Osteoporosis

Abstract

Osteoporotic fractures are common and result in extensive morbidity and mortality. It is possible to decrease the risk of fracture in postmenopausal, male, and glucocorticoid-induced osteoporosis with appropriate screening and treatment. The assessment of fracture risk, for which bone densitometry is only 1 component, should be the main focus of patient evaluation. Epidemiologically derived risk-assessment tools such as World Health Organization Fracture Risk Assessment Tool (FRAX) provide physicians with a way to determine the 10-year risk of osteoporotic fracture and effectively choose candidates for therapy. A number of potent skeletal antiresorptive and anabolic drugs have become available to treat osteoporosis and prevent up to 70% of fractures. Here, we provide a detailed update on clinical osteoporosis, the contribution of bone densitometry, and the approach to patients using risk assessment in the consideration of treatments. Progress in osteoporosis is an example of successful bench-to-bedside research benefitting populations worldwide.

Androgen-deprivation therapy and bone loss in prostate cancer patients: a clinical review

“…5 Androgen deprivation therapy and bone loss Marc Bienz and Fred Saad fracture death rates reach 30% within the first 6 months and even more so for men. 9 In addition, in men with low bone mass, studies have demonstrated that fractures are not uncommon even when the T-score does not reflect a need for treatment. 13 To improve fracture risk assessment, the World Health Organization has computed a FRAX algorithm that accounts for demographic risk factors, alcohol/tobacco/glucocorticoid use and other relevant past personal or familial history.…”

“…Men with risk factors should, however, be tested between the ages of 50-and 69-year old. 9 An expert panel consensus on bone health and prostate cancer published in 2006 recommends a risk stratification of patients at the initiation of ADT. High-risk stratification includes one of the following risk factors: 46 months on ADT, previous fractures, a positive family history for osteoporosis, low body weight, smoking, excessive alcohol consumption, corticosteroid use, medical comorbidities and low vitamin D levels.…”

“…Bone quality cannot be readily assessed in a clinical setting but depends on qualifiable factors such as bone architecture, mineralization, accumulated discrete areas of damage and the quality of the collagen and minerals forming the bone's matrix. 9 Conversely, bone density is conventionally evaluated with a bone-mass density (BMD) measurement obtained through Dual-energy X-ray absorptiometry (DXA). However, DXA accounts for only 40% of the overall fracture risk for patients, the residual risk being associated with bone quality-associated factors.…”

α-1 Antitrypsin Inhibits RANKL-induced Osteoclast Formation and Functions

“…The bone ends were cut off with scissors and the marrow cavities were flushed with 3 mL of MEM-α through one end of the bone using a sterile 27-gauge needle. The bone marrows were filtered with 70 μm nylon mesh filter (Fisher Scientific, Pittsburgh, PA, USA), centrifuged to collect the pellet and treated with 1-2 mL of NH 4 …”

“…disproportionate osteoclast proliferation and activation can lead to excessive bone resorption. This can subsequently lead to chronic systemic bone diseases such as osteoporosis, which is a serious public health problem affecting an estimated 34 million Americans and causing 2 million fractures annually (3,4). Strategies to inhibit excessive osteoclast formation and/or function have proven to have therapeutic usefulness for the treatment of osteoporosis (1).…”