Chapter 6

Bone Densitometry

William D. Leslie and Bruce E. Roe

Pathophysiology of Bone Loss and Osteoporotic Fractures

Pathophysiology of Bone Loss

Bone is a dynamic tissue consisting of cellular, organic and inorganic components with a complex internal structure (Fig. 1). It is much more than passive scaffolding for the rest of the body and undergoes considerable metabolic activity and remodeling. The mature skeleton consists of a mixture of cortical bone (85%) and trabecular bone (15%). The relative amounts of these vary widely between different anatomic sites (Fig. 2).

Bone tissue reacts to stress and injury through a well-orchestrated sequence for removing old bone and building new tissue. Bone remodeling is carried out by the basic multicellular unit (BMU), which consists of both osteoclasts and osteoblasts. The BMU typically takes 3-6 months to complete a cycle (Fig. 3). Bone remodeling affects 3-5% of cortical bone per year, but involves up to 25% of trabecular bone due in part to its greater relative surface area. The osteoclast, a multinucleated cell of monocyte origin, resorbs bone through the release of acid and enzymes such as cathepsin K from its ruffled border. Osteoblasts, derived from mesenchymal cells, enter the resorption pit and lay down organic matrix (osteoid). The osteoblast then dies or enters a dormant stage and is known as an osteocyte (if trapped within calcified tissue) or a lining cell (if found on the surface of calcified tissue). The osteoid is subsequently mineralized over a period lasting several months. There is close coupling of osteoclast and osteoblast activities, although the intercellular signaling involved is incompletely understood. It is clear, however, that processes which stimulate (or suppress) one cell type result in stimulation (or suppression) of the other. For example, after menopause, osteoblast activity increases in an attempt to compensate for increased osteoclastic resorption. On the other side of the equation, antiresorptive treatments targeted at suppressing osteoclast activity are only able to achieve a slight gain in bone mass as there is a parallel reduction in osteoblast activity (Fig. 4). The bone remodeling cycle is regulated by a myriad of factors, including growth factors and interleukins. A new molecule, osteoprotegerin ligand (OPGL), has recently been discovered and shown to be the primary regulator of osteoclast activity. Estrogen deficiency, glucocorticoid excess and vitamin D deficiency are common conditions where bone metabolism is altered.

Bone cell activity can be evaluated through the measurement of biochemical markers. Osteoblasts produce type I collagen (the primary collagen of bone tissue), non-collagenous proteins (such as osteocalcin) and enzymes (such as alkaline phosphatase). Many of these are measured in the serum as indices of bone formation.

Nuclear Medicine, edited by William D. Leslie and I. David Greenberg. ©2003 Landes Bioscience.

Figure 1. Scanning micrograph showing normal trabecular bone (left) and osteoporotic bone (right).

Figure 2. Percent of trabecular bone in skeletal sites commonly assessed with bone densitometry.



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