Abstract

Although the association between periodontitis and obesity is well explored, it is unclear whether obesity is associated with a worse therapeutic outcome after periodontal treatment. The aim of this study was to investigate the effects of obesity on bone healing with and without the application of regeneration-promoting molecules. A standardized bone fenestration-type defect was created over the root of the mandibular first molar in 15 Wistar rats. Ten animals received a high-fat, high-sucrose diet (HFSD), while the remaining five animals were fed a standard diet. During surgery, the fenestration defects from half of the HFSD-fed, i.e., obese animals, were treated with regeneration-promoting molecules (enamel matrix derivative; EMD). After four weeks, bone healing was evaluated by histomorphometry, TRAP staining and immunohistochemistry for RUNX2 and osteopontin. The analyses revealed that the spontaneous healing of the periodontal defects was compromised by obesity. Application of EMD partially compensated for the negative effect of obesity. Nevertheless, EMD-stimulated bone healing in obese animals was not better than the spontaneous healing in the obesity-free control group, indicating that obesity may also inhibit the stimulatory effects of regeneration-promoting molecules. Our results show that obesity can negatively influence bone healing and suggest that bone healing may be compromised in humans.

Highlights

  • IntroductionPeriodontitis is a chronic multifactorial inflammatory disease that affects the periodontium, i.e., the tooth-supporting tissues, and can lead to tooth loss if left untreated [1,2,3]

  • Periodontitis is a chronic multifactorial inflammatory disease that affects the periodontium, i.e., the tooth-supporting tissues, and can lead to tooth loss if left untreated [1,2,3].Bacteria in a dysbiotic subgingival biofilm induce an immunoinflammatory response, but this host reaction is too long, strong, weak or misdirected

  • We demonstrated that the beneficial effects of enamel matrix derivative (EMD) on a number of cellular functions critical for periodontal regeneration are partially enhanced by adiponectin [41]

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Summary

Introduction

Periodontitis is a chronic multifactorial inflammatory disease that affects the periodontium, i.e., the tooth-supporting tissues, and can lead to tooth loss if left untreated [1,2,3]. Bacteria in a dysbiotic subgingival biofilm induce an immunoinflammatory response, but this host reaction is too long, strong, weak or misdirected. The bacteria, their constituents and products, and the immunoinflammatory processes further degrade subgingival structures of the periodontium, including the periodontal ligament and alveolar bone, clinically characterized by periodontal pockets, bleeding on probing, increased tooth mobility and migration and tooth loss [1,2,3]. Strong evidence demonstrates that periodontitis affects masticatory function, aesthetics and self-esteem, but that chronic periodontal inflammation exerts a negative effect on numerous diseases of the whole organism [5,6]. It is known that periodontitis is causally associated with increased intima-media thickness of the carotid artery, poorer endothelial function of the brachial artery, increased pulse wave velocity, cardiovascular diseases, obesity, hyperlipidemia, diabetes mellitus, rheumatoid arthritis, as well as neurodegenerative and other diseases [7,8,9,10,11,12,13]

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