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. 1997 Jul;289(1):125-35.
doi: 10.1007/s004410050858.

Disturbances of the secretory stage of amelogenesis in fluorosed deer teeth: a scanning electron-microscopic study

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Disturbances of the secretory stage of amelogenesis in fluorosed deer teeth: a scanning electron-microscopic study

H Kierdorf et al. Cell Tissue Res. 1997 Jul.

Abstract

Structural changes resulting from fluoride-induced disturbances of the secretory stage of amelogenesis were studied in fluorosed dental enamel of ten permanent premolars and molars from roe deer (Capreolus capreolus) and red deer (Cervus elaphus). The fluorosed enamel exhibited surface hypoplasias of different depths and extents and an associated loss of its normal prism/interprism structure. The occurrence of such aprismatic enamel either was restricted to grossly accentuated and hypomineralized incremental (calciotraumatic) bands or affected more extended areas to the bottom of the hypoplastic lesions. The fluoride-induced disturbance of the secretory functions of the cells had thus been either temporary or permanent. Layers of aprismatic enamel were regarded as denoting periods of reduced enamel matrix formation by secretory ameloblasts lacking the distal, i.e., the prism-forming, portions of their Tomes processes. Our observations also indicated that the transition from the presecretory to the secretory stage of amelogenesis could be affected by fluoride, thereby preventing the ameloblasts from achieving their normal secretory function and from establishing fully formed Tomes processes. Aprismatic enamel was formed throughout the secretory stage of amelogenesis at these locations. The most severe ameloblast reaction that could be deduced from our findings was an abrupt cessation of enamel matrix secretion. Some of the pathological changes observed in fluorosed deer enamel showed striking similarities to those reported in rodents after acute parenteral fluoride dosing. Thus, periods of especially elevated plasma-fluoride levels in chronically fluoride-stressed deer can cause a disruption in the function of secretory ameloblasts similar to that following acute fluoride dosing in rodents.

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