Journal of Oral Biology and Craniofacial Research 12 (2022) 68–73

Contents lists available at ScienceDirect

Journal of Oral Biology and Craniofacial Research

journal homepage: www.elsevier.com/locate/jobcr

Research Paper

Role of nonsurgical periodontal therapy on leptin levels and total

antioxidant capacity in chronic generalised periodontitis patients – A
clinical trial
Swet Nisha a, Avinash Bettahalli Shivamallu b, *, Akila Prashant c, Manish Kumar Yadav d,
Sheela Kumar Gujjari b, Pratibha Shashikumar b, *
a
Dept of Periodontology, Haldia Institute of Dental Sciences & Research, Haldia, West Bengal, India
b
Dept. of Periodontology, JSS Dental College & Hospital, JSS Academy of Higher Education & Research, Mysuru, Karnataka, India
c
Dept. of Biochemistry, JSS Medical College, JSS Academy of Higher Education & Research, Mysuru, Karnataka, India
d
Wake Forest Institute of Regenerative Medicine, Wake Forest University, Winston Salem, NC, 27101, USA

A R T I C L E I N F O A B S T R A C T

Keywords: Introduction: Periodontitis causes oxidative stress and reduce total antioxidant levels. The aim of this study was to
Leptin determine the effect of non-surgical periodontal treatment on leptin levels and total antioxidant capacity in
Nonsurgical periodontal therapy chronic periodontitis.
Periodontitis
Materials and methods: A total of 35 chronic periodontitis (ChP) patients and 35 systemically and periodontal
Saliva
Total antioxidant capacity
healthy subjects were enrolled in this study. Further, the ChP group received nonsurgical periodontal therapy
Oxidative stress (NSPT). Leptin and total antioxidant capacity (TAOC) was measured in serum and saliva samples at baseline, 3
months and 6 months after non-surgical periodontal therapy. Clinical parameters measured were measured at
baseline, 1, 3 and 6 months interval.
Results: The mean serum leptin and TAOC levels in control group were significantly higher compared to chronic
periodontitis group (p < 0.05). The control group had lower mean salivary leptin levels and higher mean salivary
TAOC levels as compared to periodontitis group(p < 0.05). Clinical parameters were improved in ChP group post
therapy (p < 0.05). However, the periodontal treatment showed insignificant changes in serum and salivary
leptin and TAOC levels.
Conclusion: Chronic periodontitis is significantly associated with serum and salivary TAOC and leptin levels. Non
surgical periodontal therapy didn’t alter the local and systemic TAOC and leptin levels.

1. Introduction condition there lies a balance between antioxidants and oxidants,

however, as oxidative stress sets in, it results in an imbalance and shift
Periodontitis is a chronic inflammation which causes destruction of towards increase production of harmful oxidants which causes tissue
periodontal tissues as a result of host microbial interaction. The host destruction. Measuring the total antioxidant capacity gives us an idea of
cells releases proinflammatory cytokines (mainly Interleukin 1 beta, the oxidative stress and suggests role of antioxidants as interventional
Interleukin 6, tumor necrosis factor-alpha) which causes poly­ measures in treatment and prevention of periodontal diseases.3
morphonuclear neutrophils (PMNs) migration towards inflammatory Research on biomarkers to detect periodontal tissue destruction
site. PMNs releases proteolytic enzymes which causes oxidative burst which can help in early diagnosis and treatment planning has estab­
and release of oxygen radical known as reactive oxygen species (ROS). lished matrix metalloproteinase − 8, 9, interleukin 1 beta as potential
These ROS causes microorganisms destruction, at the same time it ini­ markers of periodontal inflammation.4 Certain biomarkers are specific
tiates undesirable periodontal tissue destruction.1,2 to link periodontitis to systemic diseases, like C-reactive protein (CRP),
Antioxidants delays or prevents oxidation of substrates, thereby cortisol, leptin.5 Depending on the severity of periodontal disease, these
provides protection to human cells against oxidative damage. In healthy inflammatory mediators may show positive/negative variations as the

* Corresponding authors.
E-mail addresses: [email protected] (A. Bettahalli Shivamallu), [email protected] (P. Shashikumar).

https://doi.org/10.1016/j.jobcr.2021.10.002
Received 4 March 2021; Accepted 4 October 2021
Available online 28 October 2021
2212-4268/© 2021 Craniofacial Research Foundation. Published by Elsevier B.V. All rights reserved.

Downloaded for ahana maity maity ([email protected]) at Kasturba Medical College Manipal from ClinicalKey.com by
Elsevier on February 21, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.
S. Nisha et al. Journal of Oral Biology and Craniofacial Research 12 (2022) 68–73

disease progress. patients with Stage II Grade B periodontitis were recruited in this study.
Among of these leptin is a biomarker of interest as it is expressed by Subjects were instructed to maintain oral hygiene throughout the
gingival tissues.6 Leptin is a nonglycosylated peptide primarily pro­ study period, using soft bristle toothbrush and toothpaste.
duced by adipocytes.7
Placenta, gastric epithelium,T-cells, osteoblasts and intralobular 2.4. Saliva collection
ducts of major salivary glands are other sources of leptin secretion.8
Leptin is involved in endocrine axis regulation, thermoregulation, lipid, Saliva sample was collected before clinical examination to avoid
glucose and bone metabolism, cardiovascular functions.9 It is also sen­ blood contamination. The subjects were instructed to follow overnight
sitive to immune inflammatory response suggesting its possible role in fast of 8 hours, avoid brushing and intake of any food in the morning
periodontal inflammation.10 hours before sample collection. Whole unstimulated salivary sample
Studies have shown lower leptin concentration in gingiva, gingival (~5 ml) were collected in a polypropylene centrifuge tube (15 ml Falcon
crevicular fluid (GCF) and saliva in periodontitis.11,12 However, higher tube) according to splitting method. The collected sample were pipette
serum leptin levels were found in serum in periodontitis patients and out in an eppendorf tube and centrifuged at 4000 rotations per minute
NSPT significantly reduced the serum leptin level.10 (rpm) for 10 minutes to remove the cell debris and the supernatant was
There are very few interventional studies investigating on possible stored in aliquots with code numbers at 80 ◦ C until further analysis.
role of leptin and total antioxidant capacity in periodontitis. In this view,
the present study aimed at evaluation of local and systemic levels of
2.5. Serum collection
leptin and total antioxidant capacity levels in patients with chronic
periodontitis and its effect on periodontal treatment.
2 ml of blood was drawn from the ante cubital fossa by venipuncture
with a 5 ml of syringe. The serum was separated from blood by centri­
2. Materials and methods
fuging at 3000 g rpm for 5 minutes and the extracted serum was stored
in aliquots with code numbers at 80 ◦ C until further analysis.
2.1. Subjects and study design

The sample population consisted of a total of 35 subjects with ChP 2.6. Periodontal intervention
and 35 healthy subjects attending department of Periodontology during
February 2016 to November 2016. Table 1 shows demographic char­ NSPT involved oral hygiene instructions, scaling and root planing
acteristics of the subjects enrolled in this study. Subjects with >20 teeth (SRP) by ultrasonic scaler (UDS-K ultrasonic scaler (Guilin Woodpecker
present and diagnosed as ChP according to the classification by the Medical Instrument Co. Ltd, Guilin, China) and hand gracey curettes
American Academy of Periodontology,13 normal body mass index (Hu-friedy Chicago, IL, U.S.A) and the entire procedure was completed
(BMI),14 systemically healthy were included in the study. Patients within 2 weeks of baseline recording of clinical parameters. On the day
suffering from xerostomia, past history of use of mouthwash or intake of of saliva sample collection at baseline, 3 months and 6 months interval
any medication in last 3 months, had received any periodontal treat­ after sample collection, before recording clinical parameters and initi­
ment, pregnancy, lactating mother and smokers were excluded. ation of SRP, subjects were provided snacks and the serum samples were
Written informed consent was obtained from the subjects and the collected after the treatment procedure. This protocol was followed
study was approved by the Institutional Review Board and registered at throughout the study period. At 1 month completion of SRP only clinical
Clinical Trials Registry-India(CTRI/2017/10/010171). parameters were measured.
The study timeline consisted of four visits – first one at baseline - case
2.2. Clinical parameters measured history, clinical parameter measurement, saliva and serum sample
collection. Second visit – 1 month following SRP- oral hygiene rein­
The clinical parameters measured were plaque index (PI),15 gingival forcement and clinical parameters recorded. Third and fourth visit-3
index (GI),16 bleeding on probing (BOP),17 probing depth (PD), clinical months and 6 months post NSPT, clinical parameter measured, saliva
attachment level (CAL). All the measurement was done by single and serum samples collected (Fig. 1).
examiner (SN) using UNC 15 probe (Hu-Friedy, Chicago, IL) and at six All subjects included in the study were having moderate periodon­
sites (mesiobuccal, distobuccal, mesiolingual, lingual and distolingual) titis and any subject with progressive bone loss, > 5 mm probing depth
of each tooth excluding the third molars. The intra-examiner agreement even after 3 months of NSPT were excluded from the study and neces­
was assessed by kappa coefficient (k), which was >0.95 for all the sary treatment was provided to such subjects at periodontal surgery
periodontal clinical parameters. clinic.

2.3. Group 1 consisted of 35 systemically and periodontally healthy 2.7. Leptin assay
subjects
The leptin levels were estimated using Weldon Leptin –Elisa kit (DRG
Group 2 consisted of 35 ChP subjects, having >4 mm probing depth, Instrument GmbH, Germany)according to the manufacturer’s in­
CAL >5 mm at 3–4 sites in more than four teeth in each quadrant with structions. It was performed using quantitative sandwich enzyme
evidence of radiographic bone loss. According to recent classification immunoassay technique. The monoclonal antibody specific for leptin
precoated onto the wells of the microtitre plate. Calibrated solution,
Table 1 serum and saliva samples were pipette into the wells and bounded to the
Demographic parameters of different groups in the study. immobilized antibody. An enzyme polyclonal antibody specific for
Variables Healthy controls Group A ChP leptin was added to the wells following washing of the unbound
Group B substance.
Age in years(Mean ± S.D) 46 ± 0.62 44 ± 0.84
Elisa microreader was used for analysis using 450 nm as the primary
Gender 20 20 wavelength. Comparison of samples mean optical density with the
Male 12 11 standard curve yielded the salivary concentration of leptin. The lower
Female 8 9 limit of detection was 0.5 ng/ml. The leptin level was determined in
BMI 20.5 ± 1.33 21.4 ± 1.42
picrograms (pg) and the sample concentration was calculated by
S.D-Standard deviation, ChP-chronic periodontitis. dividing the leptin amount by the sample volume (pg/mL).

69

Downloaded for ahana maity maity ([email protected]) at Kasturba Medical College Manipal from ClinicalKey.com by
Elsevier on February 21, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.
S. Nisha et al. Journal of Oral Biology and Craniofacial Research 12 (2022) 68–73

Fig. 1. Participants flowchart.

2.8. Total antioxidant assay Wilcoxon signed-rank test. Statistical significance was kept at p < 0.5.
Statistical package for social science (SPSS windows version 16, Chi­
The total antioxidant assay were estimated using FRAP(Ferric cago, IL) was used for data analysis.
Reducing Ability of Plasma) assay by Benzie and Strain.18 This method is
based on the principal of ferric(Fe3+) reducing capacity of plasma to 3. Results
ferrous(Fe2+) ion at low pH. This in turn leads to blue coloured ferrous
tripyridyltriazine (Fe2± TPTZ) complex formation and absorption at Height and weight were recorded for evaluation of body mass index.
593 nm. Elisa microplate reader was used for reading and results were The mean body mass index among group 1 was 20.4 ± 1.38 and in group
expressed as mmol/l (Mm/l). 2 was 21.2 ± 1.44. This difference was insignificant (p < 0.05) (Table 1).
All the clinical parameters are illustrated in Table 2.
2.9. Randomisation Leptin and TAOC were detected in all the serum and saliva samples.
The control group had lower mean salivary leptin levels and higher
Sample was randomised using computerised random number mean salivary TAOC levels as compared to ChP group at baseline. The
generator (Graphpad) in 1:1 allocation ratio. This was done by the mean difference observed was statistically significant in both the groups
investigator (ABS) and the subjects were enrolled in the study by clini­ (p<0.05) (Tables 3 and 4). Baseline levels of mean serum leptin and
cian at the study site. TAOC levels in control group were significantly higher compared to ChP
group (p<0.05) (Tables 3 and 4).
2.10. Sample size determination The relationship between serum leptin levels and periodontal clinical
parameters.
The sample size was calculated based on the primary outcome of the There was a significant positive correlation between serum leptin
study, two tailed unpaired t-test with effect size of 0.5, power of the concentration and all clinical parameters which indicated decrease in
study was 0.8 and the allocation ratio 1:1. The calculated sample size leptin levels from health to periodontal disease. However, NSPT didn’t
was 68 (34 subjects in each group). Attrition rate of 20% was expected, show any significant change in serum leptin levels in ChP group at 3 and
so the final sample size was 82 (41 subjects in each group). After the 6 months post therapy (p>0.05) (Table 5).
drop outs in each group 35 subjects were assessed. The relationship between salivary leptin levels and periodontal
clinical parameters.
2.11. Statistical analysis There was a significant negative correlation between salivary leptin
concentration and clinical parameters suggesting decrease in leptin
Differences in clinical parameter, salivary and serum TAOC and levels in saliva from periodontal healthy to disease condition. Further,
leptin levels between group 1 and 2 were analyzed using the Mann- NSPT had no significant changes in salivary leptin levels in ChP group at
Whitney U test. Spearman rank correlation analysis was used to anal­ 3 and 6 months post therapy (p>0.05) (Table 5).
yse correlations between clinical parameter and the leptin and TAOC The relationship between serum TAOC levels and periodontal clin­
levels. Intragroup differences before and after NSPT was analyzed using ical parameters.

70

Downloaded for ahana maity maity ([email protected]) at Kasturba Medical College Manipal from ClinicalKey.com by
Elsevier on February 21, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.
S. Nisha et al. Journal of Oral Biology and Craniofacial Research 12 (2022) 68–73

Table 2 Table 4
Periodontal parameters among the study groups Serum and Saliva total antioxidant capacity levels.
Clinical parameters Healthy controls ChP p value Variable Healthy controls Group A ChP p value
Group B
Group A Group B
Mean±S.D Mean±S.D Saliva 952.14 ± 32.02 543.12 ± 23.10 <0.05
TAOC (pg) baseline 567.32 ± 25.20 >0.05
PI
3 month 546.22 ± 28.12 >0.05
baseline 0.24 ± 0.13 2.47 ± 0.32 NS
6 month
1 month - 1.12± 0.22 <0.05
p value*
3 month - 0.56± 0.28 <0.05
Serum 1045.03 ± 82.23 623.18 ± 76.24 <0.05
6 month - 0.58±0.26 <0.05
TAOC (pg) baseline 724.12 ± 56.14 >0.05
p value* <0.05
3 month 713.16 ± 64.26 >0.05
GI
6 month
baseline 0.42 ± 0.26 1.91 ± 0.12 NS
p value*
1 month - 1.12± 0.13 <0.05
3 month - 0.45± 0.13 <0.05 TAOC - total antioxidant capacity, p-probability value, statistically significance
6 month - 0.43±0.12 <0.05 at p < 0.05. .* Repeated measure Anova analysis for intragroup comparison.
p value* <0.05
PD
baseline 2.34 ± 0.32 4.75 ± 0.43 NS Before the NSPT in ChP group, there was a positive correlation be­
1 month - 3.25± 0.33 <0.05 tween serum leptin levels and TAOC levels which indicated a decrease in
3 month - 2.81± 0.37 <0.05 serum leptin and TAOC levels from health to periodontal disease.
6 month - 2.77±0.33
However, post therapy didn’t show any significant changes at 3 and
<0.05
p value* <0.05
CAL months. Between the saliva leptin levels and TAOC levels before ther­
baseline 1.45 ± 0.12 4.07± 0.53 NS apy, there was a negative correlations seen. Furthermore, no significant
1 month - 3.85± 0.43 <0.05 changes were seen post therapy (p>0.05) (Table 5).
3 month - 2.67± 0.37 <0.05
6 month - 2.64±0.32 <0.05
p value* >0.05
4. Discussion
BoP %
baseline 1.02 ±0 .26 4.7±0.53 NS This study evaluated the 6 months effects of NSPT on the serum and
1 month - 0.83±0.34 <0.05 saliva levels of leptin and total antioxidant capacity in patients with
3 month - 0.56±0.23
ChP. The serum leptin and TAOC levels were associated with the
<0.05
6 month - 0.42±0.15 <0.05
p value* <0.05 severity of ChP and non surgical periodontal therapy didn’t have any
significant changes. We tried to observe the correlation between serum
PI-Plaque index ,GI- Gingival index ,PD- Probing depth ,CAL - clinical attach­
and salivary leptin and TAOC levels. Several studies have reported as­
ment level, BoP - bleeding on probing, ChP-chronic periodontitis , S.D-Standard
sociation between leptin and periodontitis.19,20 Serio et al. demon­
deviation, p-probability value, NS- non significant , statistically significance at
p<0.05.*repeated measure anova analysis for intragroup comparison. strated presence of leptin within healthy and inflamed gingiva.6 The
leptin concentration was found highest in healthy gingiva in the solu­
bilised gingival biopsies. Karthikeyan et al. showed positive association
Table 3 between GCF leptin, gingivitis and periodontitis in Indian population.21
Serum and Saliva leptin levels. Our study also found positive association of serum leptin and peri­
Variable Healthy controls Group A ChP p value odontitis. Purwar et al. studied salivary leptin levels in periodontitis and
Group B found lower salivary leptin levels in periodontitis as compared to
Saliva leptin(μM) 0.29 ± 0.22 0.34 ± 0.27 <0.05
healthy subjects.22 This is in accordance with our study, we also found
baseline – 0.30 ± 0.24 >0.05 significantly lower salivary leptin levels in periodontitis. However,
3 month 0.29 ± 0.21 >0.05 NSPT didn’t show any significant changes in either serum or salivary
6 month >0.05 leptin levels.
p value*
Leptin is a peptide hormone which has a structural homolog to
Serum leptin(μM) 0.36 ± 0.21 0.23 ± 0.26 <0.05
baseline – 0.24 ± 0.31 >0.05 cytokine family and shows cytokine like expressions during inflamma­
3 month 0.23 ± 0.22 >0.05 tion.23 It also has a role in insulin and glucose metabolism, endothelial
6 month >0.05 functions and vascular tone. It acts as a proinflammatory cytokine and
p value*
has synergistic action along with IL-6, IL-1 which explains the increase
ChP-Chronic periodontitis, p-probability value, statistically significance at p < in leptin expression during inflammation and infections like periodon­
0.05. .* Repeated measure Anova analysis for intragroup comparison. titis.24 Leptin mediates local periodontal inflammation by modulating
immunocytes like T-cells, monocytes and natural killer cells and has a
There was a significant positive correlation between serum TAOC direct stimulatory effect on bone growth through osteoblast prolifera­
concentration and all clinical parameters which indicated decrease in tion and differentiation thereby regulating alveolar bone loss.25 Thus,
TAOC levels from health to periodontal disease. However, NSPT didn’t periodontal disease can cause changes in leptin levels locally and
show any significant change in serum TAOC levels in ChP group at 3 and systemically.
6 months post therapy (p>0.05) (Table 5). In our study also we found association between serum and salivary
The relationship between salivary TAOC levels and periodontal leptin levels and periodontitis, however NSPT didn’t show any
clinical parameters. improvement. This result was contradicted by Purwar et al. who found
There was a significant positive correlation between salivary TAOC that non-surgical therapy can increase the leptin levels in the saliva of
concentration and all clinical parameters which indicated decrease in chronic periodontitis patients.22 Such variation might be due to varia­
TAOC levels from health to periodontal disease. However, NSPT didn’t tions in host immune response in different individuals, duration of
show any significan change in salivary TAOC levels in ChP group at 3 follow up as only 12 weeks follow up was done in this study. There lies a
and 6 months post therapy (p>0.05) (Table 5). possibility that post therapy the serum and saliva leptin levels get
Correlation between serum and saliva leptin levels and TAOC levels. altered however they are not sustained in long term follow up and so in
our study post 3 and 6 months no significant changes were noted.

71

Downloaded for ahana maity maity ([email protected]) at Kasturba Medical College Manipal from ClinicalKey.com by
Elsevier on February 21, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.
S. Nisha et al. Journal of Oral Biology and Craniofacial Research 12 (2022) 68–73

Table 5
Spearman’s Rank correlation (r) coefficient in ChP group.
Serum leptin Saliva leptin PD CA loss Serum TAOC Saliva TAOC

Serum leptin Correlation Coefficient 1.000

Baseline
3 months
6 months
P value
Baseline
3 months
6 months
Saliva leptin Correlation Coefficient − 0.346 1.000
Baseline − 0.312
3 months − 0.311
6 months
P value <0.05
Baseline >0.05
3 months >0.05
6 months
PD Correlation Coefficient 0.324 − 0.223 1.000 0.363 –
Baseline 0.313 − 0.212 0.312 0.361
3 months 0.324 − 0.234 0.345 0.314
6 months 0.323
P value <0.05 <0.05 <0.05 <0.05
Baseline >0.05 >0.05 >0.05 >0.05
3 months >0.05 >0.05 >0.05 >0.05
6 months
CA loss Correlation Coefficient 0.367 − 0.345 1.000 0.365 − 0.342
Baseline 0.234 − 0.314 0.324 − 0.344
3 months 0.213 − 0.322 0.313 − 0.347
6 months
P value <0.05 <0.05 <0.05 <0.05
Baseline >0.05 >0.05 >0.05 >0.05
3 months >0.05 >0.05 >0.05 >0.05
6 months
Serum TAOC Correlation Coefficient 0.232 0.312 0.324 1.000
Baseline 0.234 0.322 0.327
3 months 0.245 0.314 0.318
6 months
P value <0.05 <0.05 <0.05
Baseline >0.05 >0.05 >0.05
3 months >0.05 >0.05 >0.05
6 months
Saliva TAOC Correlation Coefficient − 0.315 − 0.213 − 0.245 1.000
Baseline − 0.312 − 0.234 − 0.234
3 months − 0.322 − 0.215 − 0.243
6 months
P value <0.05 <0.05 <0.05
Baseline >0.05 >0.05 >0.05
3 months >0.05 >0.05 >0.05
6 months

PD- Probing depth, CAL - clinical attachment level, TAOC - total antioxidant capacity, p-probability value, statistically significant at p < 0.05.

Another study by Shimada et al. on effects of periodontal treatment on discarded. In the present study we evaluated serum and salivary TAOC
serum leptin and interleukins levels post 1 month follow up after levels between health and periodontitis patients. A significant difference
nonsurgical therapy showed decreased levels of proinflammatory in­ was seen between the healthy and periodontitis group in serum and
terleukins and leptin levels.26 Again the results are having short follow salivary TAOC levels (p < 0.05). However, post NSPT at 3 and 6 months
up and they found positive correlation between serum leptin levels and no significant changes were seen at serum and saliva (p > 0.05). This
periodontal clinical parameters which was also observed in the present result is similar to Sculley et al. where they found decrease salivary
study. Gonclaves et al. found no significant effect of NSPT in circulating TAOC levels is associated with periodontitis.30 Another study by Chap­
levels of leptin which is in accordance to our study.27 ple et al. and Brock et al. showed decrease level of serum TAOC levels
Leptin in saliva has physiologic effects on oral keratinocytes, wound which is in agreement with the present study.31,32 However, post ther­
healing, haematopoiesis, angiogenesis, osteogenesis, immune and in­ apy at 6 and 12 months no significant changes were seen (p > 0.05).
flammatory reactions. It also has protective effect on gingival tissues.28 Similar results were seen by Kim et al. where total antioxidant status
Antioxidants are a substance which scavenges the free radicals decreased directly after NSPT. With time, it increased slightly and was
released from enzymes and protects the normal cells from oxidation.29 relatively unchanged compared to the baseline at 3 months.33 The re­
They help in maintaining a balance between antioxidant-oxidant stress. sults of this study gives an insight that changes in antioxidant levels
This oxidative stress can be measured by various methods and might be time dependent event, post intervention the levels might seems
measuring each reactive oxygen species is crumble some and expensive, changed but over a long follow up the changes seems subtle. Akpinar
so we decided to measure total antioxidant capacity as a representative et al. showed reduce serum oxidative stress post periodontal treatment
of reactive oxygen species which causes oxidative stress. FRAP method which contradicts our study.34 The findings also suggest that significant
was used to determine the TAOC levels. The advantage of this method is relationships are present between oxidant–antioxidant status and peri­
it is sensitive to blood and any contamination of samples can be odontal parameters in the pathology of periodontitis. However, further

72

Downloaded for ahana maity maity ([email protected]) at Kasturba Medical College Manipal from ClinicalKey.com by
Elsevier on February 21, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.
S. Nisha et al. Journal of Oral Biology and Craniofacial Research 12 (2022) 68–73

studies are needed to confirm whether oxidant status is a cause of 7 Wajchenberg BL, Nery M, Cunha MR, Silva ME. Adipose tissue at the crossroads in
the development of the metabolic syndrome, inflammation and atherosclerosis. Arq
periodontitis. Such studies might lead to targeting oxidant status as a
Bras Endocrinol Metabol. 2009;53:145–150.
therapy for periodontitis. 8 Masuzaki H, Ogawa Y, Sagawa N. Non adipose tissue production of leptin: leptin as a
The limitation of the present study is the short term follow up, in­ novel placenta-derived hormone in humans. Nat Med. 1997;3:1029–1033.
dividual reactive oxygen species was not measured rather total antiox­ 9 Lago R, Gomez R, Lago F, Gomez-Reino J, Gualillo O. Leptin beyond body weight
regulation–Current concepts concerning its role in immune function and
idant capacity was taken as a representative of all ROS. inflammation. Cell Immunol. 2008;252:139–145.
10 Shimada Y, Komatsu Y, Ikezawa-Suzuki I, Tai H, Sugita N, Yoshie H. The effect of
periodontal treatment on serum leptin, interleukin-6, and C-reactive protein.
5. Conclusion
J Periodontol. 2010;81:1118–1123.
11 Purwar P, Khan MA, Mahdi AA, et al. Salivary and serum leptin concentrations in
There lies a significant association between serum and salivary total patients with chronic periodontitis. J Periodontol. 2014;24:1–10.
antioxidative capacity, leptin levels and clinical parameters in chronic 12 Mendoza-Azpur G, Castro C, Pena L, et al. Adiponectin, leptin and TNF-alpha serum
levels in obese and normal weight Peruvian adults with and without chronic
periodontitis patients when compared with control. Non-surgical peri­ periodontitis. J Clin Exp Dent. 2015;7(3):e380–386.
odontal therapy seems to restore the periodontal health, however its role 13 Armitage GC. Development of a classification system for periodontal diseases and
in local and systemic TAOC and leptin levels remains uncertain and conditions. Ann Periodontol. 1999;4:1–6.
14 WHO Expert Consultation. Appropriate body-mass index for Asian populations and
future multicentre longitudinal trials are needed to explore its relation. its implications for policy and intervention strategies. Lancet. 2004;363:157–163.
15 Loe H, Silness J. Periodontal Disease in pregnancy. I. Prevalence and severity. Acta
Contribution Odontol Scand. 1963;21:533–551.
16 Silness J, Loe H. Periodontal Disease in pregnancy. II. Correlation between oral
hygiene and periodontal condition. Acta Odontol Scand. 1964;22:121–135.
Swet Nisha: Concepts, Design, Literature search, Clinical studies, 17 Muhlemann HR, Son S. Gingival sulcus bleeding–a leading symptom in initial
Experimental studies, Data acquisition, Data analysis, Statistical anal­ gingivitis. Helv Odontol Acta. 1971;15(2):107–113.
18 Benzie IFF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of
ysis, Manuscript preparation, Manuscript editing, Manuscript review, ‘antioxidant power’: the FRAP assay. Anal Biochem. 1996;239:70–76.
Avinash Bettahalli Shivamallu: Concepts, Design, Definition of intel­ 19 Wang Z, Chen Z, Fang F, Qiu W. The role of adiponectin in periodontitis: current
lectual content, Literature search, Data acquisition, Manuscript prepa­ state and future prospects. Biomed Pharmacother. 2021;137:111358.
20 Zhu J, Guo B, Gan X, et al. Association of circulating leptin and adiponectin with
ration, Manuscript review, Akila Prashant: Design, Literature search, periodontitis: a systematic review and meta-analysis. BMC Oral Health. 2017;17:
Data analysis, Manuscript editing, Manuscript review, Manish Kumar 1–14.
Yadav and Sheela Kumar Gujjari-Literature search, data acquisition, 21 Karthikeyan BV, Pradeep AR. Gingival crevicular fluid and serum leptin: their
relationship to periodontal health and disease. J Clin Periodontol. 2007;34:467–472.
manuscript editing,manuscript review, Pratibha Shashikumar: Con­ 22 Purwar P, Khan MA, Gupta A, et al. The effects of periodontal therapy on serum and
cepts, Design, Definition of intellectual content, Manuscript editing, salivary leptin levels in chronic periodontitis patients with normal body mass index.
Manuscript review,Guarantor. Acta Odontol Scand. 2015;73:633–641.
23 Procaccini C, Jirillo E, Matarese G. Leptin as an immunomodulator. Mol Aspect Med.
2012;33(1):35–45.
Declaration of competing interest 24 Ay ZY, Kirzioglu FY, Tonguc MO, Sutcu R, Kapucuoglu N. The gingiva contains leptin
and leptin receptor in health and disease. Odontology. 2012;100(2):222–231.
25 Li W, Huang B, Liu K, Hou J, Meng H. Upregulated leptin in periodontitis promotes
No conflict of interest. inflammatory cytokine expression in periodontal ligament cells. J Periodontol. 2015;
86(7):917–926.
26 Shimada Y, Komatsu Y, Ikezawa-Suzuki I, Tai H, Sugita N, Yoshie H. The effect of
Acknowledgement periodontal treatment on serum leptin, interleukin-6, and C - reactive protein.
J Periodontol. 2010;81:1118–1123.
Nil 27 Goncalves TE, Feres M, Zimmermann GS, et al. Effects of scaling and root planing on
clinical response and serum levels of adipocytokines in patients with obesity and
chronic periodontitis. J Periodontol. 2015;86(1):53–61.
References 28 Fantuzzi G, Faggioni R. Leptin in the regulation of immunity, inflammation, and
hematopoiesis. J Leukoc Biol. 2000;68(4):437–446. Oct.
1 Guentsch A, Preshaw PM, Bremer-Streck S, Klinger G, Glockmann E, Sigusch BW. 29 Chapple ILC, Matthews JB. The role of reactive oxygen and antioxidant species in
Lipid peroxidation and antioxidant activity in saliva of periodontitis patients: effect periodontal tissue destruction. Periodontol 2000. 2007;43:160–232.
of smoking and periodontal treatment. Clin Oral Invest. 2008;12:345–352. 30 Sculley DV, Langley-Evans SC. Periodontal disease is associated with lower
2 Halliwell B, Whiteman M. Measuring reactive species and oxidative damage in vivo antioxidant capacity in whole saliva and evidence of increased protein oxidation.
and in cell culture: how should you do it and what do the results mean? Br J Clin Sci (Lond). 2003;105:167–172.
Pharmacol. 2004;142:231–255. 31 Chapple IL, Mason GI, Garner I, et al. Enhanced chemiluminescent assay for
3 Akalin FA, Baltacioglu E, Alver A, Karabulut E. Lipid peroxidation levels and total measuring the total antioxidant capacity of serum, saliva and crevicular fluid. Ann
oxidant status in serum, saliva and gingival crevicular fluid in patients with chronic Clin Biochem. 1997;34(Pt 4):412–421.
periodontitis. J Clin Periodontol. 2007;34:558–565. 32 Brock GR, Butterworth CJ, Matthews JB, Chapple IL. Local and systemic total
4 Renvert S, Lindahl C, Roos-Jansaker AM, Lessem J. Short-term effects of an anti- antioxidant capacity in periodontitis and healthy. J Clin Periodontol. 2004;31(7):
inflammatory treatment on clinical parameters and serum levels of C-reactive protein 515–521.
and proinflammatory cytokines in subjects with periodontitis. J Periodontol. 2009;80: 33 Kim SC, Kim OS, Kim OJ, Kim YJ, Chung HJ. Antioxidant profile of whole saliva after
892–900. scaling and root planing in periodontal disease. J Periodontal Implant Sci. 2010;40:
5 Buduneli N. Biomarkers in saliva and serum samples for periodontal disease and 164–171.
interactions with systemic health. Curr Oral Health Rep. 2019;6:31–36. 34 Akpinar A, Toker H, Ozdemir H, Bostanci V, Aydin H. The effects of non-surgical
6 Johnson RB, Serio FG. Leptin within healthy and diseased human gingiva. periodontal therapy on oxidant and anti-oxidant status in smokers with chronic
J Periodontol. 2001;72:1254–1257. periodontitis. Arch Oral Biol. 2013;58:717–723.

73

Downloaded for ahana maity maity ([email protected]) at Kasturba Medical College Manipal from ClinicalKey.com by
Elsevier on February 21, 2023. For personal use only. No other uses without permission. Copyright ©2023. Elsevier Inc. All rights reserved.