Effects of aluminum on rat bone cell populations

• Published in: Calcified tissue international 1993-11, Vol.53 (5), p.357-361
• Main Authors: KIDDER, L. S, KLEIN, G. L, GUNDBERG, C. M, SEITZ, P. K, RUBIN, N. H, SIMMONS, D. J
• Format: Article
• Language: English
• Subjects: Aluminum - pharmacology; Animals; Biological and medical sciences; Bone Development - drug effects; Bone Marrow - drug effects; Bone Marrow Cells; Calcium - metabolism; Cell Division - drug effects; Cells, Cultured; Chemical and industrial products toxicology. Toxic occupational diseases; DNA - biosynthesis; Male; Medical sciences; Metals and various inorganic compounds; Osteoblasts - drug effects; Osteocalcin - metabolism; Osteomalacia - chemically induced; Rats; Rats, Sprague-Dawley; Stromal Cells - drug effects; Toxicology
• ISSN: 0171-967X; 1432-0827
• DOI: 10.1007/BF01351843

Aluminum (Al) loading is associated with reduced bone formation and osteomalacia in human and certain animal models. However, uncertainty exists as to the cellular effect(s) of Al as both inhibition and stimulation of osteoblast proliferation have been reported. Furthermore, the extent to which Al affects osteoprogenitor cell populations is unknown. To determine the cellular effects of Al in the rat, an animal model in which Al bone disease has been produced, we compared the in vitro effect of 10-50 microns Al on the proliferation and hydroxyproline collagen formation of marrow osteoprogenitor stromal cell populations and perinatal rat calvarial osteoblasts. In subconfluent cultures, Al suppressed proliferation of both marrow fibroblast-like stromal cells and calvarial osteoblasts. In confluent cultures, however, Al selectively stimulated periosteal fibroblast and osteoblast DNA synthesis and collagen (hydroxyproline) production, both in the presence or absence of 1,25-dihydroxyvitamin D. Osteocalcin was not detected in osteoblast-conditioned media or extracellular matrix. These observations suggest that the bone formation defect associated with Al toxicity in growing rats may be a function of impaired patterns of osteoprogenitor/osteoblast proliferation. Furthermore, the Al-stimulated increase in collagen formation is consistent with the development of osteomalacia in Al-toxic humans and animals. The mechanism by which Al stimulated DNA synthesis and collagen production in more mature cultures awaits further study.