Juvenile Idiopathic Arthritis (JIA)

Hala Etayari
Etiology and Pathogenesis
JIA is characterized by chronic inflammatory process involving the synovial membrane, bone and cartilage. Histologically what is found is the infiltration of the synovium by lymphocytes, plasma cells, macrophages and dendritic cells. Another prominent feature is the proliferation of fibroblasts and macrophage-like synoviocytes.
Th1 cells driven by population of cytokine and chemokine producing T-cells are believed to mediate the inflammation in JIA.
The most important cytokines that play a role in JIA and targeted by the most recent drugs developed for the treatment are Tumor necrotizing facor-a (TNF-a), IL-1 and IL-6.
Antigen-driven T cells also play a central role in the pathogenesis of JIA.
Systemic onset JIA histologically can be classified as a subtype of JIA but pathologically better classified as an autoinflammatory syndrome.
What causes the inflammation in JIA is unknown, but it is believed to be multifactorial. Some of the factors that may play a role are:
• Maternal smoking which increase the risk of developing JIA.
• Breast feeding decrease the risk of developing JIA.
• Infections by many bacteria and viruses plays a role in the initiation and the augmentation of the symptoms of JIA.
• Vaccines may act as disease triggers.
• Vitamin D deficiency also may play a role.
The causal relationship between JIA and environmental factors is obscure and requires more investigation.
Also genetics play a role where several genetic loci have been proposed to be associated with susceptibility to and severity of JIA.

Juvenile Idiopathic Arthritis (JIA) Juvenile Idiopathic Arthritis (JIA) 05/11/2016
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