Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Impact of cytokines and T lymphocytes upon osteoclast differentiation and function. | Available online http content 9 2 103 Commentary Impact of cytokines and T lymphocytes upon osteoclast differentiation and function Matthew T Gillespie St Vincent s Institute of Medical Research Princes Street Fitzroy 3065 Victoria Australia Corresponding author Matthew T Gillespie mgillespie@ Published 21 March 2007 This article is online at http content 9 2 103 2007 BioMed Central Ltd Arthritis Research Therapy 2007 9 103 doi ar2141 Abstract Historically the osteoblast has been considered the master cell in the control of osteoclast development and therefore bone resorption. Now the interactions between cells of the immune system and bone cells have redefined our thinking on the regulation of bone resorption. Moreover the crosstalk between these cell types has special significance in inflammatory conditions such as rheumatoid arthritis. This report highlights the contribution that T lymphocytes make in regulating osteoclast formation and bone resorption. Rheumatoid arthritis the most common chronic autoimmune disease ultimately presents with joint destruction as a consequence of an inflammatory process. Whilst the pathogenesis for onset of this disease is not understood the final steps in the process leading to bone destruction have been recently resolved. It has been a long held view that infiltrating synovial cells are responsible for juxta-articular bone loss although it is now clear that the osteoclast is the only cell capable of resorbing bone. The recognition of this exclusive role for the osteoclast in all pathologies involving bone loss osteoporosis arthritis periodontal disease has identified a single cell whose function can be modulated to enhance or reduce bone loss 1 . The identification of the osteoclast and its role in bone destruction permits targeted therapy to reduce its resorptive capacity. Such therapies include the use of agents that can interfere with receptor activator of NFkB .
