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

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 Involvement of SOCS3 in Regulation of CD11c+ Dendritic Cell-Derived Osteoclastogenesis and Severe Alveolar Bone Loss

2009 ◽  
Vol 77 (5) ◽  
pp. 2000-2009 ◽  
Author(s):  
Xiaoxia Zhang ◽  
Mawadda Alnaeeli ◽  
Bhagirath Singh ◽  
Yen-Tung A. Teng
Keyword(s):  
T Cells ◽  
Dendritic Cell ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Expression Profiles ◽  
Critical Role ◽  
Alveolar Bone Loss ◽  
Cytokine Signaling ◽  
Periodontal Inflammation ◽  
Socs3 Expression

ABSTRACT To investigate the role of suppressor of cytokine signaling (SOCS) molecules in periodontal immunity and RANKL-mediated dendritic cell (DC)-associated osteoclastogenesis, we analyzed SOCS expression profiles in CD4+ T cells and the effect of SOCS3 expression in CD11c+ DCs during periodontal inflammation-induced osteoclastogenesis and bone loss in nonobese diabetic (NOD) versus humanized NOD/SCID mice. Our results of ex vivo and in vitro analyses showed that (i) there is significantly higher SOCS3 expression associated with RANKL+ T-cell-mediated bone loss in correlation with increased CD11c+ DC-mediated osteoclastogenesis; (ii) the transfection of CD11c+ DC using an adenoviral vector carrying a dominant negative SOCS3 gene significantly abrogates TRAP and bone-resorptive activity; and (iii) inflammation-induced TRAP expression, bone resorption, and SOCS3 activity are not associated with any detectable change in the expression levels of TRAF6 and mitogen-activated protein kinase signaling adaptors (i.e., Erk, Jnk, p38, and Akt) in RANKL+ T cells. We conclude that SOCS3 plays a critical role in modulating cytokine signaling involved in RANKL-mediated DC-derived osteoclastogenesis during immune interactions with T cells and diabetes-associated severe inflammation-induced alveolar bone loss. Therefore, the development of SOCS3 inhibitors may have therapeutic potential as the target to halt inflammation-induced bone loss under pathological conditions in vivo.

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.

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.

1728-P: Inhibition of PKC-Theta in Prediabetic NOD Mice Prevents Diabetes Onset and Increases Regulatory CD4 T Cells in a Subset of Animals

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1728-P
Author(s):  
JAMES E. DILISIO ◽  
NOAH MISHKIN ◽  
BRENDAN PODELL
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Nod Mice ◽  
Diabetes Onset

EFFECTS OF ALENDRONATE THERAPY ON CYCLOSPORINE INDUCED ALVEOLAR BONE LOSS : A MORPHO-METRIC AND BIO-CHEMICAL STUDY IN RATS

2016 ◽  
Vol 4 (4) ◽  
pp. 947-955
Author(s):  
Sneha R Bhat ◽  
◽  
Aravind R Kudva ◽  
Dhoom S Mehta ◽  
◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Chemical Study ◽  
Alveolar Bone Loss

3,4,5-Trihydroxybenzoic acid attenuates ligature-induced periodontal disease in Wistar rats.

2020 ◽  
Vol 19 ◽  
Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek
Keyword(s):  
Bone Loss ◽  
Gallic Acid ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Collagenase Activity ◽  
Osteoblastic Activity ◽  
Cell Counts ◽  
Experimental Periodontitis ◽  
Anti Inflammatory

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.

scholarly journals Gram-positive bacteria cell wall-derived lipoteichoic acid induces inflammatory alveolar bone loss through prostaglandin E production in osteoblasts

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tsukasa Tominari ◽  
Ayumi Sanada ◽  
Ryota Ichimaru ◽  
Chiho Matsumoto ◽  
Michiko Hirata ◽  
...  
Keyword(s):  
Cell Wall ◽  
Bone Loss ◽  
Alveolar Bone ◽  
Osteoclast Differentiation ◽  
Lipoteichoic Acid ◽  
Alveolar Bone Loss ◽  
Gram Negative Bacteria ◽  
Gram Positive ◽  
Gram Negative ◽  
Gram Positive Bacteria

AbstractPeriodontitis is an inflammatory disease associated with severe alveolar bone loss and is dominantly induced by lipopolysaccharide from Gram-negative bacteria; however, the role of Gram-positive bacteria in periodontal bone resorption remains unclear. In this study, we examined the effects of lipoteichoic acid (LTA), a major cell-wall factor of Gram-positive bacteria, on the progression of inflammatory alveolar bone loss in a model of periodontitis. In coculture of mouse primary osteoblasts and bone marrow cells, LTA induced osteoclast differentiation in a dose-dependent manner. LTA enhanced the production of PGE2 accompanying the upregulation of the mRNA expression of mPGES-1, COX-2 and RANKL in osteoblasts. The addition of indomethacin effectively blocked the LTA-induced osteoclast differentiation by suppressing the production of PGE2. Using ex vivo organ cultures of mouse alveolar bone, we found that LTA induced alveolar bone resorption and that this was suppressed by indomethacin. In an experimental model of periodontitis, LTA was locally injected into the mouse lower gingiva, and we clearly detected alveolar bone destruction using 3D-μCT. We herein demonstrate a new concept indicating that Gram-positive bacteria in addition to Gram-negative bacteria are associated with the progression of periodontal bone loss.

scholarly journals The Protective Effect of Rhizoma Dioscoreae Extract against Alveolar Bone Loss in Ovariectomized Rats via Regulating Wnt and p38 MAPK Signaling

Nutrients ◽  
2014 ◽  
Vol 6 (12) ◽  
pp. 5853-5870 ◽  
Author(s):  
Zhiguo Zhang ◽  
Lihua Xiang ◽  
Dong Bai ◽  
Wenlai Wang ◽  
Yan Li ◽  
...  
Keyword(s):  
Bone Loss ◽  
Protective Effect ◽  
P38 Mapk ◽  
Alveolar Bone ◽  
Mapk Signaling ◽  
Alveolar Bone Loss ◽  
Ovariectomized Rats
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