Abstract
Osteoporosis is defined as a disease characterized by low bone mass and microarchitectural deterioration of bone tissue leading to enhanced bone fragility and consequent risk of fracture [1]. It is the most common metabolic bone disease of postmenopausal women in the Western world. Like other diseases of unknown causation, the aetiology of osteoporosis is considered to be multifactorial. Age, genetic and reproductive history, body weight and various life-style factors, including diet, have been associated with the disease and can predict risk [2]. The disease may also arise as a consequence of other diseases, e.g. Cushing’s syndrome, hypogonadism and hyperparathyroidism, or treatment, e.g. corticosteroids. Peak bone mass is achieved by the fourth decade of life and thereafter there is a slow decrease in both sexes. Rate of bone loss in women, however, is markedly increased around the menopause, and hormone replacement therapy is the most effective way of slowing down this loss [3].
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References
Conference Report. Consensus Development Conference: prophylaxis and treatment of osteoporosis. Am J Med. 1991;90:107–110.
Eastell R, Riggs BL. Endocrinology and aging: calcium homeostasis and osteoporosis. Endocrinol Metab Clin N Am. 1987;16:829–842.
Department of Health. Advisory Group on Osteoporosis Report. London: Department of Health; 1994.
Jee WSS. Introduction of skeletal function: structural and metabolic aspects. In: Bronner F, Worrell RV, eds. A Basic Science Primer in Orthopaedics. Baltimore: Williams & Wilkins; 1991:3–34.
Pouilles JM, Tremollieres F, Ribot C. The effects of menopause on longitudinal bone loss from the spine. Calcif Tissue Int. 1993;52:340–343.
Bronner F. Calcium and osteoporosis. Am J Clin Nutr. 1994;60:831–836.
Dawson-Hughes B. Calcium supplementation and bone loss: a review of controlled clinical trials. Am J Clin Nutr. 1991;54:274S–280S.
Hegsted DM. Calcium and osteoporosis. J Nutr. 1986;116:2316–2319.
Sowers MF. Epidemiology of calcium and vitamin D in bone loss. J Nutr. 1993;123:413–417.
Strain JJ. A reassessment of diet and osteoporosis — possible role for copper. Med Hypoth. 1988;27:333–338.
Dollwet HHA, Sorenson JRJ. Roles of copper in bone maintenance and healing. Biol Trace Elem Res. 1988;18:39–48.
Yee CD, Kubena KS, Walker M, Champney TH, Sampson HW. The relationship of nutritional copper to the development of postmenopausal osteoporosis in rats. Biol Trace Elem Res. 1995;48:1–11.
Rajendran KG, Sood A, Spielvogel BF, Hall IH, Norwood VM, Morse KW. Antiosteoporotic activity of metal-complexes of amine carboxyboranes. Appl Organometal Chem. 1995;9:111–119.
Wink CS, Rossowska MJ, Nakamoto T. Effects of caffeine on bone-cells and bonedevelopment in fast-growing rats. Anatom Rec. 1996;1:30–38.
Strause LG, Hegenauer J, Salman P, Cone R, Resnick D. Effects of long-term dietary manganese and copper deficiency on rat skeleton. J Nutr. 1986;116:135–141.
Birchall JD, Bellia JP, Roberts NB. On the mechanisms underlying the essentiality of silicon interactions with aluminium and copper. Coord Chem Rev. 1996;149:213–240.
Suttle NF, Angus KW, Nisbet DI, Field AC. Osteoporosis in copper-depleted lambs. J Comp Pathol. 1972;82:93–97.
Suttle NF, Angus KW. Effects of experimental copper deficiency on the skeleton of the calf. J Comp Pathol. 1978;88:137–148.
Pond WG, Krook LP, Klevay LM. Bone pathology without cardiovascular lesions in pigs fed high zinc and low copper diet. Nutr Res. 1990;10:871–885.
Beattie JH, Avenell A. Trace elements and bone metabolism. Nutr Res Rev. 1992;5:167–188.
Thompson KG, Audige L, Arthur DG et al. Osteochondrosis associated with copper deficiency in young farmed red deer and Wapiti x red deer hybrids. NZ Vet J. 1994;42:137–143.
Reiser K, McCormick RJ, Rucker RB. Enzymatic and non-enzymatic cross-linking of collagen and elastin. FASEB J. 1992;6:2439–2449.
Rucker RB, Romero-Chapman N, Wong T et al. Modulation of lysyl oxidase by dietary copper in rats. J Nutr. 1996;126:51–60.
Rico H. Minerals and osteoporosis. Osteoporosis Int. 1991;2:20–25.
Danks DM. Copper deficiency in humans. Ann Rev Nutr. 1988;8:235–257.
Fife RS, Moody S, Houser D, Proctor C. Studies of copper transport in cultured bovine chondrocytes. Biochim Biophys Acta. 1994;1201:19–22.
Paterson CR, Burns J. Copper deficiency in infancy. J Clin Biochem Nutr. 1988;4:175–190.
Guler AH, Sapan N, Ediz B, Genc Z, Ozkan K. Effect of copper on liver and bone metabolism in malnutrition. Turk J Pediatr. 1994;36:205–213.
Howard G, Andon M, Bracker M, Saltman P, Strause L. Low serum copper, a risk factor additional to low dietary calcium in postmenopausal bone loss. J Trace Elem Exp Med. 1992;5:23–31.
DiSilvestro RA. Influence of dietary copper, copper injections and inflammation on rat serum caeruloplasmin activity levels. Nutr Res. 1990;10:355–358.
Strause L, Saltman P, Smith KT, Bracker M, Andon MB. Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J Nutr. 1994;124:1060–1064.
Eaton-Evans J, Mcllrath EM, Jackson WE, McCartney H, Strain JJ. Copper supplementation and the maintenance of bone mineral density in middle-aged women. J Trace Elem Exp Med. 1996;9:87–94.
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Strain, J.J. (1998). Copper and postmenopausal osteoporosis. In: Rainsford, K.D., Milanino, R., Sorenson, J.R.J., Velo, G.P. (eds) Copper and Zinc in Inflammatory and Degenerative Diseases. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3963-2_12
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DOI: https://doi.org/10.1007/978-94-011-3963-2_12
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