Periodontal disease may induce liver fibrosis in an experimental study on Wistar rats.
liver fibrosis
matrix metalloproteinase 8
oxidative stress
periodontal disease
Journal
Journal of periodontology
ISSN: 1943-3670
Titre abrégé: J Periodontol
Pays: United States
ID NLM: 8000345
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
03
10
2018
revised:
05
12
2018
accepted:
31
12
2018
pubmed:
29
1
2019
medline:
9
4
2020
entrez:
29
1
2019
Statut:
ppublish
Résumé
The aim was to assess the effects of periodontal disease in promoting liver fibrosis in a rat model of ligature-induced periodontitis. Twenty-four Wistar rats were divided into four groups: control (CTRL), experimental periodontitis group at day 7 (PER7), at day 14 (PER14), at day 21 (PER21). Experimental periodontitis was induced by the placement of a silk ligature around mandibular incisors. The following parameters were assessed: gingival index, tooth mobility; liver status, and portal vein caliber by ultrasound examination; bone retraction, bone mineral density (BMD), bone volume/tissue volume (BV/TV) by micro-CT analysis; aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT); oxidative stress (malondialdehyde [MDA], reduced glutathione/oxidative glutathione ratio [GSH/GSSG]), and matrix metalloproteinase-8 (MMP-8) levels; and histopathological evaluation of periodontal and liver tissues. Periodontal parameters showed the development of periodontitis in experimental groups. Micro-CT results indicates an increase of bone retraction and BMD values and a decrease of BV/TV value in PER groups. Liver fibrosis could not be diagnosed with ultrasound examination in any of the groups. Elevated levels of ASAT and ALAT in PER groups compared with CTRL group were found. MDA have indicated elevated levels and a decrease of GSH/GSSG ratio in PER group compared with the CTRL group. Levels of MMP-8 have indicated high values in PER21 compared with the other groups. Histological analysis of the periodontal and liver tissues sustains the link between periodontal and hepatic injury. This study demonstrates a positive correlation between periodontal lesions and liver disease. Periodontitis may be an independent risk factor for liver fibrosis.
Sections du résumé
BACKGROUND
The aim was to assess the effects of periodontal disease in promoting liver fibrosis in a rat model of ligature-induced periodontitis.
METHODS
Twenty-four Wistar rats were divided into four groups: control (CTRL), experimental periodontitis group at day 7 (PER7), at day 14 (PER14), at day 21 (PER21). Experimental periodontitis was induced by the placement of a silk ligature around mandibular incisors. The following parameters were assessed: gingival index, tooth mobility; liver status, and portal vein caliber by ultrasound examination; bone retraction, bone mineral density (BMD), bone volume/tissue volume (BV/TV) by micro-CT analysis; aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT); oxidative stress (malondialdehyde [MDA], reduced glutathione/oxidative glutathione ratio [GSH/GSSG]), and matrix metalloproteinase-8 (MMP-8) levels; and histopathological evaluation of periodontal and liver tissues.
RESULTS
Periodontal parameters showed the development of periodontitis in experimental groups. Micro-CT results indicates an increase of bone retraction and BMD values and a decrease of BV/TV value in PER groups. Liver fibrosis could not be diagnosed with ultrasound examination in any of the groups. Elevated levels of ASAT and ALAT in PER groups compared with CTRL group were found. MDA have indicated elevated levels and a decrease of GSH/GSSG ratio in PER group compared with the CTRL group. Levels of MMP-8 have indicated high values in PER21 compared with the other groups. Histological analysis of the periodontal and liver tissues sustains the link between periodontal and hepatic injury.
CONCLUSION
This study demonstrates a positive correlation between periodontal lesions and liver disease. Periodontitis may be an independent risk factor for liver fibrosis.
Identifiants
pubmed: 30689209
doi: 10.1002/JPER.18-0585
doi:
Substances chimiques
Malondialdehyde
4Y8F71G49Q
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
911-919Informations de copyright
© 2019 American Academy of Periodontology.