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Systematic Review Wit Hmeta Anlysis on Obesity and Periodontal Disease

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Influence of obesity on the effect of non-surgical periodontal therapy - a systematic review

  • Philipp Sahrmann1,
  • Oliver A. Schmidlin2,
  • Christian Heumann3,
  • Jürg Hans Beer2 &
  • Patrick R. Schmidlini

BMC Oral Health volume 16, Article number:90 (2016) Cite this article

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Abstract

Groundwork

Obesity and periodontitis are of import chronic wellness problems. Obesity is associated with an increased prevalence of periodontitis. Whether obesity also affects the result of not-surgical periodontal therapy is to engagement nevertheless unclear.

Methods

A systematic review of studies referenced in SCOPUS, MEDLINE, PubMed, Cochrane, CINAHL, Biosis and Web of Scientific discipline was performed. Titles, abstracts and finally full texts were scrutinized for possible inclusion by ii independent investigators. Quality and heterogeneity of the studies were assessed and the study designs were examined. Probing pocket depth reduction was analyzed as primary surrogate parameter for therapeutic success after not-surgical periodontal therapy.

Results

One-hundred-and-fifty-nine potentially qualifying studies were screened. Eight studies fulfilled the inclusion criteria and were analyzed. 3 of viii studies failed to evidence an influence of obesity on pocket depth reduction after non-surgical therapy. The remaining five studies documented a clear negative event on the consequence of non-surgical periodontal therapy. The finally included studies did not correspond to the highest level of quality (RCTs). Due to the heterogeneity of the data a meta-analysis was not possible.

Conclusion

The literature on the effect of obesity on the treatment effect of non-surgical periodontal therapy remains controversial. The information, nonetheless, support that obesity is non only a factor associated with poorer periodontal health but might besides result in inferior response to non-surgical treatment of periodontitis.

Peer Review reports

Groundwork

The prevalence of obesity is increasing worldwide and is becoming one of the almost important health hazards [1], every bit obesity is highly associated with increased overall morbidity and bloodshed [ii].

Obesity is divers with a trunk mass index (BMI; body weight in kilogram divided past the foursquare of the tiptop in meters (kg/m2)) of at to the lowest degree 30.0 kg/m2 [3], whereas overweight is defined with a BMI of 25–29.ix kg/mii. Normal weight is characterized by a BMI ranging between 19 to 24.ix kg/1000ii [4]. In this context, BMI seems a valuable parameter to predict obesity-related illness risks in a wide range of populations [2]. In that location are, notwithstanding, some limitations: Firstly, risk assessment past BMI is less applicable in persons over 65 years of age because they generally have a college torso fat content for the aforementioned BMI. Secondly, the abdominal (fundamental, visceral, android) type of obesity, which is more than often seen in men, is associated with higher morbidity than the rather female person type of gluteofemoral (peripheral, gynoid) obesity and, thirdly, the BMI cut-off points for overweight and obesity are too high for Asian people [2]. In addition, current large studies have indicated that measurement of waist circumference (WC) or waist-to-hip-ratio (WHR) may be a better disease risk predictor than BMI [5, six]. There is, notwithstanding, currently intensive inquiry and debate every bit to whether BMI, WC, WHR, or all of them should be used to assess disease hazard [two].

For the purpose of this systematic review, however, but BMI is the most frequently reported information of obesity in a large number of studies.

Adipose tissue contains usually 5-10 % macrophages, but the adipose tissue of obese patients shows up to 60 % macrophage infiltration [iv]. Adipocytes secrete bioactive molecules called adipokines, that can modify or trigger inflammation and fat metabolism locally or systemically as signaling molecules to liver, muscle and endothelium [4]. Therefore, the adipose tissue can be considered as an important metabolically agile endocrine organ [four].

This explains how obesity acts every bit a chance factor for several chronic diseases: Hypertension, type 2 diabetes, dyslipidemia, and coronary centre disease are so closely related to obesity that obesity itself is often considered to exist a systemic affliction. This disease also affects dental wellness [7]. Accordingly obese persons require attention of physicians and dentists [2].

Amid dental pathologies, periodontitis is a very mutual, primarily bacterial inflammatory disease, which destroys teeth surrounding soft tissues and bone. Information technology leads to pocket germination and ultimately to loss of teeth if no constructive treatment is applied [eight]. Periodontitis is no longer considered only an oral wellness event only as well a public health problem, equally it constitutes a risk cistron for cardiovascular conditions, poor glycemic control in diabetics and agin effect of pregnancy [4, 8]. These correlations coincide with obesity and general health.

Recently, information technology has been suggested that obesity is a possible risk factor for periodontitis [eight]. One report identified obesity even every bit the second strongest risk factor for periodontitis preceded only past smoking [9]. The first written report on the human relationship between obesity and periodontal disease appeared in 1977. Perlstein and co-workers [10] institute greater alveolar bone resorption in obese than in non-obese rats. Under salubrious oral conditions, obesity itself did non promote periodontal damage, but in the presence of bacterial plaque accumulation periodontal inflammation was more severe in obese than in non-obese animals. With concomitant arterial hypertension, plaque accumulation caused fifty-fifty more than pronounced periodontal destruction than with obesity alone. These results advise that a combination of risk factors, such as the i divers by the metabolic syndrome, elicit a more astringent periodontal event [10, 11]. Chaffee et al. [12] found in their meta-analysis an increased prevalence odds ratio for obesity amongst subjects with periodontal disease of approximately i-tertiary, a greater hateful clinical attachment loss (CAL) among obese individuals, a higher BMI among subjects with periodontal affliction, and a trend for linear increment in the odds of periodontal illness with increasing BMI [4, 12]. Finally the association reported betwixt obesity and periodontitis was less potent than that reported between periodontal disease and agin pregnancy outcomes [12, 13] or cardiovascular events [12, 14]. There seems, still, to be a stronger obesity-periodontitis association in women, non-smokers and younger individuals than in the general adult populations [12]. In add-on, smoking remains some other well-studied predisposing cistron for periodontitis [12, 15, 16]. Thus, BMI and smoking share a complex human relationship [17]. This relationship tin can be inverse in certain populations [12, 18, nineteen].

The biological mechanism by which obesity predisposes to periodontitis is not fully understood [8]. Compared to individuals with normal weight individuals with obesity have college levels of circulating tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-half dozen), which are also secreted from adipose tissue and are involved in the pathophysiology of both obesity and periodontitis. Non surprisingly, serum levels of these cytokines subtract with loss of weight [xx].

The objective of this systematic review was to study the hypothesis whether the clinical issue, in terms of pocket depth reduction, subsequently non-surgical periodontal therapy in not-obese is amend than in obese individuals. To verify this hypothesis, we systematically reviewed all retrievable, qualitatively adequate clinical investigations, which focused on this topic.

Methods

The review was conducted according to the PRISMA criteria [21]. The research question was explored using the PICO method [22). The focused question addressed was:

Does non-surgical periodontal therapy (I) have a different outcome in obese chronic periodontitis patients (P), than in not-obese chronic periodontitis patients (C), regarding periodontal pocket depth reduction as the chief clinical periodontal parameter (O).

Search strategy and review process

An electronic search of SCOPUS, MEDLINE, PubMed, Cochrane, CINAHL, Biosis and Web of Science was carried out considering articles published up to January 2016 in English language or German linguistic communication. The search was performed in two steps. The first electronic search started at 20.xi.14 and an update has been washed at v.ane.16.

This is shown in Table i. For the database search, a combination of subject headings (MeSH terms and CINAHL headings) and costless text search was used. An example of a detailed strategy (Medline/OvidSP) is shown in Table 2.

Tabular array 1 Search protocols with the respective number of references dated from November eleven 2014 (ane) and Jan 1 2016 (2)

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Table 2 Medline search strategy

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The same search protocol was practical to all databases.

Two of the authors (FAG, PRS) screened the titles for potential eligibility co-ordinate to the inclusion criteria. Based on the abstract screening, 18 studies were selected for total text review. Scores were independently allocated past both authors to each publication according to their suitability for the present review (see inclusion criteria). Whatsoever discrepancies were resolved by consensus.

Inclusion criteria

To be included studies had to be clinical interventional studies regarding the outcome of non-surgical periodontal therapy in obese or non-obese patients. The studies had to display the diagnosis of chronic periodontitis. Key parameters to be reported were data for pocket probing depth (PPD) and BMI.

Exclusion criteria

Studies were excluded for the following reasons: animal studies, case reports, commentaries, unsuitable exposure or effect measures, confounding medical diagnoses (e.g. pregnancy or any systemic disease, such every bit diabetes, in add-on to metabolic syndrome), misreckoning systemic medical treatments such every bit immunosuppressive treatments, cortisone or antibody treatment as well as confounding local treatments such as treatment of peri-mucositis, gingival overgrowth or surgical periodontal handling. Studies including either the diagnosis of aggressive periodontitis or of peri-implantitis were excluded as well.

Consequence measures

The primary outcome measure is PPD after non-surgical periodontal treatment.

Data extraction

A list with exclusion reasons for each newspaper was generated. Total number of patients, demographic data, origin of written report, outcome measurements two, 3, 6 and 12 months after therapy and the impact of obesity on the treatment-outcome were extracted. In addition, the exact definition of chronic periodontitis, the assessment of the periodontal illness and the number of smokers included in the studies were summarized. Data on the individual definition of obesity and the systemic examinations were also nerveless. Non-surgical periodontal treatment measures, treatment time, periodontal maintenance and agin events were also recorded for each written report separately (Tables iii, 4, 5, six and vii).

Table three Excluded studies

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Table 4 Probing pocket depth (PPD [mm]) every bit master outcome variable

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Table 5 Definition of periodontitis, periodontal assessment and definition of smoking

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Tabular array vi Definition of obesity and systemic examination

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Table seven Not-surgical periodontal treatment, treatment time and limitations

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The quality of the included studies was assessed through the Newcastle-Ottawa Quality Cess Scale (Tabular array 8).

Table 8 Newcastle – Ottawa Quality Assessment Scale

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Results

Choice of studies

Initially, 159 studies were identified by electronic search by the ii reviewers (FAG, PRS). Full text analysis of the 18 potentially qualified reports led to exclusion of ten other studies. Additional five titles [23–27] were identified by hand search but after full text analysis, all these articles had to exist excluded based on the inclusion and exclusion criteria (Tabular array iii). Therefore, 8 publications [8, 28–34] from the electronic and mitt search fulfilled the criteria. Notwithstanding, it was not possible to compare the raw data and so that we had to reduce our assay to a qualitative analysis. This process is summarized in a flow-chart (Fig. 1).

Fig. 1
figure 1

PRISMA 2009 flow diagram

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Summary of studies: characteristics (PICO)

Total number of patients, demographic information, origin of study, outcome measurements 2, iii, 6 and 12 months later on therapy and the touch of obesity on the handling-outcome are summarized in Table 4.

Definition of chronic periodontitis, periodontal assessment and the amount of smokers included are depicted in Table 5.

The definition of obesity and systemic examination were summarized in Tabular array six. Non-surgical periodontal treatment, treatment fourth dimension, periodontal maintenance and limitations are shown in Tabular array vii.

Population

Of the eight finally analyzed studies, clinical trials comprised 516 participants. One study [viii] enrolled only women. The prevalence of smoking among male person patients affected with periodontitis was so high that Al-Zahrani and co-workers [eight] were unable to correct for smoking in the male population. Accordingly, only women were included in their study. Overall the studies comprised betwixt 26 upwards to 260 subjects (Tabular array 4).

The inclusion criteria "historic period" was divers in all but one study [30]. 3 investigations [28, 33, 34] defined the age ≥xviii years. The other studies defined a minimum historic period of thirty years [31, 32] or 35 years [viii]. Duzagac et al. divers an age range from 25 to 55 years (Table 4).

Suvan et al. [34] included smokers into their written report. Lakkis et al. [33] and Eldin et al.(30] did not mention the smoking condition of the patients. All other studies [8, 28, 29, 31, 32] excluded smokers (Table 5).

Patients with diabetes, another important modifier of periodontal health or disease [35] were excluded in 7 studies [8, 28–32, 34]. Lakkis et al. [33] did not report the presence or absence of diabetes.

Intervention/Comparison

Each paper described the periodontal intervention as a not–surgical therapy. All studies [8, 28–34] practical scaling and root planing. Ultrasonic instruments and/or hand instruments were used in all studies (Table 7).

2 papers (8,34] reassessed the PPD 2 months after therapy. Two studies [29, 30] reassessed their patients after iii months. Another two papers [28, 31] re-evaluated the patients later on three and half dozen months and ane study [32] reassessed the PPD three, six and 12 months after therapy. Just Lakkis et al. [33] measured the periodontal pocket depths already iv to 6 weeks later on non-surgical therapy (Tabular array 3). Oral hygiene was instructed additionally to the non–surgical periodontal therapy in all studies (Tabular array seven).

Due to the heterogeneity of the written report designs with respect to issue measures and treatment protocol, every bit well as variation in study population, sample size, and/or statistical methods, a statistical synthesis of the results of the included studies was non possible. And so the authors decided to analyze the papers on a qualitative way [22]. A meta-assay was not possible.

Outcome

Generally obese patients were found to have deeper periodontal pockets at baseline in all studies.

Iii [8, 29, 30] of the eight papers [8, 28–34] reported no major negative bear upon of obesity on response to periodontal therapy in terms of PPD reduction (mm). Al-Zahrani et al. [8] assessed the reduction of PPD (mm) comparison obese with normal–weighted women. At that place was no statistically significant event of obesity on handling outcome. Duzagac et al. [29] assessed the clinical response to non-surgical periodontal treatment, according to the severity of periodontitis based on probing depth < 4 mm vs. ≥ iv mm. Patients with and without obesity showed similar clinical healing in terms of per centum and number of sites with probing depth < 4 mm and ≥ 4 mm. So they failed to show an effect of obesity on the treatment outcome dependent on the severity of the affliction. Eldin et al. [thirty] likewise institute no result when comparison an overweight group with an obese group. The departure between the groups in reduction of PPD was not significant (Table four).

Five [28, 31–34] of the eight papers showed a negative result of obesity on the healing afterward not-surgical periodontal therapy. Bouaziz et al. [28] revealed that normal-weight patients had a better response to periodontal treatment than obese patients. This upshot was specially observed for moderate-to-deep pockets. This fact suggests that the more than severe the periodontitis the more pronounced is the negative consequence of obesity on periodontal treatment outcome. They showed in the multivariate assay that obesity was significantly associated with percentage changes of PD > 5 mm and numbers of improving sites (p ≤ 0.05). In the univariate analysis all periodontal parameters improve more in patients suffering from more astringent periodontitis at baseline. Other patient characteristics, like age, sexual practice, obesity, and WHR, were not associated with periodontal parameter changes. Gonçalves et al. [31] showed that patients with obesity and chronic periodontitis had a lower PDD reduction than patients without obesity. The measurement of the reduction in PPD (mm) at full-mouth sites showed later 3 months a non statistically significant difference (p = 0.08) between the obese group compared to the group without obesity. However after 6 months there was a statistically meaning difference (p = 0.04). At this time point, especially deep sites (PPD ≥ 7 mm) showed a significantly better result in the group without obesity (p = 0.04). Another study of Gonçalves et al. [32] reported that patients with obesity had a significantly greater mean PD (half dozen months p-value = 0.04, 12 months p value = 0.03) than patients without obesity at six and 12 months postal service-therapy. The data of a written report past Suvan et al. [34] corroborated these findings and showed that obesity was an contained impact value of poorer periodontal treatment outcome 2 months after therapy. The extent of the clan between poorer periodontal treatment and obesity was like to that of smoking (p = 0.02). They worked with 260 patients. This secondary analysis consisted of individuals participating in five clinical studies of non-surgical periodontal therapy over a 7-year menstruum. Lakkis et al. [33] selected thirty patients who were obese; fifteen of them had previously undergone bariatric surgery, whereas the other half (n = fifteen) did not loose any weight and served as a control group. The bariatric surgery group reached a statistically pregnant greater mean PPD reduction (0.45 mm versus 0.28 mm) compared with the control (no surgery) group (p = 0.007; Table 4).

Limitations

Some patients could not be reviewed or discontinued the study for personal reasons [28, 29, 31]. Weight loss and pregnancy were additional reasons to exist excluded in the written report of Duzagac et al. [29] (Table vii).

The quality of the included studies was evaluated through the Newcastle-Ottawa Quality Assessment Calibration (Table viii).

Discussion

This review focused on obesity and the outcome after not-surgical periodontal therapy and has shown that currently there is no really robust scientific evidence to reach solid conclusions and recommendations.

Three papers [8, 29, 30] were institute, which did not find whatever statistically significant negative bear on of obesity on the response to not-surgical periodontal therapy, whereas five papers [28, 31–34] showed the opposite, i.eastward. a conspicuously negative influence of obesity on the treatment outcomes.

With regard to the quality of prove, seven included papers [8, 28, 29, 31–34] reported some limitations.

Al-Zahrani et al. [8] included only women. Gonçalves and co-workers [31] did non consistently apply the accepted definitions of overweight and obesity, but rather included the waist-to-hip-ratio (WHR) for their definitions, probably leading to inclusion of patients with a BMI inferior to xxx kg/mtwo into the obesity grouping. Thus the results are hard to interpret and compare with the other studies and are therefore not applicable for patients with a BMI ≥forty kg/thousand2 [31]. All the same, these studies still show a conspicuously ameliorate tendency with regard to the treatment response for patients without obesity every bit divers in their written report. Lakkis et al. [33] chose another interesting manner to find an impact of obesity on the outcome of non-surgical periodontal treatment. They compared obese people who had undergone bariatric surgery (BS) with obese who did not. Afterward weight loss in the BS grouping, a reduction in total adipocytes might have resulted in a decrease in adipokines and pro-inflammatory mediators released by those adipose cells. This systemic inflammatory reduction might take played a role in reducing the insulin resistance resulting in a improve outcome after periodontal therapy every bit suggested by the authors [33]. Some limitations in the specific contour of the obese patients (nondiabetic, non-smoker) in the paper of Bouaziz et al. (28) may restrict the extrapolation of the results to the whole obese population. Furthermore, the small sample size may too limit the power of this study. Duzagac et al. [29] failed to include a control group of periodontally good for you controls with obesity. Additionally the hateful periodontitis parameters were inside the limits of "moderate" periodontitis, and the WHR and BMI values of these obese patients were predominantly below those characterizing morbid obesity. So, the results of this written report may not be extrapolated to those with astringent periodontitis or morbid obesity. The 2nd included study of Gonçalves and co-workers [32] assumes that the high inter-patient variance in adipokine levels may reduce the statistical power to detect handling effects, equally previously reported. The results presented by Suvan et al. [34] may take been influenced by study limitations linked with unequal numbers in BMI categories and sample size. In addition, at that place may take been limitations with regard to the interpretation associated with the post hoc secondary analysis experimental design, although variation in clinical assessment and treatment was minimized past examiner and treatment clinician stability. This study did not plant a higher level of evidence in the context of testify-based wellness care levels of scientific show [34].

Overall, obesity is an obvious, visible stigma and so that the studies cannot be considered blinded. This may be another possible bias in each of the studies.

Five studies [viii, 28, 29, 31, 32] excluded smokers. Since smoking influences periodontal health these studies are biased [ix] and may non exist fully representative for the typical overall population. Overall it appears, nevertheless, that a positive event of normal weight is present in not-smokers [28, 31, 32] and in smokers [34].

Equally mentioned before, the included studies differed in statistical methods, populations, sample sizes, definition of chronic periodontitis, definition of obesity, fourth dimension of upshot measurement, smoking status, periodontal assessment and not-surgical periodontal therapy. Therefore, it was not only impossible to perform a meta-assay just also draw articulate conclusions.

Nonetheless at that place is a consensus in the studies that obesity is associated with different baseline PPD levels. The large cohort in the written report of Suvan et al. [34] and the long term results of Gonçalves et al. [31, 32] may lead to the conclusion that obesity is an important negative factor which influences non-surgical periodontal therapy.

In summary, all studies [viii, 28, 29, 31–34] included in this review validated the efficacy of non-surgical periodontal therapy, except the study of Eldin and co-workers [30] who did not study any efficacy of the therapy (Table iii). Clinically, it appears obvious that a therapy is necessary to reach periodontal health independent of the patient's body mass index.

Considering this systematic review provided only moderate evidence that obesity is an important factor for not-surgical periodontal therapy, future prospective cohort studies are needed to confirm these findings [36]. Such trials should exist of loftier methodological quality. They should control important confounding factors such as smoking condition, severity of chronic periodontitis, severity of obesity. Every patient should become the aforementioned periodontal treatment and periodontal maintenance. Overall, there is a possibility to solve the research question even though blinding of the examiners to obesity or non-obesity status is non practically possible.

Clinicians should know that obesity may accept some influence on periodontal status and are likely to have a negative touch on on the clinical outcome of conservative treatment, even if this systematic review found only five [28, 31–34] out of 8 papers [viii, 28–34] corroborating the influence of obesity on the clinical periodontal effect focusing on PPD as surrogate parameter for periodontal healing.

Clinicians might consider a weight reduction diet every bit an boosted handling for periodontal health with a positive consequence expected after vi and 12 months [31, 32]. Also it should not be neglected that weight control has substantial other beneficial health effects which on their ain justify such a recommendation.

Conclusion

This systematic review indicates a possible negative human relationship between obesity and poorer treatment event in obese patients afterwards not-surgical therapy based on the results of five out of eight studies. Three of these studies denied an impact of obesity on the treatment. The potentially junior healing response could be based on pathophysiological inflammatory models.

Baseline levels showed also a poorer periodontal health in patients with obesity compared with not-obese patients.

No study found any better dental health parameters in obese than in non-obese individuals, and although dental wellness may not be the most of import target for arriving at a about normal body weight, a person who tin keep his or her body weight nigh normal might, in addition to all other established health benefits, count on having meliorate periodontal health than if they are obese.

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Acknowledgment

The authors would similar to thank Mrs. Dr. Martina Gosteli, librarian of the main library of the Academy of Zurich who performed the electric literature search.

This study was supported by the Clinic of Preventive Dentistry, Periodontology and Cariology (Center of Dental Medicine) of the University of Zurich.

Authors' contributions

FAG and PRS conceived the study, participated in its design, did the literature search and drafted the manuscript. PS helped to supervise the methodological correctness of the performed study and the coordination. OAS and JHB provided the required medical theoretical background for this report and participated in the written report design. CH helped with the statistical evaluation of the papers and the tables. All authors carefully read and approved the concluding text.

Competing involvement

The authors declare that they take no competing interests.

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Affiliations

  1. Dispensary of Preventive Dentistry, Periodontology and Cariology, Heart of Dental Medicine, University of Zurich, Plattenstrasse xi, CH-8032, Zurich, Switzerland

    Fabienne A. Gerber, Philipp Sahrmann & Patrick R. Schmidlin

  2. Department of Internal Medicine, Cantonal Hospital Baden, Baden, Switzerland

    Oliver A. Schmidlin & Jürg Hans Beer

  3. Department of Statistics, Ludwig-Maximilians-University of Munich, Munich, Germany

    Christian Heumann

Corresponding author

Correspondence to Patrick R. Schmidlin.

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Gerber, F.A., Sahrmann, P., Schmidlin, O.A. et al. Influence of obesity on the result of non-surgical periodontal therapy - a systematic review. BMC Oral Health 16, 90 (2016). https://doi.org/ten.1186/s12903-016-0272-2

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  • DOI : https://doi.org/10.1186/s12903-016-0272-ii

Keywords

  • Obesity
  • Chronic periodontitis
  • Non-surgical periodontal therapy
  • Outcome

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