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   Table of Contents    
ORIGINAL ARTICLE
Year : 2017  |  Volume : 21  |  Issue : 4  |  Page : 291-295  

Impact of nonsurgical periodontal therapy on total antioxidant capacity in chronic periodontitis patients


1 Department of Periodontology, Divya Jyoti College of Dental Sciences and Research, Ghaziabad, India
2 Department of Periodontics and Community Dentistry, Dr Ziauddin Ahmad Dental College, Aligarh Muslim University, Aligarh, Uttar Pradesh, India
3 Department of Periodontics, Postgraduate Institute of Dental Sciences, Rohtak, Haryana, India

Date of Submission13-Aug-2015
Date of Acceptance16-Nov-2017
Date of Web Publication29-Jan-2018

Correspondence Address:
Dr. Neha Bansal
K-16, Ada Bank Colony, Pala Road, Aligarh - 202 001, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jisp.jisp_281_15

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   Abstract 

Aim: The aim of this study was to determine the utility of plasma total antioxidant capacity (TAC) as marker of periodontal disease by estimating TAC of periodontally healthy and chronic periodontitis patients and the impact of scaling and root planning on total antioxidant status of periodontitis patients. Materials and Methods: Blood plasma samples were collected from randomly selected eighty individuals (40 periodontally healthy controls and 40 chronic periodontitis patients), with an age range of 20–45 years and were analyzed for TAC by ferric reducing antioxidant power assay. Scaling and root planing was performed in periodontitis patients, and TAC level was measured again after 3 weeks. Data were analyzed with t-test, using SPSS software (PSAW, Windows version 18.0). Results: The mean plasma TAC was significantly lower (792.33 ± 124.33 μmol/L, P < 0.001) in chronic periodontitis patients compared to healthy control (1076.08 ± 193.82 μmol/L). Plasma TAC level increased significantly (989.75 ± 96.80, P < 0.001) after scaling and root planing. Conclusions: An inverse relationship exists between plasma TAC and severity of chronic periodontitis suggesting disturbed oxidant-antioxidant balance in chronic periodontitis. Scaling and root planing resulted in the restoration of TAC to normal levels. These results are important from the perspective of including antioxidants in periodontal therapy regime to boost up body's antioxidant defense system and to reduce oxidative stress-mediated periodontal tissue damage. We concluded that TAC can be used as a biomarker to evaluate the health of periodontium.

Keywords: Antioxidants, chronic periodontitis, lipid peroxidation, oxidative stress, reactive oxygen species, total antioxidant capacity


How to cite this article:
Bansal N, Gupta ND, Bey A, Sharma VK, Gupta N, Trivedi H. Impact of nonsurgical periodontal therapy on total antioxidant capacity in chronic periodontitis patients. J Indian Soc Periodontol 2017;21:291-5

How to cite this URL:
Bansal N, Gupta ND, Bey A, Sharma VK, Gupta N, Trivedi H. Impact of nonsurgical periodontal therapy on total antioxidant capacity in chronic periodontitis patients. J Indian Soc Periodontol [serial online] 2017 [cited 2019 Nov 20];21:291-5. Available from: http://www.jisponline.com/text.asp?2017/21/4/291/223968


   Introduction Top


Chronic periodontitis is a complex inflammatory disease which involves intricate interaction of biofilm with host immune-inflammatory response and subsequent alterations in bone and connective tissue homeostasis.[1] It is initiated by the periodontal pathogens, but the abnormal host response to these pathogens appears to be determinant in progression of disease.[2],[3],[4] In attempt to eliminate the infection/noxious stimuli, host inflammatory cells primarily polymorphonuclear leukocytes (PMNs) release a number of reactive oxygen species (ROS) in event of oxidative burst.[5],[6] These ROS particularly hydroxyl ions react with and cause oxidative damage of cellular molecules such as DNA, proteins, and lipid.[7],[8] They also promote cell apoptosis, matrix degradation and hamper the cell cycle progression, and growth of gingival fibroblasts.[9],[10] ROS accelerate bone resorption by acting as an intracellular signaling molecule during osteoclastogenesis.[11] Oxidative cell damage is mediated by various pathways as caspase pathway, protein kinase-like ER kinase/nuclear factor E2-related factor 2 pathway, nicotinamide adenine dinucleotide phosphate oxidase 4 pathway, and c-Jun N-terminal kinases/mitogen-activated protein kinase pathway.[12] Many investigators described increase in lipid, protein, and DNA oxidation products in chronic periodontitis patients displaying increase in ROS-mediated damage to the supporting periodontal tissue as well as advancing periodontal inflammation.[13],[14],[15],[16],[17],[18],[19],[20],[21],[22]

To prevent the detrimental effects of ROS, body's antioxidant defense system get activated. When the physiologically/pathologically generated ROS overwhelm the endogenous antioxidant system of the body, oxidative stress occurs.[23] In recent years, various studies pointed out that oxidative stress is strongly linked with periodontitis and may be a key factor in determining the extent of destruction associated with the disease.[24],[25],[26],[27] The total capacity of all antioxidants present in our body to neutralize the ROS, is known as total antioxidant capacity (TAC). TAC was first described by Miller et al.[28] as “measure of the antioxidant capacity of all antioxidants in a biological sample and not just the antioxidant capacity of a single compound.” In the present study, we correlated TAC with periodontal disease and therapy. This can provide a basic understanding of pathogenesis and impact of oxidative destruction seen in chronic periodontitis. We postulated that periodontal therapy, especially scaling and root planing reduces oxidative stress by minimizing the induced ROS in response to bacterial load. This helps in restoration of body's antioxidant levels and TAC.


   Materials and Methods Top


Study group

In this case–control study, eighty participants (20–45 years of age) were randomly recruited from patients who were referred to the department of periodontics and community dentistry due to periodontal problems or for routine periodontal examination. Patients were informed about the study, and written informed consent was obtained from all patients before the study. Ethical approval was taken from institutional ethical committee.

Selected participants were divided equally into two groups. The control group (C) (n = 40) consisted of periodontally healthy participants and test group (P) (n = 40) included chronic periodontitis patients. The detailed case history and medical history were recorded for all participants. Patients were clinically and radiographically evaluated for chronic periodontitis according to the criteria accepted by the American Academy of Periodontology in 1999. Loe and Sillness plaque index, Sillnes and Loe gingival index, pocket probing depth, and clinical attachment level were recorded at six sites per tooth using a PCP-UNC 15 periodontal probe (Hu-Friedy, Chicago, US). The bone level was assessed with intraoral periapical and panoramic radiographs. Inclusion criteria for periodontitis patients were generalized chronic periodontitis with a probing depth ≥5 mm at minimum six different teeth. In control group, no probing pocket depth ≥4 mm and no radiographic bone loss was recorded. The control group displayed good oral hygiene and no clinical signs of gingival inflammation.

Participants having systemic disease, having received periodontal treatment or antibiotics in the past 6 months, smokers, alcoholics, and pregnant or lactating mothers were excluded from the study. In addition, participants who have taken antioxidants or vitamin therapy within the past 3 months were also excluded from the participant sample.

Study design

After clinical assessment, venous blood sample was taken. Collection of samples and the assay of biochemical indices were performed in all participants before treatment. In periodontitis group, initial full-mouth scaling and root planing (SRP) were performed. After 3 weeks of SRP, measurement of periodontal status, collection of samples, and the assay of biochemical indices were repeated.

Biochemical analysis

The ferric reducing antioxidant power described by Benzei and Strain was used to measure the TAC of plasma.[29] The results were expressed as μmol/L.

Statistical analysis

The data were summarized as mean ± standard deviation. Groups were compared by one-way analysis of variance, and the significance of the mean difference between the groups was done by Tukey post hoc test. Groups were also compared by independent Student's t-test. The pre- and post-data were compared by paired t-test. A two-sided (α = 2) P < 0.05 was considered statistically significant. Analyses were performed on SPSS software version 18.0 (IBM Corp., Armonk, NY).


   Results Top


The TAC levels in control group and SRP-treated test groups are summarized in [Table 1] and [Figure 1]. The results showed that mean plasma TAC was significantly lower in periodontitis patients (792.33 ± 124.33 μmol/L, P < 0.001) compared to age- and sex-matched healthy control (1076.08 ± 193.82 μmol/L). Severity of periodontitis was found to be inversely related to TAC values in test group. TAC increased significantly in periodontitis patients after nonsurgical therapy (989.75 ± 96.80 μmol/L).
Figure 1: Total antioxidant capacity levels of controls, pretreatment test group, and post treatment test group, *** P<.001 very highly significant, ns – Non significant, SRP – Scaling & Root planing

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Table 1: Total antioxidant capacity levels (mean±standard deviation) of controls, pretreatment and posttreatment scaling, and root planing treated test group

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[Table 2] and [Figure 2] display comparison of the mean difference in plasma TAC levels between control and test group. On comparing, t-test revealed 19.9% increase (197.42 ± 87.51 μmol/L) in the mean TAC level after SRP as compared to pretreatment group. Posttreatment TAC concentration was comparable to control group.
Figure 2: Pretreatment and post treatment total antioxidant capacity levels of test group treated with scaling and root planing, *** P<.001 very highly significant

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Table 2: Comparison of mean difference in total antioxidant capacity levels between control and both test groups by Tukey post hoc test

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   Discussion Top


In the present study, we correlated plasma TAC with chronic periodontitis and impact of scaling and root planing on TAC. Oxidative stress is found to be cardinal in many inflammatory diseases.[12] Various studies have proved a direct association of periodontal disease with total oxidative stress.[15],[30] When there is derangement of physiological equilibrium between ROS and antioxidant defense system, oxidative stress occurs. It can be accessed directly by estimating generated ROS or indirectly by measuring TAC level. ROS which is produced during inflammatory response are nonstable and react with cellular molecules or get neutralized by antioxidants. Therefore, estimation of oxidant levels may be complicated and unreliable. According to Collins,[31] measurement of TAC is a promising tool for the assessment of oxidative stress. TAC is not a simple aggregate of all known and unknown antioxidants present in the body, but rather an integrated parameter which evidences the complex interactions among all antioxidants and their effect on the redox potential.[32] TAC was utilized as a tool to determine oxidative stress in cardiovascular disease, depression, cancer, male infertility, and other inflammatory conditions.[32],[33],[34],[35] It can be postulated that heightened oxidative damage leads to depletion of salivary and plasma antioxidants.

Our results demonstrated that plasma TAC is significantly lower in chronic periodontitis patients compared to age- and sex-matched controls. Our results are supported by earlier studies revealing reduction of plasma/serum TAC in periodontal disease and its negative correlation with disease severity.[36],[37],[38],[39],[40],[41],[42],[43],[44] Brock et al. demonstrated decreased levels of peripheral and salivary TAC in periodontitis; however, the difference was significant for plasma only.[45] The authors deduced that host response to periodontopathogens could ensue a low-grade systemic inflammation that leads to attenuation in TAC of plasma, or it may be an inherent feature of chronic periodontitis.

The alteration in TAC is further supported by recent studies that demonstrated the presence of hyperreactive peripheral PMNs in chronic periodontitis patients leading to increased production of ROS in response to Fc gamma-receptor stimulation.[46] This disturbance in antioxidant status may lead to increased ROS mediated tissue destruction and progression of disease at faster rates.

Zhang et al. reported that there is no significant correlation between periodontopathic bacterial load and salivary TAC/total oxidant status. They suggested that changes in antioxidant capacity in periodontitis patients are probably due to a dysregulated immune response and not related with increased bacterial load.[47] Liskmann et al. observed reduction in TAC in peri-implantitis cases.[48] Recently, Punj et al. evaluated relationship between periodontitis and ischemic heart disease by measuring TAC. The authors demonstrated decreased level of antioxidant enzymes and TAC in saliva and serum in both disease group patients.[49] However, few investigators revealed higher levels of plasma TAC in the periodontitis group as compared to control.[50] Disparity in results may be due to difference in method of analysis and varied dietary habits.[51],[52]

It has been shown that periodontal disease is associated with reduced levels of antioxidants enzymes [53],[49] as superoxide dismutase (SOD), catalase, glutathione peroxidase, and nonenzymatic antioxidants as glutathione (major antioxidant molecule),[54],[55],[56] albumin,[13] and Vitamins C.[56] After periodontal therapy, oxidative stress decreased and antioxidant enzyme levels were significantly increased compared to basal levels while no improvement in any parameter was found in oral hygiene reinforcement group.[39],[57],[58] However, some investigators reported higher levels of enzymatic antioxidant which decreased significantly after periodontal therapy.[21],[59],[60]

This results show that 3 weeks after thorough SRP, there was increase in plasma TAC level restoring to level comparable to control. Earlier studies have shown similar results.[37],[61] Thomas et al. evaluated TAC in periodontitis and gingivitis patients before and after periodontal therapy. They revealed that TAC increased significantly after periodontal therapy.[39] Chapple et al. demonstrated no change in plasma TAC levels after nonsurgical therapy.[62] Increase in TAC after scaling and root planing seems to occur due to reduced oxidative stress. After therapy, as the noxious stimuli are removed, there will be lesser generation of ROS. This shifts the equilibrium toward coherent antioxidant system, and it facilitates an environment conducive to periodontal health.


   Conclusions Top


The mean plasma TAC level was lower in chronic periodontitis patients compared to healthy controls which increases after nonsurgical periodontal therapy. Nonsurgical therapy can restore and control the antioxidant capacity by locally and systemically modifying the levels of ROS generated and antioxidant molecules. TAC can be used as a biomarker to evaluate the health of periodontium. Further longitudinal studies are required to establish whether oxidative stress and plasma antioxidant concentrations are true risk factors for periodontal disease.

Acknowledgement

The author would like to thank members of the Department of Biochemistry, Jawaharlal Nehru Medical College, for their assistance.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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