The fact that RASFs are found in such abundance in the spleens of the rheumatoid arthritis mice provides strong evidence that RASFs travel through the blood stream to do their damage rather than just secrete chemicals that go into the blood stream.Recent research has provided tantalizing evidence as to how rheumatoid arthritis spreads.On one flank, the mice received healthy, normal human cartilage; on the other, they received cartilage loaded with human RASFs. The mice which developed rheumatoid arthritis had spleens packed with RASFs.[Editor's note.

I personally think this is one of the most exciting bits of news in a long time and the authors should be commended for such fine work.Researchers at Justus-Liebig University in Bad Nauheim, Germany recently published the results of their work in Nature Medicine demonstrating the critical role of rheumatoid arthritis synovial fibroblasts in the spread of the disease. Jeckyll knitted fabric manufacturers into Mr Hyde.These turned-on fibroblasts, now known as rheumatoid arthritis synovial fibroblasts, are present in abundance in the synovium- the lining of the joint. However, when turned on in a particular fashion, they morph from Dr. They are responsible for the laying down of connective tissue.

Apparently RASFs can travel via the blood stream and then leave by crawling through the spaces between cells that form the lining of the blood vessels to invade other joints and other organ systems. These RASFs become very destructive and are felt to be one of the major culprits responsible for the damage to cartilage found in rheumatoid arthritis. The implantations were done in the flanks.The scientific findings have therapeutic implications since treatments designed to prevent RASFs from entering the bloodstream, traveling through the blood stream, or leaving the blood stream to attack healthy tissue could potentially prevent the spread of rheumatoid arthritis. Also, because internal organs may be affected, it is a disease that carries with it substantial morbidity complications as well as mortality (death).When the researchers look at the joints of the sacrificed mice, they didnt find RASFs. The hallmark of the disease is its symmetrical joint involvement. This would explain why it often takes many months for rheumatoid arthritis to spread. They hypothesized that it takes time for the RASFs to travel to other joints and can only enter cartilage if there is already some minor damage.One of the mysteries in the understanding of a complicated disease like rheumatoid arthritis is how does it attack so many joints? What causes it to spread?Rheumatoid arthritis is a chronic, systemic, autoimmune condition that usually starts in a single joint but then spreads to involve multiple joints.

Rheumatoid arthritis is very different from the other common form of arthritis, osteoarthritis, which is basically a wear and tear problem localized to weight-bearing joints.A control group of mice who received normal healthy cartilage in both flanks showed minimal damage, as did mice that received implants of fibroblasts from patients with osteoarthritis. Osteoarthritis does not produce the destructive changes that are characteristic of rheumatoid disease.Fibroblasts are a type of cell that is primarily involved in the wound healing process.To elucidate the mechanism by which RASFs could spread arthritis from joint to joint, lead author Elena Neumann and her colleagues took human cartilage and implanted it under the skin of mice genetically engineered not to reject tissue from a different species.Another striking discovery occurred when the researchers sacrificed the mice and examined the spleens. The spleen is the major organ responsible for filtering blood.