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Demineralized tooth enamel microporosities represent the pathological alteration of the dental enamel's crystalline structure, primarily composed of hydroxyapatite. These porosities occur when organic acids produced by cariogenic bacteria, such as Streptococcus mutans, lower the local pH, leading to the dissolution of calcium and phosphate ions from the enamel subsurface (Pitts et al., 2017). Clinically, these areas often manifest as white spot lesions due to the increased light scattering within the porous volume compared to sound enamel. These microporosities serve as the primary therapeutic target for non-invasive and micro-invasive dentistry. Drugs and agents like fluoride and CPP-ACP interact with these sites by facilitating the redeposition of minerals, often forming a more acid-resistant fluorapatite layer (Featherstone, 2000). Alternatively, low-viscosity resin infiltrants are designed to penetrate these microporosities via capillary action, sealing the internal surface area to prevent further acid diffusion and arrest lesion progression (Paris & Meyer-Lueckel, 2010). The management of these porosities is critical in preventing the transition from reversible incipient lesions to irreversible cavitated caries.
Promotion of remineralization via ion deposition into the porous matrix and physical sealing of pores to arrest acid diffusion.
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