Calcium ion release from calcium hydroxide stimulated fibronectin gene expression in dental pulp cells and the differentiation of dental pulp cells to mineralized tissue forming cells by fibronectin.

AIM: The effect of calcium ions on dental pulp cells was examined and the mechanism of dentine bridge formation by calcium hydroxide was investigated. METHODOLOGY: Human dental pulp cells were treated with high concentration of calcium or magnesium ions for 24 h and fibronectin gene expression was measured by the quantitative PCR method. Human dental pulp cells were then cultured on fibronecin-coated dishes for 24 h, and osteocalcin and osteopontin gene expression, which are typical phenotypes of mineralized tissue forming cells, were measured by the quantitative PCR method. RESULTS: Fibronectin gene expression was stimulated by calcium ions dose-dependently. On the other hand, magnesium ions did not influence fibronectin gene expression. Furthermore, pulp cells cultured on fibronectin-coated dishes enhanced the expression of phenotypes of mineralized tissue forming cells. CONCLUSIONS: Calcium ions released from calcium hydroxide stimulates fibronectin synthesis in dental pulp cells. Fibronectin might induce the differentiation of dental pulp cells to mineralized tissue forming cells that are the main cells to form dentine bridges, via contact with cells.

Muscle sympathetic nerve activity in patients with lumbar spinal canal stenosis.

The present study aimed to measure sensory nerve conduction velocity (SNCV) and muscle sympathetic nerve activity (MSA) in both normal subjects and patients with lumbar spinal canal stenosis (LSCS), and to determine what sensory and sympathetic nerve systems relate to the development of abnormal sensation in the lower limbs of the patients. The study population was 12 patients and 10 age-matched healthy control subjects. A statistical difference in the mean MSA intervals was found between the LSCS patients and the normal subjects. There was a fairly large difference between them in the values of the standard deviations as one of the parameters to determine the degree of fluctuation of MSA. These results suggest the LSCS patients have shorter MSA intervals and narrower fluctuations of MSA than normal subjects. As for the range of fluctuation of the MSA intervals and SNCV, the faster the SNCV, the wider the range of fluctuation of MSA intervals in the normal subjects. Many patients with LSCS seem to maintain a correlation between SNCV and MSA intervals. This suggests that even in cases of LSCS, human homeostasis works to keep the relationship between sympathetic nerve function and somato sensory nerve function to some extent. A few LSCS patients showed no correlation between MSA and SNCV. These patients were rather old, suffered spinal stenosis in the relatively higher levels of the spinal canal, and had suffered from the disease for longer than the mean period of all the patients. When the peripheral nerves or cauda epuina are chronically compressed, the nerve systems can not maintain the relationship between them, which finally results in failure. It is suggested that the disrupted coordination between sympathetic nerve function and somato sensory nerve function is one of the reasons why abnormal sensations occur in the lower extremities of LSCS patients.

Transient osteoporosis of the hip during pregnancy.

We report the clinical features of and MRI findings in transient osteoporosis of the hip during pregnancy. The study population consisted of 4 patients with a mean age of 33 years. The mean gestational age at onset was 31 weeks (range: 27 to 35 weeks). The main symptoms consisted of a weight-bearing pain in the hip and gait disturbance. The pain occurred suddenly and was of unknown cause and became severe within 2 to 3 weeks. X-ray examinations showed diffuse osteoporosis in the femoral head and neck. Moreover in 3 patients, similar lesions were also found in the lumbar spine or the knee. MRI obtained from 3 patients revealed a mottled low-signal lesion extending from the femoral head and neck on T1-weighted images and a high-signal lesion in the bone marrow suggesting edema on T2-weighted images. Mild elevation of C- reactive protein was shown in 2 patients. Conservative treatments with the limitation of weight bearing and bed rest were performed for all patients, and nonsteroidal anti-inflammatory drugs were given to 3 patients. The hip pain began to decline from 8 to 14 weeks after the onset, and completely disappeared from 14 to 24 weeks. X-ray examinations showed that osteoporotic lesions tended to improve at 10 to 14 weeks, on MRI, a high-signal lesion suggesting bone marrow edema resolved together with relief of the pain. No recurrence was found in any patients at mean follow-up of 70.8 months.

Essential role of neural Wiskott-Aldrich syndrome protein in neurite extension in PC12 cells and rat hippocampal primary culture cells.

Neural Wiskott-Aldrich syndrome protein (N-WASP) is an actin-regulating protein that induces filopodium formation downstream of Cdc42. It has been shown that filopodia actively extend from the growth cone, a guidance apparatus located at the tip of neurites, suggesting their role in neurite extension. Here we examined the possible involvement of N-WASP in the neurite extension process. Since verprolin, cofilin homology and acidic region (VCA) of N-WASP is known to be required for the activation of Arp2/3 complex that induces actin polymerization, we prepared a mutant (Deltacof) lacking four amino acid residues in the cofilin homology region. The corresponding residues in WASP had been reported to be mutated in some Wiskott-Aldrich syndrome patients. Expression of Deltacof N-WASP suppressed neurite extension of PC12 cells. In support of this, the VCA region of Deltacof cannot activate Arp2/3 complex enough compared with wild-type VCA. Furthermore, H208D mutant, which has been shown unable to bind to Cdc42, also works as a dominant negative mutant in neurite extension assay. Interestingly, the expression of H208D-Deltacof double mutant has no significant dominant negative effect. Finally, the expression of the Deltacof mutant also severely inhibited the neurite extension of primary neurons from rat hippocampus. Thus, N-WASP is thought to be a general regulator of the actin cytoskeleton indispensable for neurite extension, which is probably caused through Cdc42 signaling and Arp2/3 complex-induced actin polymerization.

Sonographic findings in muscle strain injury: clinical and MR imaging correlation.

Both sonography and magnetic resonance imaging were performed in 57 patients with clinically suspected strain injury in lower extremity muscles. Sonography demonstrated normal findings in nine patients (16%), hyperechoic infiltration in 31 patients (54%), mass in nine patients (16%), and compound lesions of infiltration and mass in eight patients (14%). Clinically grade 2 lesions ranged from small infiltration to large compound lesions on both sonography and magnetic resonance imaging. Hyperechoic infiltration was not demonstrated on T1-weighted magnetic resonance images and with less than 50% cross-sectional muscle involvement. The mass and compound lesions were ascertained to be moderate or severe injury because the masses of the lesions had obvious hemorrhage or hematoma on magnetic resonance images.