Inflammation markers are predictive of fractures

The inflammation of aging hypothesis purports that aging is the accumulation of damage, which results, in part, from chronic activation of the inflammatory process. This process is believed to play an important role in deterioration of the cardiovascular system and skeleton. Cytokines play major roles in regulating bone remodeling in the bone microenvironment, but their relationship to fractures is uncertain.

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FSH directly regulates bone mass

Postmenopausal osteoporosis is usually solely attributed to a drop in ovarian estrogen secretion. However, while estrogen is used in the therapy of osteoporosis, the primary mechanism of its action at the cellular level remains unclear.

A recent study challenges this dogma of the sole responsibility of estrogens [1]. Indeed, the decline in ovarian secretion of estrogens and inhibins relieves a negative feedback exerted by these hormones on the pituitary, and is accompanied by an overproduction of the pituitary-derived hormone FSH. Sun et al therefore hypothesized that FSH per se might affect bone remodeling. Several lines of evidence support such a hypothesis: first, plasma FSH concentrations are well correlated to markers of bone resorption in postmenopausal women; second, mice missing the estrogen receptor, but not estrogens, have only mild bone loss; third, the bone loss following an ovariectomy in the mouse occurs only if the pituitary is intact.

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Bone mineral density in childhood

The 2000 NIH Consensus Development Conference on Osteoporosis Prevention, Diagnosis, and Therapy identified bone mineral accretion during childhood as a critical determinant of osteoporosis risk later in life. Consequently, there is interest in monitoring the impact of behavioral modifications for maximizing bone mineral content (BMC) and density (BMD) during childhood and adolescence with the aim of preventing osteoporosis later in life. For children with chronic disorders, identifying ways to increase bone mineral accrual is of particular importance because many have been found to have low BMC and BMD.
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Long-term proton pump inhibitor therapy and risk of hip fracture

Hip fracture is the main manifestation of senile osteoporosis, which results from secondary hyperparathyroidism associated with calcium malabsorption, low calcium intake, and other factors. Among the various forms of low-trauma fractures, hip fracture leads to the most devastating consequences.

The advent of potent acid-suppressive medications such as proton pump inhibitors (PPIs) has revolutionized the management of acid-related diseases such as gastroesophageal reflux disease (GERD). Significant hypochlorhydria, particularly among the elderly population who may have decreased PPI clearance and may be more likely to have hypochlorhydria at baseline due to higher prevalence of Helicobacter pylori infection, could theoretically result in calcium malabsorption.

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