Calcification of aging articular cartilage in man.

Calcification of the articular cartilage was studied ultrastructually using normal femoral heads obtained from necropsies of persons ranging in age from 11 months to 80 years. Mineral crystals which appeared during the initial stages of deposition were morphologically divided into two types. Type A crystals were slender, twisted and curved, measuring from 100 nm to 360 nm in length. Type B crystals were short, needle-like and slightly curved, measuring from 30 nm to 160 nm in length. Type A crystals were found mainly in the developing epiphysis during childhood. Type B crystals were generally found in the calcified zone of adult articular cartilage. Both types of crystals initially appeared in close proximity to extracellular membrane-invested electron dense particle called "matrix vesicles", and gradually increased in number to form calcified cartilage matrix. The morphological differences between type A and B crystals might be caused by biochemical alterations of the cartilage matrices and/or biomechanical changes in the joints of children and adults.

Ultrastructure of the deep zone of degenerative osteoarthritic cartilage.

The deep zone of articular cartilage obtained from 22 surgical cases with advanced osteoarthritis of the hip joint and from additional 14 necropsy cases with normal hip joint were studied by aids of ultrastructural, electron histochemical and elemental analytic techniques. The deep zone of osteoarthritic cartilage showed significant degenerative changes of the extracellular matrix including fibrillar or non-fibrillar components and/or abnormal calcification. The electron histochemical method used revealed prominently decreased concentration of proteoglycan complex in the osteoarthritic cartilage as compared with that in the normal articular cartilage.

Vitamin D sclerosis in rats.

The early fine structural changes in the arteries of rats induced by excess vitamin D3 perorally or parenterally were essentially similar, except the latter had a more prominent toxic effect to the vascular wall. The ultrastructural features, incidental to calcification, included the appearance of increased ground substance with a separation of collagenous and elastic fibrils, and degenerative changes in smooth muscle cells. Atherosclerosis was greatly accelerated at the sites of vascular injury when cholesterol, cholic acid and thiouracil were added to the basal diet. Calcification was initially observed in relation to elastic fibrils or degenerated cells in the upper and middle layers of the arteries, although there were few such deposits in the thickened intima of the coronary arteries. Calcium deposition could not be a direct effect of hypercalcemia, but the functional activity of smooth muscle cells did seem to promote the mineralization of calcium and phosphate. Furthermore, vitamin D-induced sclerosis did not prevent intimal thickening of the arteries when vitamin D3 was withdrawn.

Measurement of endothelial fibrinolytic activity in aorta and vena cava in rabbits: a fibrin-agar plate method.

The fibrin-agar plate method was used to estimate fibrinolytic activity from the luminal surfaces of aorta and vena cava with or without denudation of endothelium in rabbits. Diffuse endothelial denudation was accomplished by air-dry injury to the luminal surfaces for 24 hours prior to sacrifice. The segments individually obtained from the aorta and vena cava were immediately turned inside out in a cylindrical fashion and soaked in a vial containing plasminogen-rich solution. The vials were kept in a refrigerator at 4 degrees C for 4 hours. Five microliter of the solution was dropped on a fibrin-agar plate containing 0.08% fibrinogen (plasminogen free) and 1.4% agar in 0.01 M phosphate buffer with a pH of 7.4. A thrombin solution was then added to the plates, which were incubated for 18 hours at 37 degrees C in a moist chamber. The fibrinolytically digested areas revealed no comparative difference in fibrinolytic activity between the aorta and the vena cava either in the experimental or control group. However, a plasminogen activator was detected on the luminal surfaces of both the aorta and the vena cava with endothelial denudation as well as in normal controls. These results suggest that luminal fibrinolytic activity may be located not only in endothelial cells but possibly in other sources as well. Further examination of the interaction between the tissue activator and the inhibitor and determination of their localization are needed. Thrombogenesis may be an important factor in atherogenesis; in certain circumstances, detachment of the endothelial cells exposes underlying collagen fibrils and subsequently initiates the aggregation of platelets and cellular proliferation in the intima. There are, however, many unresolved questions concerning the precise mechanisms of development, resolution and organization of thrombi.

Mast cells in human aorta.

Aortic specimens from 111 autopsy and 23 surgical cases were examined by light and electron microscopy. Differential mast cell counts were made of three aortic segments (ascending, thoracic, and abdominal) and layers (intimal, medial, adventitial). The mast cell counts varied considerably from case to case and sector to sector and generally showed no correlation with age, sex, or atherosclerotic severity. However, intimal mast cells were fewer in number in areas of lipid accumulation than in areas of diffuse intimal thickening without lipid accumulation. The reduction in the number of intimal mast cells may play a part in the localization of atherosclerosis.