A process has been developed for the in situ formation of the mineral phase of bone. Inorganic calcium and phosphate sources are combined to form a paste that is surgically implanted by injection. Under physiological conditions, the material hardens in minutes concurrent with the formation of dahllite. After 12 hours, dahllite formation was nearly complete, and an ultimate compressive strength of 55 megapascals was achieved. The composition and crystal morphology of the dahllite formed are similar to those of bone. Animal studies provide evidence that the material is remodeled in vivo. A novel approach to skeletal repair is being tested in human trials for various applications; in one of the trials the new biomaterial is being percutaneously placed into acute fractures. After hardening, it serves as internal fixation to maintain proper alignment while healing occurs.

CT-guided percutaneous RF ablation of osteoid osteoma is a safe and effective technique.

No abstract

Osteoporosis is a known consequence of anorexia nervosa (AN) in adults, but the mechanism of bone loss is not established, and there have been no studies of bone mass in women developing AN before attaining peak bone mass. To investigate the causes of bone loss in AN and to determine the consequences of developing AN during adolescence on bone mass, we compared the effects of AN on cortical and trabecular bone in 26 women with AN (19 adults, 18-42 yr old, and 7 adolescents, 14.9-17.0 yr old) using direct radial photon absorptiometry and both single and dual energy spinal computed tomography. The adult AN patients had marked spinal osteopenia [mean bone density, 120 +/- 28 (+/- SD) mg K2HPO4/cm3] compared with age-matched normal women (mean, 176 +/- 26 mg K2HPO4/cm3; P = 0.0001), which was severe (greater than 2 SD below the normal mean) in 50% of patients. Adult AN patients with the onset of amenorrhea before age 18 yr had significantly (P = 0.04) lower spinal bone density than those developing amenorrhea later (mean, 103 +/- 25 vs. 129 +/- 25 mg K2HPO4/cm3) independent of other variables correlated with bone density (duration of amenorrhea or urinary cortisol excretion). We found a negative correlation between spinal bone density and duration of amenorrhea (P = 0.006; r = -0.53). To determine the contribution of endogenous cortisol excess to the pathogenesis of the osteoporosis, urinary cortisol was measured. Urinary cortisol/creatinine clearance was significantly (P = 0.001) higher in AN patients than in normal women (mean, 2.7 +/- 1.2 vs. 1.0 +/- 0.3 nmol/L) and was negatively correlated (P = 0.03; r = -0.43) with bone mass. We conclude that AN affects trabecular bone and that both the onset of AN before attainment of peak bone mass and prolonged duration of amenorrhea result in more severe osteopenia. In addition to the significant contribution of hypogonadism, the cortisol excess that occurs in AN patients may contribute to the development of osteoporosis in these patients.