Literature DB >> 11570525

T-cell contributions to alveolar bone loss in response to oral infection with Porphyromonas gingivalis.

P J Baker1, J Garneau, L Howe, D C Roopenian.   

Abstract

We have previously shown that mice lacking CD4+, but not CD8+, T cells lose less alveolar bone loss in response to oral infection with Porphyromonas gingivalis than do immunocompetent mice of the same genetic background, indicating that CD4+ T cells contribute to bone resorption. The CD4+ and CD8+ T-cell knockouts were produced by targeted deletions of, respectively, major histocompatibility complex II (MHCII) or beta2-microglobulin (producing non-expression of MHCI). Because MHC deletions can have other effects in addition to those on T-cell selection, we wanted to confirm that the lessened bone loss was truly an effect of the lack of T cells. Consequently, we repeated our experiments with C57B1 /6J-Tcra mice that have a targeted deletion of the alpha chain of the T-cell receptor (Tcra). Six weeks after oral infection with P. gingivalis ATCC 53977 the total bone loss at buccal maxillary sites was 0.28 mm in infected immunocompetent mice (P=0.002 compared with sham-infected mice), whereas in Tcra knockouts the bone loss was only 0.08 mm (P=0.04 compared with shams). The T-cell-deficient mice thus lost 70% less bone after infection than did genetically matched immunocompetent mice (P =0.003). These experiments confirm that T cells, and their responses to oral infection with P. gingivalis, help to push bone remodeling in the direction of net loss of bone.

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Year:  2001        PMID: 11570525     DOI: 10.1080/00016350152509247

Source DB:  PubMed          Journal:  Acta Odontol Scand        ISSN: 0001-6357            Impact factor:   2.331


  15 in total

1.  Blockade of protease-activated receptors on T cells correlates with altered proteolysis of CD27 by gingipains of Porphyromonas gingivalis.

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2.  Soluble RANKL Cleaved from Activated Lymphocytes by TNF-α-Converting Enzyme Contributes to Osteoclastogenesis in Periodontitis.

Authors:  Hiroyuki Kanzaki; Seicho Makihira; Maiko Suzuki; Takenobu Ishii; Alexandru Movila; Josefine Hirschfeld; Hani Mawardi; Xiaoping Lin; Xiaozhe Han; Martin A Taubman; Toshihisa Kawai
Journal:  J Immunol       Date:  2016-10-07       Impact factor: 5.422

3.  Immune and inflammatory pathways are involved in inherent bone marrow ossification.

Authors:  Umut Atakan Gurkan; Ryan Golden; Vipuil Kishore; Catherine P Riley; Jiri Adamec; Ozan Akkus
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4.  Porphyromonas gingivalis induces RANKL in T-cells.

Authors:  Georgios N Belibasakis; Durga Reddi; Nagihan Bostanci
Journal:  Inflammation       Date:  2011-04       Impact factor: 4.092

Review 5.  The oral microbiome and the immunobiology of periodontal disease and caries.

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Journal:  Infect Immun       Date:  2021-01-19       Impact factor: 3.441

Review 7.  The potential of p38 MAPK inhibitors to modulate periodontal infections.

Authors:  Keith L Kirkwood; Carlos Rossa
Journal:  Curr Drug Metab       Date:  2009-01       Impact factor: 3.731

8.  Protease-activated receptor 2 has pivotal roles in cellular mechanisms involved in experimental periodontitis.

Authors:  David M Wong; Vivian Tam; Roselind Lam; Katrina A Walsh; Liliana Tatarczuch; Charles N Pagel; Eric C Reynolds; Neil M O'Brien-Simpson; Eleanor J Mackie; Robert N Pike
Journal:  Infect Immun       Date:  2009-11-23       Impact factor: 3.441

9.  Dental tissue repair: novel models for tissue regeneration strategies.

Authors:  Alastair J Sloan; Christopher D Lynch
Journal:  Open Dent J       Date:  2012-12-28

10.  B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection.

Authors:  Pamela J Baker; Nicole Ryan Boutaugh; Michaela Tiffany; Derry C Roopenian
Journal:  Interdiscip Perspect Infect Dis       Date:  2009-10-25
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