Antimicrobial‐induced oral dysbiosis exacerbates naturally occurring alveolar bone loss
| Autor: | Caroline Westwater, Matthew D Carson, J. Ignacio Aguirre, Amy J Warner, Joy E Kirkpatrick, Chad M. Novince, Alexander V. Alekseyenko, Alexa Corker, Brooks A Swanson, Jessica D. Hathaway-Schrader |
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| Rok vydání: | 2021 |
| Předmět: |
Male
medicine.drug_class Antibiotics Alveolar Bone Loss digestive system Biochemistry Article Proinflammatory cytokine Mice Osteoclast Genetics Animals Medicine Molecular Biology Dental alveolus Innate immune system Host Microbial Interactions business.industry Chlorhexidine Minocycline respiratory system medicine.disease Anti-Bacterial Agents Gastrointestinal Microbiome Mice Inbred C57BL medicine.anatomical_structure Immunology Dysbiosis Female business Biotechnology medicine.drug |
| Zdroj: | FASEB J |
| ISSN: | 1530-6860 0892-6638 |
| Popis: | Periodontitis-mediated alveolar bone loss is caused by dysbiotic shifts in the commensal oral microbiota that upregulate proinflammatory osteoimmune responses. Study purpose was to determine whether antimicrobial-induced disruption of the commensal microbiota has deleterious effects on alveolar bone. We administered an antibiotic cocktail, minocycline, or vehicle-control to sex-matched C57BL/6T mice from age 6- to 12-weeks. Antibiotic cocktail and minocycline had catabolic effects on alveolar bone in specific-pathogen-free mice. We then administered minocycline or vehicle-control to male mice reared under specific-pathogen-free and germ-free conditions, and we subjected minocycline-treated specific-pathogen-free mice to chlorhexidine oral antiseptic rinses. Alveolar bone loss was greater in vehicle-treated specific-pathogen-free vs. germ-free mice, demonstrating that the commensal microbiota drives naturally occurring alveolar bone loss. Minocycline- vs. vehicle-treated germ-free mice had similar alveolar bone loss outcomes, implying that antimicrobial-driven alveolar bone loss is microbiota dependent. Minocycline induced phylum-level shifts in the oral bacteriome and exacerbated naturally occurring alveolar bone loss in specific-pathogen-free mice. Chlorhexidine further disrupted the oral bacteriome and worsened alveolar bone loss in minocycline-treated specific-pathogen-free mice, validating that antimicrobial-induced oral dysbiosis has deleterious effects on alveolar bone. Minocycline enhanced osteoclast size and interface with alveolar bone in specific-pathogen-free mice. Neutrophils and plasmacytoid dendritic cells were upregulated in cervical lymph nodes of minocycline-treated specific-pathogen-free mice. Paralleling the upregulated proinflammatory innate immune cells, minocycline therapy increased T(H)1 and T(H)17 cells that have known pro-osteoclastic actions in alveolar bone. This report reveals that antimicrobial perturbation of the commensal microbiota induces a proinflammatory oral dysbiotic state that exacerbates naturally occurring alveolar bone loss. |
| Databáze: | OpenAIRE |
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