Bone resorption pathways

"Bone resorption pathways" is not the name of a specific molecule or receptor but rather refers to a collection of molecular signaling cascades that regulate the breakdown and removal of old or damaged bone tissue by specialized cells called osteoclasts. The most prominent among these is the RANK/RANKL/OPG pathway, where receptor activator of nuclear factor kappa-B ligand (RANKL) produced by osteoblasts binds to its receptor RANK on preosteoclasts to stimulate their maturation into active osteoclasts that mediate resorption. This process is tightly regulated by other factors such as Wnt signaling—which can suppress excessive resorptive activity—and molecules like citrate that participate in energy metabolism during both formation and breakdown phases. These interconnected pathways are central targets for osteoporosis therapies; drugs such as bisphosphonates and denosumab act by inhibiting key steps within these cascades to reduce fracture risk. However, "bone resorption pathways" itself does not refer to a single druggable target but rather an entire network involved in skeletal homeostasis.[1][3][4][5]

Other names

Bone resorption signaling pathwaysBone remodeling pathwaysBone metabolic pathways

- Inhibition of osteoclast-mediated bone resorption (bisphosphonates, denosumab, calcitonin) - Modulation of RANKL-RANK pathway to reduce osteoclast activity and promote bone formation (denosumab)