Increasing evidence suggests that periodontitis, characterized by oral dysbiosis, is a critical player in the progression of multiple systemic diseases in humans. However, there is still a lack of a proper mouse model of periodontitis with the colonization of human periodontitis-associated bacteria. We here established a new mouse periodontitis model by combining ligation of the second molars with application of subgingival plaques from periodontitis patients. Using 16S rRNA gene sequencing and Taxonomic classification, we found that human periodontitis-associated bacteria efficiently colonized in the mouse model and were enriched in both ligature silk and mouse saliva. Furthermore, the well-recognized periodontal pathogens including , , , and were enriched in the new model, but not in ligature-induced periodontitis model or Sham mice. The human periodontitis-associated bacteria potently aggravated mouse periodontitis, as demonstrated by more severe bone resorption and higher expression of inflammatory and osteoclastogenesis genes. In summary, the new mouse periodontitis model paves the way for studying human periodontitis-associated bacteria in oral diseases and systemic diseases.
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http://dx.doi.org/10.3389/fcimb.2022.842845 | DOI Listing |
J Dent Res
January 2025
Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Cellular senescence has emerged as one of the central hallmarks of aging and drivers of chronic comorbidities, including periodontal diseases. Senescence can also occur in younger tissues and instigate metabolic alterations and dysfunction, culminating in accelerated aging and pathological consequences. Senotherapeutics, such as the combination of dasatinib and quercetin (DQ), are being increasingly used to improve the clinical outcomes of chronic disorders and promote a healthy life span through the reduction of senescent cell burden and senescence-associated secretory phenotype (SASP).
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2024
Laboratory of Tissue Regeneration and Immunology and Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, PR China. Electronic address:
Obesity and its related metabolic disorders seriously threaten our health and significantly reduce our life expectancy. The aim of the present study was to explore the effects of bone marrow mesenchymal stem cells (BMSCs) on high-fat diet (HFD)-induced obesity mice. The results demonstrated that BMSCs significantly reduced body weight, improved glucose tolerance and insulin sensitivity in obese mice.
View Article and Find Full Text PDFJCI Insight
January 2025
Center for Precision Medicine, Department of Medicine, and.
The role played by anionic channels in diabetic kidney disease (DKD) is not known. Chloride channel accessory 1 (CLCA1) facilitates the activity of TMEM16A (Anoctamin-1), a Ca2+-dependent Cl- channel. We examined if CLCA1/TMEM16A had a role in DKD.
View Article and Find Full Text PDFExp Ther Med
February 2025
Central Research Institute, Wakunaga Pharmaceutical Co., Ltd., Akitakata, Hiroshima 739-1195, Japan.
Periodontal disease is recognized as a chronic multifactorial inflammatory condition initiated by dysbiosis within subgingival plaque biofilms. Antimicrobial peptides exhibit a wide spectrum of antimicrobial action, and thus, provide one of the first lines of host defense against oral pathogens. Aged garlic extract (AGE) is effective for preventing the progression of periodontal disease.
View Article and Find Full Text PDFAnim Cells Syst (Seoul)
December 2024
Department of Oral Biochemistry, Dental and Life Science Institute, School of Dentistry, Pusan National University, Yangsan, Republic of Korea.
(), a periodontal pathogen, has been implicated in the impairment of anti-tumor responses in colorectal cancer (CRC). The tumor microenvironment in CRC involves tumor-associated macrophages (TAMs), which are pivotal in modulating tumor-associated immune responses. The polarization of TAMs towards an M2-like phenotype promotes CRC progression by suppressing the immune system.
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