Primary hyperparathyroidism: lessons from bone histomorphometry.

Abstract

The chronic excessive hypersecretion of parathyroid hormone (PTH) in primary hyperparathyroidism (PHPT) has significant impact on bone remodeling. Bone turnover increases by about 50%, leading to increased resorption at the endosteal envelope, increased cortical porosity, and thinning of cortical bone. In cancellous bone a different response is seen. Despite stimulation of bone resorption and formation at the tissue level, osteoclastic resorption and osteoblastic bone formation at individual bone multicellular units (BMUs) are reduced. This causes reduced erosion depth, reduced bone formation rate, and decreased thickness of bone structural units (BSUs), and bone balance at individual BMUs is preserved and may even improve. Thus, PHPT causes cortical bone loss. At the same time, however, cancellous bone structure remains unchanged or even improved, which may offset cortical bone loss. This probably explains the preservation of bone mass demonstrated in long-term follow-up studies of patients with mild PHPT (S-Ca2+ < 2.80 mM). In severe cases of PHPT (S-Ca2+ > 3.00 mM), the negative effects on cortical bone may override the positive impact on cancellous bone, and lead to bone loss and increased risk of fracture.