Project Details
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Effects of Obesity on Periodontal Tissues Subjected to Biomechanical Forces

Subject Area Dentistry, Oral Surgery
Term from 2017 to 2022
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 387270868
 
Final Report Year 2022

Final Report Abstract

Obesity is characterized by excessive accumulation of adipose tissue, which has a negative impact on overall health. Obesity has been shown to be associated with periodontitis, a chronic inflammatory disease of bacterial origin characterized by the progressive destruction of the tooth-supporting tissues (periodontium). Periodontopathogens trigger an inflammatory immune response in the periodontium that can lead to tooth loss. The periodontium is subject to occlusal forces, i.e. biomechanical loading. Therefore, it should be clarified whether obesity also modulates the response of periodontal cells and tissues to biomechanical forces caused, for example, by orthodontic therapy. The main objective of this in-vivo and in-vitro projects was to investigate the effects of obesity and adipokines on the actions of biomechanical forces on periodontal cells and tissues in the presence and absence of bacterial infection. Our in-vitro and in-vivo studies demonstrated that the proinflammatory adipokine resistin is produced by periodontal cells and tissues, and that microbial and inflammatory stimuli lead to increased resistin expression and production in the periodontium. In addition, this adipokine negatively affected soft and hard tissue metabolism, suggesting that this adipokine may play a significant role in the negative effects of obesity and microorganisms on the periodontium. Further in-vivo studies showed that obesity may affect the proteomic profile of the periodontal ligament (PDL) in ligature-induced periodontitis. In addition, obesity also affected the proteomic profile of the PDL tissues from animals subjected to orthodontic forces. Our studies also demonstrated that obesity impairs alveolar bone remodeling during orthodontic tooth movement. Further in-vitro and in-vivo studies focused on the role of proinflammatory and apoptosis-related molecules in periodontal cells and tissues under microbial and biomechanical conditions. Orthodontic or biomechanical forces modulated the expression of pro-inflammatory and chemotactic cytokines and anti-apoptotic molecules in periodontal infections. Therefore, orthodontic therapy could lead to an altered host response in periodontal tissues, which in turn could promote the progression of periodontitis. When bacteriastimulated cells were biomechanically stressed, the gene expression for some proinflammatory mediators decreased. Biomechanical stress also decreased gene expressions induced by adipokines alone or in combination with bacteria. These results suggest that biomechanical forces may impair the synthesis of chemotactic molecules in the presence of periodontal infection and/or obesity, thereby potentially leading to an inadequate host response that could promote periodontal destruction. Overall, the in-vitro and in-vivo studies of this joint DFG/FAPESP project demonstrated that obesity exerts regulatory effects on periodontal cells and tissues, that obesity interacts with biomechanical/orthodontic forces as well as periodontal infections, and that specific molecules may play key roles in these processes.

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