Chemically induced in vitro lesions in dental enamel

Larsen, Mona

doi:10.1111/j.1600-0722.1974.tb00407.x

Cited by 31 publications

(33 citation statements)

References 37 publications

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“…When the aqueous phase is unsaturated with respect to fluorapatite a surface layer is not formed at all and the lesion developed is therefore not a caries-like lesion. It is an erosion [Larsen, 1974;Pearce, 1983].…”

mentioning

confidence: 99%

“…The experimental background for the effect of fluoride in the caries process is that as enamel dissolves due to an undersaturation with respect to hydroxyapatite the aqueous phase remains supersaturated with respect to fluorapatite which is formed in the surface layers of the enamel [Larsen, 1973[Larsen, , 1974. The more supersaturated with respect to fluorapatite the thicker and more mineralized becomes the surface layer and the less demineralized the lesion body enamel [Larsen, 1974;ten Cate and Duijsters, 1983;Pearce, 1983]. When the aqueous phase is unsaturated with respect to fluorapatite a surface layer is not formed at all and the lesion developed is therefore not a caries-like lesion.…”

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confidence: 99%

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Prevention by Means of Fluoride of Enamel Erosion as Caused by Soft Drinks and Orange Juice

Larsen¹

2001

Caries Res

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Fluoride has been suggested to prevent erosion of the teeth, either after a topical treatment of the teeth or by addition of fluoride to the acidic drink. The main aim of the present study was to describe the dissolution of calcium fluoride in some soft drinks and orange juice and compare it with the amounts of calcium fluoride left on the enamel surfaces after a topical treatment. A further aim was to describe the dissolution of enamel in soft drinks and juice saturated for 3 days with solid calcium fluoride. Solid calcium fluoride was suspended in each of 10 soft drinks and orange juices and gently agitated for 72 h, after which the drinks were analyzed for calcium, phosphate and fluoride and pH was determined. To examine the erosion–preventive effect of the calcium fluoride–rich drink, intact teeth were exposed to the drinks with or without calcium fluoride. It was found that from 6 to 45 mg of calcium fluoride was dissolved per liter of drink. The more acidic the drink, the more calcium fluoride was dissolved, presumably due to HF formation. The teeth exposed to the soft drinks all showed erosion–like lesions. Very little effect of the 4–6 ppm ionic fluoride dissolved in the soft drinks was observed. In orange juice, however, the dissolved calcium fluoride established a saturation with respect to fluorapatite and consequently, the erosion–like lesion was replaced by a caries–like lesion. In conclusion, the acidic soft drinks are capable of dissolving considerable amounts of calcium fluoride and the erosion–preventive effect of even high fluoride concentrations is limited.

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confidence: 99%

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Prevention by Means of Fluoride of Enamel Erosion as Caused by Soft Drinks and Orange Juice

Larsen¹

2001

Caries Res

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“…For example gelatin/lactic acid [von Bartheld, 1961;Silverstone, 1967], hydroxyethyl cellulose/lactic acid [Gray, 1966], partial hy droxyapatite saturation/lactic acid [Larsen, 1974], and diphosphonate/lactic acid [Fran cis et al, 1973;Featherstone et al, 1978a] have been shown to produce subsurface le sions in human and bovine enamel with the characteristics of natural carious lesions.…”

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confidence: 99%

Relative Rates of Progress of Artificial Carious Lesions in Bovine, Ovine and Human Enamel

Featherstone¹,

Mellberg²

1981

Caries Res

166

104

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Artificial carious lesions were produced by a gelatin/lactic acid system in deciduous bovine, permanent bovine, deciduous human and permanent human enamel over periods up to 8 days, and the progress measured by dye imbibition studies. Artificial carious lesions were produced in bovine, ovine and human permanent enamel using a diphosphonate/lactic acid system over periods up to 30 days, progress was assessed by depth measurement, and overall diffusion coefficients were calculated. The rate of lesion progress was linear with the square root of time for both systems of assessment. Lesion progress as measured by dye imbibition was in the ratio 3.7: 2.9: 1.5:1.0 for bovine deciduous: bovine permanent: human deciduous: human permanent, respectively. Bovine permanent, ovine permanent and abraded bovine permanent lesions progressed at equal rates and in the ratio 3.0: 1.0 to human permanent enamel, as measured by overall diffusion coefficients. The results provide an approximate basis for the use of bovine, ovine and human artificial carious lesion data in the quantitative discussion of the caries process.

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“…Studies on in vitro and in vivo formation of surface layer in enamel showed that pellicle is essential for formation of surface layer (60). However results from other studies revealed that pellicle did not play a crucial role in subsurface demineralization in vitro (56,87,88). Similar reports were also obtained from the in vitro experimental data of Ten Cate and Duysters (83,84), Borsboom and Arends (14), and Theuns et al (86) who found that subsurface lesion can occur even in the absence of the pellicle.…”

Section: Mechanism Of Subsurface Lesion Formation and Progressmentioning

confidence: 89%

“…Various other studies with acidic, unsaturated calcium phosphate solution by Larsen (56) and Moreno and Zahradnik (65) finally demonstrated gels were not needed for surface layer formation. The presence or absence of stirring on surface layer formation is irrelevant, although stirring affects the rate of surface layer formation (56). Studies on in vitro and in vivo formation of surface layer in enamel showed that pellicle is essential for formation of surface layer (60).…”

Section: Mechanism Of Subsurface Lesion Formation and Progressmentioning

confidence: 99%

Early Enamel Lesion: Part II. – Histo-morphology and Prevention

Kudiyirickal

Ivančaková

2008

Acta Med. (Hradec Kralove, Czech Repub.)

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The enamel demineralization defect has a lower mineral distribution in the surface layer in comparison to the adjacent sound enamel and also a lower interprismatic mineral content. The first stage of enamel demineralization is characterized by removal of interprismatic mineral content and in the subsequent stages a well defined surface layer formation occurs which constitutes early caries lesion (4).Although early investigators like Hollander and Saper (47) in 1935 had noticed this subsurface demineralization white opaque spot, they mistook it to be a photographic artifact. However the work of various other researchers like Applebaum, Thewlis, Besic, Coolidge et al., Gray and Francis (3,12,21,41,87), on white opaque enamel lesion and new experimental techniques like microradiography (42), polarized light experiments (23, 78), microhardness data (30), and electron microscopy shed new light in understanding the early caries lesion in enamel. These studies have demonstrated that a porous and mineral-rich surface layer covers an enamel lesion and the morphology differs a little from that of sound enamel while body of the lesion which comprises the subsurface area has low mineral content (10-70 vol %). The early caries lesion in enamel is characterized by a prominent perikymata pattern and focal holes (6,44,88). The main drawback of the numerous experimental techniques is that they are static measurements of caries progression at a particular time period whereas the carious process is time-dependent and is in a constant state of dynamic equilibrium wherein a balance is struck between demineralization and remineralization. Surface layer (SL) covering early enamel lesionsThe early investigators who observed the white opaque spots attributed the presence of these lesions to artifacts. They believed that the surface layer (SL) could be due to sound enamel which has a higher mineral content. These explanations were proved false by subsequent investigations by Langdon et al. (55). Their studies on pressed pellets of hydroxyapatite demonstrated that subsurface lesion could occur in an acidic gel system with 2 ppm fluoride. They also concluded that organic matrix is not important for subsurface lesion formation, and that neither a preferred crystallite orientation in the enamel prisms nor an uneven ion/mineral distribution in enamel were essential for the formation of a subsurface lesion since these are absent in pressed apatites. This is in contrast to earlier reports by Brudevold et al. (15). Mechanism of subsurface lesion formation and progressThe bacteria in the oral plaque are acidogenic and form organic acids, including lactic, formic, acetic, and propionic acids from fermentable carbohydrates which diffuse into the enamel (30), dentin, or cementum, partially dissolving the mineral crystals (57). When this process goes unchecked minerals like calcium and phosphate diffuse out of the tooth resulting in frank cavitation. In the initial stages, demineralization can be reversed by influx of calcium, phosphate, and fluoride...

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Chemically induced in vitro lesions in dental enamel

Cited by 31 publications

References 37 publications

Prevention by Means of Fluoride of Enamel Erosion as Caused by Soft Drinks and Orange Juice

Prevention by Means of Fluoride of Enamel Erosion as Caused by Soft Drinks and Orange Juice

Relative Rates of Progress of Artificial Carious Lesions in Bovine, Ovine and Human Enamel

Early Enamel Lesion: Part II. – Histo-morphology and Prevention

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