Gut microbiota and metabolic profile changes unveil the deterioration of alveolar bone inflammatory resorption with aging induced by D-galactose.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
30 10 2024
Historique:
received: 27 03 2024
accepted: 09 10 2024
medline: 31 10 2024
pubmed: 31 10 2024
entrez: 31 10 2024
Statut: epublish

Résumé

The global aging population has led to a rise in age-related health issues, such as malnutrition, metabolic disorders, and even immune decline. Among these concerns, periodontitis holds particular significance for the well-being of the elderly. This study aimed to investigate the impact of aging on inflammatory resorption of alveolar bone in mice with periodontitis, with a specific focus on alterations in the intestinal microenvironment. To achieve this, we established a D-galactose (D-gal)-induced aging mouse model with periodontitis and employed histopathological staining, oxidative stress, and inflammatory factors analyses to assess the severity of periodontitis and the health status. Additionally, the 16S rRNA sequencing and untargeted metabolomics analysis were employed to investigate alterations in the intestinal microbiota and metabolites. Our results showed that D-gal-induced aging mice with periodontitis experienced more pronounced alveolar bone inflammatory resorption and disruptions in the gut barrier, accompanied by an overall decline in physical condition. The microbial composition and structure of aged mice also underwent significant modifications, with a decreased Firmicutes/Bacteroidetes (F/B) ratio. Furthermore, metabolomics analysis demonstrated that D-gal-induced aging primarily influenced lipids and lipid-like molecules metabolism, and enrichment observed in the rheumatoid arthritis and histidine metabolism pathways. These findings provide further evidence that the aging process exacerbates age-related alveolar bone loss (ABL) through disturbances in intestinal homeostasis.

Identifiants

pubmed: 39477973
doi: 10.1038/s41598-024-75941-w
pii: 10.1038/s41598-024-75941-w
doi:

Substances chimiques

Galactose X2RN3Q8DNE
RNA, Ribosomal, 16S 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

26135

Subventions

Organisme : Department of Education of Guizhou Province
ID : Young scientific and technological talents growth project of Guizhou Provincial Department of Education (NO:Qian Jiao He KY[2022]276)
Organisme : Zunyi Medical University
ID : New academic talents Project of Zunyi Medical University (QKHPTRC [2018]5772-010)
Organisme : Department of Science and Technology of Guizhou Province
ID : the Science and Technology Program of Guizhou Province (QKHJC-ZK [2022]-591)

Informations de copyright

© 2024. The Author(s).

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Auteurs

Fangzhou Liu (F)

School of Stomatology, Zunyi Medical University, Zunyi, China.

Yanzi Yao (Y)

School of Stomatology, Zunyi Medical University, Zunyi, China.
Department of Stomatology, Luoyang Maternal and Child Health Hospital, Luoyang, China.

Yue Huang (Y)

School of Stomatology, Zunyi Medical University, Zunyi, China.

Liangliang Luo (L)

School of Preclinical Medicine, Zunyi Medical University, Zunyi, China.

Qian Wang (Q)

School of Stomatology, Zunyi Medical University, Zunyi, China.
Microbial Resources and Drug Development Key Laboratory of Guizhou Tertiary Institution, Zunyi Medical University, Zunyi, China.

Bin Chen (B)

School of Stomatology, Zunyi Medical University, Zunyi, China.
Microbial Resources and Drug Development Key Laboratory of Guizhou Tertiary Institution, Zunyi Medical University, Zunyi, China.

Huan Hu (H)

School of Stomatology, Zunyi Medical University, Zunyi, China. huhuan1990@163.com.
Microbial Resources and Drug Development Key Laboratory of Guizhou Tertiary Institution, Zunyi Medical University, Zunyi, China. huhuan1990@163.com.

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