Low Turnover Osteoporosis Research Articles

Osteoporosis and Diabetes: Lessons from the Diabetic BB Rat

The spontaneously diabetic BB rat was used to study the effect of diabetes on bone. Short-term diabetes (3-4 weeks) resulted in a state of low bone turnover, characterized by a severe decrease in osteoblast/osteoid surface and bone mineral apposition rate on histology, and in serum osteocalcin concentrations. If diabetes was long-term (12 weeks), the parameters of low bone formation were associated with histological evidence of osteoporosis and a decreased bone strength; the relative bone calcium concentration remained normal in diabetes. We conclude that long-standing diabetes results in a low-turnover osteoporosis.

胃切除後骨障害について

This paper describes the study of bone rarefaction in 37 patients with low back pain, bone fracture and dental rarefaction after gastrectomy. Our investigations included laboratory tests and radiological measurements of bone mineral content.Serum calcium and phosphate levels were maintained within normal range but alkaline phosphatase was elevated in 8 patients and the level was a good correlation with the degree of bone rarefaction. PTH was impaired in 14 patients and was just below the normal range in 12 patients.Vertebral compression fractures were present 19.5% in males, and 21.1% in females. Bone mineral content was severely decreased in 3 patients and was slightly or moderately decreased in 23 patients, but was normal in 11 patients. Bone rarefaction after gastrectomy was assessed in 26 patients and was attributed to low turn-over osteoporosis.

Increases in bone density during treatment of men with idiopathic hypogonadotropic hypogonadism.

To assess the effects of gonadal steroid replacement on bone density in men with osteoporosis due to severe hypogonadism, we measured cortical bone density in the distal radius by 125I photon absorptiometry and trabecular bone density in the lumbar spine by quantitative computed tomography in 21 men with isolated GnRH deficiency while serum testosterone levels were maintained in the normal adult male range for 12-31 months (mean +/- SE, 23.7 +/- 1.1). In men who initially had fused epiphyses (n = 15), cortical bone density increased from 0.71 +/- 0.02 to 0.74 +/- 0.01 g/cm2 (P less than 0.01), while trabecular bone density did not change (116 +/- 9 compared with 119 +/- 7 mg/cm3). In men who initially had open epiphyses (n = 6), cortical bone density increased from 0.62 +/- 0.01 to 0.70 +/- 0.03 g/cm2 (P less than 0.01), while trabecular bone density increased from 96 +/- 13 to 109 +/- 12 mg/cm3 (P less than 0.01). Cortical bone density increased 0.03 +/- 0.01 g/cm2 in men with fused epiphyses and 0.08 +/- 0.02 g/cm2 in men with open epiphyses (P less than 0.05). Despite these increases, neither cortical nor trabecular bone density returned to normal levels. Histomorphometric analyses of iliac crest bone biopsies demonstrated that most of the men had low turnover osteoporosis, although some men had normal to high turnover osteoporosis. We conclude that bone density increases during gonadal steroid replacement of GnRH-deficient men, particularly in men who are skeletally immature.

Pulse Amplitude and Frequency Modulation of Parathyroid Hormone in Plasma*

Inconclusive reports on pulsatile secretion of PTH in man have been published. In this study PTH was measured by intact and PTH-(44-68) assays. Central venous blood sampling was performed every 2 min in 10 healthy men between 6-9 h and in 3 male patients with osteoporosis for over 6 h. Pulsatile PTH secretion was identified for healthy men and controls. Narrow pulses and bursts of narrow pulses (broad pulse) could be distinguished. Six narrow pulses per h with 26 +/- 16 ng/L amplitude and 1 burst of narrow pulses/h were detected for the intact hormone. One narrow pulse/h with 25 +/- 12 ng/L amplitude and 1 burst of narrow pulses (broad pulse) every 2 h were found (Pulsar) for PTH-(44-68). Intact and PTH-(44-68) exhibit in part a concordant pattern. Results from 3 patients with osteoporosis show a decreased amplitude and frequency of pulsatile PTH secretion. The same decreased pattern was demonstrated in a postmenopausal osteoporotic woman. A constant decline in ionized calcium elicits major secretory episodes of PTH, and ionized calcium increases after major secretory episodes of PTH. We conclude that pulsatile secretion of PTH in healthy young men is the physiological mode of secretion. Low pulsatile secretion of PTH might be related to low turnover osteoporosis.

Increase of vertebral density by combination therapy with pulsatile 1-38hPTH and sequential addition of calcitonin nasal spray in osteoporotic patients

Combination therapy with the biologically active (1-38) human parathyroid hormone peptide and calcitonin using pulsatile and sequential activation of the skeleton for 14 months in patients with low-turnover osteoporosis resulted in an increase in trabecular bone mass. These favorable responses were observed without any significant changes in cortical (forearm) bone mass content.

Serum and urinary markers of bone remodeling: assessment of bone turnover.

It appears that at present, serum BGP is the one bone protein that has the most promise for assisting in the diagnosis and management of high turnover metabolic bone disease states. If further studies confirm its usefulness in osteoporosis as a predictor of rapid bone loss without the need for bone biopsy, this serum marker will then not only allow early detection but also an appropriate choice of therapy in osteoporosis, i.e. the use of specific inhibitors of high turnover states such as estrogen, calcitonin, or bisphosphonates. In addition, it may also permit more accurate follow-up of patients suffering from diseases such as primary hyperparathyroidism after surgery. In low turnover osteoporosis, it may also serve a useful function to observe whether the osteoblast can be stimulated to enhance bone formation with therapies such as fluoride, anabolic steroids, PTH, etc. As yet, additional measurements, such as bone histomorphometry and other bone mineral markers, are required for definitive diagnosis. Hopefully, the availability of specific well-characterized antibodies against BGP may define its role more accurately. Recently, several other new bone proteins have been identified but at present they have very limited clinical application. Future studies into the structure-function relationship of these bone proteins may identify those markers which will be most relevant to the diagnosis and treatment of metabolic bone disease.

Deficit of Trabecular and Cortical Bone in the Radius in Low-Turnover Osteoporosis

Deficit of Trabecular and Cortical Bone in the Radius in Low-Turnover Osteoporosis