Metabolic bone disease

Most of the literature on metabolic bone disease is steeped in biochemistry, physiology, histology, internal medicine, and other arcane pursuits that can be quite confusing for a poor radiology resident who just wants a few pearls and illustrations. Frankly, it’s a tough topic. I will, by necessity, keep it simple, but this is an important topic about which every radiologist should have at least a superficial fund of knowledge. I have excluded disorders such as pseudo- and pseudo-pseudo hypoparathyroidism that are unlikely to be seen, and I have tried to cover the more commonly seen disorders.

Osteoporosis

Osteoporosis is diminished bone quantity in which the bone is otherwise normal. This contrasts with osteomalacia, in which the bone quantity is normal but the bone itself is abnormal in that it is not normally mineralized. Osteomalacia results in excess nonmineralized osteoid. It is not possible in the vast majority of cases to distinguish between osteoporosis and osteomalacia on plain films.

The causes of osteoporosis are myriad, the most common of which was senile osteoporosis (a term that is not considered politically correct and is no longer used), or osteoporosis of aging. The preferred term for this type of osteoporosis is primary osteoporosis. This is seen most commonly in postmenopausal females and is a major public health concern because of the increase of spinal and hip fractures in this patient population.

Secondary osteoporosis implies that an underlying disorder, such as thyrotoxicosis or renal disease, has caused the osteoporosis. Only about 5% of osteoporosis has an underlying cause. The differential diagnosis for secondary osteoporosis is long and probably should not be memorized, because one cannot even be sure if it is osteoporosis or osteomalacia based on the plain films. Therefore the differential for presumed osteoporosis would have to include the causes of osteomalacia. The list gets too long to be of any real help to anyone.

The main radiographic finding in osteoporosis is thinning of the cortex. This is best demonstrated in the second metacarpal at the middiaphysis (Figures 7-1 and 7-2). The normal metacarpal cortical thickening should be approximately one fourth to one third the thickness of the metacarpal (Figure 7-3). In osteoporosis this cortical thickness is decreased. The metacarpal cortex (and all bony cortices, for that matter) decreases normally with age and is less for women than for men of the same age. Several tables have been published that give the normal metacarpal cortical measurement, with age and sex adjustments to allow determination of normal. Unfortunately these tables determine only the mineralization of the peripheral skeleton and do not seem to correlate to whether or not spinal or hip fractures will occur.

FIGURE 7-1 Mild osteoporosis. Mild cortical narrowing (arrows) at the mid-second metacarpal is noted in this patient with renal osteodystrophy. Compare this cortical width with that of the normal width in Figure 7-3.

FIGURE 7-2 Marked osteoporosis. Marked cortical narrowing (arrows) of the mid-second metacarpal cortex is present in this patient with severe osteoporosis. Also note the intracortical tunneling, which occurs with more rapid forms of osteoporosis.

FIGURE 7-3 Normal mineralization. Note the cortical width (arrows) of the mid-second metacarpal in this patient with normal mineralization. The width of the cortex is easily greater than one third of the total width of the metacarpal.

Measurement of the axial bone mineral content can be done by one of several methods that use computed tomography (CT) to assess the bone quantity in the spine. There is some debate over which method is superior and even whether or not knowing the bone mineral content is clinically helpful, because merely knowing the age and sex of the patient is fairly accurate for predicting the bone mass quantity. Nevertheless, it is generally agreed that if a quantitative CT (QCT) measurement shows bone mass to be 2 standard deviations below normal, that person is at high risk for spinal and hip fractures. Bone densitometry is widely used to identify patients, especially postmenopausal women, who are osteoporotic so that treatment can be instituted. Bisphosphonates have been widely used for treating osteoporosis with excellent results for the most part. A complication of long-term bisphosphonate therapy is fracture of the proximal femur.¹ These fractures occur on the lateral aspect of the proximal femoral diaphysis and are often bilateral (Figure 7-4). If not treated, they can go on to complete fractures.

FIGURE 7-4 Femoral fracture secondary to bisphosphonate therapy. This postmenopausal woman had been taking bisphosphonates for many years and sought treatment for left thigh pain. Focal cortical thickening (arrow) is characteristic for the appearance of femur fractures related to bisphosphonate therapy. These can go on to a complete fracture if not protected or treated.

Exercise and proper diet (whatever that is) seem to help delay the onset of primary osteoporosis as much as anything. Calcium additives alone have not been shown to reverse the process of primary osteoporosis.²

Because we cannot accurately give the causes of osteoporosis by looking at a radiograph and cannot even differentiate it from osteomalacia, it is a topic that is frustrating for many radiologists to deal with. Most of us would rather comment on something we can give a diagnosis on or at least a short differential. In general, when decreased bone mass is present on a radiograph, the odds are that osteoporosis is present. However, because the disease process could just as easily be osteomalacia, it is recommended that the term osteopenia be used. This is a generic term that includes both osteoporosis and osteomalacia. When used, it also implies that the observer knows he or she cannot separate the two entities and is an educated person.

A type of osteoporosis that can be seen in a patient of any age is disuse osteoporosis. It results from immobilization from any cause, most commonly after treatment of a fracture. The radiographic appearance of disuse osteoporosis is different from primary osteoporosis in that it occurs somewhat more rapidly and gives the bone a patchy or even a permeative appearance (Figure 7-5). This is from the osteocytic resorption in the cortex, causing intracortical holes. If allowed to continue with disuse, the bone would resemble any bone with marked osteoporosis (i.e., severe cortical thinning).

FIGURE 7-5 Aggressive osteoporosis. A diffuse permeative pattern throughout the proximal femur is noted in this patient, who has recently had an amputation. Note that the cortices are riddled with holes, which would indicate that this is not a true intramedullary process but an intracortical process. This is distinctive for aggressive osteoporosis and causes a pseudopermeative pattern that can be mistaken for a more sinister process.

Occasionally aggressive osteoporosis from disuse can mimic a permeative lesion, such as a Ewing’s sarcoma or multiple myeloma, because of the severe cortical patchy or permeative pattern that projects over the medullary space and resembles a medullary permeative process (Figure 7-6). The way to differentiate a true intramedullary permeative process from an intracortical process such as osteoporosis is to observe the cortex and see if it is solid or riddled with holes (Figure 7-7). If it is solid, you can assume the permeative process is emanating from the medullary space (Figure 7-8); if it has multiple small holes, you have to assume the permeative pattern is from the cortical process. I call a permeative appearance that is secondary to cortical holes a pseudopermeative process to distinguish it from a true permeative process.