Summary
The final clinical outcome of the osteoporotic process is a fracture, which can occur as a result of minimal trauma or even spontaneously. At present low bone mass is regarded as the main contributor to bone fragility, but possible qualitative changes in the bone matrix must also be considered. Two factors which determine the level of bone mass at any age are the obtained peak bone mass and duration and rate of bone loss. Peak bone mass is achieved during the first three decades of life. Genetic and nutritional factors as well as mechanical stress on the skeleton obviously play crucial roles in determining peak bone mass. Two phases of bone loss—age-related and menopause-related—dictate the final bone mass at old age. Postmenopausal osteoporosis is a particular example of unbalanced bone resorption leading to net bone loss. An increasing number of systemic and local factors have been found to participate in the regulation of bone remodeling.
Similar content being viewed by others
References
Riggs BL, Melton LJ III (1986) Involutional osteoporosis. N Engl J Med 314:1676–1686
Riggs BL, Melton LJ III (1983) Evidence for two distinct syndromes of involutional osteoporosis. Am J Med 75:899–901
Riggs BL, Melton LJ III (1990) Clinical heterogeneity of involutional osteoporosis: implications for preventive therapy. J Clin Endocrinol Metab 70:1229–1232
Glastre C, Braillon P, David L, Cochat P, Meunier PJ, Delmas PD (1990) Measurement of bone mineral content of the lumbar spine by dual energy X-ray absorptiometry in normal children: correlations with growth parameters. J Clin Endocrinol Metab 70:1330–1333
Evans RA, Marel GM, Lancester EK, Kos S, Evans M, Stanley YP (1988) Bone mass is low in relatives of osteoporotic patients. Ann Intern Med 109:870–873
Nordin BEC, Need AGA, Chatterton BE (1990) The relative contributions of age and years since menopause to postmenopausal bone loss. J Clin Endocrinol 70:83–88
Eriksen E, Steiniche T, Mosekilde L, Melsen F (1989) Histomorphometric analysis of bone in metabolic bone disease. Endocrinol Metab Clin North Am 18:919–954
Reeve J (1986) A stochastic analysis of iliac trabecular bone dynamics. Clin Orthop 213:264–278
Aaron JE, Makins NB (1987) The microanatomy of trabecular bone loss in normal ageing men and women. Clin Orthop 215:260–271
Frost HM (1964) Dynamics of bone remodeling. In: HM Frost (ed) Bone Biodynamics. Little, Brown, Boston, p. 315
Martin TJ, Ng SK, Suda T (1989) Bone cell physiology. Endocrinol Metab Clin North Am 18:833–858
Mundy GR, Roodman GD (1987) Osteoclast ontogeny and function. In: Peck WA (ed) Bone and mineral research V. Elsevier, Amsterdam, pp 209–280
Lakkakorpi P, Tuukkanen J, Hentunen T, Järvelin K, Väänänen K (1989) Organization of osteoclast microfilaments during the attachment to bone surface in vitro. J Bone Miner Res 4:817–825
Horton MA, Davies J (1989) Adhesion receptors in bone. J Bone Miner Res 4:803–808
Vaes G (1988) Cellular biology and biochemical mechanism of bone resorption. A review of recent developments on the formation, activation, and mode of action of osteoclast. Clin Orthop 231:239–271
Blair HC, Teitelbaum SL, Ghiselli R, Gluck S (1989) Osteoclastic bone resorption by a polarized vacuolar protyon pump. Science 245:855–857
Bekker PJ, Gay CV (1990) Biochemical characterization of an electrogenic vacuolar proton pump in purified chicken osteoclast plasma membrane vesicles. J Bone Miner Res 5:569–579
Väänänen HK, Karhukorpi E-K, Sundquist K, Wallmark B, Roininen I, Hentunen T, Tuukkanen J, Lakkakorpi P (1990) Evidence for the presence of a proton pump of the vacuolar H+-ATPase type in the ruffled borders of osteoclasts. J. Cell Biol 111:1305–1311
Sundquist K, Lakkakorpi P, Wallmark B, Väänänen K, (1990) Inhibition of osteoclast proton transport by bafilomycin A1 abolishes bone resorption. Biochem Biophys Res Commun 168:309–313
Eeckhout Y, Delaisse JM (1988) The role of collagenase in bone resorption. An overview. Pathol Biol (Parr's) 36:1139–1146
Bonewald LF, Mundy GR (1989) Role of transforming growth factor beta in bone remodeling: a review. Connect Tissue Res 23:201–208
Marcus R (1989) Estrogens and progestins in the management of primary hyperparathyroidism. Endocrinol Metab Clin North Am 18:715–722
Calvo MS, Kumar R, Heat H III (1990) Persistently elevated parathyroid hormone secretion and action in young women after four weeks of ingesting high phosphorus, low calcium diets. J Clin Endocrinol Metab 70:1334–1340
Tiegs RD, Body JJ, Wahner HW, Barta J, Riggs BL, Heath H III (1985) Calcitonin secretion in postmenopausal osteoporosis. N Engl J Med 312:1097–1100
Hurley DL, Tiegs RD, Wahner HW, Heath H III (1987) Axial and appendicular bone mineral density in patients with long-term deficiency or excess of calcitonin. N Engl J Med 317:537–541
Gallagher JC, Jerpbak CM, Jee WSS, Johnson KA, DeLuca HF, Riggs BL (1982) 1,25-Dihydroxyvitamin D3: short- and long-term effects on bone and calciuim metabolism in patients with postmenopausal osteoporosis. Proc Natl Acad Sci USA 79:3325–3329
Eriksen EF, Colvard DS, Berg NJ, Graham ML, Mann KG, Spelsberg TC, Riggs BL (1988) Evidence of estrogen receptors in normal human osteoblast-like cells. Science 241:84–86
Colvard DS, Eriksen EF, Keeting PE, Wilson EM, Lubahn DB, French FS, Riggs FB, Spelsberg TC (1989) Identification of androgen receptors in normal human osteoblast-like cells. Proc Natl Acad Sci USA 86:854–857
Mundy G (1989) Calcium homeostasis: hypercalcemia and hypocalcemia. Martin Dunitz, London
Canalis E, McCarthy TL, Centrella M (1989) The role of growth factors in skeletal remodeling. Endocrinol Metab Clin North Am 18:903–918
Raisz LG (1988) Local and systemic factors in the pathogenesis of osteoporosis. N Engl J Med 318:818–828
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Väänänen, H.K. Pathogenesis of osteoporosis. Calcif Tissue Int 49 (Suppl 1), S11–S14 (1991). https://doi.org/10.1007/BF02555080
Issue Date:
DOI: https://doi.org/10.1007/BF02555080