Decalcification Agents Research Articles

PREVENTION OF EXPERIMENTAL RAT CARIES

In succession with the previous report, more detailed observation on two lesions, absent Pb-mark and infected tubulus in the fissure caries of rats, was reported in the present paper. Chronological observation of these lesions showed that the absent Pb-mark appeared earlier, being called the early lesion, and the infectious lesion was found at later stage of experiment in highest incidence, being called the late lesion, a successor of the early lesion.The early lesion often accompanied with half-moon shaped hematoxylin-phobe dentin matrix, brown pigmentation of dentin, bacterial crowd at the dentinoenamel junction, bacterial plaque in the fissure and bacterial invasion in the enamel binding above two bacterial settlements. The findings concluded that the once marked Pb-line in dentin did not remove spontaneously during 110 days after marking, but in vitro examination proved that removal of Pb-mark was easily resulted after action of decalcification agents, either acid or chelator. Therefore, the half moon shaped discoloration of the early lesion may probably be a track of decalcification. And decalcifying agents may sent from the bacterial crowd existing in the dentinoenamel junction. In dentin caries, however, the early lesion may follow the pre-early lesion characterized by the intact Pb-mark, the bacterial crowd and brown pigmentation.Instead of the early lesion, progress of infectious process in the late lesion may need action of neither acids nor chelators as bacterial products. The late lesion was often found under the cavity, exposing dentinal lesion toward the bottom of the fissure. In additional findings, at the summit caries, only the late type of lesion was found from the first. The differences between the early and late lesion in the mechanism of their production could be assumed from point of view on the different growth environment of bacteria existing, i-e. beneath the thick enamel layer and in dentinal tubulus under the open cavity where oxygen supply to bacteria may be much better than the dentinoenamel junction. Now carious progress in rat dentin may assume that in the early stage, after some lag phase of pre-early pictures, it proceeds exclusively decalcification by acid or chelator produced from bacterial crowd in the dentinoenamel junction, which in the later stage, invades into dentinal tubulus under the environment of better supply of oxygen and organic nutrient.

Succinic dehydrogenase in ameloblasts during formation and maturation of enamel

Enamel organs from upper incisor teeth of adult rats were dissected free of hard tissue and placed in appropriate incubating media for the demonstration of succinic dehydrogenase by means of the tetrazolium method. No fixative or decalcifying agents were employed prior to incubation of tissue, although some tissues were frozen prior to being incubated. At the growing end of the tooth, in ameloblasts that are engaged in matrix production, succinic dehydrogenase was found at the basal end of the cell. In shorter ameloblasts related to the maturation of enamel, intense succinic dehydrogenase activity was found throughout the cell, except for the nuclei and distal processes. In a more incisal part of the enamel organ where the ameloblasts begin to accumulate yellow pigment, succinic dehydrogenase activity was greatest in the basal end of the cell. Near the gingiva, where the ameloblasts are still shorter, succinic dehydrogenase was found throughout the cell. These observations are interpreted as indicating that cells related to maturation of enamel are metabolically very active, and suggest that the activity of ameloblasts in maturation of enamel may be multiphasic.