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Metabolic Bone Diseases

Upon viewing a skeleton, one thinks of bone as an inert framework upon which the remainder of the body is constructed. Nothing could be more incorrect, since bone is a dynamic living organ which is capable of constant turnover, weight-bearing, and sustaining the remarkable stresses incurred in running, jumping, and other daily activities. Bone is constantly being formed and reformed (modeled and remodeled), is continuously serving as a reservoir of the divalent minerals (calcium, phosphate, and magnesium), and, in children, is constantly undergoing growth. In this article, the disorders that affect bone will be reviewed. These conditions fall under the general rubric metabolic bone disease and generally comprise a group of disorders in which impaired formation, enhanced resorption, or altered turnover of bone prevails (Table 1).

The human skeleton is composed of a collagen-containing (and noncollagen protein-containing) matrix, or osteoid, upon which is deposited a crystalline mineral phase. This mineral component of bone contains calcium and phosphate in various inorganic chemical compounds, the major one being hydroxyapatite. However, this hydroxyapatite is deep within bone trabeculae and ordinarily inaccessible. The rapidly exchangeable pool and accessible mineral phase of bone is composed of newly formed, but incomplete, hydroxyapatite crystals and amorphous calcium phosphate.¹

This article has been cited by other articles:

				R. W. Chesney A New Form of Rickets During Infancy: Phosphate Depletion-Induced Osteopenia Due to Antacid Ingestion Arch Pediatr Adolesc Med, December 1, 1998; 152(12): 1168 - 1169. [Full Text] [PDF]

				E. K. Pivnick, N. C. Kerr, R. A. Kaufman, D. P. Jones, and R. W. Chesney Rickets Secondary to Phosphate Depletion: A Sequela of Antacid Use in Infancy Clinical Pediatrics, February 1, 1995; 34(2): 73 - 78. [Abstract] [PDF]