Biophysical Analyses of Sequential Bands of Enamel Related to Ruffle-ended and Smooth-ended Maturation Ameloblasts

McKee, Marc D.; Martin, Jared; Landis, William J.

doi:10.1177/00220345890680020101

Cited by 7 publications

(3 citation statements)

References 35 publications

(40 reference statements)

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“…Exactly how it occurs, what controls it, and what the two morphologies mean functionally to changes occurring within the enamel layer between successive modulations are unknown. For the most part, investigators have NOT been able to establish any obvious quantitative chemical difference in the amounts or types of minerals and/or proteins present in enamel vs. the apical morphology displayed by ameloblasts covering the enamel surface at equivalent time points in maturation (Sasaki et al, 1987b;Bawden et al, 1988;McKee et al, 1989a). However, there have been empirical observations for many years that some, perhaps physical, difference exists "underneath" the modulating ameloblasts, because mineral and protein phases of maturing enamel selectively bind certain stains and dyes, depending upon whether a patch of enamel is covered by ameloblasts that are ruffle-ended or smooth-ended, or are in the process of re-creating the ruffled border after being smooth-ended (e.g., Boyde and Reith, 1981;Takano et al, 1982a;losephsen, 1983;Warshawsky, 1986a, 1989;Smith et al, 1987;McKee et al, 1989b).…”

Section: Modulationmentioning

confidence: 99%

Cellular and Chemical Events During Enamel Maturation

Smith

1998

Critical Reviews in Oral Biology & Medicine

636

836

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This review focuses on the process of enamel maturation, a series of events associated with slow, progressive growth in the width and thickness of apatitic crystals. This developmental step causes gradual physical hardening and transformation of soft, newly formed enamel into one of the most durable mineralized tissues produced biologically. Enamel is the secretory product of specialized epithelial cells, the ameloblasts, which make this covering on the crowns of teeth in two steps. First, they roughly "map out" the location and limits (overall thickness) of the entire extracellular layer as a protein-rich, acellular, and avascular matrix filled with thin, ribbon-like crystals of carbonated hydroxyapatite. These initial crystals are organized spatially into rod and interrod territories as they form, and rod crystals are lengthened by Tomes' processes in tandem with appositional movement of ameloblasts away from the dentin surface. Once the full thickness of enamel has been formed, ameloblasts initiate a series of repetitive morphological changes at the enamel surface in which tight junctions and deep membrane infoldings periodically appear (ruffle-ended), then disappear for short intervals (smooth-ended), from the apical ends of the cells. As this happens, the enamel covered by these cells changes rhythmically in net pH from mildly acidic (ruffle-ended) to near-physiologic (smooth-ended) as mineral crystals slowly expand into the "spaces" (volume) formerly occupied by matrix proteins and water. Matrix proteins are processed and degraded by proteinases throughout amelogenesis, but they undergo more rapid destruction once ameloblast modulation begins. Ruffle-ended ameloblasts appear to function primarily as a regulatory and transport epithelium for controlling the movement of calcium and other ions such as bicarbonate into enamel to maintain buffering capacity and driving forces optimized for surface crystal growth. The reason ruffle-ended ameloblasts become smooth-ended periodically is unknown, although this event seems to be crucial for sustaining long-term crystal growth.

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Section: Modulationmentioning

confidence: 99%

Cellular and Chemical Events During Enamel Maturation

Smith

1998

Critical Reviews in Oral Biology & Medicine

636

836

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“…The reason why certain fractions of the transported Ca ions can stay in labile or loosely bound forms within the extracellular space is ascribed to the blocking effects of the growth sites by abundant matrix proteins which retard the incorporation of Ca 2+ (and other ionic constituents) into the lattice positions. To date, however, analytical approaches (McKee et al ., 1989) failed to provide quantitative information about the corresponding calcium pool or compositional changes associated with the cyclic zones during maturation enamel. Also, the use of radioisotope gives the uptake pattern of 45 Ca but does not allow us to differentiate the labile Ca pool from total Ca uptake, due to precipitation or isotopic exchange onto the existing crystals.…”

Section: (10) Assessment Of the Exchangeable Calcium Pool Located On mentioning

confidence: 99%

Dental Fluorosis: Chemistry and Biology

Aoba

Fejerskov²

2002

Critical Reviews in Oral Biology & Medicine

395

296

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ABSTRACT:This review aims at discussing the pathogenesis of enamel fluorosis in relation to a putative linkage among ameloblastic activities, secreted enamel matrix proteins and multiple proteases, growing enamel crystals, and fluid composition, including calcium and fluoride ions. Fluoride is the most important caries-preventive agent in dentistry. In the last two decades, increasing fluoride exposure in various forms and vehicles is most likely the explanation for an increase in the prevalence of mild-to-moderate forms of dental fluorosis in many communities, not the least in those in which controlled water fluoridation has been established. The effects of fluoride on enamel formation causing dental fluorosis in man are cumulative, rather than requiring a specific threshold dose, depending on the total fluoride intake from all sources and the duration of fluoride exposure. Enamel mineralization is highly sensitive to free fluoride ions, which uniquely promote the hydrolysis of acidic precursors such as octacalcium phosphate and precipitation of fluoridated apatite crystals. Once fluoride is incorporated into enamel crystals, the ion likely affects the subsequent mineralization process by reducing the solubility of the mineral and thereby modulating the ionic composition in the fluid surrounding the mineral. In the light of evidence obtained in human and animal studies, it is now most likely that enamel hypomineralization in fluorotic teeth is due predominantly to the aberrant effects of excess fluoride on the rates at which matrix proteins break down and/or the rates at which the by-products from this degradation are withdrawn from the maturing enamel. Any interference with enamel matrix removal could yield retarding effects on the accompanying crystal growth through the maturation stages, resulting in different magnitudes of enamel porosity at the time of tooth eruption. Currently, there is no direct proof that fluoride at micromolar levels affects proliferation and differentiation of enamel organ cells. Fluoride does not seem to affect the production and secretion of enamel matrix proteins and proteases within the dose range causing dental fluorosis in man. Most likely, the fluoride uptake interferes, indirectly, with the protease activities by decreasing free Ca 2+ concentration in the mineralizing milieu. The Ca 2+ -mediated regulation of protease activities is consistent with the in situobservations that (a) enzymatic cleavages of the amelogenins take place only at slow rates through the secretory phase with the limited calcium transport and that, (b) under normal amelogenesis, the amelogenin degradation appears to be accelerated during the transitional and early maturation stages with the increased calcium transport. Since the predominant cariostatic effect of fluoride is not due to its uptake by the enamel during tooth development, it is possible to obtain extensive caries reduction without a concomitant risk of dental fluorosis. Further efforts and research are needed to settle the currently uncertain ...

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“…The main signal of the Al 2p spectrum in Al-NPCC was at 73.8 eV, which is attributed to the presence of Al2O3 [43] . The Ca 2p spectrum of Ca-NPCC consisted of two bands associated with Ca 2p3/2 (347.4 eV) and Ca 2p1/2 (350.9 eV) [44] . However, no clear characteristic 2p signals of Fe, K, and Co could be observed in the respective Fe-NPCC, K-NPCC, and Co-NPCC samples.…”

Section: Resultsmentioning

confidence: 99%