Dental caries is a disease that causes the destruction of the tooth due to the metabolic bacterial processes that take place within the oral biofilm. The term "caries" identifies the actual pathology, while the notation "carious lesion" indicates the sign of the disease. The damage is consequent to a demineralization process: in most individuals, it proceeds very slowly and remains active thanks to the presence of events that can modify the physiological and dynamic balance between the mineral component and saliva. In fact, when the oral pH drops due to the release of acids produced by the bacteria located within the dental biofilm the solubility of hydroxyapatite increases favoring demineralization, which will continue until a neutral pH is restored. When the rate of demineralization decreases, the opposite event, remineralization, can occur. Enamel dissolution (demineralization) and precipitation (remineralization) are events that, during the day, continually follow one another, depending on pH variations, without necessarily hesitating in a carious lesion: for example, if the bacterial biofilm is partially or totally removed, the mineral loss can be stopped or even reversed favoring remineralization. Therefore, the absence of a clinically visible lesion does not necessarily imply that demineralization has not occurred. The extent of the carious lesion is variable, as it can occur both as an initial loss of mineral substance at an ultrastructural level, and as a complete destruction of the tooth. The initial phase of each carious lesion appears as a non-cavitated hypo-mineralized area confined to the more superficial layers of the enamel known as white spot or initial enamel carious lesion. The progression of these lesions can be stopped or reversed by remineralization, by using specific materials capable of supplying ions necessary for the repair of the enamel. The study intends to evaluate, in vitro, the remineralizing capacity of amorphous calcium phosphate (ACP) in two different forms: conjugated with casein phosphopeptides (CPP-ACPF) or citrate (C-ACP).
MATERIALS AND METHODS
Thirty sound dental crowns were embedded in self-curing acrylic resin. The enamel surface was polished with abrasive paper in order to remove a thin layer of 100 µm thick. The baseline surface microhardness (Baseline) was measured for all the specimens using the Vickers microhardness testing machine. Artificial enamel carious lesions were created by inserting the specimens in de-mineralizing solution for 96 hours. Demineralized surface microhardness (T1) was measured again for all the specimens. The 30 samples were then divided into 3 groups: Group A - CPP-ACPF (Mi Paste Plus, GC Italia Srl, Milan, Italy), Group B - C-ACP (Biosmalto, Mousse azione d’urto, Curasept SpA, Varese, Italy) and Group C - Control. The samples were subjected to 10 days pH-cycling regimen, in which demineralization and remineralization continuously occured in order to simulate the normal oral cavity pH fluctuations. The surface micro-hardness was re-measured at the end of the treatment (T2).
RESULTS
Groups A and B showed a significant microhardness recovery compared to Group C. Tendency towards remineralization was observed in both groups A and B.
CONCLUSIONS
Considering the limits, the present study demonstrated the efficacy of CPP-ACPF and C-ACP as anticariogenic agents. The treated samples showed a tendency towards remineralization.
CLINICAL SIGNIFICANCE
Both agents can be used for the prevention and treatment of early carious lesions.
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