Metabolic bone diseases include skeletal disorders related to abnormalities of the anabolic and catabolic biochemical reactions in the body. They are a diverse group of diseases that affect bone mass, bone turnover, bone mineral homeostasis, or bone growth. The causes can be genetic, nutritional, or acquired. Such metabolic bone disorders include, but are not limited to, endocrine dysfunctions, Paget disease, and osteoporosis. The focus of this chapter is to discuss several of the more common metabolic bone diseases with emphasis on review of their imaging features and differential diagnosis.
Parathyroid hormone (PTH) is intimately involved in calcium homeostasis. Not only does PTH regulate the release of calcium from bone through its combined effects on osteoblasts and osteoclasts, it also stimulates bone remodeling. Hyperparathyroid states, reflecting excess circulating levels of PTH, are traditionally divided into three types: primary, secondary, and tertiary. Primary hyperparathyroidism is characterized by the excessive production of PTH by one or more of the parathyroid glands, most commonly a solitary hyperfunctioning adenoma (up to 80% of cases). Primary hyperparathyroidism may rarely be caused by a parathyroid carcinoma (<1%).1 Other causes of primary hyperparathyroidism include diffuse hyperplasia of the parathyroid gland and multiple hyperfunctioning adenomas. Secondary hyperparathyroidism results from prolonged hypocalcemia, as in cases of chronic renal failure or intestinal malabsorption. Tertiary hyperparathyroidism may result from long-standing secondary hyperparathyroidism, with the development of autonomous activity due to parathyroid hyperplasia and loss of the glands’ response to levels of serum calcium. Secondary hyperparathyroidism is more common than primary hyperparathyroidism.2
Hyperparathyroidism is characterized by an increased ratio of osteoclasts to osteoblasts. Because osteoclasts do not express a PTH receptor, the skeletal effects of hyperparathyroidism are mediated through the osteoblasts that communicate with the osteoclasts.3 Skeletal manifestations of hyperparathyroidism are varied, and include osteitis fibrosa (vascular fibrous tissue replacement), osteitis fibrosa cystica (coalescence into cysts), cysts, brown tumors, thinned cortices, distorted trabeculae, infarction, and fracture.
The most common radiographic bone abnormality in patients with hyperparathyroidism, regardless of cause, is bone resorprtion. The most often recognized skeletal findings of hyperparathyroidism in 95% of patients are recognized in hand.4 The most characteristic type of bone resorption associated with hyperparathyroidism is subperiosteal (Figure 8-1), although intracortical, endosteal, subchondral, subphyseal, subligamentous, and subtendinous resorption may be noted. Other bony findings may include brown tumors and osteosclerosis. There is an association of primary hyperparathyroidism with calcium pyrophosphate dihydrate crystal deposition disease (CPPD), and rarely with gout.5
Hyperparathyroidism. PA view of the hand demonstrates subperiosteal resorption (arrows) in a characteristic location along the radial aspect of the index and long middle phalanges.
Subperiosteal resorption of cortical bone can be found in many locations, including the medial aspects of the proximal tibia, humerus, ...