Calcium in the human body exists as calcium phosphate complexes in the skeleton and as its free ion (ionized calcium) or bound complexes in the blood. Serum ionized calcium levels are tightly controlled to ensure proper function of various physiological processes. Control of calcium homeostasis depends on bone turnover. Hyperparathyroidism, a pathological condition characterized by increased activity of the parathyroid glands leading to excessive excretion of parathyroid hormone, causes disturbance in calcium homeostasis and metaboLic bone disease. Hyperactivity of the parathyroid glands may directly result from an intrinsic change in the parathyroid glands (primary hyperparathyroidism) or indirectly from other pathological or metaboLic disorders such as chronic renal disease or vitamin D deficiency (secondary hyperparathyroidism). A third-type (tertiary) hyperparathyroidism is also proposed to describe hypercalcemic hyperparathyroidism as seen in X-Linked hypophosphatemia, which results from prolonged secondary hyperparathyroidism. This article discusses the pathological mechanism of these metaboLic diseases and current treatments.