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Hydroxyapatite formation via calcium and hydroxide ion release from calcium silicate cements

Molecular classification
Other
01

Overview

This target describes the process by which **hydraulic calcium silicate cements** (such as mineral trioxide aggregate) facilitate **hydroxyapatite formation** at the application site, primarily through the release of calcium and hydroxide ions during hydration of tri- and dicalcium silicates. These ions increase local alkalinity, react with phosphate from tissue fluids, and induce the precipitation of calcium phosphate, which ultimately transforms into hydroxyapatite—the principal mineral of bone and dentin. This process promotes hard tissue regeneration and provides a seal, with additional antimicrobial properties resulting from alkaline pH. The mechanism is foundational to the clinical application of these materials in endodontics and bone repair, although this is a *bioactive material behavior* rather than a distinct molecular target or receptor[1][3][5][6][7].

02

Mechanism of action

Release of calcium and hydroxide ions increases local pH, dissolves phosphate esters, and promotes precipitation of calcium phosphate, leading to hydroxyapatite formation[1][3][5][7]. Formation of hydroxyapatite enhances sealing and supports hard tissue cell attachment and differentiation[1][3][5][6].

03

Biological functions

Hard tissue regenerationTissue sealingBioactivity (apatite formation)Promotion of osteogenesis and cementogenesisAntimicrobial environment (due to alkaline pH)
04

Disease associations

Dental hard tissue repair (e.g., pulp capping, root-end filling)Bone defect repairEndodontic regeneration
05

Safety considerations

Initial cytotoxicity due to high pH immediately after material placement[6]Extended setting time can limit applicability in some clinical contexts[7]Material-dependent tissue response variability, especially with modified or new-generation cements[1]

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