In studies with mice, scientists have found evidence that osteoporosis-like bone disorders and inflammatory intestinal disorders are both caused by the abnormal regulation of a common protein. Dr. Simon R. Carding from the University of Leeds in England and colleagues report their study in the December issue of the journal Immunity. Autoimmune-related bone disease and intestinal inflammation are closely linked with the deregulation and the hyperactivation CD4 T cells, which are involved in the body's defense system, or immune response, they report. "How these T cells are activated and mediate disease is not clear." Mice that were genetically engineered to lack a key regulator of CD4 T cells have overactive T cells and spontaneously develop ulcerative colitis and the loss of bone cells, the scientists explain. Carding and colleagues' experiments indicate that this is caused by increased production of a protein called RANKL. "We find that the hyperactive CD4 T cells produce too much of this protein, which then contributes to bone breakdown and bowel inflammation," Carding said. Treating mice with osteoprotegerin, a protein that prevents RANKL from binding to its receptor, reversed this bone loss and improved colitis. "This study shows that some bone diseases and intestinal problems may share a common cause," Carding told. "If similar mechanisms occur in humans, then osteoprotegerin might prove a useful treatment for intestinal disorders such as ulcerative colitis and Crohn's disease," he said, which are both often accompanied by bone loss.