July 22, 2005
Osteoarthritis of the temporomandibular joint (TMJ) - where the jaw and skull bones meet on both sides of the head - is one of the more common of the over 20 pathologic conditions that are known to affect this joint. Typically, those who develop this condition receive a diagnosis only when damage to the TMJ is so advanced that it is visible with current imaging techniques. Prior to this point, dentists and doctors have no way of detecting an early and potentially more easily treatable arthritic condition. That’s why scientists continue to search for molecular clues that one day might offer an early warning of trouble to come. Fueling these investigations are three types of specially bred laboratory mice whose arthritic conditions in the TMJ broadly mimic those in people. Now, in the July issue of the journal Osteoarthritis and Cartilage, NIDCR scientists and colleagues report success in developing a fourth mouse model that will further enable the research. The latest mouse model cannot make the proteoglycans biglycan and fibromodulin, both of which play an important role in regulating the formation of filament-like collagen fibrils, a key structural component of bone and other mineralized tissues. According to the scientists, the absence of these proteoglycans seems to accelerate osteoarthritis, possibly by altering the biomechanical properties of the joint. Before the appearance of visible osteoarthritis, the scientists also identified a marked decrease in cell proliferation within the cartilaginous portions of the jawbone’s ball-like condyle. They now can pursue this lead in greater detail, possibly allowing them valuable insights into the earliest stages of the disease process.