Molecular imaging techniques for rheumatology: paving the way for novel molecular therapies

نویسنده

  • Luke L Gompels
چکیده

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease, primarily characterized by inflamed synovial tissue in multiple joints leading to localized destruction of cartilage and bone. It is a severe disabling disease that affects approximately 1% of the population on a worldwide basis [1]. RA is characterized by hyperplasia of the synovial lining layer and marked infiltration of synovium by lymphocytes, macrophages and plasma cells. Locally produced inflammatory mediators and the subsequent upregulation of adhesion molecules at sites of inflammation are pivotal to RA pathogenesis. Normal synovium is a highly vascular tissue that protects the joint, and provides oxygen, and nutrients to the synovial tissue, and to the relatively avascular cartilage. The normal synovium consists of an intimal lining, which is composed of macrophageand fibroblast-like cells that are loosely associated without a definite underlying basement membrane, and a relatively acellular sublining, which merges with the joint capsule and contains loose connective tissue containing fibroblasts, macrophages, adipocytes and vascular endothelial cells. In RA, the synovium is altered to a thickened and invasively growing tissue several cell layers thick, which covers and erodes the adjacent cartilage, bone and tendon. Histologically, the inflamed synovium shows pronounced angiogenesis, cellular hyperplasia and influx of inflammatory cells. Significant advances in understanding the underlying etiology of RA have been made. For example, a predominant role for major histocompatibility complex class II-dependent immune activation is supported by powerful evidence for antibody reactivity to proteins modified by citrullination [2]. Epidemiological and genetic studies of RA in relation to anticitrulline immunity have demonstrated significant differences in subsets of patients with and without the presence of antibodies to citrullinated protein antigens (ACPA). Antibodies to citrullinated proteins can be found in approximately 60% of RA patients but only in 2% of the normal population, making them highly specific for RA [3–5]. The occurrence of ACPA is linked to the HLA-DRB1 shared epitope alleles [6]. In addition to the previously established risk posed by smoking, there are further associations between those who are HLA-DRB1 positive and a close segregation with those who are ACPA positive [6]. Such progress in our understanding of the pathogenesis of RA has led to the introduction of novel biological therapies in RA, such as those that target TNF-a and other specific biological targets [7,8].

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تاریخ انتشار 2012