Bone and cartilage are important in providing functional rigidity to the body, but have central function in modulating mineral metabolism in the body. Both tissues are subject to toxic and genetically determined influences on mucopolysaccharide (ground substance) synthesis, hormonal changes and defects in mineral homeostasis. In prenatal development, skeletal development is sensitive to abnormalities in the intrauterine environment and in the availability of
S
‐amino acids, trace metals and vitamin balances. Animal models have provided beneficial information on mechanisms of teratogenesis involving cartilage and bone, notably on the action of salicylates and hypervitaminosis, both of which involve impairment in mucopolysaccharide synthesis, ossification and osteoclast activity. Toxic changes in adult skeletal tissues are largely associated with functional impairment of bone as a source of minerals—calcium, phosphate, zinc, and so on, and the property of calcium hydroxyapatite to bind xenobiotic cations including lead and cadmium with no trace metal nutrient value. Toxic changes range from osteoporosis, and impairment in bone strength and functional capacity. Radioactive bone‐seeking metals including
90
Sr are a potential cause of bone tumours. Much remains to be understood concerning the interaction between the calcium‐binding capacity of hydroxyapatite and the putative nutritional importance of silicon and strontium. Further studies are needed to investigate the cytotoxic action of lead and cadmium in bone and cartilage and to understand the implication of chronic exposure to low levels of these and toxic metals on bone structure and function.
