The Effects of Obesity on Non Surgical Periodontal Therapy (EONSPT)

The investigators' earlier study reported a high prevalence of chronic periodontitis among obese Malaysian adult population. Non-surgical periodontal therapy (NSPT) has been shown to effectively reduce microbial load and contributes to reduction in periodontal parameters and inflammatory burden up to 6 months post-therapy. This study will cast light on the effects of obesity on chronic periodontitis (CP) patients following NSPT. The objectives of the study were to quantify and to compare the periodontal pathogens, serum and salivary interleukins in obese and non obese with CP following NSPT.

Obesity is a health concern, associated with complex diseases such as diabetes, hypertension as well as chronic periodontitis. The prevalence is estimated as 24% worldwide, 3% for South East Asia, and 27.2% for Malaysia. Prevalence of CP is increasing, with 10-15% reported in various adult populations and estimated 5-20% categorised as severe CP. In Malaysia, the prevalence of severe CP is estimated as 18%. The first paper on the relationship between obesity and periodontal disease reported that obese-hypertensive rats are more likely to have periodontal tissue deterioration than normal rats. Subsequent study reported an induction of expression of Tumour Necrosis Factor (TNF) -a gene in obese mice and thus proposed TNF-α represents a key mediator of obesity-linked insulin resistance. This was strongly supported by an extension study on human adipose tissue. A model was proposed linking inflammation to obesity, diabetes, and periodontal infection in 2005. Subsequent studies found association between obesity and increased risk for CP in the United States, Japanese and Jordanian adult populations. Adipose tissue produces a number of adipokines linked to inflammation, including adiponectin, interleukin (IL)-1β, IL-6, TNF-α, Monocyte Chemoattractant Protein (MCP)-1 and Macrophages Migrant Inhibitory Factor (MIF). Increased in circulating levels of pro-inflammatory cytokines such as TNF-α and IL-6 are strongly correlated with obesity, insulin resistance, hyperglycemia and diabetes mellitus. These cytokines also stimulate the synthesis of C-reactive protein (CRP) and fibrinogen by liver, as CRP is known for its role in inflammation, atherosclerosis and insulin resistance. In addition, these cytokines are also secreted from adipose tissues are involved in the pathophysiology of both obesity and periodontitis. Obese individuals have higher levels of circulating TNF-α and IL-6 when compared to normal weight individuals. This may increase the risk of destructive periodontal diseases development. Interestingly, studies on the immune response to periodontal pathogens showed that TNF-α enhanced the immune response to these pathogens. Periodontal health is accomplished through non-surgical periodontal therapy (NSPT), which includes oral hygiene education (OHE) and scaling and root planing (SRP). NSPT has been reported to effectively reduce microbial load and contributes to reduction in periodontal parameters and inflammatory burden up to 6 months post-therapy. In a general population, NSPT has been shown to induce a shift from a pre-dominant gram-negative to a gram-positive subgingival microbiota. The total bacteria count and positives sites of Porphyromonas gingivalis (P gingivalis) and Tannerella forsythia (T forsythia) were significant decreased in treated group compared to control groups. In addition, SRP has markedly reduced these periodontal pathogens: Porphyromonas gingivalis, Tannerella forsythia as well as Prevotella intermedia 24 months post NSPT. Molecular mechanisms between inflammatory cytokines and CP are unclear and warrant further studies to determine whether pro-inflammatory cytokines is the pathogenic factor linking obesity to periodontal infections. To date, there are not many studies that examine the changes in periodontal pathogen, salivary and serum interleukins levels in obese patients with CP following NSPT. Further prospective studies are needed to address this issue and to determine stronger evidence on the association between obesity, periodontal diseases and potential mediating factors following NSPT.

Procedure/Surgery Non surgical periodontal therapy Received OHE, scaling and root planing. OHE includes brushing and flossing techniques, chlorhexidine rinse thrice a day

Procedure/Surgery Non surgical periodontal therapy Received OHE, scaling and root planing. OHE includes brushing and flossing techniques, chlorhexidine rinse thrice a day

Changes in clinical attachment level (CAL) (mean in mm, as a measure of periodontal parameter) in obese and non obese, with chronic periodontitis following NSPT

Changes in microbial profile (mean count of Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia and Actinobacillus actinomycetemcomitans quality and quantity) in obese and non obese, with chronic periodontitis before and after NSPT

Changes in serum interleukins levels (mean value in ng/mL, of TNF-α, IL-1, IL-6 and resistin) in obese and non obese, with chronic periodontitis before and after NSPT

Changes in salivary interleukins levels (mean value in ng/mL, of TNF-α, IL-1, IL-6 and resistin) in obese and non obese, with chronic periodontitis before and after NSPT

Inclusion Criteria: Those who are obese Those whose age are 30 years and above Those who have at least 12 teeth present Exclusion Criteria: Those who have received periodontal treatment within the last 4 months Those who have been on antibiotics within the past 4 months Those who require prophylactic antibiotic coverage, on systemic or topical steroidal anti-inflammatory drugs for the past 4 months, Those who are pregnant or intend to be pregnant Those lactating mothers, mentally handicapped

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