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Immunolocalization of heat shock protein 70 during reparative dentinogenesis.

OBJECTIVE: To investigate the immunolocalization of heat shock protein 70 (hsp 70) during reparative formation and to discuss the role of heat shock response in dental pulp injury and repair. METHODS: A single cavity was prepared in the mesial surface of the first molars of both maxilla and mandible in Wistar rat. The animals were sacrificed at 3, 15, and 30 days post-operation. After the histological process, the paraffin sections were reacted with monoclonal antibodies against rat hsp 70 using the strept-avidin-biotin-peroxidase complex method. RESULTS: Immunolocalization demonstrated heavy staining for hsp 70 in normal pulp and at different stages of dental pulp repair. In normal pulp, immunoreactivity was visualized in the odontoblasts and the pulp fibroblast. In the group sacrificed at 3 days, heavy staining was located in the odontoblast process and cytoplasm. After 15 days, the newly formed odontoblast-like cells were strongly stained. At 30 days, the same staining intensity was observed in odontoblast-like cells and in pulp cells. No staining was seen in reparative dentin. CONCLUSION: These results demonstrated that heat shock protein 70 might play an important role as a molecular chaperone during reparative dentin formation.

Animals↗

Dentinogenesis and the calciotraumatic response to the injection of lead or fluoride ions.

A number of ions can disturb the formation of dentine resulting in a calciotraumatic response. The calciotraumatic response following the injection of sodium fluoride was investigated using backscattered electron imaging in the scanning electron microscope and compared with the response to lead acetate. With fluoride, there was formation of a hypermineralized band succeeded by a relatively hypomineralized band, but with lead acetate, only a hypomineralized band was produced. However, there were some differences in the response between the labial and lingual dentine with both ions. In the labial dentine following injection of sodium fluoride, the onset of hypermineralization was less abrupt than in the lingual dentine. Furthermore, the transition from hypermineralization to relative hypomineralization was more abrupt in the labial dentine. Sometimes there was an increased thickness of labial dentine between the hypermineralized layers towards the apex of the tooth and this dentine was less homogeneously mineralized. Normal incremental lines were occasionally seen both labially and lingually. Lead acetate produced a more severe disruption of dentine formation labially than lingually. These differences in response may be related to the pattern of mineralization labially and lingually and to the systemic effects following the injection of sodium fluoride.

Animals↗

Genetic marker study of dentinogenesis imperfecta.

DGI-II has been linked to the group specific component (Gc) on 4q and to interferon induced protein 10 (INP10) on 4q. We studied a three generation family with DGI-II along with a four generation DGI-II family to more precisely place DGI-II in the existing genetic map of 4q and to determine if genetic heterogeneity existed between various DGI-II families. Affected family members had brownish discoloration of the teeth, enamel fracturing and radiographic evidence of coronal and radicular pulp chamber obliteration. Thirteen polymorphic markers on 4q were studied including D4S35, D4S1, ALB, Gc, MGSA, AR, INP10, ADH3, FGFB, EGF, IL2, IF, and MNS. Gc and MNS blood group antigen typing were done using commercial SERA. Restriction fragment length polymorphism analysis using Southern blotting was done on the remaining markers. Pairwise linkage analysis was performed using the procedures of Morton. Tight linkage between DGI-II and eleven genetic markers, including Gc and EGF, was excluded. The tightest linkage with DGI-II was identified with the probe INP10 at theta = 0.0 with lod = +3.91. However, INP10 RFLP differences were detected between the families, such that DGI-II correlated with different alleles in each family. Results from this study demonstrated that DGI-II may possibly arise from more than one genetic mutation.

Alleles↗