Psoriasis (Ps) is the most common chronic autoimmune disease in the United States. The immune system releases proinflammatory cytokines and growth factors that accelerate the growth of skin cells which accumulate and form thick red patches of skin on various parts of the body. About 25 percent of psoriasis patients develop inflammatory arthritis in which inflammation progresses to joints and entheses. Psoriatic Arthritis (PsA) patients exhibit joint pain, stiffness, and swelling which can affect any part of the body. PsA occurs when the immune cells release cytokines that act on healthy cells and tissues to induce skin and joint inflammation. Genetic and environmental factors interact to trigger the cellular pathways that promote skin and joint disease. Research studies on the pathophysiology of psoriatic arthritis have revealed that alterations in both immune cells and resident cells in the skin and joint characterize this disease. Dr. Christopher Ritchlin's research focuses on the links between skin and joint inflammation. His laboratory is examining the mechanisms of bone resorption and formation, the effect of anti-TNF agents on dendritic cell differentiation, and the mechanisms of bone marrow edema (a finding on MRI of the joints) observed in PsA and rheumatoid arthritis. His current research demonstrates a mechanism for the destructive pathology in psoriatic joints. The purpose of my thesis is to illustrate Dr. Ritchlin's research. It will be a 2-dimensional animation explaining normal bone remodeling and the bi-directional attack on PsA joints. Accompanying the animation is a voice over explaining what is happening on screen.
Myers, Laurel, "Mechanisms of psoriatic arthritis" (2012). Thesis. Rochester Institute of Technology. Accessed from
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