Supraphysiological Levels of Quercetin Glycosides are Required to Alter Mineralization in Saos2 Cells
Osteoporosis, characterized by low bone mineral density (BMD), is a silent disease that ultimately results in fragility fractures. Fragility fractures lead to significant morbidity and mortality worldwide. Owing to the rapidly aging population, it is estimated that one in two American adults will be at risk for osteoporosis-related fractures by the year 2020 , and bone health will continue to worsen as the population ages. Similar estimates exist for other developed countries [1,2]. It is somewhat ironic that despite the fact that obesity rates in developed countries are at their highest historical level, the quality of an individual’s diet is often not favorable for maintaining a healthy skeleton. Moreover, childhood obesity may result in a greater risk of fracture [3,4]. Bone health is classified using criteria established by the WHO, and is based on measurement of BMD using dual energy x-ray absorptiometry and calculating t-scores relative to normal peak values for BMD in young adults. The classification is as follows: normal bone density, t-score above -1.0 standard deviation (SD); osteopenia, t-score between -1.0 and -2.5 SD; osteoporosis, t-score of -2.5 or less; and severe osteoporosis, t-score of -2.5 SD or less with one or more fragility fractures . This classification does not consider bone quality, but rather is strictly based on the quantity of mineral present. Moreover, there is evidence that more than 50% of all incident fractures occur in women with osteopenia . Owing to the natural loss of BMD during aging, most individuals would be classified as having osteopenia during their lifetime. Thus, prevention strategies, as well as strategies for attenuating loss of BMD during aging, warrant attention. Peak bone mass is the maximum quantity of bone an individual acquires during their lifetime, occurring by approximately 18–25 years of age. While genetics is a major determinant of an individual’s peak bone mass, other factors, such as diet, can influence whether an individual’s genetic potential for peak bone mass is reached [7–9]. For the best defense against osteopenia, and possibly osteoporosis, an individual should strive to reach a high peak bone mass, as they will have a higher starting point when bone mass starts to decline naturally during the aging process. The natural decline in bone mass, approximately 1–3% per year, commences during adulthood. The most rapid loss of bone mass in women occurs within 5–10 years after menopause, and therefore, this is a critical time for interventions [2,10–12]. Men also experience a decline in bone mass owing to declining levels of testosterone and estrogen [10–12]. A balanced diet assists the development of a strong skeleton, in addition to a healthy body weight. While diet alone cannot prevent the loss of bone mineral and skeletal weakening that often accompanies the aging process, a diet that provides appropriate levels of nutrients – particularly calcium, vitamin D and protein – is essential to support skeletal health. Moreover, specific pharmacological agents that prevent or slow the Fragility fractures resulting from osteoporosis are a leading cause of morbidity and even mortality in developed countries. Afflicting both men and women the rates of osteoporosis are increasing in countries with aging populations. Although dietary components, particularly calcium and vitamin D, are widely recognized to be important for overall skeletal health, intakes are often lower than the recommended amount. Such lower than recommended intakes of calcium are of particular concern if diets are rich in protein, sodium and/or caffeine. Dietary components such as omega-3 fatty acids and soy isoflavones may play a positive role in bone health, and this is an active area of study. Combining healthful foods together with current pharmacological agents that preserve bone mass and strength may be an effective and safe strategy for prevention and/or treatment of osteoporosis.