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Featured researches published by J Arends.


American Journal of Orthodontics and Dentofacial Orthopedics | 1988

Orthodontic appliances and enamel demineralization. Part 1. Lesion development.

Bjørn Øgaard; Gunnar Rölla; J Arends

A clinical trial was conducted to investigate carious lesion development associated with fixed orthodontic therapy. Specially designed orthodontic bands for plaque accumulation were attached to premolars scheduled to be extracted as part of an orthodontic treatment. Visible white spot lesions were seen within 4 weeks in the absence of any fluoride supplementation. Both microradiographic and SEM examinations showed surface softening of the enamel surface--that is, a surface layer was not seen in the lesions. The clinical significance of the present study is that enamel demineralization associated with fixed orthodontic therapy is an extremely rapid process caused by a high and continuous cariogenic challenge in the plaque developed around brackets and underneath ill-fitting bands. Careful inspection of the appliance at every visit and preventive fluoride programs are therefore required.


Caries Research | 1983

Comparison of Artificial Caries-Like Lesions by Quantitative Microradiography and Microhardness Profiles

Jdb Featherstone; Jm Tencate; M. Shariati; J Arends

A direct comparison of quantitative microradiography and microhardness profiles was made using artificial caries-like lesions in human enamel. Tooth crowns with lesions were cut in half through the ce


Colloids and Surfaces | 1984

The effect of surface roughening of polymers on measured contact angles of liquids

Henk J. Busscher; A.W.J. van Pelt; P. de Boer; H.P. de Jong; J Arends

Equilibrium, advancing and receding contact angles for five different liquids have been determined on twelve commercial polymers after various surface roughening procedures. It was found that influences of surface roughening on contact angles disappear if the stylus surface roughness RA is < 0.1 μm. Surface roughening tends to increase observed contact angles, if the contact angle on the smooth surface is above 86°, whereas contact angles decrease if the contact angle on the smooth surface is below 60°. For contact angles on the smooth surface between 60° and 86°, surface roughening was found not to influence measured contact angles. These results show a broad similarity in the trend, predicted by the early Wenzel equation, describing the influence of surface roughness on contact angles, although of course the stylus surface roughness RA is not identical to the theoretical r-parameter in the Wenzel equation.


American Journal of Orthodontics and Dentofacial Orthopedics | 1988

Orthodontic appliances and enamel demineralization Part 2. Prevention and treatment of lesions

Bjørn Øgaard; Gunnar Rölla; J Arends; J.M. ten Cate

Clinical experiments were performed to investigate the effect of fluoride on carious lesion development and on lesions established during fixed orthodontic therapy. All presently available fluoride agents are developed from the concept of fluoridating the enamel in the form of fluorhydroxyapatite. Recent research has indicated, however, that calcium fluoride formation may be a major aspect of the mechanism of the cariostatic effect of topical fluoride. Therefore a fluoride solution with very low pH (1.9) that induced large amounts of calcium fluoride also was tested on lesion development underneath orthodontic bands. Daily fluoride mouth rinsing with a 0.2% solution sodium fluoride (NaF) retarded lesion development significantly, whereas the fluoride solution with low pH inhibited lesion formation completely. Fluoride applied as a mouth rinse to plaque-covered lesions underneath orthodontic bands retarded lesion progression. The remineralizing capacity of saliva was found to be rapid in the absence of any fluoride. Although white spot lesions may remineralize and even disappear, most of the emphasis should be directed against prevention of carious lesion development during treatment with fixed orthodontic appliances.


Journal of Dental Research | 1986

THE NATURE OF EARLY CARIES LESIONS IN ENAMEL

J Arends; J. Christoffersen

Since 1935, various mechanisms have been suggested for the formation of subsurface lesions and, in particular, the surface layer covering enamel lesions. The relatively intact mineral-rich and porous surface layer is most likely caused by kinetic events. The suggested mineral-rich outer layer in sound enamel, the organic matrix, the pellicle, or a non-uniform ion distribution have all been shown to be non-essential for surface layer formation; they may, however, influence the rate of surface layer formation. Models based on outer surface protection by adsorbed agents, the dissolution-precipitation mechanism, and combinations of these two models, as well as models based on porosity or solubility gradients, are discussed in this paper together with their advantages and disadvantages. Most models have not explained some important recent experimental observations on initial in vivo caries lesion formation: e.g., initial enamel lesions formed in vivo do not have a surface layer initially but develop this mineral-rich layer later on; and the fact that the F- level in the solid sound enamel is not determining the subsurface lesion formation. Furthermore, the observations that in vitro fluoride ions in the liquid at very low levels (approximately equal to 0.02 ppm) determine surface layer formation are difficult to explain. A new kinetic model for subsurface lesion formation is described, in which inhibitors such as F- or proteins play an important role. The model predicts that if lesions depth and demineralization period are denoted by df and t, lesion progress can be described by: dfp = alpha t + c, where alpha and c are constants with 1 less than or equal to p less than or equal to 3, depending on the lesion formation conditions. If lesion progress is entirely diffusion-controlled, p = 3, corresponding to low inhibitor concentrations; if the inhibitor content is so high that the progress is controlled by processes at the crystallite surface, p = 1. A kinetic mechanism for surface layer formation in vivo is proposed, based on the assumption that F- is a main inhibitor in the plaque-covered acidic in vivo situation. The inhibiting fluoride, adsorbed onto the crystallite surfaces at OH- vacancies, originates from the so-called fluoride in the liquid phase (FL) between the enamel crystallites. Under acidic conditions (plaque), we have, due to an influx of fluoride from the saliva or plaque as FL, an aqueous phase in the enamel supersaturated with respect to the mineral for a small distance (x*) only.(ABSTRACT TRUNCATED AT 400 WORDS)Since 1935, various mechanisms have been suggested for the formation of subsurface lesions and, in particular, the surface layer covering enamel lesions. The relatively intact mineral-rich and porous surface layer is most likely caused by kinetic events. The suggested mineral-rich outer layer in sound enamel, the organic matrix, the pellicle, or a non-uniform ion distribution have all been shown to be non-essential for surface layer formation; they may, however, influence the rate of surface layer formation. Models based on outer surface protection by adsorbed agents, the dissolution-precipitation mechanism, and combinations of these two models, as well as models based on porosity or solubility gradients, are discussed in this paper together with their advantages and disadvantages. Most models have not explained some important recent experimental observations on initial in vivo caries lesion formation: e.g., initial enamel lesions formed in vivo do not have a surface layer initially but develop this mineral-rich layer later on; and the fact that the F- level in the solid sound enamel is not determining the subsurface lesion formation. Furthermore, the observations that in vitro fluoride ions in the liquid at very low levels (~ 0.02 ppm) determine surface layer formation are difficult to explain. A new kinetic model for subsurface lesion formation is described, in which inhibitors such as F- or proteins play an important role. The model predicts that if lesion depth and demineralization period are denoted by df and t, lesion progress can be described by: d fp = αt + c, where a and c are constants with 1 ≤ p ≤ 3, depending on the lesion formation conditions. If lesion progress is entirely diffusion-controlled, p = 3, corresponding to low inhibitor concentrations; if the inhibitor content is so high that the progress is controlled by processes at the crystallite surface, p = I. A kinetic mechanism for surface layer formation in vivo is proposed, based on the assumption that F- is a main inhibitor in the plaque-covered acidic in vivo situation. The inhibiting fluoride, adsorbed onto the crystallite surfaces at OH- vacancies, originates from the so-called fluoride in the ljquid phase (F L ) between the enamel crystallites. Under acidic conditions (plaque), we have, due to an influx of fluoride from the saliva or plaque as F L, an aqueous phase in the enamel supersaturated with respect to the mineral for a small distance (x*) only. Deep in the lesion the solution is undersaturated. For d < x* we have, due to F L and pH, mineral precipitation; for d > x*, enamel dissolution. The surface layer thickness, about x*, depends on F L level, on pH, and on time. The results described indicate that the surface layer is formed after a considerable period if a fluoride gradient has been established in initially surface-softened enamel. The combination of this F L gradient and pH dependency of the inhibitor effectiveness results in two regions in the enamel: (1) a small surface region where, due to inhibitor action, no dissolution takes place (and possible mineral redeposition occurs), and (2) a subsurface region where dissolution takes place. The mechanism of surface layer formation is based mainly on the information available for one inhibitor: fluoride. Other inhibitors, such as proteins, can have a similar effect. The kinetic model for subsurface lesion formation can, in contrast to thermodynamic models, explain the facts that: (a) the initial lesions do not show a surface layer; (b) the thickness of the surface layer, once formed, appears to be roughly constant; (c) the fluoride level in the saliva is the main reason for the surface layer to develop; and (d) the fluoride level in the solid sound enamel does not materially influence the surface layer formation.


Journal of Dental Research | 1989

The Influence of Surface Free-energy on Planimetric Plaque Growth in Man

Marc Quirynen; Marina Marechal; Hj Busscher; Anton H. Weerkamp; J Arends; Paul Darius; D. van Steenberghe

The purpose of this study was to examine the change in plaque area over nine days in vivo on four materials with different surface free-energies (s.f.e.). Twelve healthy dental students participated in a crossover, split-mouth, double-blind study. Supragingival plaque formation was recorded over a nine-day period, on four different materials: fluorethylenepropylene (Teflon) (FEP), parafilm (PAR), cellulose acetate (CA), and enamel (E) with s.fe. of 20, 26, 57, and 88 erg/cm2, respectively. Strips made from the first three materials were stuck to the buccal surface of an upper incisor. The remaining incisor was carefully polished and served as an enamel surface. The increase in plaque was evaluated after three, six, and nine days. A planimetrical analysis was used so that the plaque area could be expressed as a percentage of the total buccal tooth surface. This procedure was repeated on each subject, so that at the end, each pair of central or lateral incisors received the four tested materials. The results indicated that the adherence of micro-organisms on pellicle-coated substrata was influenced by the materials s.f.e.; there was an association between the s.f.e. of the substrata and the supragingival plaque extension in vivo. High surface free-energy substrata in the oral cavity attracted more micro-organisms than did low energetic materials. Additionally, the bacterial adhesion seemed very weak on surfaces with a low s.f.e.


Caries Research | 1978

Remineralization of Artificial Enamel Lesions in vitro

Jm Tencate; J Arends

To investigate the mechanism of remineralization, artificial (HEC) lesions in bovine enamel and etched bovine enamel were remineralized in a pH-stat controlled system at 25, 37 and 50 °C. In all exper


Journal of Colloid and Interface Science | 1983

EFFECT OF SPREADING PRESSURE ON SURFACE FREE-ENERGY DETERMINATIONS BY MEANS OF CONTACT-ANGLE MEASUREMENTS

H.J. Busscher; A.W.J. van Pelt; H.P. de Jong; J Arends

Abstract Contact angle measurements have been carried out on various solid substrates using water-propanol mixtures and α-bromonaphthalene as wetting liquids. These substrates were: polytetrafluorethylene, Parafilm, polyethylene, polyurethane, polystyrene, polymethylmethacrylate, fluorapatite, and hydroxyapatite. The dispersion and the polar components of the surface free energy, γsd and γsp have been calculated from the geometric mean equation. Two approaches have been considered: (1) neglecting the spreading pressure πe and (2) taking πe into account (Danns method). The results show that both approaches actually yield the same results for the surface free energy, γs, if a proper interpretation of the approaches is considered. All data indicate, that approach (1) gives γs values determined on the adsorbed liquid layer, whereas in approach (2) the free energies of the bare solid surfaces are found.


Caries Research | 1985

LESION FORMATION AND LESION REMINERALIZATION IN ENAMEL UNDER CONSTANT COMPOSITION CONDITIONS - A NEW TECHNIQUE WITH APPLICATIONS

J.A.K.M. Buskes; Jørgen Christoffersen; J Arends

A new apparatus for the de- and remineralization of enamel in vitro under constant composition conditions is described. A de- or remineralizing solution flows over the specimens at a controlled rate.


Journal of Dental Research | 1994

Orientational Micro-Raman Spectroscopy on Hydroxyapatite Single Crystals and Human Enamel Crystallites

H. Tsuda; J Arends

Single crystals of synthetic hydroxyapatite have been examined by orientational micro-Raman spectroscopy. The observed Raman bands include the PO4 3-/OH- internal and external modes over the spectral range from 180 to 3600 cm-1. The Raman-active symmetry tensors (A, E1, and E2) of crystal-class C6 have been assigned to these bands. Intensities of the Raman bands are invariant to the orientation of the a- or b-axis of a single crystal, but depend solely on the c-axis orientation. Changes in the spectral profile thus reflect changes in the c-axis orientation, which, with respect to the known excitation/observation coordinates, can be determined through the angular dependencies of Raman bands due to A and E2 symmetries. The useful bands are those of the PO4 3- v4 vibrational mode, which contains relatively well-defined bands due to E2 (581 cm-1) and A (593 cm-1) symmetries. A preliminary Raman study on crystallites near the intact outer surface of human enamel has also been carried out. Strong orientational dependencies similar to those of hydroxyapatite single crystals have been observed among the bands in enamel spectra. This suggests that the crystallites in the region investigated are highly oriented. The results were consistent with an averaged orientation of the crystallite c-axis being perpendicular to the outer surface.

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J.L. Ruben

Radboud University Nijmegen

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Ag Dijkman

University of Groningen

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Awj Vanpelt

University of Groningen

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Hj Busscher

University of Groningen

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Hp Dejong

University of Groningen

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Henk J. Busscher

University Medical Center Groningen

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