Primary hyperparathyroidism (PHPT) is characterized by sustained secretion of PTH from the parathyroid glands which is excessively disproportionate to calcium levels. This leads to enhanced bone turnover, predominantly resorption, resulting in low bone mass, hypercalcemia, hypercalciuria and hypophosphatemia. Successful parathyroidectomy (PTX) reverses these pathological conditions and is the treatment of choice in PHPT. Alternatively, the bone disease in PHPT may be treated pharmacologically by using bisphosphonates which are able to diminish bone turnover. The mechanism by which PTH exerts its effects in bone and the mechanism of bone loss in PHPT in humans have not been fully explained. PHPT with enhanced PTH seems to be a suitable model to observe possible relationships between PTH, OPG and RANKL.