The effects of 1α, 24(R)-dihydroxyvitamin D₃ (1α, 24(R)-(OH)₂D₃) on trabecular bone remodeling were evaluated by histomorphometric methods in adult female beagle dogs. Oral 1α, 24(R)-(OH)₂D₃ was administered for 125 days at doses of 0.020 and 0.075μg/kg/day. Static and dynamic alterations were evaluated in vivo by calcein and teramycin double labelling of bone from the iliac crest taken before treatment and after 126 days. The dosage of 0.020 μg/kg/day reduced the values of osteoid specific volume, relative osteoid volume, bone formation rate, mineralization lag time, fractional singly or doubly labelled surface, tetracycline labelling rate, mean seam thickness, mineral apposition rate, fractional formation surface, and elevated the values of corrected mineralization lag time and bone formation period. Also, hypercalcemia was induced by the higher dose of 1α, 24(R)-(OH)₂D₃. Namely, an overdosage of 1α, 24(R)-(OH)₂D₃ decreased the rate of bone formation during trabecular bone remodeling.

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The effects of 1α-hydroxyvtitamin D₃ (1α-(OH)D₃) and 1α, 24(R)-dihydroxyvitamin D₃ (1α, 24(R)-(OH)₂D₃), active vitamin D₃ derivatives, on serum electrolytes, vitamin D metabolites, and other calcium-regulating factors in ovariectomized dogs were investigated. Oral 1α-(OH)D₃ or 1α, 24(R)-(OH)₂D₃ was administered for 2 years at dosage range of 0.02-0.05 μg/kg/day. After ovariectomy, serum concentrations of 1, 25-(OH)₂D, 24, 25-(OH)₂D, and 25-(OH)D decreased without hypocalcemia. Transient decreases in cortisol and thyroxine levels were also observed in ovariectomized dogs. The administration of 1α-(OH)D₃ resulted in a nomalization of the decreased serum concentration of 1, 25-(OH)₂D caused by ovariectomy. The decreased level of 1, 25-(OH)₂D in ovariectomized dogs given 1α, 24(R)-(OH)₂D₃ was replaced by the appearance of serum 1, 24(R)-(OH)₂D. The administrations of these active vitamin D₃ derivatives showed a tendency to nomalize the decreased level of serum 24, 25-(OH)₂D and 25-(OH)D due to ovariectomy. Continuous administration (2 or 3 weeks) of more than 0.03μg/kg/day of 1α, 24(R)-(OH)₂D₃ showed hypercalcemia.
Thus, the deficiency in vitamin D metabolites in ovariectomized dogs was inclined to be removed after continuous administration of 1α-(OH)D₃ or 1α, 24(R)-(OH)₂D₃.

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The effects of 1α-hydroxyvitamin D₃ (1α-(OH)D₃) and 1α, 24(R)-dihydroxyvitarnin D₃ (1α, 24(R)-(OH)₂D₃), active vitamin D₃ derivatives, on trabecular bone remodeling were evaluated by histomorphometric methods in ovariectomized beagle dogs. Either derivative was administered orally for 2 years at dosage of between 0.02-0.05 μg/kg/day. Static and dynamic alterations were evaluated using calcein and tetracycline in vivo double labeling of bone from the iliac crest taken before treatment and after two years. Two years after ovariectomy, the values of mean trabecular or seam thickness and mineralization lag time were elevated, and those of mineral apposition rate and bone formation rate were decreased. Treatment with 1α-(OH)D₃ or 1α, 24(R)-(OH)₂D₃ reversed these alterations due to ovariectomy back to normal levels. Furthermore, the administration of these active vitamin D₃ derivatives resulted in increases in the values of bone formation rate or mineral apposition rate and fractional resorption surface greater than those in non-treated animals.
Thus, active vitamin D₃ derivatives had a therapeutic effect on ovariectomy-induced bone remodeling changes in beagle dogs and were bone remodelers.

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There are increasing evidences that aluminum may cause a type of osteomalacia (Fracturing Dialysis Osteodystrophy) which occurs in some patients with chronic renal failure on regular hemodialysis. One of such cases is reported here.
A 39 year old woman who has been on regular hemodialysis for 11 years, developed hypercalcemio 5 years after commencing hemodialysis, She underwent parathyroidectomy at 6th year of hemodialysis with little clinical improvement. Multiple fractures developed at 9th year of dialysis and there was no tendency to heal at all in these fractures.
On iliac bone biopsy severe osteomalacia with low turnover was found. Bone aluminum content was about 300ug/dry weight, and aluminum was identified at (osteoid)/(calcified bone) interface with aluminum stain.
Treatment with a chelating agent desferrioxamine, 200mg twice a week before dialysis, seemed to have a significante effect to relieve her bone pain and her multiple fractures healed with good callus formation after 6 months treatment.

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The changes of bone density in a year in seventy seven patients with renal osteodystrophy in the treatment with 1 alpha (OH) D₃ and aluminum gel were investigated. Statistical analysis of quantitative microdensitometry showed that the main change did not occur in the cortical width but in the degree of intracortical mineralization. Serum parathyroid hormone levels were significantly higher in patients who showed the decrease of bone density than in those who made the improvement of it. Serum 25(OH)D₃ and 24, 25(OH)₂D₃ levels were normal, but serum 1, 25(OH)₂D₃ levels were still lower than normal in cases with optimum serum calcium and phosphorous levels. It was highly suspected that normalized serum 1, 25(OH)₂D₃ may provoke the hypercalcemia in these anuric patients. The partial resolution of defective vitamin D metabolism with the treatment of 1 alpha(OH)D₃ might still leave the persistent stimulation for parathyroid hormone secretion in some cases. In order to accomplish the regulation of the parathyroid function, elevation of serum 1, 25(OH)₂D₃ levels without causing the resultant hypercalcemia would be necessary.

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We report two adult cases of hypophosphatemic vitamin D resistant rickets with Ankylosing Spinal Hyperostois (ASH).
Case 1. A 52-year-old female had a short stature with bilateral bow legs and abnormalities of bone and joints since her childhood. At age 40, she manifested sensory disturbance in her lower extremities and gait disturbance. On admission, she had a peculiar short stature, 118cm in height, 35kg in weight. Laboratory examinations showed hypophosphatemia with normal serum calcium level, increased level of serum alkaliphosphatase and decreased renal reabsorption of phosphate. Radiological findings showed ossification in the pelvis, elbow, knee, especially, ASH with ossification of the posterior longitudial ligaments (OPLL) in the cervical.
Case 2. A 52-year-old female had essentially the same clinical history, physical characteristics and laboratory examinations. However, at age 30, she suffered from Filariasis and chyuria, so that, her laboratory examinations showed hypoprotenemia and hypocalcemia. Radiological examinations revealed ASH.
We guess that the cause of our cases with ASH may be in connection with hypophosphatemia, low level of (Ca×P) and high calcium retention rate for long periods. Our cases suggest that ASH may have a close relationship with abnormality of calcium and phosphate metabolism.

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Using Wistar male rats, the effects of thyroxine (T₄) on the levels of bone γ-carboxyglutamic acid-containing protein (BGP) in bone, serum, and urine were observed in relation to those of calcium metabolism. T₄-treatment increased serum and bone BGP levels in 2 weeks with the increase of bone-origin serum alkaline phosphatase activity indicative of the activity of bone formation. After 7 weeks treatment of T₄, no significant change was observed in these levels, however a significant loss of travecular bone was observed in T₄-treated tibia. Moreover, the excretion of urinary calcium and inorganic phosphorus was stimulated by T₄-treatment with the increase of urine BGP excretion. These results suggest that BGP level in urine, as well as in serum, reflects bone metabolism.

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Bone mineral content was measured by a densitometer on x-ray films of second metacarpal bone with an alminum wedge standard (D-Method). This was tested on 28 patients with lumbago, stiff shoulder and postgastrectomy. These measured values were compared with values obtained by photonabsorptionmetory (BMC).
A close correlation was found between the D values and BMC values (γ=0.94) and also between D values and MD values, especially in the indices GSmin (γ=0.92), SGS and SGS/D (γ=0.9) which reflected well bone density.
It was suggested that method would be a simple, safe, reproducible and economical method in quantifying bone mineral content for the routine clinical use.

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