Normal Bone Remodelling and Its Disruption in Metastatic Bone Disease
- 56 Downloads
Bone is a metabolically active tissue which is continually being remodelled by a process involving the removal of microscopic packets of calcified matrix and their subsequent replacement at the same site by new bone. This normal physiological process can be disturbed by the direct local and/or the distant systemic effects of tumour cell products released by neoplastic cells. Recent research has indicated that many of the factors that may be involved in the regulation of bone remodelling and are produced by normal cells in the bone micro-environment can also be produced in excessive amounts by neoplastic cells. Thus metastatic malignant cells could directly interfere with the function of normal bone cells and so disrupt the bone micro-architecture.
KeywordsBone Resorption Bone Remodelling Metastatic Bone Disease Stimulate Bone Resorption Normal Bone Remodelling
Unable to display preview. Download preview PDF.
- Baron R, Vignery A, Horowitz M (1983) Lymphocytes, macrophages and the regulation of bone remodelling. In: Peck WA (ed) Bone and mineral research, Annual 2. Elsevier, New York, pp 175–246Google Scholar
- Berrettoni BA, Carter JR (1986) Mechanisms of cancer metastasis to bone. J Bone Joint Surg [Am] 68:308–312Google Scholar
- Boyce BF (1990) Bone biopsy and histomorphometry in metabolic bone disease. In: Stevenson JC (ed) New techniques in metabolic bone disease. Wright, London, pp 110–131Google Scholar
- Chambers TJ (1980) The cellular basis of bone resorption. Clin Orthop Rel Res 151:283–293Google Scholar
- Chambers TJ (1982) Osteoblasts release osteoclasts from calcitonin-induced quiescence. J Cell Sei 57:247–260Google Scholar
- Frost HM (1973) The origin and nature of transients in human bone remodelling dynamics. In: Frame B, Parfitt AM, Duncan H (eds) Clinical aspects of metabolic bone disease. Excerpta Medica; Amsterdam, pp 124–137Google Scholar
- Martin TJ, Partridge NC, Greaves M, Atkins D, Ibbotson KJ (1979) Prostaglandin effects on bone and role in cancer hypercalcaemia. In: Maclntyre I, Szelke M (eds) Molecular Endocrinology Elsevier, North-Holland, Amsterdam, pp 251–264Google Scholar
- Sabatini M, Bonewald L, Chavez J, Mundy GR (1989) Production of GM-CSF by a human tumour associated with leukocytosis and hypercalcemia induces cytokine production by host cells. J Bone Miner Res [Suppl 1] 4:S155 (abstr)Google Scholar
- Sakamoto S, Sakamoto M (1986) Bone collagenase, osteoblasts and cell-mediated bone resorption. In: Peck WA (Ed) Bone and mineral research vol 4 Elsevier, Amsterdam, pp 49–102Google Scholar
- Valentin Opran A, Edouard C, Charhon S, Meunier PJ (1980) Histomorphometic analysis of iliac bone metastases of prostatic origin. In: Donath A, Huber H (eds) Bone and tumours. Medicine et hygiene, Geneve, pp 24–28Google Scholar
- Wo Z, Bonewald LF, Oreffo ROC et al. (1990) The potential role of procathepsin D secreted by breast cancer cells in bone resorption. In: Cohn DV, Glorieux FH, Martin TJ (eds) Calcium regulation and bone metabolism. Elsevier, North-Holland, Amsterdam, pp 304–310Google Scholar