Marked bone changes can be produced by severe, prolonged hyperthyroidism. Attention was first drawn to this by Von Recklinghausen in 1891 when he described a young woman of 23 years of age who had had clinical evidence of Basedow's disease for five years. She complained of constant pain in her back and limbs and had a severe kyphoscoliosis. At autopsy seven years later her bones were thin, the cortices of the long bones were striated, and histologically there was evidence of increased osteoclasis and fibrosis. Such florid bone disease is virtually unknown now because of early diagnosis and treatment of hyperthyroidism, and the bone changes of this disease can only be detected by specialised investigation. However, while this is true of the majority of patients, bone changes in some do occur where the diagnosis of hyperthyroidism has been overlooked. This is especially true in elderly patients who are most susceptible to the effect of excess thyroid hormone on bone. The frontispiece shows severe spinal osteoporosis in a 69-year old patient who had mistakenly been treated with thyroxine in a dose of 0.4 rag/day. The vertebral compressions led to a loss of 4-} inches in height in four years. On a reduced dose of thyroxine (0.2 rag/day) no further loss of height occurred in the next three years. In addition to the effects on bone, changes in serum calcium, phosphorus, protein, and in calcium absorption, endogenous calcium secretion, and calcium balance are recorded. Increased loss of calcium in urine and sweat are known to occur. There is a raised excretion of hydroxyproline in the urine, aiad there are changes in the renal handling of phosphorus. Generally, these changes are of secondary importance clinically, but on rare occasions hypercalcaemia can lead to the development of serious clinical symptoms.