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Dentinal tubules are microscopic, fluid-filled channels that traverse the dentin layer of the tooth, connecting the internal pulp to the outer enamel or cementum (Brännström, 1963). When these tubules become exposed through enamel loss or gingival recession, they serve as the primary pathway for stimuli to reach pulpal nerves, leading to dentin hypersensitivity. Demineralized dentin hydroxyapatite surfaces refer to the mineral component of the tooth that has undergone ion loss due to acidic challenges, creating a porous substrate (Cochrane et al., 2010). These structures are the therapeutic targets for desensitizing agents and remineralizing treatments. Drugs targeting these surfaces typically function by occluding the tubule orifices to prevent fluid movement or by providing mineral precursors to restore the hydroxyapatite lattice (Cummins, 2009). Furthermore, the integrity and chemical state of these surfaces are vital for the success of dental adhesives and restorative materials in clinical practice (Markowitz & Pashley, 2008).
Therapeutic agents act by physically occluding the dentinal tubules to prevent fluid movement (hydrodynamic theory), chemically inducing remineralization of the hydroxyapatite surface, or reducing the excitability of pulpal nerves through ion-mediated depolarization.
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