Osteoclast

An osteoclast is a multinucleated cell that breaks down bone tissue. It develops from the monocyte–macrophage lineage and works with bone-forming osteoblasts to remodel the skeleton.

RANKL: RANKL is a signaling protein that promotes osteoclast formation, activation, and survival. It binds RANK on osteoclast precursors, driving their differentiation.
Monocyte: A monocyte is a circulating white blood cell that can develop into macrophages and related cell types. Osteoclast precursors arise from cells in the monocyte lineage.
Osteoporosis: Osteoporosis is a skeletal disorder characterized by reduced bone strength and increased fracture risk. Excess resorption by osteoclasts can contribute to the loss of bone mass.
Caffey disease: Caffey disease is an inherited disorder involving episodic inflammation and excessive bone formation in infancy. Some cases involve altered RANK signaling, linking osteoclast regulation to abnormal bone growth.
RANK: RANK is a cell-surface receptor in the tumor necrosis factor receptor family. Its activation by RANKL initiates the signaling needed for osteoclast development.
Macrophage: A macrophage is a tissue-resident immune cell that engulfs microbes, debris, and damaged cells. Osteoclasts share developmental ancestry and molecular features with macrophages.
Bisphosphonate: Bisphosphonates are drugs that bind bone mineral and suppress osteoclast-mediated resorption. They reduce osteoclast activity and are widely used to treat osteoporosis.
Pycnodysostosis: Pycnodysostosis is a rare inherited skeletal disorder caused by deficient cathepsin K activity. Its impaired matrix degradation shows the importance of osteoclast-secreted cathepsin K.
Osteoprotegerin: Osteoprotegerin is a soluble decoy receptor that binds RANKL. By sequestering RANKL, it limits osteoclast formation and bone resorption.
Osteoblast: An osteoblast is a cell that forms new bone by producing and mineralizing bone matrix. Osteoblasts counterbalance osteoclast resorption during bone remodeling.

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