There have been many arguments on the irritating mechanisms of the composite resin on the dental pulp. While the direct irritative effect of the resin has been prefered, some authors considered that the marginal microleakage and the resulting bacterial infection play a more important role in inducing the complicating pulp irritation. We developed a new filling technique, called the direct inlay restoration method, which could prevent the marginal leakage associated with the polymerization shrinkage of the adhesive composite resin.
In this study, we tried to apply our method clinically. None of the 440 cases which were filled with the adhesive composite resin and 60 cases out of 64 cases in which the pulps were directly capped with the adhesive composite resin developed any signs and symptoms of pulp irritation . The other 4 cases developed signs of pulp irritation. Two of those 4 cases were pulpectomized due to spontaneous pain and the other 2 cases turned out to be well after re-restoration. With the informed consent of the patients, the direct pulp capping using the adhesive composite resin was experimentally performed on 6 caries-free 3rd molars and the histopathological examination of these capped molars revealed that neither significant degenerative nor inflammatory changes were brought about in the dental pulp.
These clinical and histopathological observations suggest that the dental pulp irritation after resin filling is not induced by the composite resin itself.
In this study, ultrastructural and immunohistochemical studies were performed on the adult rat (15 weeks old) mandibular condyle, with particular attention to the matrix fibers in the condylar cartilage. The fibrous zone had thick collagen fibrils which formed fibril bundles. These collagen fibrils consisted mainly of Type I collagen. From the proliferative zone to the mature zone, the density of the collagen fibrils became higher. In the hypertrophic zone, thick collagen fibrils were formed around the chondrocytes. Immunohistochemical study indicated that these collagen fibrils consisted mainly of Type I collagen. Therefore, it was confirmed that the hypertrophic chondrocytes in this tissue had one of the osteoblastic phenotypes.
To clarify the mechanism of the high incidence of ischemic heart disease in the diabetics, we studied the particle size of the lipoprotein with particular attention to the structural abnormality. Using high performance liquid chromatography, the particle size of the lipoprotein was determined with elution volume, which was precisely correlated with the particle size. The particle size of low density lipoprotein (LDL) from the diabetics with normolipidemia is larger than that from the nondiabetics (p<0.001) in the elution pattern of triglyceride. The examination of the elution pattern of the triglyceride and cholesterol revealed that this large LDL was composed of a large amount of triglyceride. These characteristics of the large LDL resembled that of the atherogenic intermediate density lipoprotein. The particle size of high density lipoprotein (HDL) from the diabetics with normolipidemia was larger than that from the nondiabetic controls (p< 0.00l), detected by the elution pattern of triglyceride. The comparison of the triglyceride and cholesterol elution pattern indicated that also the large HDL in the diabetics with normolipidemia was rich with triglyceride, which was reported to inhibit the activity of the lipid transfer protein.
These facts revealed that the disorder of the lipid metabolism not accompanied with hyperlipidemia produced the large LDL and HDL, which might lead to the excess mortality rate of the ischemic heart disease in the diabetics even with normolipidemia.