Osteocytes, RANKL and bone loss

RANKL From Osteocytes Contributes to Periodontal Bone Loss

Periodontal bone loss results from bacterial infection and the associated host response. The ligand for the receptor activator of NF-κB (RANKL) induces the differentiation of osteoclasts, resulting in periodontal bone loss. The role of osteocytes in periodontal bone loss was investigated in this study. Transgenic mice expressing RANKL under the control of dentin matrix protein 1 (DMP1) were inf...

Role of RANKL and RANK in bone loss and arthritis.

The tumour necrosis factor family molecule RANKL (RANKL, TRANCE, ODF) and its receptor RANK are key regulators of bone remodelling and regulate T cell/dendritic cell communications, and lymph node formation. Moreover, RANKL and RANK are expressed in mammary gland epithelial cells and control the development of a lactating mammary gland during pregnancy and the propagation of mammalian species. ...

RANK, RANKL and osteoprotegerin in arthritic bone loss.

Rheumatoid arthritis is characterized by the presence of inflammatory synovitis and destruction of joint cartilage and bone. Tissue proteinases released by synovia, chondrocytes and pannus can cause cartilage destruction and cytokine-activated osteoclasts have been implicated in bone erosions. Rheumatoid arthritis synovial tissues produce a variety of cytokines and growth factors that induce mo...

Contribution of Rankl Regulation to Bone Resorption Induced by Pth Receptor Activation in Osteocytes

RANKL inhibition through osteoprotegerin blocks bone loss in experimental periodontitis.

BACKGROUND Prevention of alveolar bone destruction is a clinical challenge in periodontal disease treatment. The receptor activator of nuclear factor-kappa B ligand (RANKL) inhibitor osteoprotegerin (OPG) inhibits osteoclastogenesis and suppresses bone resorption. METHODS To study the effects of RANKL inhibition on alveolar bone loss, an experimental ligature-induced model of periodontitis wa...