Periodontitis and metabolic syndrome

Background + Aims

• Periodontal diseases have been linked to systemic conditions, including obesity. Meta-analyses show significant associations between chronic periodontitis and obesity, with obese patients exhibiting 81% higher odds of periodontitis compared to normal-weight individuals.
• Metabolic syndrome, encompassing obesity, insulin resistance, and other components, further increases periodontitis risk by 71–109%. However, most studies are cross-sectional, limiting causality insights.
• Biological mechanisms connecting obesity to periodontal health include proinflammatory cytokines, adipokines, and immune system alterations. Obesity-induced inflammation, oxidative stress, and dysregulated cytokine production may exacerbate periodontal destruction. Additionally, white adipose tissue actively produces inflammatory mediators, such as TNF-α and IL-6, which may influence periodontitis progression. Obesity is also linked to altered immune responses, potentially increasing susceptibility to infections, including periodontal disease.
• While the association between obesity and periodontitis is well-documented, the impact of obesity on the response to periodontal treatment remains unclear.
• This systematic review assessed whether treatment outcomes, assessed through periodontal, inflammatory, metabolic, or anthropometric measures, differ among obese, overweight, or normal-weight patients.

Materials + Methods

• Eligibility criteria included both randomised controlled trials (RCTs) and non-RCTs.
• Comprehensive searches were conducted, with no restrictions on language, publication year, or status. References of included articles were manually screened, and authors were contacted for additional data.
• Study selection involved screening titles, abstracts, and full texts, with disagreements resolved by a third reviewer.
• Data were independently extracted into a pre-defined form, focusing on four outcome categories: periodontal, inflammatory, metabolic, and anthropometric parameters.
• Primary outcomes were clinical attachment loss (CAL) and probing pocket depth (PPD), while secondary outcomes included all other parameters.
• The risk of bias for RCTs was assessed using the Cochrane tool, and non-RCTs were evaluated with a modified Downs and Black checklist.
• Quantitative synthesis included pooling studies with comparable weight groups and outcomes.
• A random-effects model was used for meta-analysis, considering heterogeneity assessed through tau² and I² statistics. Prediction intervals were calculated for meta-analyses with three or more trials.

Results

• After screening, 15 studies were included in the review:
  • 10 directly comparing obese/ overweight individuals with normal-weight patients
  • 5 providing additional data upon author request
  • The included studies consisted of 4 RCTs and 11 non-RCTs, all conducted in university settings
• The risk of bias varied, with high risk noted in outcome blinding and allocation concealment for some studies. Non-RCTs displayed serious limitations in methodological design.
• Meta-analyses distinguished between systemically healthy and diabetic patients due to potential differences in periodontal treatment response.
  • For systemically healthy patients:
    • No significant differences were observed in periodontal parameters, except for a greater decrease in TNFα and glycated haemoglobin levels in overweight/obese patients in isolated studies.
  • For patients with diabetes:
    • Significant increases in adiponectin (an anti-inflammatory protein) and decreases in leptin (a pro-inflammatory protein) levels were noted in overweight/obese groups compared to normal-weight groups.
• The overall quality of evidence was rated low or very low due to inclusion of non-RCTs, inconsistent findings, and small sample sizes.
• Subgroup and sensitivity analyses were limited, with additional exploratory analyses suggesting further research is needed to clarify the influence of obesity on periodontal treatment outcomes.

Limitations