This ScienceDaily release provides insight into present mainstream research into the mechanisms of osteoporosis and rheumatoid arthritis: a matter of scientists investigating and debating mechanisms to find the next and better target for viable drug development. "Bone is continually recycled to maintain its strength through the competing action of osteoclasts, cells that break down aging bone, and osteoblasts, which build new bone. Osteoclasts also play a central role in common diseases that erode bone, where two signaling molecules, TNF-alpha and RANKL, cause too much bone breakdown. ... the current study argues that TNF-alpha and RANKL have different effects on levels of a key inhibitory protein [called] NF-kappaB p100 ... We believe NF-kappaB p100 limits not only osteoclast maturation, but also the number of inflammatory cells attracted to the joints in response to TNFalpha. If confirmed, it would mean that p100 has more than one role in more than one major bone disease, and thus would create new opportunities to reverse disease by manipulating p100 levels."