The following variables are categorized as static. The terms and abbreviations used are consistent with the recommendation of the Bone Histomorphometry Nomenclature Committee of the American Society for Bone and Mineral Research.13

The following variables are categorized as dynamic.

Table 55-1 indicates how each of these variables is altered in different disease states.

Bone is remodeled continuously throughout life—old, worn out bone is replaced by new bone. Approximately 25% of trabecular bone and 3% of cortical bone is replaced annually. The remodeling process is a quantum phenomenon because it occurs in discrete units or “packets.” Osteoclasts resorb a preprogrammed volume of old bone. Shortly thereafter, the osteoclasts are replaced by osteoblasts, which refill the resorption cavity with a new packet of bone. The group of cells (osteoclasts and osteoblasts) that creates one new packet of bone is called a bone remodeling unit. In normal trabecular bone, ˜900 bone remodeling units are activated each day. In cortical bone, the activation frequency is ˜180 per day.2,14,15 and 16

Elevated circulating levels of parathyroid hormone (PTH) stimulate the activation frequency of bone remodeling units, resulting in increased numbers of osteoclasts in bone and, because of the coupling process, increased numbers of osteoblasts. Consequently, quantitative analysis of a biopsy specimen from a patient with either primary or secondary hyperparathyroidism reveals increases in eroded surface, osteoid surface, and mineralizing surface (see Fig. 55-4).10,17,18 and 19 The extension of surface double labeled by tetracycline has allowed precise determination of the mineral apposition rate, which has been shown to be reduced. Because the osteoid thickness is normal in this disorder, the reduction in mineral apposition rate indicates a decreased rate of organic matrix production by the osteoblasts, rather than a defect in calcification. However, the extension of mineralizing surface overcompensates for the decrease in mineral apposition rate, so that the overall bone formation rate, the product of these two variables, is still increased. Thus, in hyperparathyroidism, bone resorption and formation rates are increased, which is a situation commonly referred to as a “high turnover” state. Bone turnover is higher in hyperthyroid patients with vitamin D insufficiency.18a Despite the rapid remodeling that occurs in primary hyperparathyroidism, the balance between resorption and formation is generally conserved because cancellous bone volume is normal or may even be increased, and trabecular connectivity is preserved.19 Often accompanying the increased bone turnover rate are increased deposition of immature (woven) bone and marrow fibrosis. These features are particularly prominent in severe secondary hyperparathyroidism.

Because the hallmarks of excessive remodeling activity (e.g., increased eroded surface) accumulate in bone over time, the biopsy can be a sensitive indicator of parathyroid gland hyper activity, especially when this is mild or intermittent. However, the biopsy alone does not distinguish between primary and secondary hyperparathyroidism.

Numerous causative mechanisms underlie osteomalacia (see Chap. 63 and Chap. 70). Most of the mechanisms involve processes that decrease the circulating calcium × phosphate product below the levels required for bone mineralization. Although calcification of the organic matrix is inhibited, the osteoblasts continue to synthesize and secrete the matrix. An accumulation of unmineralized matrix (“osteoid”) results (Fig. 55-6). The cancellous bone volume is normal in osteomalacia, but as the osteoid volume is increased, the amount of mineralized bone is actually reduced.