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Advances in Dental Research
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Adv Dent Res 8:144-157, July, 1994
© 1994 SAGE Publications

In Vivo Caries Models-Mechanisms for Caries Initiation and Arrestment

A. Thylstrup

Department of Cariology and Endodontics School of Dentistry, Health Science Faculty University of Copenhagen 20 Nørre Allé DK-2000 Copenhagen N, Denmark

C. Bruun

Department of Cariology and Endodontics School of Dentistry, Health Science Faculty University of Copenhagen 20 Nørre Allé DK-2000 Copenhagen N, Denmark

L. Holmen

Department of Cariology and Endodontics School of Dentistry, Health Science Faculty University of Copenhagen 20 Nørre Allé DK-2000 Copenhagen N, Denmark

The effects of intra-oral mechanical forces on caries initiation, progression, and arrestment are evaluated by examination of different in vivo caries models. The models are grouped in four categories: (1) a population study, (2) short-term clinical trials, (3) clinical experiments, and (4) controlled clinical observations. Taken together, these in vivo studies convincingly demonstrate that partial or total elimination of the intra-oral mechanical forces operating during mastication or toothbrushing leads to evolution of cariogenic plaque, resulting in localized carious enamel dissolution. In addition, they show that re-exposure to the partly or totally eliminated mechanical forces not only arrests further lesion progression, but also results in partial lesion regression. The data from in vivo caries studies also show that the clinical and structural changes associated with lesion arrestment or partial regression are not related to any salivary repair mechanism, but are solely the result of mechanical removal of the cariogenic biomass which is physically interrelated with the eroded surface of the active, dull-whitish enamel lesion. No indications of superficial mineral deposition or "blocking" of the external intercrystalline spaces are seen in the surface layer of lesions arrested in vivo. For this reason, the conventional usage of the terminology 'remineralization' is considered absolutely misleading when used to describe the mechanisms responsible for the arrest of lesion progression in vivo.

Advances in Dental Research, Vol. 8, No. 2, 144-157 (1994)
DOI: 10.1177/08959374940080020401


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