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Oral acids refer to the collection of acidic substances present within the mouth, primarily lactic acid produced by the bacterial fermentation of dietary carbohydrates and various organic acids introduced through the diet [1, 12]. These acids are not considered a specific molecular target like a protein or receptor; rather, they constitute a chemical environmental factor that influences dental hard tissue integrity [10]. When oral acids reduce the pH of the tooth surface below the critical threshold of approximately 5.5, they facilitate the demineralization of hydroxyapatite, leading to dental caries and erosive lesions [3, 11]. Therapeutic strategies focus on neutralizing these acids with buffers like sodium bicarbonate, strengthening enamel via fluoride therapy, or increasing salivary flow to restore a neutral pH [10, 13]. Additionally, oral acids serve as the chemical stimulus for the sour taste modality, which is biologically detected by the proton-selective ion channel Otopetrin 1 (OTOP1) [4, 9].
The primary therapeutic mechanisms involve the chemical neutralization of hydrogen ions, the enhancement of salivary buffering capacity to raise oral pH, and the promotion of enamel remineralization (e.g., formation of fluorapatite) to increase resistance against acid-induced dissolution [1, 10, 11].
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