B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease - Wikidata - wikimedia - TriplyDB

B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease

B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease

http://www.wikidata.org/entity/Q35222008

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Activated human T cells express alternative mRNA transcripts encoding a secreted form of RANKL The role of "bone immunological niche" for a new pathogenetic paradigm of osteoporosis Paget's disease of bone: an osteoimmunological disorder?Host response mechanisms in periodontal diseases The role of osteoimmunology in periodontal disease Periodontal disease: linking the primary inflammation to bone loss Osteoimmunology: Major and Costimulatory Pathway Expression Associated with Chronic Inflammatory Induced Bone Loss HIV: inflammation and bone Periodontal disease immunology: 'double indemnity' in protecting the host Functional Local Renin-Angiotensin System in Human and Rat Periodontal Tissue Porphyromonas gingivalis suppresses adaptive immunity in periodontitis, atherosclerosis, and Alzheimer's disease Defective neutrophil recruitment in leukocyte adhesion deficiency type I disease causes local IL-17-driven inflammatory bone loss.Activation of Toll‐like receptor 9 inhibits lipopolysaccharide‐induced receptor activator of nuclear factor kappa‐ B ligand expression in rat B lymphocytes.The potential of p38 MAPK inhibitors to modulate periodontal infections.Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis.Identification of immunological parameters associated with the alveolar bone level in periodontal patients.B cells promote obesity-associated periodontitis and oral pathogen-associated inflammation Daidzein prevents the increase in CD4+CD28null T cells and B lymphopoesis in ovariectomized mice: a key mechanism for anti-osteoclastogenic effect.Impact of the Oral Commensal Flora on Alveolar Bone Homeostasis.Alterations in the immuno-skeletal interface drive bone destruction in HIV-1 transgenic rats.How B cells influence bone biology in health and disease PKA-induced receptor activator of NF-kappaB ligand (RANKL) expression in vascular cells mediates osteoclastogenesis but not matrix calcification Constitutive expression of TNF-related activation-induced cytokine (TRANCE)/receptor activating NF-κB ligand (RANK)-L by rat plasmacytoid dendritic cells.Cytokine-mediated bone destruction in rheumatoid arthritis.Infection of RANKL-primed RAW-D macrophages with Porphyromonas gingivalis promotes osteoclastogenesis in a TNF-α-independent manner.Transcriptional profiling of bone marrow stromal cells in response to Porphyromonas gingivalis secreted products Dysregulated B cell expression of RANKL and OPG correlates with loss of bone mineral density in HIV infection Antibody to receptor activator of NF-κB ligand ameliorates T cell-mediated periodontal bone resorption.Using tetracyclines to treat osteoporotic/osteopenic bone loss: from the basic science laboratory to the clinic.RNAi-mediated silencing of Atp6i and Atp6i haploinsufficiency prevents both bone loss and inflammation in a mouse model of periodontal disease 18β-glycyrrhetinic acid inhibits periodontitis via glucocorticoid-independent nuclear factor-κB inactivation in interleukin-10-deficient mice.Role of periodontal pathogenic bacteria in RANKL-mediated bone destruction in periodontal disease.Review of osteoimmunology and the host response in endodontic and periodontal lesions.T-cells and B-cells in osteoporosis Do γδ T cells predict osteonecrosis of the jaw?Inflammation and uncoupling as mechanisms of periodontal bone loss Selective serotonin reuptake inhibitors attenuate the antigen presentation from dendritic cells to effector T lymphocytes.Tumour-infiltrating regulatory T cells stimulate mammary cancer metastasis through RANKL-RANK signalling.Cytokine mRNA profiling identifies B cells as a major source of RANKL in rheumatoid arthritis.Bone-immune cell crosstalk: bone diseases.

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B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease

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Cory W O Ernst

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Leticia A Miranda

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Makoto Seki

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Selective diapedesis of Th1 cells induced by endothelial cell RANTES

Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation

Osteoprotegerin: a novel secreted protein involved in the regulation of bone density

RANK is essential for osteoclast and lymph node development

Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families

Bone resorption by osteoclasts

Potassium channel-blockers as therapeutic agents to interfere with bone resorption of periodontal disease

OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis

Osteoclast differentiation and activation

Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand

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