ArticleInterdisciplinary perspectives on infectious diseases2009
B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection.
Article in Interdisciplinary perspectives on infectious diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- Trial
- Immunopathogenesis and immunotherapy of diabetes-associated periodontitis.Clinical oral investigations · 2025Review
- Oral microbiota-host interaction: the chief culprit of alveolar bone resorption.Frontiers in immunology · 2024Review
- Osteoimmunology in Periodontitis and Orthodontic Tooth Movement.Current osteoporosis reports · 2023Review
- Review
- Update on B Cell Response in Periodontitis.Advances in experimental medicine and biology · 2022Article
- An emphasis of T-cell subsets as regulators of periodontal health and disease.Journal of clinical and translational research · 2021Review
- Effects ofMedicina (Kaunas, Lithuania) · 2021Article
- Maintaining homeostatic control of periodontal bone tissue.Periodontology 2000 · 2021Review
- B-Cell Deficiency Exacerbates Inflammation and Bone Loss in Ligature-Induced Experimental Periodontitis in Mice.Journal of inflammation research · 2021Article
- Revisiting the Page & Schroeder model: the good, the bad and the unknowns in the periodontal host response 40 years later.Periodontology 2000 · 2017Review
- Immune cells link obesity-associated type 2 diabetes and periodontitis.Journal of dental research · 2014Review
- Divergence of the systemic immune response following oral infection with distinct strains of Porphyromonas gingivalis.Molecular oral microbiology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Periodontal disease is one of the most common infectious diseases of humans. Immune responses to infection trigger loss of alveolar bone from the jaw and eventual tooth loss. We investigated the contribution of B cell IgD to alveolar bone loss by comparing the response of B cell normal BALB/cJ mice and IgD deficient BALB/c-Igh-5(-/-J) mice to oral infection with Porphyromonas gingivalis, a gram-negative periodontopathic bacterium from humans. P. gingivalis-infected normal mice lost bone. Specific antibody to P. gingivalis was lower and oral colonization was higher in IgD deficient mice; yet bone loss was completely absent. Infection increased the proportion of CD69(+) activated B cells and CD4(+) T cells in immune normal mice compared to IgD deficient mice. These data suggest that IgD is an important mediator of alveolar bone resorption, possibly through antigen-specific coactivation of B cells and CD4(+) T cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.