Risedronate decreases osteoporotic fracture incidence; however, its effects remain unclear in elderly osteoporotic patients. Vitamin K mediates carboxylation of osteocalcin (OC), and high undercarboxylated osteocalcin (ucOC) levels indicate vitamin K deficiency and increased osteoporotic fracture risk. We aimed to evaluate the effects of risedronate alone or combined with vitamin K2 on serum ucOC, OC, and incidence of vertebral fractures in elderly osteoporotic patients. A total of 101 women with postmenopausal osteoporosis aged >60 years were randomly stratified into two groups-R group (n = 51), treated with risedronate alone; and R + K group (n = 50), treated with risedronate and vitamin K2. Serum ucOC, OC and incidence of vertebral fractures were evaluated before treatment and at 6 and 12 months post-treatment. Decreased ucOC rates at 6 and 12 months were not significant between groups. However, at 6 and 12 months, decreased OC rates in the R group (p < 0.01 and 0.05, respectively) were significantly higher than in the R + K group, and ucOC/OC change rates in the R group (p < 0.05 and 0.001, respectively) were significantly lower than in the R + K group. Vertebral fracture incidence was not significantly different between the groups at 6 and 12 months. ucOC levels in patients with incident vertebral fractures were significantly higher than in patients without incident vertebral fractures in the R group at 6 months (p < 0.05). Although no significant difference was observed for ucOC decrease rate and incidence of vertebral fractures between treatments, ucOC levels in patients with incident vertebral fractures were significantly greater than in patients without when using risedronate alone.

Endothelial cells are stable and quiet in normal animals. They arrange regularly and have a smooth lumen surface and thin endothelial wall. According to Thoma's principle (1893) and Kamiya and Togawa's principle (1980) on the relationship of the vascular diameter to flow alteration, blood flow is in equilibrium to the diameter and in a physiological state. That is to say, there is no fast flow or slow flow. To understand the nature of the endothelial cells, we should investigate endothelial cells under flow alteration to break the equilibrium state. Endothelial cells under increased flow were studied in arteries with an arteriovenous fistula or in the capillaries of myocardium with volume-overloaded hearts or of the skeletal muscle by electrical stimulation. Those under decreased flow were studied by the closure of the fistula or by ceasing the stimulation. Endothelial cells in the coarctation of the arteries were also observed. Endothelial cells were activated by increased flow in the arteries and capillaries, while they were inactivated by decreased flow. Endothelial activation is characterized as lumen protrusions, increase of cytoplasmic organelles, abluminal protrusions, basement membrane degradation, internal elastic lamina degradation in the arteries, and sproutings in the capillaries. These are ultrastructurally comparable to angiogenesis. Endothelial inactivation is characterized by the decrease of endothelial cell number with apoptosis, which is ultrastructurally comparable to angioregression. We assume that endothelial cells respond to increased flow by angiogenesis and to decreased flow by angioregression.

Physiological angiogenesis occurs in electrically stimulated skeletal muscles. It is known to start as capillary sproutings, but has not yet been well characterized as ordinary angiogenesis. To characterize the sprouting process during physiological angiogenesis, we carried out an ultrastructural 3-D reconstruction study for the extensor digitorum longus of three adult rabbits under electrical stimulation for 7 days. In addition, hemodynamic and morphological studies were carried out after stimulation for 3, 7, and 14 days. The electrical stimulation induced a twofold increase in femoral artery blood flow and tissue blood flow. This was associated with an increase in capillary density of the muscle by more than twofold at 7 and 14 days. Sproutings frequently appeared at 7 days (4.3 +/- 1.4 x 10(3) sproutings per mm3, 13.3 +/- 6.9 microm in length). All sprouting tips consisted of endothelial cytoplasmic protrusions (ECP). Besides sproutings, there were communicating networks consisting segmentally of ECP (11.6 +/- 5.6 x 10(3) networks per mm3). Endothelial cytoplasmic protrusions began to appear at 3 days, were frequent at 7 days, and disappeared at 14 days, which corresponded well to the changes in blood flow and capillary density. We consider that in physiological angiogenesis, sproutings start as ECP, which contact other capillaries to form networks and become hollowed to form new capillary networks.

The current definition of atypical femoral fractures (AFFs) excludes periprosthetic fractures. However, a few cases of bisphosphonates (BPs) -associated periprosthetic atypical femoral fractures (PAFFs) have been reported in the literature. Here, we report two rare cases of PAFFs that fulfilled the major criteria for AFFs in patients with prolonged use of BPs. Both cases progressed to a complete fracture with minor trauma from an incomplete fracture at the distal tip of the well-fixed femoral stem. The femoral stem effect on lateral femoral cortical bone, together with the decreased bone elastic resistance induced by BPs, was considered the cause of onset. In each case, we performed open reduction and internal fixation using a locking plate with cable grip and postoperatively prescribed teriparatide and low-intensity pulsed ultrasound (LIPUS). Both cases had a good clinical course. However, as conservative treatment was not effective in these cases, treatment such as non-weight-bearing exercises during hospitalization or prophylactic surgery may be necessary. Further studies are needed to determine the optimal treatment strategy.

An autopsy case of aortic sarcoma who died of acute myocardial infarction caused by coronary involvement is reported. The patient was a 54 year old woman who was admitted because of an undiagnosed fever and general fatigue of 6 months duration. Magnetic resonance imaging (MRI) showed a tumor in the aortic arch. Total aortic arch replacement was performed. It was diagnosed as a malignant mesenchymal tumor of the aorta. The patient died of acute myocardial infarction 10 months after the operation. At autopsy, the tumor had invaded the luminal surface and intima of the proximal anastomosis (the remnant ascending aorta and the graft), the aortic valves, the distal anastomosis (surgical line of the thoracic aorta plus the graft), and the coronary arteries. The left main coronary artery showed complete obstruction by fibrin thrombus with tumor invasion in the intima, which was responsible for acute myocardial infarction. Primitive and bizarre tumor cells proliferated with many slit-like tissue spaces. Most of the tumor except for its luminal surface showed necrosis. Ultrastructurally, there were spaces between tumor cells, suggesting lumen formation, and some of them had microvilli. This sarcoma was considered to be the so-called aortic intimal sarcoma.