Bone is composed of two types of structural tissues, cortical (or compact) tissue and trabecular (or cancellous) tissue. Dense cortical tissue (80% of skeleton) covers trabercular tissue (20% of skeleton) (Lee and Nieman, 2003; Anderson, 2004). The active metabolism of bone, which involves two types of cells: osteoblasts and
osteoclasts, is called bone modeling, bone turnover and bone remodeling. Osteoblasts secrete a collagen protein matrix, which forms the support structure of the bone, and bone mineral, which strengthens the bone. This mineral consists of calcium and phosphorus, called hydroxyapatite (Ca10(PO4)6(OH)2). Osteoclasts continually break
down bone in areas where bone is not needed. This activity leads to bone turnover and causing bone loss, while osteoblasts conduct bone remodeling (Wardlaw, Hampl, & DiSilvestro, 2004).
Bone mineral density and bone quality are used to measure bone strength. Bone quality relates to bone architecture, bone turnover, mineralization, and the accumulation
of bone damage. Bone mineral density (BMD) accounts for approximately 70% of bone strength (Lee and Nieman, 2003). BMD, expressed as grams per centimeter squared (g/cm2), shows the relative value of mineral content in bone for the measured area. Bone mass (called bone mineral content, BMC) refers to the absolute amount of
hydroxyapatite measured in grams, and is also used to describe bone strength.
The three periods in skeletal development over the life span are rapid growth, stabilization, and bone mass decline. The rapid growth period is the time during early childhood and adolescence. The stabilization period is achieved in young adults, i.e. age 20 to 35 years, after which time bone mass will decline. Having a high BMD at age 50 lowers the risk of age-related bone fractures in women and men (Kanis et al., 2001).
Women lose their bone mass faster than men. The bone mass loss in women is caused by the alteration of calcium absorption due to the change of hormones at menopause when estrogen is no longer formed. Estrogen can possibly stimulate bone loss by several possible mechanisms, such as changes in serum levels of parathyroid hormone, calcitonin, and vitamin D metabolites (Kaptoge et al., 2003; Anderson, 2004).
Physical activity improves the peak bone mass, which is reached during the growth. Evidence shows that physical activity is beneficial for BMD during childhood, but excess exercise during puberty can result in lower BMD. Physical activity is effective at high calcium intake, at least 1000 mg/day (Gilsanz, 1999). Region-specific interaction between calcium intake and physical activity in pre-pubescent girls was found by Iuliano-Burns, Naughton, Gibbons, Bass, and Saxon (2003).
Calcium makes up 39-40% of the entire mineral in the body. More than 99% of calcium in the body is located in bones and teeth (Wardlaw et al., 2004; Matkovic, Crncevic-Orlic, & Landoll, 2003). Calcium is critical to the structural integrity of both trabecular and cortical bone. Another 1% of calcium is in the cellular and extracellular fluid. The other roles of calcium are participating in blood clotting, transmission of nerve impulses to target cells, muscle contraction, and regulating the activity of several enzymes, including those that synthesize glycogen. The task of calcium in cellular and extracellular fluid is very important. When dietary intake is low, calcium is withdrawn from the skeleton to maintain normal calcium concentrations in blood. Adequate
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calcium consumption throughout life optimizes peak bone mass and minimizes age- related bone loss later in life (Wardlaw et al., 2004).
When blood calcium and vitamin D are low, the parathyroid gland releases parathyroid hormone, which then stimulates the synthesis of 1,25 dihyroxyvitamin D (calcitriol) in kidneys. Calcitriol then interacts with specific cells in the small intestine, bone, and kidney. In the small intestines, calcitriol promotes calcium absorption. In bone, calcitriol and parathyroid hormone stimulate osteoclasts to release calcium from bone to the blood. In kidney cells, both of them also prevent calcium loss in urine excretion (Wardlaw, 2004; Dawson-Hughes, 2003).
High blood levels of phosphate suppress the conversion of vitamin D to its active form in the kidneys. Since phosphorus level maintenance is not as tight as calcium, serum phosphate levels can rise slightly with a high phosphorous diet, especially after meals. High blood phosphate levels reduce the formation of the active form of vitamin D (calcitriol) in the kidneys, reduce blood calcium, and lead to increased PTH release. However, high serum phosphorus levels also lead to decreased urinary calcium excretion. If sustained, elevated PTH levels could have an adverse effect on bone
mineral content, but this effect has only been observed in humans in diets that were high in phosphorus and low in calcium (Knochel, 2003).
Milk, which contains 300 mg calcium in a 250 mL serving, is a good source of absorbable calcium. Dairy foods provide 75% calcium in the North American diet generally (Weaver, 2003; Wardlaw et al., 2004) and more than 55% calcium in the adolescents’ diet especially (Iuliano-Burns, Whiting, Faulkner, & Bailey, 1999). From all milk products, fluid milk alone contributed at least 40% as calcium source in
teenagers’ diet. The calcium rich plants in the kale family (broccoli, bok choy, cabbage, mustard, and turnip greens) contain calcium that is as bioavailable as that in milk (Weaver, 2003; Wardlaw et al., 2004).
Some food components have been found to inhibit the absorption of calcium. Oxalic acid (oxalate) is the most potent inhibitor of calcium absorption, and is found in high concentrations in spinach and rhubarb and somewhat lower concentrations in sweet potato and dried beans. Phytic acid is a less potent inhibitor of calcium absorption than oxalate. Yeasts possess an enzyme (phytase) which breaks down phytic acid in grains
during fermentation, lowering the phytic acid content of breads and other fermented foods. Only concentrated sources of phytate such as wheat bran or dried beans substantially reduce calcium absorption (Weaver, 2003).