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Table of Contents   
ORIGINAL RESEARCH  
Year : 2020  |  Volume : 31  |  Issue : 4  |  Page : 520-525
GCF and serum levels of omentin in periodontal health and disease of diabetic and non-diabetic individuals: A comparative study


1 Department of Periodontology, Dr. D.Y. Patil Dental College and Hospital, Dr. D.Y. Patil Vidyapeeth, Pune, Maharashtra, India
2 Public Health Dentistry, Dr. D.Y. Patil Dental College and Hospital, Dr. D.Y. Patil Vidyapeeth, Pune, Maharashtra, India

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Date of Submission24-Oct-2018
Date of Decision09-Aug-2019
Date of Acceptance29-Oct-2019
Date of Web Publication16-Oct-2020
 

   Abstract 


Background: Omentin is an adipocytokine secreted by visceral adipose tissue cells associated with the action of insulin-increasing, insulin-facilitated glucose uptake. Aim: The aim of this study was to compare and evaluate the levels of omentin in gingival crevicular fluid (GCF) and serum of periodontally healthy individuals and chronic periodontitis (CP) patients with and without type 2 diabetes mellitus (T2DM). Settings and Design: A hospital-based comparative study was conducted amongst 40 subjects of age group 30–50 years. Methods: Subjects were divided into four groups, group I (10 healthy individuals), group II (10 T2DM), group III (10 CP only) and group IV (10 patients with CP and T2DM). Clinical and systemic parameters assessed were gingival index (GI), plaque index (PI), probing pocket depth (PPD), periodontal attachment level (PAL) and glycated haemoglobin (HbA1c). Serum and GCF samples were collected and analysed for omentin levels using the enzyme-linked immunosorbent assay (ELISA). Results: Although the mean GCF omentin levels were highest in group I and lowest in group IV, it was not statistically significant. However, the serum omentin levels were statistically significant, showing the highest mean level in group I and lowest in group IV and serum levels were statistically significant. Also, the serum omentin levels had a negative correlation with HbA1c. Conclusion: The levels of omentin reflect the diabetic status of an individual, which suggests that omentin can be a potential anti-inflammatory marker and a therapeutic agent for conditions like CP and T2DM.

Keywords: Diabetes, GCF, periodontitis, serum

How to cite this article:
Bagwe S, Gopalakrishnan D, Mehta V, Mathur A, Kapare K, Deshpande A. GCF and serum levels of omentin in periodontal health and disease of diabetic and non-diabetic individuals: A comparative study. Indian J Dent Res 2020;31:520-5

How to cite this URL:
Bagwe S, Gopalakrishnan D, Mehta V, Mathur A, Kapare K, Deshpande A. GCF and serum levels of omentin in periodontal health and disease of diabetic and non-diabetic individuals: A comparative study. Indian J Dent Res [serial online] 2020 [cited 2020 Nov 24];31:520-5. Available from: https://www.ijdr.in/text.asp?2020/31/4/520/298420



   Introduction Top


The complex interaction between the oral microbial biofilm present on the tooth and host immunoinflammatory response gives rise to an irreversible disease termed periodontitis, which results in the destruction of the soft and hard tissue components of the periodontium, ultimately, resulting in tooth loss.[1] Once regarded as a disease of the oral cavity, periodontitis in recent times has shown to be a hub of chronic infection spreading systemically. It has been linked to systemic diseases, such as cardiovascular diseases (CVDs), obesity, pregnancy, chronic kidney disease (CKD), metabolic syndrome, rheumatoid arthritis (RA) and diabetes mellitus (DM).[2],[3]

DM, an endocrinal metabolic disorder, which is characterised by chronic hyperglycaemia, is steadily making its presence felt globally with 422 million cases of diabetes,[4] as per the World Health Organization (WHO) in 2016. Periodontitis is suggested as the sixth complication of DM,[5] and a bi-directional relationship has been established between periodontitis and T2DM.[3] Thus, the presence of periodontal disease in a diabetic patient holds a serious threat to health, proven by studies that state that periodontitis leads to worsening of the glycaemic status and further complications.[3]

Omentin is an adipocytokine secreted by visceral adipose tissue cells consisting of 313 amino acids and weighs 40 kDa, exhibiting a variety of biological properties that are anti-inflammatory, anti-atherogenic and anti-diabetic in nature.[6],[7] Omentin as an anti-inflammatory adipokine has been studied in rheumatoid arthritis (RA) by Senolt et al.[8] and Crohn's disease by Schäffleret al.,[9] and it has shown to enhance the action of insulin by increasing insulin-facilitated glucose uptake by subcutaneous tissue and omental adipocytes.[10]

Pro-inflammatory mediators like interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-α) are common to both chronic periodontitis (CP) and type 2 diabetes mellitus (T2DM). Omentin inhibits the TNF-α-induced cyclooxygenase (COX2) expression[11] and is also independently associated with T2DM as reported by Yan et al.[12] However till date, there is no study reported to estimate the levels of omentin in periodontal health and disease associated with T2DM. It may also aid in relating T2DM and CP.

Hence, the aim of this study is to evaluate and compare the levels of omentin in gingival crevicular fluid (GCF) and serum of healthy individuals and CP patients with and without T2DM.


   Materials and Methods Top


Forty subjects aged 30–50 years (15 males, 25 females) were selected from the out-patient department (OPD) of periodontology in a period of 1 year. CP patients were selected on the basis of gingival index (GI)[13] ≥1, plaque index (PI)[14] ≥1 and probing pocket depth (PPD) ≥5 mm by measuring the distance from the gingival margin to the bottom of the periodontal sulcus on the buccal, lingual, mesial and distal surface of each tooth, periodontal attachment level (PAL) ≥3 mm and the distance from the cementoenamel junction to the bottom of the periodontal sulcus on the buccal, lingual, mesial and distal surface of each tooth and evidence of radiographic bone loss on orthopantomogram (OPG).[15]

Patients were excluded if there was a history of prolonged use of antibiotics/steroids/immunosuppressive agents/aspirin/anti-coagulants in the preceding 3 months; systemic diseases, such as hypertension and HIV; bone disorders; renal disorders; radiation therapy; infectious diseases; aggressive periodontitis; cancer patients; pregnant/lactating women, patients with T1DM or patients who have received periodontal therapy in preceding 6 months.

The subjects were divided into four groups as follows:

  1. Group I (10 healthy individuals)
  2. Group II (10 T2DM only)
  3. Group III (10 CP patients only)
  4. Group IV (10 patients with CP and T2DM)


Detailed case history and clinical and radiographical examination were done for each patient and informed consent was obtained.

Full mouth periodontal examination was conducted for the selected patients that included the clinical parameters, and they were assessed for bone loss using OPG. The glycated haemoglobin (HbA1c) test was done for patients in all the groups. Patients with moderately controlled T2DM and with HbA1c in range of (7.0 - 8.0 gm %)[16] were selected for groups II and IV.

Gingival crevicular fluid samples

Before the collection of GCF, to avoid its contamination with blood associated with bleeding on probing of inflamed sites, the GCF was collected on the subsequent day. In groups I and II, to ensure that an adequate amount of GCF was collected, multiple sites with the absence of inflammation were sampled. In groups III and IV, a single site showing PAL ≥3 mm and PPD ≥5 mm, signs of clinical inflammation along with radiographic loss of bone was confirmed, and the site was selected for sampling. In all four groups, maxillary sites were selected for GCF collection to prevent contamination of saliva. After drying the selected site with a blast of air, the supragingival plaque was removed without touching the marginal gingiva, and the selected area was then isolated using cotton rolls. This was followed by GCF collection in black-coloured volumetric capillary pipettes (Sigma-Aldrich), which were calibrated from 1–5 μL. The collected GCF was immediately transferred to plastic vials containing phosphate buffer solution and stored at −70°C until time of assay.[17]

Serum samples

Two millilitres of blood was collected from the antecubital fossa by venepuncture using a 20-gauge needle with a 2 ml syringe and immediately transferred to the test tube. A blood sample was allowed to clot at room temperature and after 1 h was centrifuged at 3,000 revolutions per minute (rpm) for 15 min to separate the serum component. The serum was stored at −70°C until the time of the assay.[17]

Laboratory diagnosis of omentin

The omentin levels in GCF and serum were measured using a commercially available enzyme-linked immunosorbent assay (ELISA) kit (Elab Science) as instructed by the manufacturer.

Statistical analysis

The data was analyzed with Statistical Package for Social Sciences (SPSS) for Windows, version 26.0 (IBM Corp., Armonk, N.Y., USA). Confidence intervals (CIs) were set at 95% and values of P < 0.05 were interpreted as statistically significant. Intergroup analysis was carried out using one-way analysis of variance (ANOVA) and Tukey's posthoc test. An unpaired t-test was applied to compare PPD and PAL for groups III and IV. Spearman's rank correlation (r) coefficient test was used to evaluate the correlation between omentin and HbA1c.


   Results Top


[Table 1] and [Figure 1] show age and demographic information for all the groups. The impact of age and gender on omentin levels was nullified by including the same number of men and women in each group and selecting participants who were in the age group of 30–50 years. Although the mean GCF omentin levels were highest in group I and lowest in group IV, it was not statistically significant. However, serum omentin levels were statistically significant, showing the highest mean level in group I and lowest in group IV and serum levels were statistically significant (P < 0.05). PPD and PAL measured for groups III and IV, [Table 2] showed no statistically significant results. On co-relating serum omentin with GI and PI, it was found to be weak but positive with group II. The GCF levels were weak and positive when correlated with GI levels in groups III and IV. The GCF omentin level was weak and negative in group I when compared with PI but weak and positive in group II, III and IV. A weak correlation was observed between serum and GCF omentin levels and clinical parameters, as shown in [Table 3]. The relation between HbA1c and serum omentin levels are shown in [Figure 2] and [Figure 3]. Statistically significant relation is seen in serum omentin levels and HbA1c(P < 0.05). No statistically significant relation was seen between GCF omentin and HbA1c.
Table 1: Descriptive statistics of the study population

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Figure 1: Comparison between all the groups

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Table 2: Comparison of variables between the various study groups

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Table 3: Results of Spearman's rank correlation (r) coefficient test

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Figure 2: Scatter plot showing the correlation between HbA1cand omentin serum concentration in group III * HbA1c = Glycated haemoglobin

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Figure 3: Scatter plot showing the correlation between HbA1cand omentin serum concentration in group IV HbA1c = Glycated haemoglobin

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   Discussion Top


Owing to a steep rise in patients with T2DM, adipose tissue has gained recognition as an endocrine organ, which produces adipokines that are bioactive in nature and play a crucial role in insulin sensitivity.[18] Certain adipokines exhibit pro-inflammatory properties (resistin and visfatin) and some exhibit anti-inflammatory properties like (adiponectin) while a few display both.[19]

As most of these adipokines act on insulin sensitivity and inflammation, their altering effects have been demonstrated on patients with T2DM as an increase of the pro-inflammatory adipokines and decrease in their anti-inflammatory counterparts. T2DM and periodontitis display a bi-directional relationship during which certain pro-inflammatory mediators like TNF-α, IL-1 and IL-6 are released, which cause destruction of the alveolar bone, as well as cause insulin resistance systemically, thus, hampering the overall health of the individual.[3]

A recent study by Ogawa et al.[20] has highlighted the role of adipokines in T2DM and periodontitis. While the levels of certain pro-inflammatory adipokines like resistin[21] and visfatin[22] have been observed to be elevated in subjects with T2DM with CP, their anti-inflammatory equivalents like adiponectin[23] reduced in the subjects with the same condition. However, the role of newly discovered adipokines in CP is yet to be learnt.

Of late, the role of omentin in CP needs to be studied. Omentin is a unique adipokine that has been identified from a cDNA library from visceral omental adipose tissue by Yang et al.[24] in 2003. The gene for omentin is placed at 1q22–q23, a chromosomal region that has been linked to type 2 diabetes populations.[25],[26]

Omentin has two homologous isoforms omentin-1 and omentin-2, of which, omentin-1 is the major circulating form in plasma.[9] Omentin has been identified as a “good” adipokine,[7] and it has played a pivotal role in diabetes,[27] atherosclerosis,[28] obesity,[29] end-stage renal disease,[30] RA,[8] osteoarthritis,[31] Crohn's disease,[9] polycystic ovary syndrome (PCOS),[32] acute myocardial infarction,[33] pulmonary diseases[34] and cancer.[35]

Omentin regulates the inflammatory process by acting as an anti-inflammatory cytokine by inhibiting the TNF-α-induced COX2 expression via inhibiting c- Jun N-terminal kinase signal through activation of 5xs242; adenosine monophosphate-activated protein kinase (AMPK)/endothelial nitrate synthetase (eNOS)/nitric oxide (NO) pathway.[11] Anin vitro study by Yang et al.,[10] has explained the uptake of glucose by insulin in the presence of omentin by cultured adipocytes.

The role of omentin in periodontal disease is not completely explored. Only one study has described the levels of omentin.[19] in the GCF of periodontally healthy and CP patients with and without T2DM before and after non-surgical periodontal therapy (NSPT). However, they have not described the serum levels of omentin as periodontitis also plays a role in systemic inflammation. Our study investigates and compares the level of omentin in GCF and serum of periodontally healthy individuals and CP patients with and without T2DM.

In the present study, it was observed that the GCF and levels of omentin were highest in group I (individuals with healthy periodontium) and least in group IV (CP subjects with T2DM). The results of this study corroborated with a similar study conducted by Doǧan et al.,[19] where the GCF levels of omentin-1 were decreased before non-surgical periodontal therapy but increased after the treatment. This low GCF level of omentin can be attributed to inflammation in CP and T2DM, which is responsible for altering the immune-inflammatory equilibrium of the host[36] by releasing cytokines that can downregulate the levels of omentin. However, a statistically significant difference was not observed in the GCF levels of omentin owing to the similarity in the balance between proinflammatory and anti-inflammatory mediators in healthy individuals and T2DM subjects as described in a review by Javed et al.[37]

The serum levels of omentin were decreased in T2DM with CP subjects, which were similar to the serum omentin levels in patients with impaired glucose regulation, T2DM, 36 gestational diabetes mellitus (GDM),[38] T2DM with ischemic heart disease,[39] diabetic retinopathy (DR),[40] RA[8] and Crohn's disease.[9]

In this study, the levels of omentin were assessed in GCF. As the GCF passes through the inflamed tissue, it seems to carry molecules implicated in the process of destruction.[41] As omentin is an anti-inflammatory systemic marker, serum samples were collected. Shibata et al.[42] has suggested that omentin could serve as a biomarker for metabolic and CVDs. A review article by Tan et al.[43] has stated that omentin has been patented to diagnose diseases like obesity, obesity-associated subacute inflammation, CVDs and metabolic diseases.

The strength of this study is that it is one of the few studies highlighting the level of omentin in CP patients with and without T2DM in both GCF and serum. A weak correlation suggests that large sample size is required. Also, patients with only T2DM were included. Patients with CVDs or RA with periodontal diseases should have been included.


   Conclusion Top


The levels of omentin were highest in the group of systemically as well as periodontally healthy subjects and lowest in subjects who had T2DM with CP, which suggests that both these conditions play a role in decreasing the GCF and serum concentration of this anti-inflammatory marker. The levels of omentin also reflect the diabetic status of an individual. Omentin can thus serve as a biomarker in periodontitis and be developed at the molecular level as an anti-inflammatory therapeutic agent to combat the effect of periodontal inflammation.

Grant information

Grant number: N0.3/3/March-2016/PG-Thesis-HRD (23)

The thesis manuscript titled “GCF and Serum Levels of Omentin in Periodontal Health and Disease of Diabetic and Non-diabetic individuals: A Comparative Study” received a grant of INR 25,000/- (Twenty-five thousand only) from the Indian Council of Medical Research (ICMR), New Delhi in 2016.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Correspondence Address:
Dr. Vini Mehta
Department of Public Health Dentistry, Dr. D.Y. Patil Dental College and Hospital, Pune - 411018, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijdr.IJDR_796_18

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