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This coupled ALPL activity alters the P i/PP i ratio in the bone microenvironment to favor bone mineralization.
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This facilitates bone ECM mineralization in two ways: first, it reduces the level of a mineralization inhibitor, and second, in the process generates P i, an activator of ECM mineralization. Alkaline phosphatase (ALPL), an ectoenzyme tethered to the osteoblast cell membrane, cleaves inorganic pyrophosphate (PP i), a small, but potent mineralization inhibitor. Serum calcium (Ca 2+), inorganic phosphate (P i) levels, and a mineral scaffolding collagen-rich extracellular matrix (ECM) are important determinants of bone mineralization. The current review will discuss the key determinants of ECM mineralization in bone and propose a unified model explaining this process.Ĭopyright © 2018 Cold Spring Harbor Laboratory Press all rights reserved. More recently, intracellular enzyme regulators of skeletal tissue mineralization have been identified. These pathways regulate the homeostasis of ionic calcium and inorganic phosphate-two mineral components required for bone mineral formation, the synthesis of mineral scaffolding ECM, and the maintainence of the levels of the inhibitory organic and inorganic molecules controlling the process of mineral crystal formation and its growth. However, the explosion of genetic studies during the past decades has established that this process is essentially controlled by multiple genetic pathways.
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For a long time, extracellular matrix (ECM) mineralization in the vertebrate skeleton was considered as a passive process. Mineralized "hard" tissues of the skeleton possess unique biomechanical properties to support the body weight and movement and act as a source of essential minerals required for critical body functions.