Smoking promotes the development of rheumatoid arthritis
Erlangen medical scientists present new research findings
Smoking increases the risk of developing rheumatoid arthritis. However, in addition to genetic factors other external influences also play a major role in the development of the autoimmune disease. Knowledge about the various triggers and molecular mechanisms involved in the development of rheumatoid arthritis are advancing the development of new and more effective therapies. Dr. Georg Schett, director of Medical Clinic 3 at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and specialist colleagues from other renowned universities speak about the current state of research progress in two review articles published in the renowned specialist journals Nature Medicine and New England Journal of Medicine.
Rheumatoid arthritis belongs to the group of the diseases whereby immune cells attack the body’s own cells. The disease is a result of a complex interplay of genetic factors, environmental influences and infections. Pain and swelling in the finger joints are often the first external symptoms of the disease. The underlying inflammation can cause damage to the bone and joint system, and as the disease progresses it can also lead to various organ disorders.
On the basis of genetic studies, research scientists have been able to prove that genetic predisposition is not the only factor to influence the development of rheumatoid arthritis. Infections such as inflammation of the gums (periodontitis) and the Epstein-Barr virus, and habits such as smoking can also increase the risk of developing rheumatoid arthritis. Experimental studies have revealed that cigarette smoke affects the immune system: nicotine attaches itself to specific receptors found on the surface of immune cells which can in part lead to their activation. Furthermore, cigarette smoke can also trigger a reaction that alters the body’s own proteins. The immune system then recognises these proteins as foreign and attacks them.
Several molecular interactions which are responsible for inflammatory response and bone damage have already been explored. The results of which have made a significant contribution to the development of new clinical therapies. “In order to develop new, effective and sustainable treatment methods – by more accurately localising the inflammation of the bones – we have to close the existing knowledge gap and better understand the triggers and molecular mechanisms at play”, explains Professor Schett. “In order to achieve this goal the existing experimental models require further development. Ultimately we need models with a holistic approach.”
Research into the development process of autoimmune diseases poses a great problem in terms of fundamental research, as the trigger event must first be generated artificially and does not necessarily correspond to the actual mechanisms at work. Furthermore, autoimmune models should take into account the chronological sequence of a disease in accordance with the human disorder. The creation of a disease model that is representative of a clinical phenotype could help accelerate research into the development of rheumatoid arthritis and guarantee the more rapid implementation of research findings into clinical practice as well as the development of new diagnosis and treatment methods. Ultimately, this could result in the more effective relief of patient suffering and attenuate disease activity. In addition, this step fuels hopes of implementing new preventive diagnostic measures.
More information for the media:
Prof. Dr. Georg Schett
uni | media service | research No. 11/2012 on 29.3.2012