SYSTEMIC OSTEOPENIA AND MINERALIZATION DEFECT IN PATIENTS WITH ANKYLOSING-SPONDYLITIS

Objective. Low bone mass, vertebral osteopenia, and fractures have bee n recognized in patients with ankylosing spondylitis (AS). However, th ere are few data about bone histology and histomorphometric changes in these patients. To shed light on bone alterations of these patients, we carried out a study including static and dynamic variables of bone of patients with AS, using iliac crest bone biopsy. Methods. 16 white men with AS, mean age 34+/-3 years (15 to 55), mean duration of diseas e 11+/-2 years (6 months to 27) underwent bone biopsy for mineralized bone histology and evaluation of histomorphometric variables. Results. 14 patients presented osteopenia, 10 mineralization defects, and 3 os teomalacia. Trabecular bone mass, trabecular wall thickness, trabecula r plate, and wall thickness were significantly lower than the control values. Comparing bone formation variables we found that the relative osteoid volume and the thickness of osteoid were significantly greater than control values (p <0.05); comparing bone resorption variables we found that the bone osteoclast interface and the eroded surface were similar to that obtained in male controls. Analyzing dynamic variables , we observed that mineral apposition rate and doubly labeled osteoid were significantly less than the control group (p <0.05), and minerali zation lag time was statistically greater than the control group (p <0 .01). There was positive correlation between the duration of disease w ith relative (r=0.513, p <0.05) and absolute osteoid volume (r=0.590, p <0.05). There was negative correlation between disease duration and eroded surface (r=-0.616, p <0.01) and bone osteoclast interface (r=-0 .481, p <0.05). There was positive correlation between duration of dis ease and singly labeled trabeculae (r=0.680, p <0.01), duration of dis ease and singly labeled osteoid seam, and duration of disease and mine ralization lag time (r=0.439, p <0.05). Conclusion. Low bone mass in m ale patients with AS may also be related to mineralization defect. As bone resorption variables were normal in our patients, it is possible that the reduced bone mass seen in AS is due to a depression in bone f ormation rather than an increase in bone resorption.