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The **dentino-enamel junction** (DEJ) is the complex interface where **enamel**—the hardest and most mineralized tissue of the tooth—meets the underlying **dentin**, a slightly softer and less mineralized tissue[1][2][3][4]. The DEJ is not a discrete molecule or receptor but a structural boundary with unique architecture crucial for mechanical robustness of the tooth. It is characterized by a supramolecular assembly of mineral (hydroxyapatite crystals), collagen fibrils from dentin, and specific enamel and dentin extracellular matrix proteins (such as amelogenin, enamelin, and dentin matrix acidic phosphoprotein 1)[1]. This interface dissipates mechanical stress, provides crack resistance, and integrates two mechanically contrasting tissues—hard enamel and flexible dentin—ensuring long-term durability under repeated occlusal forces[1][3][4][5]. **Note:** - The "tooth enamel/dentin mineral interface" is not a single gene, receptor, or druggable molecular entity, but a histological and biomechanical region, making it unsuitable as a classical therapeutic target. - Any search for interacting drugs, biomarkers, or targeted therapies is not applicable[1][2][3][4][5]. - If a molecular target within this interface is needed, consider components like "Amelogenin", "Dentin matrix protein 1", or enzymes like "Matrix metalloproteinase-20 (MMP20)", which participate in enamel or dentin matrix modulation.
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