The above findings identify a role for Wnt-7b in arthritic processes. Arthritic diseases manifest differently depending on the type, with RA exhibiting inflammation of the synovium and loss of cartilage and bone and OA exhibiting narrowing of joint space, loss of protective cartilage, and growth of bone cysts (or osteophytes).
Interestingly, Wnt-7b was strongly upregulated within joints at sites of disease manifestation: mainly in synovium of RA but in synovium, cartilage, osteophyte, and bone of OA. In addition, the findings that Wnt-7b was frequently found at sites of inflammation and elicited an inflammatory response are consistent with inflammation as a hallmark of RA disease.
Co-author Dr. Yukio Nakamura is an Orthopedic Surgeon at Shinshu University School of Medicine and is currently at Howard Hughes Medical Institute/Case Western Reserve University as a research associate. Nakamura has been studying the biological activities and signaling pathway of a Wnt-related gene that causes severe joint degenerative disease in humans.
"More specific analyses such as gain-of-function and loss-of-function study of Wnt-7b will give us a clue which Wnt-7b would be an important pathobiological factor in rheumatoid arthritis," added Nakamura. Future studies will investigate the role of Wnt and its signaling partners in arthritic joint destruction. Further delineation of the Wnt signaling pathway in arthritic progression may provide future therapies for the growing number of arthritis suffers.
According to The National Center for Health Statistics, over 42 million US adults, or 20% of the population, complained of arthritic symptoms in 2002.