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Do periodontal defects affect periodontal inflammation and destruction? Histological/microbiological changes and gene expression profiles of a pilot study in beagle dogs

Authors
 Yin-Zhe An  ;  Kyung-A Ko  ;  Chang-Sung Kim  ;  Reinhard Gruber  ;  Xinhong Wang  ;  Jung-Seok Lee 
Citation
 JOURNAL OF PERIODONTOLOGY, Vol.92(7) : 1007-1017, 2021-07 
Journal Title
JOURNAL OF PERIODONTOLOGY
ISSN
 0022-3492 
Issue Date
2021-07
MeSH
Alveolar Bone Loss* / genetics ; Alveolar Bone Loss* / surgery ; Alveolar Process* ; Animals ; Dogs ; Female ; Guided Tissue Regeneration, Periodontal ; Inflammation / genetics ; Pilot Projects ; Transcriptome
Keywords
dental plaque ; gingivitis ; periodontal disease ; periodontal pocket ; periodontitis
Abstract
Background: The present study focused on the inflammatory disease progress after periodontal defect induction and aimed to specifically determine periodontal tissue responses following dental plaque accumulation by ligatures on a site with/without standardized periodontal defect induction.

Methods: After 1 month from extraction of the adjacent teeth, semi-circumferential defects were surgically created in the unilateral second and fourth premolars (test group), whereas no defects were being induced at the contralateral sites (control group). One week later, silk was used to ligate the tooth cervix at both sites to encourage the accumulation of dental plaque. Four weeks later, the tissue samples were collected for histological/histomorphometric and microarray analysis. Microbiological analysis was performed before defect induction and at ligatures, and after 4 weeks of dental plaque accumulation.

Results: Remarkable inflammation was clinically and histologically observed in both groups after plaque accumulation, and the intrabony type of periodontal defect exaggerated inflammatory cell infiltration into the connective tissue layer. Expression of genes related to inflammation such as IL-1 was highly up-regulated in test sites. However, these inflammatory infiltrations did not invade to a boundary of periodontal ligament and connective tissue attachment in both groups, and histomorphometric results corresponds to these observational results. Bacterial findings also showed no significant differences in detected microbiome compositions between control and test groups at three-time points.

Conclusion: Intrabony defect might exaggerate the plaque-induced inflammation in the aspect of inflammatory cell infiltration and the related gene expression, but both dental plaque and the pre-existing periodontal defect negligibly disrupt periodontal attachment and the underlying alveolar bone.
Full Text
https://aap.onlinelibrary.wiley.com/doi/10.1002/JPER.20-0508
DOI
10.1002/JPER.20-0508
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Periodontics (치주과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Chang Sung(김창성) ORCID logo https://orcid.org/0000-0003-3902-1071
Lee, Jung Seok(이중석) ORCID logo https://orcid.org/0000-0003-1276-5978
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/184641
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