Metabolic bone diseases are a diverse group of diseases that result in abnormalities of (a) bone mass, (b) structure mineral homeostasis, (c) bone turnover, or (d) growth. Osteoporosis, the most common metabolic bone disease, results in generalized loss of bone mass and deterioration in the bone microarchitecture. Impaired chondrocyte development and failure to mineralize growth plate cartilage in rickets lead to widened growth plates and frayed metaphyses at sites of greatest growth. Osteomalacia is the result of impaired mineralization of newly formed osteoid, which leads to characteristic Looser zones. Hypophosphatasia is a congenital condition of impaired bone mineralization with wide phenotypic variability. Findings of hyperparathyroidism are the result of bone resorption, most often manifesting as subperiosteal resorption in the hand. Renal osteodystrophy is the collection of skeletal findings observed in patients with chronic renal failure and associated secondary hyperparathyroidism and can include osteopenia, osteosclerosis, and "rugger jersey spine." Hypoparathyroidism is most commonly due to iatrogenic injury, and radiographic findings of hypoparathyroidism reflect an overall increase in bone mass. Thyroid hormone regulates endochondral bone formation; and congenital hypothyroidism, when untreated, leads to delayed bone age and absent, irregular, or fragmented distal femoral and proximal tibial epiphyses. Soft-tissue proliferation of thyroid acropachy is most often observed in the hands and feet. The findings of acromegaly are due to excess growth hormone secretion and therefore proliferation of the bones and soft tissues. Vitamin C deficiency, or scurvy, impairs posttranslational collagen modification, leading to subperiosteal hemorrhage and fractures. ©RSNA, 2016.