Osteoporosis is a prevalent disease worldwide, with 1 in 3 women and 1 in 5 men older than 50 years of age at risk for an osteoporotic fracture.1,2 For women, the risk for osteoporotic fractures is greater than the cumulative risk for stroke, heart attacks, and breast cancer combined.3 Having a fracture places a patient at much higher risk for sustaining additional fractures.
In the United States, the direct costs associated with osteoporosis treatment rose 118% between 1998 and 2000, to $73.6 billion, with the costs distributed between ambulatory care, inpatient care, and prescription drugs.4 The conundrum for primary care practitioners is how to screen women appropriately to detect younger postmenopausal women who may not meet the known criteria for osteoporosis screening.
Risk Factors for Osteoporosis
In addition to the well-known risk factors for osteoporosis, new studies show there are novel risk factors that can be ascertained with thorough history and physical information.5,6 Primary care providers can counsel women about risk factors and how to avoid the development of osteopenia and osteoporosis (Table 1).5,6
Age of menarche, dietary habits, and laboratory values of calcium, parathyroid hormone, and vitamin D are important diagnostic considerations. For example, moderate (more than 720 mL) to frequent (more than 1180 mL) daily consumption of sugary soft drinks has been associated with the development of osteoporosis in women.7,8 In addition, Shieh et al reported that high levels of follicle-stimulating hormone (FSH) may be an independent predictor of ongoing or imminent bone loss during the perimenopausal and menopausal phases.7 Shieh et al also found that high levels of FSH and low levels of estradiol were associated with loss of bone mineral density (BMD) at both the lumbar spine and femoral neck in perimenopausal women.7 Late menarche has been associated with lower BMD in later life as well.8
Normal Bone Physiology
Osteoporosis occurs when bone loss (resorption) outpaces the growth of new bone (formation), making the bones more prone to fracture. The structure of bone consists of a tubular shape, with a strong outer shell (cortical layer) surrounding the spongier bone in the core (trabecular layer).2 Peak bone mass occurs in early adulthood, usually late 20s or early 30s.2 As aging occurs, the minerals on the inside of the cortical bone are resorbed, and trabecular bone is lost, causing a widening of the bone cavity.2 Although bones may be getting thicker, they are not becoming denser.
On a cellular level, 2 cell types — osteoclasts and osteoblasts — are responsible for resorption and growth of bone. Osteoclasts break down bone by lowering the pH of their microenvironment,2 causing the bone material to dissolve. Osteoblasts then lay down new bone, which is a longer process; thus, any increase in remodeling activity leads to loss of bone. Multiple hormones are implicated in bone health: parathyroid hormone, testosterone, and estrogen, with the latter having the most direct effect on bone cells. When women enter perimenopause, bones become less dense because of the withdrawal of larger amounts of estrogen, predisposing them to fractures.7
This article originally appeared on Clinical Advisor