Osteoporosis is a disabling disorder that is characterized by decreased bone strength, which predisposes patients to an increased risk of bone fracture. Peak bone mass (maximum bone strength and density) is normally attained by age 20-25. Age, race, sex, environment, and lifestyle factors such as physical activity and diet are important determinants of bone density. With the increase in age, the rate at which bone tissue is replaced is reduced in comparison to the rate at which it is lost, which increases the risk for fractures.
As bone loss is a gradual and painless process, osteoporosis is often diagnosed only after the occurrence of a fracture, which makes it challenging to reliably estimate the patient population that is at risk for developing this disease. Worldwide, 200 million people are estimated to suffer from osteoporosis (Cooper, 1999). While the overall number of fractures is increasing worldwide according to the report from World Health Organization, several reports from population-based studies have shown that recent progress in the diagnosis and treatment of osteoporosis has been effective at reducing the number of hip fractures (Jaglal et al., 2005).
Pharmacological and nutritional factors may help to prevent bone loss with increasing age. Nutritional factors may be especially important in the prevention of osteoporosis (Bonjour et al., 1996; Yamaguchi, 2002, 2006). While chemical factors in food and plants may also help to prevent bone loss with increasing age, these factors are poorly understood.
There has been a major increase in lifestyle-related diseases due to the fact that we are living longer and have adopted a Western diet.
In Japan, osteoporosis is currently treated with active form of vitamin D3 (Orimo et al., 1994; Schacht, 1999), estrogen (Lufkin et al., 1992; Weinstein et al., 2003), calcitonin (Body, 2002; Kopaliani, 2005), ipriflavone (Nakamura et al., 1992), vitamin K2 (Sakamoto et al., 2005; Steven et al., 2005), bisphosphonate (Hamdy et al., 2005; Matsumoto, 2004; Perez-Lopez, 2004), and related compounds. However, although these drugs are used to treat osteoporosis, they cannot prevent it. In addition, some of these drugs, such as calcitonin, are not easily administered, and the emergence of drug resistance has been observed. The active form of vitamin D3 is not effective for treating hypercalcemia, and bisphospho-nate inhibits bone formation. The use of estrogen should be careful, while estrogen administration for even just 6 months has been observed to result in abdominal bloating, breast pain, digestive symptoms, and irregular vaginal bleeding (Barkhem et al., 1998). These limitations of medications suggest that the prevention of osteoporosis through diet is very important.
Bone health and the prevention of osteoporosis-related fractures are key elements in the strategy for managing patients undergoing menopause. A detailed knowledge of bone health and related diagnostic and therapeutic options falls within the domain of the gynecologist as part of a multidisciplinary approach.
Osteoporosis-related fractures are common and will affect at least one-third of women over 50 years of age (Johnell and Kanis, 2005). It is estimated that osteoporosis affects 75 million people in Europe, the United States, and Japan, and this is estimated to increase by 240% by 2050.
Bone metabolism is characterized by two opposing activities: bone formation and bone resorption (Martin, 2002). Once formed, the bones in adults are continuously remodeled, and the remodeling rate is between 2% and 10% of the skeletal mass per year. Bone mass depends on the balance between resorption and formation within the remodeling unit. As osteoporosis is characterized by a decrease in bone mass with deterioration in the architecture of bones, it is the result of an imbalance between bone formation and resorption.
Bone remodeling is disturbed under a variety of pathologic conditions that affect the skeleton, including postmenopausal osteoporosis and rheumatoid arthritis, in which there is a local and/or systemic alteration in the levels of hormones or proinflammatory cytokines that are known to stimulate or inhibit bone resorption in vitro and in vivo. Parathyroid hormone has been recognized as a stimulator of bone resorption since the early 1980s (Rodan and Martin, 1981). Studies with genetically altered mice and other animal models of bone diseases over the past 10 years have greatly increased our knowledge of factors that regulate the formation and activity of osteoclasts. In particular, identification of the receptor activator of nuclear factor-kB ligand (RANKL)/RANK/osteoprotegerin signaling system in the mid- to late-1990s represented a major breakthrough that clarified the role played by osteoblasts in this process. Moreover, it has become increasingly clear that osteoclasts are not simply trench-digging cells; instead, they have important regulatory functions as immunomodulators in pathologic states and also help to control osteoblast function (Martin and Slims, 2005).
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