Bone remodeling osteocalcin

Levormeloxifene induces an increase in lumbar and tibial bone mass in a rat model and is associated with a decrease in osteocalcin and cholesterol levels, while it has a neutral effect on the uterus (Bain et al. 1997 Nowak et al. 1998). In monkeys, a decrease in bone remodeling with prevention of bone loss has... 

An estimated 75 million people are affected by osteoporosis to some degree in the United States, Europe, and Japan. Osteoporosis is a systematic skeletal disease characterized by bone mass and microarchitectural deterioration with a consequent increase in bone fragility and susceptibility to fracture. Operationally, osteoporosis can be defined as a certain level of bone mineral density. The definition of osteoporosis is somewhat arbitrary and is based on epidemiological data relating fracture incidence to bone mass. Uncertainty also is introduced due to variability in bone densitometry measurements. Other clinical measures to assess the skeleton include collagen cross-links (measure of bone resorption) and levels of bone-specific alkaline phosphatase and osteocalcin (bone formation). A list of biochemical markers of bone remodeling is provided in Table 37-3. Measurement of total serum alkaline phosphatase level and urinary hydroxyproline or calcium levels is of limited value. 

Much evidence exists to support the contention that boron has beneficial effects on bone. The effects of boron, however, are most evident in the presence of suboptimal status of another nutrient important in bone formation or remodeling. In chicks, boron deprivation (0.465 mgkg diet) exacerbates the distortion of marrow sprouts (location of calcified scaffold erosion and new bone formation) and delay in imtiation of cartilage calcification in bones during marginal vitamin D deficiency (Hunt 1996). In humans, estrogen therapy to maintain bones increases serum 17P-estra-diol this increase is depressed when dietary boron intake is low (0.25-0.35 g per day) (Nielsen 1996, 1997). Boron deprivation also can exacerbate the increase in serum calcitonin and osteocalcin caused by low dietary copper and magnesium in humans. 

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