Researchers at Stanford University have identified a protein-producing gene that acts as a form of tartar control for joints. When the gene mutates the result is a build up of excessive mineral deposits in joints which commonly leads to many arthritic conditions. The findings are the first to confirm a theory that researchers have speculated on for 20 years.
The protein appears to govern the flow of mineral-reducing pyrophosphate into joint tissues. Pyrophosphate is the substance used in toothpaste to control calciferous plaque on tooth surfaces. The researchers, led by Dr. David M. Kingsley, believe that their findings could offer powerful new insights into the basic mechanisms that underlie some forms of arthritis—a group of diseases that afflicts half of people 65 and older and accounts for $100 billion in medical costs and lost productivity each year. The new study was published in the July 14th issue of Science magazine.
Although the joint disease in the mice is more severe and widespread than that seen in humans, many of the pathological processes involved resemble those seen in human arthritis. “By studying a severe form of disease in an animal model, we hoped we might be able to identify basic molecular mechanisms that may apply to milder forms of disease as well,” said Kingsley.
Kingsley and his colleagues, were able to track changes in articular cartilage, an area of the skeleton which is normally free of deposits. The team observed that the mice with thedefective gene had abnormal mineral deposits “ultimately leading to loss of mobility, inflammation and joint destruction.”
Further studies of the ank gene in both animals and humans could offer important new insights into arthritic diseases as well as disorders of soft tissue calcification outside of joints.