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 Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 6  |  Issue : 1  |  Page : 3-6

Evaluation of the serum antioxidant status in patients with chronic periodontitis


1 Department of Periodontics, Himachal Institute of Dental Sciences, Paonta Sahib, Himachal Pradesh, India
2 Department of Oral and Maxillofacial Pathology, HP GDC, Shimla, Himachal Pradesh, India
3 Department of Conservative Dentistry, Government Dental College, Rohtak, Haryana, India

Date of Web Publication11-Aug-2016

Correspondence Address:
Parveen Dahiya
Department of Periodontics, Himachal Institute of Dental Sciences, Paonta Sahib - 170 325, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2229-6360.188213

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  Abstract 

Aim: The aim of this study was to evaluate any measurable change in antioxidant and free radical scavenger status in periodontal disease.
Materials and Methods: A total of forty subjects consisting of twenty test subjects and twenty controls were recruited for the study. The antioxidant defense status in serum (in terms of superoxide dismutase (SOD), glutathione peroxidase [GSHPx] and catalase [CAT]), serum lipid peroxidation (in terms of malondialdehyde), and free radical scavengers (Vitamin C) was assessed.
Results: Significant differences were noted between tests and controls. Negative correlation was observed between the values of lipid peroxidation and that of SOD, GSHPx, and CAT. Our study confirmed that lowered level of SOD, CAT, and GSHPx is associated with hyper lipid peroxidation in periodontal disease.
Conclusion: It is now clear that the free radicals play a critical role in the initiation and progression of periodontal disease. Furthermore, the results of the present study may have important therapeutic implications in terms of the use of the antioxidants in periodontal therapy to prevent tissue destruction.

Keywords: Catalase, lipid peroxidation, periodontal disease, reactive oxygen species, Vitamin C


How to cite this article:
Dahiya P, Kamal R, Gupta R, Saini H. Evaluation of the serum antioxidant status in patients with chronic periodontitis. Indian J Multidiscip Dent 2016;6:3-6

How to cite this URL:
Dahiya P, Kamal R, Gupta R, Saini H. Evaluation of the serum antioxidant status in patients with chronic periodontitis. Indian J Multidiscip Dent [serial online] 2016 [cited 2019 Jan 17];6:3-6. Available from: http://www.ijmdent.com/text.asp?2016/6/1/3/188213


  Introduction Top


Periodontitis is an inflammatory disease caused by opportunistic bacteria residing in the oral cavity, leading to the loss of supporting tissues of teeth. [1] It has been observed that various invading bacteria trigger the release of cytokines such as interleukin 8 and tumor necrosis factor-α, leading to elevated numbers and activity of polymorphonuclear leukocytes (PMNs). As a result of stimulation by bacterial antigens, PMN produces the reactive oxygen species (ROS) superoxide via the respiratory burst as part of the host response to infection. Patients with periodontal disease display increased PMN number and activity. It has been suggested that this proliferation results in a high degree of ROS release, culminating in heightened oxidative damage to gingival tissue, periodontal ligament, and alveolar bone. Hydroxyl radical is most active in damaging important molecules such as DNA, proteins, and lipids, whereas hydrogen peroxide, even not being considered a potent ROS, is capable of crossing the nuclear membrane and also damaging DNA. [2]

Antioxidant defense system is very dynamic and responsive to any disturbance taking place in redox balance of the body. Antioxidants can be upregulated and neutralize free radical formation that could take place due to oxidative stress. [3] The human body does contain an array of antioxidant defense mechanisms (nonenzymatic and enzymatic antioxidants) to remove harmful ROS as soon as they are formed and to prevent their deleterious effects. The nonenzymatic antioxidants include Vitamins E and C, and reduced glutathione (GSH), whereas the enzymatic antioxidants include superoxide dismutase (SOD), catalase (CAT), and GSH peroxidase (GSHPx).

The possible mechanisms by which antioxidants may offer protection against free radical damage include: [4]

  • Prevention of formation of free radicals
  • Interception of free radicals by scavenging the reactive metabolites and converting them to less reactive molecules
  • Facilitating the repair of damage caused by free radicals
  • Providing a favorable environment for effective functioning of other antioxidants.
In recent years, more attention has been focused on the role of ROS, lipid peroxidation products, and antioxidant systems in the pathology of periodontitis. Recent medical and dental research in this area is geared toward the prevention of free radical-mediated diseases by using specific nutrient antioxidants.


  Materials and Methods Top


The present study was conducted in the Department of Periodontics, Himachal Institute of Dental Sciences, Paonta Sahib, Himachal Pradesh (India), with an objective to evaluate any measurable change in antioxidant and free radical scavenger status in periodontal disease. A total of 40 subjects (aged 20-50 years) consisting of 20 test subjects (patients with chronic periodontitis, 10 males and 10 females) and 20 (healthy individuals, 10 males and 10 females) controls were recruited for the study. All the subjects in control and test groups belonged to similar socioeconomical background and were having similar dietary habits. Subjects with a history of antibiotic therapy and antioxidant therapy in the past 6 months and with current infections and other diseases (other than periodontal) were excluded from the study. Subjects and controls were not engaged in tobacco smoking or chewing, or alcohol consumption, and did not suffer from any systemic diseases. The patients were clinically and radiographically evaluated for chronic periodontitis according to the criteria accepted by the American Academy of Periodontology in 1999. It was ensured that patients had teeth with 30% periodontal bone loss and with ≥5 mm deep pockets. The gingiva showed bleeding on probing and had the characteristics of chronic inflammation.

Blood samples were obtained by venous arm puncture and collected in heparinized tubes, and the following tests were conducted.

Methods for serum levels

Estimation of serum lipid peroxidation (in terms of malondialdehyde [MDA]) (Yagi et al. method, 1976): [5]

  • Estimation of SOD [6]
  • Estimation of CAT [7]
  • Estimation of GSHPx [8]
  • Estimation of Vitamin C (Omaye et al., 1979). [9]

  Results Top


Numerical data were expressed as mean ± standard deviation, Student t-test was applied, and P < 0.01 was considered highly significant. [Table 1] represents the serum lipid peroxidation (MDA), and plasma MDA levels were significantly higher in test subjects as compared to controls. In test subjects, male had plasma MDA (n moles/dl) of 310 ± 72 and female had 306 ± 45 whereas in control group, values were 208.8 ± 21.5 and 180 ± 22.5 for males and females, respectively.
Table 1: Lipid peroxidation


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[Table 2] assesses the antioxidant defense status in serum (in terms of SOD, GSHPx, and CAT). SOD levels were significantly lower in test group than in healthy controls. The numerical values of SOD in U/mgHb are 2.1 ± 0.2 for males and 1.6 ± 0.4 for females as compared to healthy males (3.15 ± 0.25) and females (3.1 ± 0.25).
Table 2: Antioxidant defense statuses


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[Table 3] shows that there is a significant reduction in the level of Vitamin C in test group as compared to controls. The level of Vitamin C (μmol/L) is 35 ± 5 (males) and 30 ± 4 (females) in test group and 52 ± 5 (males) and 50 ± 4 (females) in controls.
Table 3: Free radical scavenger activities


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  Discussion Top


ROS are produced in animals and humans under various physiological and pathological conditions. ROS are produced continuously in living cells as byproducts of normal metabolism, during the metabolism of xenobiotics and during exposure to high temperature or radiation. They also form due to the leakage of electrons from electron transport chains and the generation of superoxide or hydrogen peroxide by peroxisomal enzymes. [3] Deliberate generation of free radicals occurs during phagocytosis as part of the bactericidal reaction. [10]

Antioxidants are present in all body fluids and tissues and protect against endogenously formed free radicals, usually produced by leakage of the electron transport system. [11] Antioxidant enzymes such as SOD and GSHPx provide protection within cells while low-molecular-weight scavenging antioxidants are present in extracellular fluid. These include ascorbic acid, α-tocopherol, and β-carotene. In addition, dietary-derived components such as uric acid, nonprotein thiols, and GSH also act as antioxidants, [11] as does albumin found in plasma and saliva. [12],[13] Ascorbic acid is believed to be the major aqueous antioxidant, while α-tocopherol protects against lipid peroxidation. [14]

In the present study, we have tried to assess free radical scavengers (Vitamin C), serum lipid peroxidation (in terms of MDA), and the antioxidant defense status in serum (in terms of SOD, GSHPx, and CAT) in patients with periodontal disease and controls. In chronic periodontitis, progressive generation of free radicals takes place leading to increased lipid peroxidation and decrease in antioxidant enzyme defense status. Our study confirms that lowered level of SOD, CAT, and GSHPx is associated with hyper lipid peroxidation in periodontal disease. Free radical-induced tissue injury has been demonstrated to be increased in individuals with periodontitis. [15] Enhanced lipid peroxidation was reported in the periodontal tissues of cats with gingivitis. [16] In preeclamptic women with periodontitis, there was a significant reduction of SOD activity in saliva, GCF, and serum. [17]

Panjamurthy et al. in their study found that the level of enzymatic antioxidant activity was significantly higher in the plasma, erythrocytes, erythrocyte membranes, and gingival tissues in the periodontitis sufferers, whereas the levels of nonenzymatic antioxidants were significantly lower (except for reduced GSH in the gingival tissues) relative to the parameters found in healthy subjects. [18] In a study carried out by Zhang et al., it was found that the levels of total oxidative status (TOS) and SOD were significantly higher in chronic periodontitis patients than in control group and after periodontal treatment, there was a significant decrease in serum, saliva, GCF TOS, and SOD level. [19]

In periodontal disease, there is an increase in MDA levels due to increase in oxidative stress and production of ROS. Increased oxidative stress releases certain compounds from the tissue membrane which activate PMN leukocytes to release more free radicals. [20] Free radical scavenger such as Vitamin C is lowered in patients than in controls. Vitamin C is a powerful reducing agent and an important water-soluble vitamin for humans and certain other animals. It has been shown to scavenge superoxide radicals, hydrogen peroxide, and singlet oxygen. Vitamin C also protects plasma lipids against lipid peroxidation and has an important role in the regeneration of α-tocopherol. [21]

Enhanced oxidative stress in cells results in the activation of free radical scavenging enzymes to neutralize the toxic effect of ROS. SOD and CAT, respectively, protect the cell against ROS by scavenging superoxide radicals and hydrogen peroxide, which cause damage to the structure and function of membrane assembly. [22] GSHPxs are major enzymes that remove hydrogen peroxide generated by SOD in the cytosol and mitochondria by oxidizing reduced GSH to its oxidized form (GSSH). GSH and GSHPx have been documented to have regulatory effects on cell proliferation. [3] Increased plasma GSHPx activity has been reported as an indirect indicator of oxidative stress. [23] It was also reported that reduced GSH effectively protects vital cell components from structural damage during hyper-inflammation. [24]

The results of the present study showed that the disturbance in the endogenous antioxidant defense system due to the over-production of lipid peroxidation products at inflammatory sites can be related to a greater degree of oxidative stress in patients with periodontitis.


  Conclusion Top


Periodontal disease is clearly an important and potentially life-threatening condition, often underestimated by health professionals and the general population. The concept of the role of free radicals in the initiation and progression of periodontal disease points to the purposefulness of including bio-oxidants and other bioregulatory substances in the pharmacological prevention of these diseases. It is now of importance to determine the possible contribution of diet to salivary antioxidant status. In the future, antioxidant supplementation may be used in the treatment or prevention of these chronic diseases of the oral cavity.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

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O'Leary TJ. The impact of research on scaling and root planing. J Periodontol 1986;57:69-75.  Back to cited text no. 1
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2.
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Yagi K. A simple fluorometric assay for lipid peroxides in plasma. Biochem Med 1976;15:212-16.  Back to cited text no. 5
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Canakci V, Yildirim A, Canakci CF, Eltas A, Cicek Y, Canakci H. Total antioxidant capacity and antioxidant enzymes in serum, saliva, and gingival crevicular fluid of preeclamptic women with and without periodontal disease. J Periodontol 2007;78:1602-11.  Back to cited text no. 17
    
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Zhang WD, Wang XL, Yang YZ, Chan CX. Lipid peroxidation levels, total oxidant status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic periodontitis patients before and after periodontal therapy. Aust Dent J 2010;55:70-8.  Back to cited text no. 19
    
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Chapple IL, Brock G, Eftimiadi C, Matthews JB. Glutathione in gingival crevicular fluid and its relation to local antioxidant capacity in periodontal health and disease. Mol Pathol 2002;55:367-73.  Back to cited text no. 24
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]


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