1 week when early recov-
ery was evaluated, and the difference between
the 2 groups was statistically significant. Pesevska
et al examined the clinical outcomes of laser ther-
apy applied to inflamed gingival tissue and dem­
onstrated that the amount of TNF-α started to de-
crease from the first day of therapy and showed a
positive correlation with the resolution of inflam-
mation.36
Hung et al reported that laser therapy followed
by nonsurgical periodontal therapy reduces gingi-
val inflammation in the early period and thereby
decreases PPD due to shrinkage. Although the
study found a positive effect of laser therapy on
inflammation, this effect is believed to be caused
by the decrease in PPD in the early period.37
In their study, Dukić et al observed a statistical­
ly significant decrease in PPD in the group that
underwent diode laser therapy in addition to non-
surgical periodontal therapy when compared to the
group that did not undergo laser therapy.38
These studies reveal the success of laser ther-
apy when performed in addition to nonsurgical
periodontal therapy. In our study it was observed
that the clinical parameter changes occurring in
the first week and at 1 month were consistent
with those reported in previous studies. In our
study both the concentration and the total value
of TNF-α were evaluated to examine the effect
of laser treatment on inflammation. The volume
of GCF and its flow rate are affected by many
factors, such as gingival trauma and repeat sam-
pling, and a change in the volume of GCF also
affects enzyme and cytokine concentrations. Ac­
cordingly, there is a widely accepted notion that
total quantity is more closely related with disease
activity.39
In a 3-month split-mouth study, de Oliveira et
al evaluated the effects of nonsurgical periodon-
tal therapy and nonsurgical periodontal therapy
combined with laser therapy on TNF-α levels and
noted a marked recovery in the treatment area
at the end of 3 months without any significant
difference between the treatment areas. They con-
cluded that laser therapy has no additional effects
on the decrease in TNF-α levels in the GCF. Al-
though total amount of TNF-α showed a decrease
over time from baseline values in the present
study, the difference between the treatment areas
at 3 months was not statistically significant.40
Conclusion
It was observed in the present study that addi-
tional laser therapy affects proinflammatory cyto-
kine levels in the short term but has no effect in
the long term. It is believed that the unfavorable
outcomes after 3 months may have been caused
by the difference in treatment protocols, the wave-
length and energy of the laser employed, the dif-
ferences in the timing of the evaluation of recovery
after therapy, the differences in the inflammatory
and immunological responses of the patients, and
the biological changes to tissues caused by diode
laser.
Acknowledgements
We thank all the members of our department for
their assistance.

8. Volume 42, Number 6/December 2020 187
Periodontal Therapy and Diode Decontamination
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