Characterization of a mouse model to study the relationship between apical periodontitis and atherosclerosis.
apical periodontitis
atherosclerosis
inflammation
Journal
International endodontic journal
ISSN: 1365-2591
Titre abrégé: Int Endod J
Pays: England
ID NLM: 8004996
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
22
08
2019
accepted:
10
02
2020
pubmed:
14
2
2020
medline:
15
5
2020
entrez:
14
2
2020
Statut:
ppublish
Résumé
First, to determine the feasibility of using the low-density lipoprotein receptor knockout (LDLR KO) mouse model to study apical periodontitis (AP). Secondly, to investigate the causal relationship between AP and atherosclerosis. It was hypothesized that it would be feasible to induce AP and atherosclerosis in LDLR KO mice and find a difference in atherosclerosis between AP and Sham groups. Using a published methodology, AP was induced in LDLR KO mice by exposing the dental pulp of the four first molars (Tx). Shams received only anaesthesia. Mice were fed a high fat, Western-type diet (WTD), to induce atherosclerosis. At 16 weeks, mice were euthanized and aortas collected to measure atherosclerosis lesion burden (oil red O staining). Periapical lesions were validated using micro-CT and histology. Systemic inflammation was measured using a cytokine array. Both groups developed a similar degree of atherosclerosis (mean lesion area 7.46 ± 0.44% in the Tx group compared with 7.65 ± 0.46%, in the Sham group, P = 0.77), and a similar degree of inflammation. Periapical lesions (PALs) in all four molars were only identified in a small subset of Tx mice. A novel mouse model, which combines AP and CVD, was created. This model allows investigation of the relationship between the two diseases, whilst avoiding other potential common confounders. Although no difference in the degree of atherosclerosis was found between the groups, more studies in which the number of periapical lesions, changes in systemic inflammation and the degree of atherosclerosis are correlated are necessary to ultimately determine the impact of AP on CVD.
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Langues
eng
Pagination
812-823Subventions
Organisme : University of Alberta
ID : Faculty of Medicine and Dentistry, Motyl Graduate Studentship in Cardiac Sciences
Organisme : University of Alberta
ID : Fund for Dentistry
Organisme : Canada Foundation for Innovation
ID : N/A
Organisme : Alpha Omega Foundation
ID : N/A
Informations de copyright
© 2020 International Endodontic Journal. Published by John Wiley & Sons Ltd.
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