Ligature‐induced peri‐implantitis and periodontitis in mice
Aim Peri‐implantitis (PI), inflammation around dental implants, shares characteristics with periodontitis (PD). However, PI is more difficult to control and treat, and detailed pathophysiology is unclear. We aimed to compare PI and PD progression utilizing a murine model. Materials and Methods Four‐...
Saved in:
Published in: | Journal of clinical periodontology Vol. 45; no. 1; pp. 89 - 99 |
---|---|
Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Blackwell Publishing Ltd
01-01-2018
|
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Aim
Peri‐implantitis (PI), inflammation around dental implants, shares characteristics with periodontitis (PD). However, PI is more difficult to control and treat, and detailed pathophysiology is unclear. We aimed to compare PI and PD progression utilizing a murine model.
Materials and Methods
Four‐week‐old male C57BL/6J mice had their left maxillary molars extracted. Implants were placed in healed extraction sockets and osseointegrated. Ligatures were tied around the implants and second molars. Controls did not receive ligatures. Mice were sacrificed 1 week, 1 and 3 months (n ≥ 5/group/time point) post‐ligature placement. Bone loss analysis was performed. Histology was performed for: haematoxylin and eosin (H&E), tartrate‐resistant acid phosphatase (TRAP), matrix metalloproteinase‐8 (MMP‐8), nuclear factor kappa‐light‐chain enhancer of activated B cells (NF‐κB), toluidine blue and calcein.
Results
PI showed statistically greater bone loss compared to PD at 1 and 3 months. At 3 months, 20% of implants in PI exfoliated; no natural teeth exfoliated in PD. H&E revealed that alveolar bone surrounding implants in PI appeared less dense compared to PD. PI presented with increased osteoclasts, MMP‐8 and NF‐κB, compared to PD.
Conclusion
PI exhibited greater tissue and bone destruction compared to PD. Future studies will characterize the pathophysiological differences between the two conditions. |
---|---|
Bibliography: | Funding information Hiyari reports grants from NIH/NIDCR T90 DE022734‐01, during the conduct of the study. Dr. Wong reports grants from Clinical and Translational Science Institute NIH grant 5TL1TR000121‐05, during the conduct of the study. Yaghsezian, Dr. Naghibi, Dr. Tetradis and Dr. Camargo have nothing to disclose. Dr. Pirih reports grants from UCLA School of Dentistry, during the conduct of the study. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Authors contributed equally to the work. |
ISSN: | 0303-6979 1600-051X |
DOI: | 10.1111/jcpe.12817 |