Background

Idiopathic adynamic bone disease (ABD) in dialysis patients is characterized by low serum parathyroid hormone (PTH) concentration. Whether ABD itself causes serious disease is controversial. Fuller understanding of both primary hypoparathyroidism and secondary hypoparathyroidism resulting in a long-standing low-PTH state may shed light on properties of ABD.

Methods

We performed histomorphometric analysis in bone specimens from biopsy in two female patients with primary hypoparathyroidism and in an autopsy specimen of bone from a male patient with secondary hypoparathyroidism related to long-term hemodialysis; respective ages, 45, 58, and 65 years; dialysis duration, 6 years, 2 months, and 30 years; lumbar bone mineral density, 2.88, 2.43, and 4.1 SD above the normal mean; and serum intact PTH, <5, <20, and <84 pg/mL (mean, 30.4). Tetracycline labeling was performed in the first two cases.

Results

Histomorphometric analysis in the first two cases indicated a diagnosis of ABD, since no tetracycline labeling could be seen along most of trabecular bone surfaces, total osteoid volume was decreased, and fibrous tissue was minimal. Bone volume was preserved, and the dense bone-trabecular connectivity was noted, with normal lamellar structure. A small number of hump-like structures protruded from the quiescent surface of trabecular bone, a pattern which has been called "minimodeling." Tetracycline label was observed in only a small area within trabecular bone in patient 1, and at a region of trabecular bone surface showing minimodeling in patient 2.

The third case was also diagnosed as ABD; cancellous lamellar structure and bone volume were normal, although trabecular connectivity was poor and island bone was relatively prominent. Minimodeling was evident. Minimodeling bone volume/total bone volume in these three cases was 9.0%, 13.1%, and 6.8%, respectively; number of minimodeling sites/total bone volume (N/mm²) was 4.9, 8.6, and 9.0, respectively.

Conclusion

Bone formation mechanism by minimodeling might contribute to preserving bone volume in dialysis patients with hypoparathyroidism, even in the absence of remodeling stimulated by PTH.