Abstract
In the past, the osteoporotic syndrome has been variably classified as “senile,” “postmenopausal,” “involutional,” “Type I,” and “Type II,” primarily on the basis of age, fracture incidence patterns, and/or fracture sites. Histological analyses of bone biopsy specimens from osteoporotic individuals also reveal a wide spectrum of cellular activity and rates of bone formation and resorption. These range from those that show an abundance of osteoblasts and osteoclasts with increments in both bone formation and bone turnover (i.e., “active” or “high-turnover” osteoporosis) to others demonstrating minimal cellular activity and relatively little active bone formation or resorption (“inactive” or “low-turnover” osteoporosis). The varied states of bone activity are reflected in associated changes in noninvasive biochemical markers of bone turnover such as circulating bone-gla-protein (BGP) or the urinary hydroxyproline/creatinine ratio (OH−Pr/Cr). Both BGP and OH−Pr/Cr are elevated in patients with high-turnover osteoporotic syndromes. The significance of this mode of categorizing osteoporotic patients is exemplified by the response to remedial therapy such as salmon calcitonin. Recent studies demonstrate a striking sensitivity of patients with high-turnover osteoporosis to calcitonin, with as much as 22% increments in vertebral bone mass recorded during a 12-month therapeutic interval. These promising results should also be compared with other forms of therapy in which an increase in vertebral bone mass of only 7–8% was sufficient to cause a significant decrease in the incidence of vertebral fracture rates.