Iliac crest bone biopsies from 62 patients (42 women, 20 men; median age 59 years; range 17-79 years) with primary hyperparathyroidism (PHP) were examined. Static and structural parameters were compared with 30 age- and sex-matched normal controls. Eighteen sex-matched younger controls were used for evaluation of the dynamic controls. On the endocortical surface increase in extension of eroded (p < 0.01) and formative (p < 0.01) surfaces was found in PHPs compared with normals. Endocortical bone formation rate was increased in PHPs (p < 0.05), but mineral appositional rate and adjusted appositional rate were normal. On the periosteal surface very little remodeling activity was found. Although bone formation rate was found increased in PHPs (p < 0.05), more than half of the labeled biopsies were without periosteal tetracycline in patients, and only 2 of 18 biopsies from normals contained periosteal tetracycline labels. No significant decreases in cortical width or relative cortical width were found in PHPs. In both patients and controls an age-related decrease in relative cortical width was noted for women (PHPs: r = -0.52, p < 0.01; controls: r = -0.59, p < 0.001), but not for men. Cortical porosity was about 30% increased in PHPs (p < 0.02). Only normal women showed a positive age-related increase in porosity (r = 0.61, p < 0.05). In a group of nine patients with bone biopsies performed 6 to 12 months after surgery significant decreases in porosity (p < 0.02), eroded surface (p < 0.02), and osteoid surface (p < 0.02) were noted. Premenopausal women with PHP had increased values of eroded (p < 0.05) and formative (p < 0.05) surfaces as well as of porosity (p < 0.05) compared with controls, but for the postmenopausal group these differences were not statistically significant. In spite of increased remodeling activity on endocortical, periosteal, and Haversian envelopes, cortical width seemed to a large extent to be preserved in the patients. The cortical bone, though, might be weakened by increased porosity and, because of the increased remodeling activity, by an increased amount of new and lightly mineralized cortical bone.