Pathogenesis of osteoporosis

Publisher Summary Pathophysiology of osteoporosis is multifactorial and includes genetic, endocrine, and lifestyle influences. This chapter reviews the role of these factors in the earlier gain and later loss of bone mass, as well as the cellular mechanisms responsible for the latter. During growth, the effect of genes is modulated by hormonal factors, which in themselves may be genetically mediated. However, there is little consistency regarding the magnitude of importance of each of these genes and the extent to which their contribution can be generalized to all populations. Nutrition is an important, modifiable factor that determines peak bone mass (PBM). Several nutrients play key roles in skeletal development, including protein, calcium, phosphorus, and vitamin D. High-impact forces applied to the skeleton appear to confer the greatest benefit. Weight-bearing exercise is associated with higher PBM in both genders. The amount of tissue in the bone mass is the integral of the amount of bone accrued during growth and consolidation and the inevitable loss of bone tissue with aging and menopause in women. Therefore, both peak bone mass, and the rate and duration of bone loss determine fracture risk. Most clinicians consider the process of loss of mass and its accompanying architectural changes to be a prerequisite to the relationship between bone mass and fracture risk in older individuals.

[1]  A. Parfitt Use of bisphosphonates in the prevention of bone loss and fractures. , 1991, The American journal of medicine.

[2]  François Duboeuf,et al.  Vitamin D3 and Calcium to Prevent Hip Fractures in Elderly Women , 1992 .

[3]  D. Dempster Perspectives bone histomorphometry in glucocorticoid‐induced osteoporosis , 1989 .

[4]  J. Feyen,et al.  Prostaglandin production by calvariae from sham operated and oophorectomized rats: effect of 17 beta-estradiol in vivo. , 1987, Endocrinology.

[5]  Kenneth G. Mann,et al.  Evidence of estrogen receptors in normal human osteoblast-like cells , 1988 .

[6]  L. Raisz,et al.  Glucocorticoid-induced osteoporosis: pathogenesis and management. , 1990, Annals of internal medicine.

[7]  R. Martin,et al.  Studies of skeletal remodeling in aging men. , 1980, Clinical orthopaedics and related research.

[8]  E. Canalis,et al.  Parathyroid hormone enhances the transcript and polypeptide levels of insulin-like growth factor I in osteoblast-enriched cultures from fetal rat bone. , 1989, Endocrinology.

[9]  G. Rodan,et al.  Estradiol effects on proliferation, messenger ribonucleic acid for collagen and insulin-like growth factor-I, and parathyroid hormone-stimulated adenylate cyclase activity in osteoblastic cells from calvariae and long bones. , 1989, Endocrinology.

[10]  J. Compston,et al.  Age-related changes in trabecular width and spacing in human iliac crest biopsies. , 1989, Bone and mineral.

[11]  S. Mohan,et al.  Bone growth factors. , 1991, Clinical orthopaedics and related research.

[12]  S. Jaglal,et al.  Past and recent physical activity and risk of hip fracture. , 1993, American journal of epidemiology.

[13]  C. Slemenda,et al.  Calcium supplementation and increases in bone mineral density in children. , 1992, The New England journal of medicine.

[14]  H. Broxmeyer,et al.  Increased osteoclast development after estrogen loss: mediation by interleukin-6 , 1992 .

[15]  E. Puscheck,et al.  Effect of surgical menopause and estrogen replacement on cytokine release from human blood mononuclear cells. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[16]  B. Riggs,et al.  The influence of age on bone mineral regulating hormones. , 1986, Bone.

[17]  R. Heaney Thinking straight about calcium. , 1993, The New England journal of medicine.

[18]  R. Weinstein,et al.  Decreased trabecular width and increased trabecular spacing contribute to bone loss with aging. , 1987, Bone.

[19]  A. Parfitt Implications of architecture for the pathogenesis and prevention of vertebral fracture. , 1992, Bone.

[20]  B. Riggs,et al.  Avian osteoclasts as estrogen target cells. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[21]  D. Kiel,et al.  Alcohol consumption and hip fractures: the Framingham Study. , 1988, American journal of epidemiology.

[22]  R. Lindsay,et al.  Maintenance of cancellous bone connectivity in primary hyperparathyroidism: Trabecular strut analysis , 1992, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[23]  S. Ralston,et al.  Estrogen inhibits release of tumor necrosis factor from peripheral blood mononuclear cells in postmenopausal women , 1990, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.