scholarly journals B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection

2009 ◽  
Vol 2009 ◽  
pp. 1-6 ◽  
Author(s):  
Pamela J. Baker ◽  
Nicole Ryan Boutaugh ◽  
Michaela Tiffany ◽  
Derry C. Roopenian
Keyword(s):  
T Cells ◽  
B Cells ◽  
Bone Loss ◽  
B Cell ◽  
Tooth Loss ◽  
Alveolar Bone ◽  
Oral Infection ◽  
Alveolar Bone Loss ◽  
Oral Colonization ◽  
Deficient Mice

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−/−Jmice to oral infection withPorphyromonas gingivalis, a gram-negative periodontopathic bacterium from humans.P. gingivalis-infected normal mice lost bone. Specific antibody toP. gingivaliswas 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.

γδ T Cells Differentially Regulate Bone Loss in Periodontitis Models

2021 ◽  
pp. 002203452110428
Author(s):  
O. Barel ◽  
Y. Aizenbud ◽  
Y. Tabib ◽  
Y. Jaber ◽  
A. Leibovich ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Bone Loss ◽  
Immune Responses ◽  
Alveolar Bone ◽  
Γδ T Cells ◽  
Oral Infection ◽  
Alveolar Bone Loss ◽  
Infection Model ◽  
The Impact

γδ T cells are nonclassical T lymphocytes representing the major T-cell population at epithelial barriers. In the gingiva, γδ T cells are enriched in epithelial regions adjacent to the biofilm and are considered to regulate local immunity to maintain host-biofilm homeostatic interactions. This delicate balance is often disrupted resulting in the development of periodontitis. Previous studies in mice lacking γδ T cells from birth ( Tcrd-/- mice) examined the impact of these cells on ligature-induced periodontitis. Data obtained from those studies proposed either a protective effect or no impact to γδ T cells in this setting. Here, we addressed the role of γδ T cells in periodontitis using the recently developed Tcrd-GDL mice, enabling temporal ablation of γδ T cells. Specifically, the impact of γδ T cells during periodontitis was examined in 2 modalities: the ligature model and the oral infection model in which the pathogen Porphyromonas gingivalis was administrated via successive oral gavages. Ablation of γδ T cells during ligature-induced periodontitis had no impact on innate immune cell recruitment to the ligated gingiva. In addition, the number of osteoclasts and subsequent alveolar bone loss were unaffected. However, γδ T cells play a pathologic role during P. gingivalis infection, and their absence prevented alveolar bone loss. Further analysis revealed that γδ T cells were responsible for the recruitment of neutrophils and monocytes to the gingiva following the exposure to P. gingivalis. γδ T-cell ablation also downregulated osteoclastogenesis and dysregulated long-term immune responses in the gingiva. Collectively, this study demonstrates that whereas γδ T cells are dispensable to periodontitis induced by the ligature model, they play a deleterious role in the oral infection model by facilitating pathogen-induced bone-destructive immune responses. On a broader aspect, this study highlights the complex immunopathologic mechanisms involved in periodontal bone loss.

scholarly journals CD4+ T Cells and the Proinflammatory Cytokines Gamma Interferon and Interleukin-6 Contribute to Alveolar Bone Loss in Mice

1999 ◽  
Vol 67 (6) ◽  
pp. 2804-2809 ◽  
Author(s):  
Pamela J. Baker ◽  
Mark Dixon ◽  
R. Todd Evans ◽  
Lisa Dufour ◽  
Ellis Johnson ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Bone Loss ◽  
Proinflammatory Cytokines ◽  
Interleukin 6 ◽  
Alveolar Bone ◽  
Adaptive Immune Response ◽  
Oral Infection ◽  
Alveolar Bone Loss ◽  
Adaptive Immune

ABSTRACT In this study, we used a mouse model to examine the role of the adaptive immune response in alveolar bone loss induced by oral infection with the human gram-negative anaerobic bacteriumPorphyromonas gingivalis. Severe combined immunodeficient mice, which lack B and T lymphocytes, exhibited considerably less bone loss than did immunocompetent mice after oral infection, suggesting that lymphocytes contribute to this process. Bone loss after oral infection was decreased in mice deficient in major histocompatibility complex (MHC) class II-responsive CD4+ T cells, but no change in bone loss was observed in mice deficient in MHC class I-responsive CD8+ T cells or NK1+ T cells. Mice lacking the cytokine gamma interferon or interleukin-6 also demonstrated decreased bone loss. These results suggest that the adaptive immune response, and in particular CD4+ T cells and the proinflammatory cytokines that they secrete, are important effectors of bone loss consequent to P. gingivalis oral infection. The studies also reinforce the utility of the mouse oral infection model in dissecting the pathobiology of periodontal disease.

scholarly journals B-Cell RANKL Contributes to Pathogen-Induced Alveolar Bone Loss in an Experimental Periodontitis Mouse Model

2021 ◽  
Vol 12 ◽  
Author(s):  
Rajendra P. Settem ◽  
Kiyonobu Honma ◽  
Sreedevi Chinthamani ◽  
Toshihisa Kawai ◽  
Ashu Sharma
Keyword(s):  
B Cells ◽  
Bone Resorption ◽  
Bone Loss ◽  
Mouse Model ◽  
B Cell ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Conditional Knockout ◽  
Wild Type ◽  
In The Wild

Periodontitis is a bacterially-induced inflammatory disease that leads to tooth loss. It results from the damaging effects of a dysregulated immune response, mediated largely by neutrophils, macrophages, T cells and B cells, on the tooth-supporting tissues including the alveolar bone. Specifically, infiltrating B cells at inflamed gingival sites with an ability to secrete RANKL and inflammatory cytokines are thought to play roles in alveolar bone resorption. However, the direct contribution of B cells in alveolar bone resorption has not been fully appreciated. In this study we sought to define the contribution of RANKL expressing B cells in periodontitis by employing a mouse model of pathogen-induced periodontitis that used conditional knockout mice with B cell-targeted RANKL deletion. Briefly, alveolar bone loss was assessed in the wild-type, B-cell deficient (Jh), or B-cell-RANKL deleted (RANKLΔB) mice orally infected with the periodontal pathogen Tannerella forsythia. The RANKLΔB mice were obtained by crossing Cd19-Cre knock-in mice with mice homozygous for conditional RANKL-flox allele (RANKLflox/flox). The alveolar bone resorption was determined by morphometric analysis and osteoclastic activity of the jaw bone. In addition, the bone resorptive potential of the activated effector B cells was assessed ex vivo. The data showed that the RANKL producing B cells increased significantly in the T. forsythia-infected wild-type mice compared to the sham-infected mice. Moreover, T. forsythia-infection induced higher alveolar bone loss in the wild-type and RANKLflox/flox mice compared to infection either in the B cell deficient (Jh) or the B-cell specific RANKL deletion (RANKLΔB) mice. These data established that the oral-pathogen activated B cells contribute significantly to alveolar bone resorption via RANKL production.

scholarly journals G(-) Anaerobes-Reactive CD4+ T-Cells Trigger RANKL-Mediated Enhanced Alveolar Bone Loss in Diabetic NOD Mice

Diabetes ◽  
2005 ◽  
Vol 54 (5) ◽  
pp. 1477-1486 ◽  
Author(s):  
D. A. Mahamed ◽  
A. Marleau ◽  
M. Alnaeeli ◽  
B. Singh ◽  
X. Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Bone Loss ◽  
Cd4 T Cells ◽  
Alveolar Bone ◽  
Nod Mice ◽  
Alveolar Bone Loss

scholarly journals Alveolar Bone Loss, Tooth Loss and Oral Cancer Mortality in Older Patients: A Retrospective Cohort Study

2020 ◽  
Vol Volume 15 ◽  
pp. 1419-1425
Author(s):  
Yifeng Qian ◽  
Huiting Yu ◽  
Weijun Yuan ◽  
Jiaqing Wu ◽  
Qingyu Xu ◽  
...  
Keyword(s):  
Cohort Study ◽  
Oral Cancer ◽  
Bone Loss ◽  
Retrospective Cohort Study ◽  
Cancer Mortality ◽  
Older Patients ◽  
Retrospective Cohort ◽  
Tooth Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss

scholarly journals T Cell Accumulation in B Cell Follicles Is Regulated by Dendritic Cells and Is Independent of B Cell Activation

2003 ◽  
Vol 197 (2) ◽  
pp. 195-206 ◽  
Author(s):  
Simon Fillatreau ◽  
David Gray
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Cell Activation ◽  
B Cell Activation ◽  
Cell Accumulation ◽  
Antigen Presenting ◽  
Deficient Mice

We investigated the mechanism of CD4 T cell accumulation in B cell follicles after immunization. Follicular T cell numbers were correlated with the number of B cells, indicating B cell control of the niche that T cells occupy. Despite this, we found no role for B cells in the follicular migration of T cells. Instead, T cells are induced to migrate into B cell follicles entirely as a result of interaction with dendritic cells (DCs). Migration relies on CD40-dependent maturation of DCs, as it did not occur in CD40-deficient mice but was reconstituted with CD40+ DCs. Restoration was not achieved by the activation of DCs with bacterial activators (e.g., lipopolysaccharide, CpG), but was by the injection of OX40L–huIgG1 fusion protein. Crucially, the up-regulation of OX40L (on antigen-presenting cells) and CXCR-5 (on T cells) are CD40-dependent events and we show that T cells do not migrate to follicles in immunized OX40-deficient mice.

Potential Application of Low-Dose Doxycycline to Treat Periodontitis in Post-Menopausal Women

1998 ◽  
Vol 12 (1) ◽  
pp. 166-169 ◽  
Author(s):  
J.B. Payne ◽  
R.A. Reinhardt
Keyword(s):  
Bone Loss ◽  
Tooth Loss ◽  
Low Dose ◽  
Alveolar Bone ◽  
Public Health Problem ◽  
The United States ◽  
Alveolar Bone Loss ◽  
Design Concepts ◽  
Significant Public Health ◽  
Post Menopausal

The purpose of this paper is two-fold: (1) to review the evidence that osteoporosis and post-menopausal estrogen deficiency are associated with progressive alveolar bone loss and an elevated risk of tooth loss; and (2) to propose the use of tetracyclines, specifically low-dose doxycycline (LDD) (and, perhaps in the future, the chemically modified tetracyclines), to mitigate alveolar bone loss in post-menopausal osteoporotic/osteopenic women. Design concepts for a randomized clinical trial to study the effects of LDD on progressive alveolar bone loss in this patient population are reviewed. Since osteoporosis affects over 20 million people in the United States, progressive alveolar bone loss in this patient group represents a potentially significant public health problem unique from common adult periodontitis. Stopping progressive alveolar bone loss is essential to prevent both tooth loss and micro-architectural deterioration of alveolar bone.

Involvement of Cot/Tp12 in Bone Loss during Periodontitis

2010 ◽  
Vol 89 (2) ◽  
pp. 192-197 ◽  
Author(s):  
T. Ohnishi ◽  
A. Okamoto ◽  
K. Kakimoto ◽  
K. Bandow ◽  
N. Chiba ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Periodontal Tissue ◽  
Rankl Expression ◽  
Periodontal Tissues ◽  
Tnf Α ◽  
Experimental Periodontitis ◽  
Deficient Mice

Periodontitis causes resorption of alveolar bone, in which RANKL induces osteoclastogenesis. The binding of lipopolysaccharide to Toll-like receptors causes phosphorylation of Cot/Tp12 to activate the MAPK cascade. Previous in vitro studies showed that Cot/Tp12 was essential for the induction of RANKL expression by lipopolysaccharide. In this study, we examined whether Cot/Tp12 deficiency reduced the progression of alveolar bone loss and osteoclastogenesis during experimental periodontitis. We found that the extent of alveolar bone loss and osteoclastogenesis induced by ligature-induced periodontitis was decreased in Cot/Tp12-deficient mice. In addition, reduction of RANKL expression was observed in periodontal tissues of Cot/Tp12-deficient mice with experimental periodontitis. Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-α mRNA expression in gingiva of mice with experimental periodontitis. Our observations suggested that Cot/Tp12 is essential for the progression of alveolar bone loss and osteoclastogenesis in periodontal tissue during experimental periodontitis mediated through increased RANKL expression.

scholarly journals Treatment of OPG-deficient mice with WP9QY, a RANKL-binding peptide, recovers alveolar bone loss by suppressing osteoclastogenesis and enhancing osteoblastogenesis

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0184904 ◽  
Author(s):  
Yuki Ozaki ◽  
Masanori Koide ◽  
Yuriko Furuya ◽  
Tadashi Ninomiya ◽  
Hisataka Yasuda ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Binding Peptide ◽  
Deficient Mice

scholarly journals Suppression of insulitis and diabetes in B cell-deficient mice treated with streptozocin: B cells are essential for the TCR clonotype spreading of islet-infiltrating T cells

2000 ◽  
Vol 12 (7) ◽  
pp. 1075-1083 ◽  
Author(s):  
Shiori Kondo ◽  
Isao Iwata ◽  
Keizo Anzai ◽  
Tomoyuki Akashi ◽  
Shigeharu Wakana ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Deficient Mice
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