Classic Papers in Geriatric Medicine with Current Commentaries (eBook)

Acknowledgments 8
Contents 9
Perspectives on General Aging 12
Palliative Care of Older Patients 31
Home- Based Care of the Older Patient 36
Education of Health Professionals 42
Dementia 55
Delirium 68
Urinary Incontinence 96
Osteoporosis 102
Health Screening and Disease Prevention 120
Pressure Ulcers 151
Depression 158
Index 171

"10 Osteoporosis (p. 95-96)

Robert J. Pignolo, MD, PhD

Commentary

Paleopathologic examinations of old skeletons confirm that osteoporosis likely existed throughout history (1), but it has been only within the last 200 years that the term was coined and that the pathology distinguished it from osteomalacia (2). As human lifespan has increased over the late nineteenth and early twentieth centuries, osteoporosis has taken on major importance as a clinical problem.

In 1940, Fuller Albright, in a communication to the Association of American Physicians, described and introduced the term "postmenopausal" osteoporosis. In that landmark publication (reproduced here), he distinguished postmenopausal osteoporosis from other forms of bone loss that were known at the time, including disuse, senile, and so-called "idiopathic" osteoporosis, the later involving primarily the spine and to a lesser extent the pelvis.

He evaluated 42 individuals with idiopathic osteoporosis who were less than 65 years of age, only two of whom were men. He also observed that several premenopausal women who were affected had undergone a surgical menopause. Thus, he correctly renamed this category of idiopathic bone loss as postmenopausal osteoporosis. In associating estrogen deprivation with postmenopausal osteoporosis, Albright acknowledged in his 1940 paper the previous work of Kyes and Potter (3), who reported that male pigeons had osteoporotic bones compared to those of ovulating females and that ossification in the skeleton of female pigeons was proportional to the size of their ovarian follicles. Albright also acknowledged the work of Pfeiffer and Gardener (4), who injected male pigeons with estrogen and corrected the deficit in bone formation relative to female birds. In the same paper Albright treated three women with estrogen therapy and noted that there was "a markedly positive calcium and phosphorus balance . . . (which) continued as long as estrogen was administered. "

Based on these findings, Albright concluded that osteoporosis is a failure of osteoblasts to form adequate bone matrix. In a subsequent paper in 1941, Albright attempted to elaborate differences between postmenopausal osteoporosis and other metabolic bone diseases (5). He made the observation that postmenopausal and senile osteoporosis rarely involves the skull, a feature which distinguishes them from mild hyperparathyroidism and osteomalacia.

Contrary to Albrights original idea that osteoblast dysfunction mediates bone loss associated with menopause, an increase in bone resorption (and not a decrease bone formation) appears primarily to underlie osteoporosis in estrogen deficient states (6,7). However, the production of new bone seen in response to mechanical loading is attenuated with estrogen deficiency, suggesting that estrogen is both an anticatabolic as well as an anabolic hormone in bone tissue (8)."