Using immunohistochemical techniques, we examined the expression of heat shock protein (HSP) appearing in murine dental pulp cells after the application of experimental orthodontic mechanical stress. We used Waldo's method, and the results demonstrate that the dental root pulp cells expressed HSP in a comparatively short time after stress. The results suggest that HSP works as one of the mechanisms to maintain homeostasis.

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Hereditary Gingival Fibromatosis (HGF) is a rare, benign disorder characterized by slowly progressive fibrous overgrowth of the gingiva. HGF occurs in several forms as a Mendelian trait (usually as an autosomal dominant condition), in malformation syndromes, in chromosomal abnormality syndromes and side effect of several pharmacological agents. Except Son of sevenless-1 (SOS1) gene mutation, molecular basis of HGF is unclear. Here, we reported the cytogenetic and SOS1 gene mutation analysis in a Turkish family with 7 affected members through three generations, whose features are consistent with the diagnosis of autosomal dominant, isolated hereditary gingival fibromatosis. To the best of our knowledge this is the first large Turkish family with hereditary gingival fibromatosis. In this study, we excluded the chromosomal abnormalities and the mutation in SOS1 gene at this family.

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Using a transmission electron microscope, we compared the ultrastructure of apatite crystals of normal calcified hard tissue to that of apatite crystals created under pathological conditions. We also sought to verify whether the process of calcification resembles that of osteogenesis after the phenotypic change of soft tissue cells into hard tissue-forming cells. Electron micrographs clearly revealed that cellular debris, plausibly originating from degenerated immune cells like macrophages as well as perivascular cells in intima of femoral artery lesions, seemed to serve in the formation of an organic envelope. This indicates that crystal formation is accompanied by the death of cells. Judging from the lattice image, we also found that the calcified deposits consisted of 2 distinct types of apatite crystals. One type has central dark lines, while the other does not have lines. In addition, the crystals were of various sizes and some showed lattice defects. From these findings, we concluded that ectopic calcification occurred in a manner different from the calcification of normal hard tissues, suggesting that cellular phenotypic change may not happen in vivo.

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Rhabdomyolysis is a disorder of striped (skeletal) muscle and is caused by several factors, and acute renal failure associated with myoglobinuria is the most serious complication of rhabdomyolysis. However, the mechanism of tubule damage caused by myoglobin is still unclear. The early histopathological changes were not examined. Myoglobin reabsorption by the proximal renal tubules has not been reported to contribute to cellular damage. We performed histological analysis in a rat rhabdomyolysis model with administration of cytochalasin B (CB), which is an inhibitor of motile cell motile processes. CB inhibits the endocytosis of myoglobin in the proximal renal tubules and the increase in the BUN level, and decreased the percentage of area that had undergone tubular necrosis. On the other hand, initial degenerative changes (shortening of microvilli and protrusion of the cytoplasm) were observed on the cell surface of the proximal tubules with glycerolinduced cellular injury, and were not inhibited by the administration of CB. In conclusion, initial glycerolinduced cellular injury of the renal proximal tubules may be caused by free iron, which is isolated from myoglobin in urine. Further, the combination of the free iron in urine and the myoglobin reabsorbed by tubular cells may lead to cell necrosis.

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The aim of the present study was to evaluate new bone formation around the periosteum within the space formed by a polytetrafluoroethylene tube on the surface of rat calvarial bone. The experimental model consisted of 40 rats divided into eight groups (five rats per group). Each group was divided into the experimental group and the control groups, and it divided on 1, 2, 6 and 8 weeks group respectively. For the experimental groups, a polytetrafluoroethylene tube was placed under a raised periosteal flap, and for the control groups, the periosteum was removed and a teflon tube was placed under the skin on the calvarial bone. All surgical sites were then sutured. We examined new bone formation using micro-computed tomography, histology by staining with hematoxylin and eosin, and immunochemistry by antibodies specific to bone morphogenetic protein-2 (BMP-2) and runt-related gene-2 (Runx2). The experimental and control groups were compared at 1, 2, 6, and 8 weeks after surgery. The histological analysis clearly demonstrated that specimens from the experimental groups showed some bone formation at 2, 6, and 8 weeks after surgery. In contrast, the control groups demonstrated new bone only at 6 and 8 weeks after surgery. New bone was produced only from the calvarial bone side; it was not observed from the periosteum side. Micro-computed tomography scan revealed that bone mineral content (BMC), bone mineral density (BMC), and bone volume/tissue volume ratio (BV/TV) all increased in a time-dependent manner in the experimental groups. In the control groups, the bone volume/tissue volume ratio, bone mineral content, and bone mineral density increased slightly from 6 to 8 weeks after surgery. In all experimental and control groups, BMP-2 positive and Runx2-positive cells appeared on the new bone. In conclusion, these results suggest that the periosteum plays a role in promoting new bone formation.

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