Relationship Between Obesity and Periodontal Disease — ROPD  

Obese Clinical Trial

Official title: Relationship Between Obesity and Periodontal Disease

Status Completed

Clinical Trial Summary

Obesity is an epidemic with increasing prevalence in the Asia Pacific region. The first Malaysian national estimate in 1996 of obesity was 5.8%. A systematic review reported a marked increase in obesity in 2003, 2004 and 2006 with 12.2%, 12.3% and 14.0% respectively.

Periodontal disease is a chronic inflammatory disease which results in gingival inflammation, irreversible attachment loss, alveolar bone destruction and eventually tooth loss. Worldwide, the prevalence of periodontitis in the adult population is about 10-15%. Periodontal disease, through inflammation and destruction of the periodontium produces clinical signs and symptoms, some of which may have a considerable impact on quality of life (QoL).

A positive association between obesity and periodontal disease was repeatedly demonstrated worldwide. Obese individuals have elevated levels of circulating TNF- α and IL-6 compared to normal weight individuals. These cytokines decrease after weight loss. Adipokines produced by adipose tissue could be one of the mechanisms mediating the association between obesity and periodontal disease. This suggests that obesity may have the potential to modify the host's immunity and inflammatory system.

This project will extend the existing information on the association between obesity and periodontal disease including QoL aspect to a Malaysia population. It will also improve knowledge on the cellular and molecular mechanisms that underpin obesity-periodontal disease relationship. By extension, this study also will cast light on the effects of periodontal interventions for the subgroup population.

Clinical Trial Description

Obesity is an epidemic with increasing prevalence in most countries in the Asia Pacific region. It is characterized by abnormal or excessive lipid deposition as a result of chronic disproportion between energy intake and energy outflow. The first Malaysian national estimate in 1996 of obesity was 5.8%. A systematic review reported a marked increase in obesity in 1996, 2003, 2004 and 2006 with 5.5%, 12.2%, 12.3% and 14.0%. Obesity is highest among adults of 40-59 years old, is greater risk in women compared to men and is highest among Indians followed by Malays, Chinese and Aboriginals.

Periodontitis and obesity are both chronic health problems, and an association between the two conditions exists. A positive association was repeatedly demonstrated between obesity and periodontal disease in multiple studies around the world.

Periodontal disease is a chronic oral infection, in which destruction of tooth supporting structures, periodontal ligament and alveolar bone occurs, leading ultimately to tooth loss. Worldwide, the prevalence of periodontitis in the adult population is about 10-15%. In Malaysia, the National Oral Health study reported 90.2% of the adults presented with some forms of periodontal conditions. About 5.5% of these subjects had deep pockets of 6 mm or more.

Periodontal disease, through inflammation and destruction of the periodontium produces a wide range of clinical signs and symptoms, some of which may have a considerable impact on quality of life (QoL). A study conducted using a community sample found a significant association between periodontal disease and quality of life (QoL). They also found that self-reported symptoms of periodontal diseases such as swollen gums, sore gums and receding gums has an apparent impact on the quality of life of the person. With the mechanism of obesity, it is expected that the obese patients may have experienced more severe periodontal diseases and hence they may experience more impact on the quality of life. However, the evidence is still lacking.

Cytokines play a role in the pathogenesis of periodontitis. They play an active role in wound repair and in transient inflammation. They also activate defence mechanisms in which they may give rise to considerable tissue damage in severe inflammation.

Adipose tissue cells namely adipocytes, preadipocytes and macrophages secrete protein signals collectively known as adipokines or adipocytokines. Adipokines are involved in inflammation and the acute-phase response. Production of adipokines increased in obesity, and raised circulating levels of several acute-phase proteins and inflammatory cytokines. This has led to the concept that obese is a state of chronic low-grade systemic inflammation causally link to insulin resistance and metabolic syndrome.

Salivary components comprising of several inflammatory and immune mediators have been identified which are involved in periodontal destruction. Among all the adipokines, resistin which is an adipocyte-derived cytokine is raised in obese mice. In humans, it is suggested that resistin is largely expressed from neutrophils, macrophages, and monocytes other than adipocytes. Resistin is identified as a proinflammatory adipokine that potentially links obesity to diabetes. It is also believed that human resistin stimulates the production and secretion of other proinflammatory molecules like tumor necrosis factor (TNF)-α and interleukin (IL)-12. Studies have shown high levels of resistin in subjects having chronic periodontitis and this may affect systemic health. In a study by Devanoorkar et al., stated that the decrease in the resistin levels was not statistically significant following non-surgical periodontal therapy.

The reason for the interest in GCF/serum levels of resistin in periodontitis lies in the fact that epidemiological research indicates that periodontitis interplays between obesity and diabetes mellitus. It is possible that raised levels of resistin in periodontitis can explain at least in part the link between periodontitis and other chronic inflammatory diseases. Therefore, the overall aim of this systematic review was to provide evidence of resistin biomarker in chronic periodontal disease which might underpin the relationship between periodontal disease, diabetes and obesity. Evidence from case-control studies are all summarized and evaluated. ;

Study Design

Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Treatment

Related Conditions & MeSH terms

• Gingival Diseases
• Obese
• Periodontal Disease
• Periodontal Diseases

• NCT number: NCT02508415
• Study type: Interventional
• Source: University of Malaya
• Status: Completed
• Phase: N/A
• Start date: February 2013
• Completion date: January 2014