EdenteV1, Main, Exploration, bibRecord, 000197

A Murine Model of Lipopolysaccharide-Induced Peri-Implant Mucositis and Peri-Implantitis.

Identifieur interne : 000197 ( Main/Exploration ); précédent : 000196; suivant : 000198

A Murine Model of Lipopolysaccharide-Induced Peri-Implant Mucositis and Peri-Implantitis.

Auteurs : Flavia Q. Pirih ; Sarah Hiyari ; Ho-Yin Leung ; Ana D V. Barroso [Brésil] ; Adrian C A. Jorge [Brésil] ; Jeniffer Perussolo [Brésil] ; Elisa Atti ; Yi-Ling Lin ; Sotirios Tetradis ; Paulo M. Camargo

Source :

The Journal of oral implantology [ 1548-1336 ] ; 2015.

RBID : pubmed:24967609

Abstract

Dental implants are a widely used treatment option for tooth replacement. However, they are susceptible to inflammatory diseases such as peri-implant mucositis and peri-implantitis, which are highly prevalent and may lead to implant loss. Unfortunately, the understanding of the pathogenesis of peri-implant mucositis and peri-implantitis is fragmented and incomplete. Therefore, the availability of a reproducible animal model to study these inflammatory diseases would facilitate the dissection of their pathogenic mechanisms. The objective of this study is to propose a murine model of experimental peri-implant mucositis and peri-implantitis. Screw-shaped titanium implants were placed in the upper healed edentulous alveolar ridges of C57BL/6J mice 8 weeks after tooth extraction. Following 4 weeks of osseointegration, Porphyromonas gingivalis -lipolysaccharide (LPS) injections were delivered to the peri-implant soft tissues for 6 weeks. No-injections and vehicle injections were utilized as controls. Peri-implant mucositis and peri-implantitis were assessed clinically, radiographically (microcomputerized tomograph [CT]), and histologically following LPS-treatment. LPS-injections resulted in a significant increase in soft tissue edema around the head of the implants as compared to the control groups. Micro-CT analysis revealed significantly greater bone loss in the LPS-treated implants. Histological analysis of the specimens demonstrated that the LPS-group had increased soft tissue vascularity, which harbored a dense mixed inflammatory cell infiltrate, and the bone exhibited noticeable osteoclast activity. The induction of peri-implant mucositis and peri-implantitis in mice via localized delivery of bacterial LPS has been demonstrated. We anticipate that this model will contribute to the development of more effective preventive and therapeutic approaches for these 2 conditions.

DOI: 10.1563/aaid-joi-D-14-00068
PubMed: 24967609

Affiliations:

Brésil

Le document en format XML

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<front><div type="abstract" xml:lang="en">Dental implants are a widely used treatment option for tooth replacement. However, they are susceptible to inflammatory diseases such as peri-implant mucositis and peri-implantitis, which are highly prevalent and may lead to implant loss. Unfortunately, the understanding of the pathogenesis of peri-implant mucositis and peri-implantitis is fragmented and incomplete. Therefore, the availability of a reproducible animal model to study these inflammatory diseases would facilitate the dissection of their pathogenic mechanisms. The objective of this study is to propose a murine model of experimental peri-implant mucositis and peri-implantitis. Screw-shaped titanium implants were placed in the upper healed edentulous alveolar ridges of C57BL/6J mice 8 weeks after tooth extraction. Following 4 weeks of osseointegration, Porphyromonas gingivalis -lipolysaccharide (LPS) injections were delivered to the peri-implant soft tissues for 6 weeks. No-injections and vehicle injections were utilized as controls. Peri-implant mucositis and peri-implantitis were assessed clinically, radiographically (microcomputerized tomograph [CT]), and histologically following LPS-treatment. LPS-injections resulted in a significant increase in soft tissue edema around the head of the implants as compared to the control groups. Micro-CT analysis revealed significantly greater bone loss in the LPS-treated implants. Histological analysis of the specimens demonstrated that the LPS-group had increased soft tissue vascularity, which harbored a dense mixed inflammatory cell infiltrate, and the bone exhibited noticeable osteoclast activity. The induction of peri-implant mucositis and peri-implantitis in mice via localized delivery of bacterial LPS has been demonstrated. We anticipate that this model will contribute to the development of more effective preventive and therapeutic approaches for these 2 conditions.</div>
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A Murine Model of Lipopolysaccharide-Induced Peri-Implant Mucositis and Peri-Implantitis.

A Murine Model of Lipopolysaccharide-Induced Peri-Implant Mucositis and Peri-Implantitis.

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