Day 1 :
Warsaw Medical University, Poland
Time : 10:00-10:40
Margaret Wisłowska, Head of The Department of Internal Medicine and Rheumatology CSK MSW is a specialist in internal medicine, rheumatology, rehabilitation medicine, hypertension, and the author of over 200 scientific papers and books. She has participated in numerous scientific meetings and is a promoter of 12 Ph.D. theses. She took training at Guy and St. Thomas’ Hospitals in London, Charity Hospital in Berlin, Rheumatology Institutes in Prague and Moscow. In 2003, she started the Department of Internal Medicine and Rheumatology, and in 2010 the Clinic of Internal Medicine and Rheumatology CSK MSW. She is a Professor at the Warsaw Medical University.
RA is a chronic inflammatory disease affecting approximately 0.5-1% of the population, characterized by symmetric, erosive arthritis of the synovial joints and variable extra-articular features. The primarily affected site is the synovium where “pannus” is gradually formed. Typical articular symptoms include pain, stiffness and swelling. The progressive destruction of the articular cartilage may lead to deformation and loss of function of affected joints. The goal of treatment is to reduce mortality and to prevent joint damage and disability. RA imposes a substantial economic burden on both patients and society. The etiopathogenesis of RA is only partially understood. Its onset is triggered by environmental factors on the basis of a genetic predisposition in combination with altered immune responses. Tobacco and infection by Porphyromonas gingivalis during periodontal diseases favor ACPA production which has a crucial role in RA pathogenesis. Cytokine networks involving TNFα, IL-1β, 6, 15 and 17, matrix metalloproteinases and many other factors participate in disease perpetuation. Bone and cartilage destruction are primarily mediated by osteoclasts and fibroblasts – like synoviocytes, respectively. Although RA is primarily considered a disease of the joints, abnormal systemic immune responses can cause a variety of extra – articular manifestations. One of the current issues in rheumatology is the type and extent of pathological changes in the heart in the course of rheumatoid arthritis. The problems with diagnosis are due to a very limited number of clinical symptoms showing that cardiac muscle is affected by a disease process and that symptoms do not always appear. The results of epidemiological studies point to the presence of an increased risk of cardiovascular disease (CVD), particularly atherosclerosis and congestive heart failure (CHF) in RA. Necropsy examinations of RA hearts revealed a higher prevalence of clinically silent myocardial nodules, restrictive pericarditis and coronary vasculitis in RA compared to non-RA patients. At least 50% of abnormalities remained asymptomatic. Pathological conditions contributing to myocardial dysfunction such as high serum levels of IL-6, C-reactive protein and TNF alpha are present both in RA and CHF patients. The most common pathological mechanism leading to the development of heart failure is left ventricular diastolic dysfunction, which remains clinically asymptomatic for a long time. The presence of heart disease in RA patients is not only dependent on concurrent heart disease but is also caused by RA disease.
University of Arizona Arthritis Center, AZ
Time : 10:40-11:20
Dr. Kwoh’s research group has had a long interest in the epidemiology of a broad spectrum of rheumatic and musculoskeletal diseases, with a particular focus on the epidemiology of, and outcome assessment in osteoarthritis. He is currently engaged in several lines of research examining biomarkers, early indicators, pain, outcome assessment, and the examination of risk factors for the development and progression of osteoarthritis. His current work focuses on the identification of biomarkers for outcomes in knee osteoarthritis. One line of research examines quantitative and semi-quantitative assessment of imaging features on MRI that are associated with the incidence of radiographic knee osteoarthritis or progression to total joint replacement. Another line of research examines the characterization of knee pain patterns and MRI features associated knee pain in osteoarthritis.
Pain is an important feature of osteoarthritis and is the most common presenting symptom. Multiple standardized measures have been developed to assess pain. The etiology of pain in osteoarthritis is unclear, however, and is likely to be heterogeneous. Osteoarthritis is recognized as being a disease of the whole joint. Cartilage is aneural, but the subchondral bone, the periosteum, peri-articular ligaments, peri-articular muscle, synovium and the joint capsule are all richly innervated and may be sources of nociceptive pain in osteoarthritis. Central sensitization may also play a role in chronic knee pain. The complexity of pain in osteoarthritis is highlighted by the apparent lack of correlation between individual’s report of pain and the changes seen on knee radiographs. Advances in magnetic resonance imaging (MRI), however, have improved our understanding of the relationship between pathology and the structural changes to cartilage, subchondral bone and the surrounding soft-tissues of joint in osteoarthritis. Relationship between morphologic features and knee pain is dependent on the specific MRI feature and method of assessing knee pain. Cross-sectional studies suggest that morphologic changes on MRI such as bone marrow lesions (BMLs), effusion-synovitis, denuded bone area and meniscal extrusion are associated with frequent knee pain and weight-bearing pain, whereas longitudinal studies suggest that incident frequent knee pain is associated with new bone marrow lesions, new denuded bone area, or enlarging bone marrow lesions and development of inflammation such as effusion-synovitis or Hoffa-synovitis. Recent studies have advanced our understanding of potential etiologies for osteoarthritis-related pain and have helped to identify potential targets for pharmacologic and non-pharmacologic treatments.