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Calcium Hydroxyapatite
Osteocalcin and bone
Wada S, Fukawa T, Kamiya S. Clin Calcium. 2007 Nov;17(11):1673-7.
Josai International Universtiy, Faculty of Pharmaceutical Sciences, Department of Clinical Sciences.
Osteocalcin (OC) is a product of osteoblasts and accumulated in the extracellular matrix of bone. It has been recognized that serum OC is a marker of osteoblast activity, and the levels reflect the rate of bone formation. The present assay system was developed to assess the major circulating forms of intact and the large N-terminal fragments. OC binds to the crystal of hydroxyapatite, at least partly, through gamma-carboxylation of three residues. Increased rate of immature undercarboxylated osteocalcin, therefore, might display risks for osteoporotic fractures in clinical studies. However, at present, measurement of OC does not substitute for bone mass measurement and only provide limited values to evaluate the conditions of patients with primary osteoporosis.
Active Absorbable Algal Calcium (AAA Ca): New Japanese technology for osteoporosis and Calcium paradox disease
FUJITA T. ;
Résumé / Abstract
Active Absorbable Algal Calcium (AAA Ca) is made by submaximally (800°C) heating cleaned oyster shell under reduced pressure and mix it with similarly heated seaweed (Cystophyllum fusiforme). AAA Ca, best absorbed from the intestine among available calcium compounds, consequently most efficiently suppresses parathyroid hormone secretion, increases bone mineral density and decreases vertebral fracture.
Aging is associated with calcium deficiency, mostly because of the decreased biosynthesis of 1,25 (OH)2 vitamin D in the kidney. Parathyroid hormone consequently increases, contributing to various diseases associated with aging such as osteoporosis or decrease of calcium in the bone, as well as hypertension, arteriosclerosis, Alzheimer's disease and osteoarthritis due to paradoxical increase of calcium in vascular walls, brain, cartilage and intracellular compartment of many kinds of cells. Mild calcium deficiency is hard to detect despite these serious consequences because of the remarkable constancy of blood calcium concentration maintained by elaborate homeostatic control. Only by successfully counteracting calcium deficiency by AAA Ca with outstanding absorbability, the phenomenon of calcium paradox becomes a recognizable reality within our reach.
Effects of vitamin K2 on osteoporosis.
Iwamoto J, Takeda T, Sato Y. Curr Pharm Des. 2004;10(21):2557-76.
Department of Sports Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. jiwamoto@sc.itc.keio.ac.jp
Vitamin K2 is a cofactor of gamma-carboxylase, which converts the glutamic acid (Glu) residue in osteocalcin molecules to gamma-carboxyglutamic acid (Gla), and is, therefore, essential for gamma-carboxylation of osteocalcin. Available evidence suggests that vitamin K2 also enhances osteocalcin accumulation in the extracellular matrix of osteoblasts in vitro.
Osteocalcin-knockout mice develop hyperostosis, suggesting that the Gla-containing osteocalcin promotes normal bone mineralization. Although the precise role of osteocalcin in bone mineralization remains obscure, it probably regulates the growth of hydroxyapatite crystals. Furthermore, vitamin K2 also inhibits the expression of the osteoclast differentiation factor (ODF)/RANK ligand, tartrate-resistant acid phosphatase activity, and mononuclear cell formation, and induces osteoclast apoptosis in vitro.
There is some evidence indicating that vitamin K2 prevents bone resorption in ovariectomized rats, retards the increase in bone turnover in orchidectomized rats, ameliorates the increase in bone resorption and decrease in bone formation in sciatic neurectomized rats, and prevents the decrease in bone formation in glucocorticoid-treated rats. These findings suggest that vitamin K2 may not only stimulate bone formation but also suppress bone resorption in vivo.
Clinically, vitamin K2 sustains the lumbar bone mineral density (BMD) and prevents osteoporotic fractures in patients with age-related osteoporosis, prevents vertebral fractures in patients with glucocorticoid-induced osteoporosis, increases the metacarpal BMD in the paralytic upper extremities of patients with cerebrovascular disease, and sustains the lumbar BMD in patients with liver-dysfunction-induced osteoporosis.
Vitamin K deficiency, as indicated by an increased circulating level of undercarboxylated osteocalcin, may contribute to osteoporotic fractures. Even though the effect of vitamin K2 on the BMD is quite modest, this vitamin may have the potential to regulate bone metabolism and play a role in reducing the risk of osteoporotic fractures. No randomized well-controlled prospective studies conducted on a sufficiently large number of patients have been reported yet, therefore, further studies are needed to confirm the efficacy of vitamin K2 in the treatment of osteoporosis.
Vitamin K and bone quality
Hara K, Akiyama Y. Clin Calcium. 2007 Nov;17(11):1678-84.
Eisai Co., Ltd., Clinical Research Center, Applied Drug Research Department, Pharmacological Evaluation Section.
Meta-analysis involving previous clinical studies showed that VK(2) decreased the incidence of fracture. In particular, the results based on the data on bone mineral density and fracture suggested that VK(2) improves bone quality. Preclinical studies regarding bone quality reported that VK(2) improved the trabecular microarchitecture (connectivity and width) in an ovariectomized model, and that VK(2) increased the bone strength without influencing the bone mineral content in a model fed a low-Mg diet and a vitamin C deficiency model, increasing the collagen level and proline hydroxylation. Thus, improvement in bone quality via actions on the bone geometry and collagen level/quality may be involved in a VK(2)-related decrease in the incidence of new fracture in clinical studies.
Guidelines for the management of osteoporosis
Pfeilschifter J. Internist (Berl). 2008 Oct;49(10):1178, 1180-2, 1184-5.
Klinik für Innere Medizin III, Lutherhaus, Alfried Krupp Klinikum, Hellweg 100, 45276, Essen, Deutschland. Johannes.Pfeilschifter@lutherhaus.de
Treatment of osteoporosis aims to reduce osteoporotic fractures and to minimize fracture-related pain and functional impairment. Components of non-drug therapy include improvement of muscle strength and coordination, treatment of modifiable causes of falls, a diet rich in calcium and sufficient in calories, adequate supply of vitamin D and an individual assessment of drugs known to increase falls or osteoporosis. Bisphosphonates, raloxifene, strontium ranelate and parathyroid hormone have been shown to reduce osteoporotic fractures in postmenopausal women. Alendronate, risedronate and parathyroid hormone are also licensed for the treatment of male osteoporosis. One of the still open questions is the optimal duration of pharmacological treatment.
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