Exposure of both small carious lesions and artificial caries-like lesions to a synthetic calcifying fluid in vitro produced a significant degree of ‘healing’ or remineralization of the lesion. Changing the calcium concentration of the calcifying fluid had a marked effect on the degree of remineralization produced. When a low calcium concentration of 1 mM was employed, remineralization occurred throughout the entire depth of a lesion. Under these conditions, there was a mean reduction of 69% in area of the body of the lesion and a mean increase of 40% in orientated mineral. The dark zone at the advancing front of the lesion showed a dramatic increase in area of 526% and was much closer to the enamel surface relative to the control. When higher calcium ion concentrations of 3 mM were used, remineralization occurred but was limited to the surface of the lesion. Under these conditions, the mean reduction in area of the body of the lesion was 20%, brought about by a mean increase in orientated mineral of 17%. Although changes were found in relation to the dark zone, these were much smaller than those found for the 1-mM fluid, the increase in area being 38%. With respect to exposure times, results obtained using ten consecutive 24-hour exposures to the synthetic calcifying fluid were similar to those obtained after ten consecutive 1-hour exposures. Remineralization, therefore, occurred within each 1-hour exposure increment. Scanning electron microscopy showed that crystal diameters for sound enamel were in the range 35–40 nm. In the body of the lesion crystal diameters were reduced and found to be in the range 10–30 nm. In lesions remineralized with the high calcium-calcifying fluid containing 3 mM calcium, crystal diameters were larger than those found in either control lesions or in sound enamel, being in the range 50–75 nm. When the low calcium-calcifying fluid was used, remineralized lesions showed crystal diameters in the range 50–150 nm with a small number of crystals having diameters of 200 nm. Calculation of the supersaturation of the calcifying fluids revealed that the low calcium-calcifying fluid having 1 mM calcium favors crystal growth as opposed to nucleation.
We investigated the development of artificial caries lesions adjacent to experimental composite resins which release fluoride by ion exchange. Overall, compared with both a commercial, non-fluoride composite and a restorative silicate cement, the cavity walls and tooth surfaces immediately adjacent to the experimental resins developed fewer and/or smaller lesions. When lesions did develop, they did not penetrate as far along the cavity walls adjacent to the experimental materials. In general, the degree of protection imparted by the fluoride composites increased with increasing fluoride content. These results demonstrate the potential of these adhesive resins for restorative and other dental applications in which an extended fluoride presence would be of benefit.
Syndesmotic sutures of the skull are formed by dense connective tissue and called "open"; they are "closed" by formation of a synostosis between adjacent bones. Open sutures are considered as areas of growth and as hinges. The importance of open sutures during the period of skull growth is reflected by pathological situations in which premature closure of the sutures occurs. As alterations of the FGF receptor have been reported in genetical disorders accompanied by premature suture closure (Bellus et al. 1996), the role of fibroblasts and connective tissue in the development of the sagittal suture of mice has been investigated by light and electron microscopy. Morphological changes of the sagittal suture at the following stages are reported: at embryonic day 18, days 1, 5, 9, 14, 20, 26, 28 after birth and in adult mice. Two skulls per stage were investigated. Early osteogenesis appeared in a thin plate, followed by a second plate underneath the first one. Both were separated by blood vessels. In general, vascularization preceded desmoid mineralization; the space around blood vessels was occupied by non-bone-forming cells leaving cavities for the presumptive bone marrow. Mineralization of the collagen-rich osteoid at the mineralizing rim of the bone plates was accompanied by apoptoses and cell disintegration. Newly formed bone was immediately covered by osteoblasts forming a sheet of bone-lining cells. At day 9, the double-layered bone plates of both sides reached the median area of the skull but were separated by non-mineralizing, collagen-rich connective tissue. From day 14 onwards, the bone plates thickened. Bone apposition, recognizable by the formation of collagen-rich osteoid and proceeding from day 14 pp onwards, occurred mainly at the outer and inner surfaces of the calvariae, but neither at bone marrow surfaces nor at the medial edges of the parietal bones. These opposite bone faces showed fewer osteoblasts and bone-lining cells, but an increased number of fibroblasts. Tendon-like collagen bundles connected both bone plates of the open suture of day 26 pp as well as in the adult mice, whereby synostotically closed areas alternated. Formation of an open, syndesmotic suture can, therefore, be described as a transition of bone-forming tissue into a bone-tendon junction. The results indicate the importance of the replacement of osteoblasts by fibroblasts at the sutural front of the bone plates in order to prevent a premature suture closure.
Prototype anion-exchanging resins were used to treat artificial carious lesion; The resins penetrate into lesion porosity, harden, and release either F or Cl ions. After second demineralization, various histological features of the lesions were measured. I progression of untreated lesions, surface zones (SZ) decreased by 75% and lesion bodie increased by 86%, while in resin-treated lesions the SZ remained essentially constant ant lesion bodies increased by only 52%. Dark zones (DZ) of F resin-treated lesions wer significantly larger than the DZ of Cl resin-treated, untreated, and initial lesions. After initiation of lesions in sound enamel, the SZ was essentially the same for botl treated and untreated enamel but slightly larger lesion bodies developed in the treate( enamel. After demineralization, the DZ of F resin-treated enamel were significantly larger than in Cl resin-treated or untreated enamel. In a separate experiment the rate of phosphate release from demineralized enamel into i pH 4.5 buffer was decreased by 85% by a F resin treatment and by 41% by a Cl resin treatment. In summary, both resins act as a barrier to demineralization and the fluoride-releasing resin appears to promote remineralization during acid attack.
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