IL1B and postmenopausal osteoporosis: Evidence from animal and in vitro studies suggests that increases in these cytokines promote bone resorption through several mechanisms, including increasing osteoclast differentiation, activation, and survival; enhancing RANKL expression; and inhibiting osteoblast survival.[32–34] TNF-α has long been implicated in osteoclast formation in postmenopausal osteoporosis through 2 mechanisms, the 1st process occurs when stromal cells are exposed to TNF-α and to amplify RANKL, M-CSF, and IL-1, which enhance osteoclast activation and differentiation.