Abstract

Peri-implantitis is an inflammatory disease that results in bone destruction around dental implants. A preclinical study using beagle models is frequently performed prior to clinical application in dentistry. Previously, we proposed an immediate peri-implantitis experimental model with a shorter experimental duration and less expense than the conventional experimental model. However, the differences in the regenerative outcomes between the immediate and conventional models were not fully revealed. In this study, we aimed to compare the regenerative outcomes between both models when ex vivo BMP2 gene therapy using autologous periodontal ligament stem cells (B2/PDLSCs) was applied to peri-implantitis defects. The results showed that the defect depths were significantly different between both models. New bone formation occurred in both models, but there were significant differences between the models. More than 70% of the defects were filled with newly formed bone in the conventional model, whereas 30–40% of the defects were filled in the immediate model. However, after adjustment for the differences in the defect depths between the models, the statistically significant differences in the regenerative outcomes between the models were lost. In conclusion, the inferior regenerative outcome of an immediate peri-implantitis model at B2/PDLSCs transplantation resulted from the defect depths, not the model itself.

Highlights

  • Peri-implantitis is an inflammatory disease that results in bone destruction around dental implants

  • Regarding the vertical bone fill, approximately 30% of the defects were re-osseointegrated in the immediate model, whereas more than 60% were re-osseointegrated in the conventional model (p = 0.016 on the buccal side; p = 0.017 on the lingual side)

  • PDL stem cells (PDLSCs) are dental originated mesenchymal stem cells (MSCs) that are isolated from root surfaces of an extracted tooth

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Summary

Introduction

Peri-implantitis is an inflammatory disease that results in bone destruction around dental implants. The inferior regenerative outcome of an immediate peri-implantitis model at B2/PDLSCs transplantation resulted from the defect depths, not the model itself. Pathogenic bacteria initiate immune and inflammatory responses in the tissues that defend against the bacteria and sequester the damaged tissues for repair[3] On this occasion, chemokines and cytokines secreted by inflammation around the implant stimulate the differentiation of monocytes into osteoclasts, leading to bone loss around the implant[4]. (Figure 1a) the conventional model is too time-consuming and expensive to validate new therapies that are at risk of failure this model shows a similar etiology and defect morphology with naturally occurring human peri-implantitis defects For experiments about regenerative therapy, it takes at least 13 months including more than 10 months of peri-implantitis induction and more than 3 months of healing after treatment to yield results. (Figure 1a) the conventional model is too time-consuming and expensive to validate new therapies that are at risk of failure this model shows a similar etiology and defect morphology with naturally occurring human peri-implantitis defects

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