Osteoporosis is a reduction in bone mass and weakening of bone architecture that increases the susceptibility of bone to fracture. Bone is a living tissue that is constantly being broken down and re-synthesized at 1 to 2 million microscopic sites in the adult skeleton. Osteoporosis occurs when the rate of breakdown is faster than the rate of resynthesis. Following menopause, the balance through the process of re-synthesis ends. 

Only estrogen has significant positive effect.   Estrogen is off patent and thus cheap.  Big PhARMA has insidiously gone after estrogen for to replace it with costly drugs.  The standard Big PhARMA pushed approach for treatment of osteoporosis with bisphosphonates doesn’t work—see article this site.   

http://www.worstpills.org/member/newsletter.cfm?n_id=616 

Osteoporosis Screening: What You Need to Know

     Worst Pills Best Pills Newsletter article November, 2008
    

As older adults face pressure from their doctors to be tested (and then possibly treated) for osteoporosis, it is important that they understand the tools used to determine their diagnosis. The development of new screening tools for osteoporosis has been helpful in estimating the 10-year risk of a hip or any osteoporotic fracture, but these tests still omit several important risk factors in their calculation and have the potential for resulting in inappropriate drug treatment for people who may not necessarily need it.

Osteoporosis is usually diagnosed in one of two ways. First, the patient can have a low Bone Mineral Density (BMD) score, represented by a so-called “T-score” less than -2.5. BMD is most commonly measured by dual-emission X-ray absorptiometry (DXA). The T-score represents the number of standard deviations (a representation of the distribution of BMD values in the population) from the average BMD of a young woman; negative T-scores represent lower BMDs than average.

The second way osteoporosis may be diagnosed is after a fragility fracture. A fragility fracture occurs when a bone breaks under a force that would not break a healthy bone, such as falling down from a standing position.

BMD peaks in the 20s and thereafter begins to decline. In women, BMD begins to decline more rapidly after menopause; this is thought to be due to loss of estrogen production by the ovaries. In order to detect women at risk for fracture, the U.S. Preventive Services Task Force recommends that all women over 65 years old (and some women 60-64 years old with risk factors mentioned in B ox 1 ) be screened for low BMD. Screening for low BMD before 65 years of age is controversial and guidelines are vague. Nonetheless, screening occurs for many women at some point between menopause and 65 years of age.

Screening for low BMD with DXA is intended to identify patients at risk for fractures so that they might be referred for treatment to prevent fractures. But, much like measuring blood pressure or cholesterol to screen for stroke or heart disease, BMD is only one aspect of the disorder; microscopic bone architecture and the likelihood of falling are crucial aspects of fracture risk, yet neither is reflected in a BMD value. While women with a low BMD are at increased risk for fractures, low BMD (T-score less than -2.5) does not adequately identify most women who will go on to develop a fracture. Only 25 to 45 percent of women who sustain a fracture have T-scores less than -2.5. Additionally, in the same patient, the T-score varies depending on what part of the skeleton is measured.

Because almost 50 percent of fragility fractures occur in patients with T-scores between -1.0 and -2.5, a condition known as “osteopenia,” the focus is shifting toward recognizing risk factors for fractures other than low BMD.  In consultation with a physician, these factors may be used to decide whether screening for low BMD is necessary.

New diagnostic tools not requiring BMD: helpful but incomplete

To address the deficiencies in using BMD alone in determining fracture risk, the World Health Organization recently released an online tool called FRAX (available at http://www.shef.ac.uk/FRAX/ ). FRAX can estimate one’s 10-year risk of hip or any osteoporotic fracture based on risk factors (such as gender, smoker status and daily alcohol consumption), and can be run with or without the results from testing for BMD.

A similar tool developed at the University of Washington (available at http://courses.washington.edu/bonephys/FxRiskCalculator.html) uses elements of FRAX combined with several other factors (for instance, do you use your arms to stand from a chair?) to provide a more detailed and technical assessment of fracture risk, but, unlike the WHO calculator, this tool requires knowledge of one’s T-score.

However, despite the usefulness of these tools, several important aspects of fracture risk are left out. For instance, exercise substantially increases BMD and reduces the likelihood of falling; yet physical activity is not accounted for in either online assessment. Falling is the antecedent to most hip fractures; however, several important determinants of one’s risk of falling were not included in FRAX.

Below, we illustrate how these tools can be used and how, surprisingly often, a BMD measurement alone would not lead to a change in treatment. The examples use the FRAX tool and are based on the assumption that only those with a risk of a hip fracture of 3 percent or greater in the next 10 years should begin treatment with medication.

Low-risk patient. Using FRAX without any BMD data, a 55-yearold white female who is five feet four inches tall and weighs 169 pounds with no risk factors has only a 0.4 percent chance of fracturing her hip in the next 10 years (before she is 65 years old). This less than 1 percent risk is obviously much less than the 3 percent risk of hip fracture that might indicate the need for medication. The same lower-than-3 percent risk would also be true for women 60 or 70 years old of the same height and weight with no risk factors.

Using FRAX with BMD information, even if the 55-year-old woman had a T-score equal to -2.5 (osteoporosis), her 10-year hip fracture risk is still only 2.6 percent. Thus, with or without the BMD results, this patient would not be a candidate for treatment.

Intermediate-risk patient. If the 55-year-old woman in the first case was a smoker and had a previous fragility fracture, without knowing her T-score, her risk of hip fracture before 65 years is 2.2 percent. However, with a T-score of -2.5, her hip fracture risk would rise dramatically to about 9 percent. For this patient, assessing BMD could lead to her being treated.

High-risk patient. If, in addition to smoking and a previous fracture, the patient drinks three alcoholic beverages per day and is on steroids for rheumatoid arthritis, even without a BMD, her 10-year fracture risk is 12 percent, high enough to merit treatment. Screening for low BMD would not alter her treatment.

In sum, while measuring BMD can be a useful diagnostic test, all too often, its deficiencies are overlooked. Consequently, far more women receive the test than are likely to benefit from it and may well be started on drug treatment based only on the results. No doubt one of the reasons for the heavy emphasis on BMD is the large industry it supports: the companies who make the equipment and the doctors who profit from doing the tests. Most of the other risk factors can be determined in the course of a routine doctor visit, but screening for low BMD requires a diagnostic test that can be reimbursed. We can achieve better application of our limited resources with a more thoughtful approach that stratifies patients according to the many risk factors that contribute to fracture, rather than relying so heavily on primarily screening for low BMD.

Box 1.

A way to compare what Worse Pill published with that of another reliable source, Wikipedia;

FROM WIKIPEDIA: 

Screening

The U.S. Preventive Services Task Force (USPSTF) recommended in 2002 that all women 65 years of age or older should be screened with bone densitometry.^[27] The Task Force recommends screening only those women ages 60 to 64 years of age who are at increased risk. The best risk factor for indicating increased risk is lower body weight (weight < 70 kg), with smoking or family history. There was insufficient evidence to make recommendations about the optimal intervals for repeated screening and the appropriate age to stop screening. Clinical prediction rules are available to guide selection of women ages 60-64 for screening. The Osteoporosis Risk Assessment Instrument (ORAI) may be the most sensitive strategy^[28]

Regarding the screening of men, a cost-analysis study suggests that screening may be "cost-effective for men with a self-reported prior fracture beginning at age 65 years and for men 80 years and older with no prior fracture".^[29] Also cost-effective is the screening of adult men from middle age on to detect any significant decrease in testosterone levels, say, below 300.

Medication

Certain medications have been associated with an increase in osteoporosis risk; only steroids and anticonvulsants are classically associated, but evidence is emerging with regard to other drugs.

• Steroid-induced osteoporosis (SIOP) arises due to use of glucocorticoids - analogous to Cushing's syndrome and involving mainly the axial skeleton. The synthetic glucocorticoid prescription drug prednisone is a main candidate after prolonged intake. Some professional guidelines recommend prophylaxis in patients who take the equivalent of more than 30 mg hydrocortisone (7.5 mg of prednisolone), especially when this is in excess of three months.^[19] Alternate day use may not prevent this complication.^[20]
• Barbiturates, phenytoin and some other enzyme-inducing antiepileptics - these probably accelerate the metabolism of vitamin D. ^[21]
• L-Thyroxine over-replacement may contribute to osteoporosis, in a similar fashion as thyrotoxicosis does.^[16] This can be relevant in subclinical hypothyroidism.
• Several drugs induce hypogonadism, for example aromatase inhibitors used in breast cancer, methotrexate and other anti-metabolite drugs, depot progesterone and gonadotropin-releasing hormone agonists.
• Anticoagulants - long-term use of heparin is associated with a decrease in bone density,^[22] and warfarin (and related coumarins) have been linked with an increased risk in osteoporotic fracture in long-term use.^[23]
• Proton pump inhibitors - these drugs inhibit the production of stomach acid; it is thought that this interferes with calcium absorption.^[24] Chronic phosphate binding may also occur with aluminium-containing antacids.^[16]
• Thiazolidinediones (used for diabetes) - rosiglitazone and possibly pioglitazone, inhibitors of PPARγ, have been linked with an increased risk of osteoporosis and fracture.^[25]
• Chronic lithium therapy has been associated with osteoporosis.^[16]

Potentially modifiable

• Excess alcohol - small amounts of alcohol do not increase osteoporosis risk and may even be beneficial, but chronic heavy drinking (alcohol intake greater than 2 units/day),^[7] especially at a younger age, increases risk significantly.^[8]
• Vitamin D deficiency^[9] - low circulating Vitamin D is common among the elderly worldwide.^[10] Mild vitamin D insufficiency is associated with increased Parathyroid Hormone (PTH) production. ^[10] PTH increases bone reabsorption, leading to bone loss. A positive association exists between serum 1,25-dihydroxycholecalciferol levels and bone mineral density, while PTH is negatively associated with bone mineral density.^[10]
• Tobacco smoking - tobacco smoking inhibits the activity of osteoblasts, and is an independent risk factor for osteoporosis.^[7][11] Smoking also results in increased breakdown of exogenous estrogen, lower body weight and earlier menopause, all of which contribute to lower bone mineral density.^[10]
• High body mass index - being overweight protects against osteoporosis, either by increasing load or through the hormone leptin.^[12]
• Malnutrition - low dietary calcium intake, low dietary intake of vitamins K and C^[9] Also low protein intake is associated with lower peak bone mass during adolescence and lower bone mineral density in elderly populations.^[10]
• Physical inactivity - bone remodeling occurs in response to physical stress. Weight bearing exercise can increase peak bone mass achieved in adolescence.^[10] In adults, physical activity helps maintain bone mass, and can increase it by 1 or 2%.^{[citation needed]} Conversely, physical inactivity can lead to significant bone loss.^[10]
• Excess physical activity - excessive exercise can lead to constant damages to the bones which can cause exhaustion of the structures as described above. There are numerous examples of marathon runners who developed severe osteoporosis later in life. {I have always recommended running no more than 2 miles—jk} In women, heavy exercise can lead to decreased estrogen levels, which predisposes to osteoporosis. Intensive training is often associated with low body mass index.^{[citation needed]}
• Heavy metals - a strong association between cadmium, lead and bone disease has been established. Low level exposure to cadmium is associated with an increased loss of bone mineral density readily in both genders, leading to pain and increased risk of fractures, especially in the elderly and in females. Higher cadmium exposure results in osteomalacia (softening of the bone).^[13]
• Soft drinks - some studies indicate that soft drinks (many of which contain phosphoric acid) may increase risk of osteoporosis;^[14] Others suggest soft drinks may displace calcium-containing drinks from the diet rather than directly causing osteoporosis.^[15]

^Pathogenesis

The underlying mechanism in all cases of osteoporosis is an imbalance between bone resorption and bone formation. In normal bone, there is constant matrix remodeling of bone; up to 10% of all bone mass may be undergoing remodeling at any point in time. The process takes place in bone multicellular units (BMUs) as first described by Frost in 1963.^[30] Bone is resorbed by osteoclast cells (which derive from the bone marrow), after which new bone is deposited by osteoblast cells. ^[5]

The three main mechanisms by which osteoporosis develops are an inadequate peak bone mass (the skeleton develops insufficient mass and strength during growth), excessive bone resorption and inadequate formation of new bone during remodeling. An interplay of these three mechanisms underlies the development of fragile bone tissue.^[5] Hormonal factors strongly determine the rate of bone resorption; lack of estrogen (e.g. as a result of menopause) increases bone resorption as well as decreasing the deposition of new bone that normally takes place in weight-bearing bones. The amount of estrogen needed to suppress this process is lower than that normally needed to stimulate the uterus and breast gland. The α-form of the estrogen receptor appears to be the most important in regulating bone turnover.^[5] In addition to estrogen, calcium metabolism plays a significant role in bone turnover, and deficiency of calcium and vitamin D leads to impaired bone deposition; in addition, the parathyroid glands react to low calcium levels by secreting parathyroid hormone (parathormone, PTH), which increases bone resorption to ensure sufficient calcium in the blood. The role of calcitonin, a hormone generated by the thyroid that increases bone deposition, is less clear and probably not as significant as that of PTH.^[5]

In hypogonadal men testosterone has been shown to give improvement in bone quantity and quality, but, as of 2008, there are no studies of the effects on fractures or in men with a normal testosterone level.^[18]

Selective estrogen receptor modulator (SERM)

SERMs are a class of medications that act on the estrogen receptors throughout the body in a selective manner. Normally, bone mineral density (BMD) is tightly regulated by a balance between osteoblast and osteoclast activity in the trabecular bone. Estrogen has a major role in regulation of the bone formation-resorption equilibrium, as it stimulates osteoblast activity. Some SERMs such as raloxifene (Evista), act on the bone by slowing bone resorption by the osteoclasts.^[38] SERMs have been proved as effective in clinical trials.^[39][40]

The role of calcium in preventing and treating osteoporosis is unclear - some populations with extremely low calcium intake also have extremely low rates of bone fracture, and others with high rates of calcium intake through milk and milk products have higher rates of bone fracture. Other factors, such as protein, salt and vitamin D intake, exercise and exposure to sunlight, can all influence bone mineralization, making calcium intake one factor among many in the development of osteoporosis.^[42] In the report of WHO(World Health Organization) in 2007, because calcium is consumed by an acid load with food, it influences osteoporosis.^[43][44].  A meta-analysis of randomized controlled trials involving calcium and calcium plus vitamin D supported the use of high levels of calcium (1,200 mg or more) and vitamin D (800 IU or more), though outcomes varied depending on which measure was used to assess bone health (rates of fracture versus rates of bone loss).^[45] The meta-analysis, along with another study, also supported much better outcomes for patients with high compliance to the treatment protocol.^[46]

Vitamin D

Some studies have shown that a high intake of vitamin D reduces fractures in the elderly,^[45][48] though the Women's Health Initiative found that though calcium plus vitamin D did increase bone density, it did not affect hip fracture but did increase formation of kidney stones.^[49]

[edit] Exercise

Multiple studies have shown that aerobics, weight bearing, and resistance exercises can all maintain or increase BMD in postmenopausal women.^[50] Many researchers have attempted to pinpoint which types of exercise are most effective at improving BMD and other metrics of bone quality, however results have varied. One year of regular jumping exercises appears to increase the BMD and moment of inertia of the proximal tibia^[51] in normal postmenopausal women. Treadmill walking, gymnastic training, stepping, jumping, endurance, and strength exercises all resulted in significant increases of L2-L4 BMD in osteopenic postmenopausal women.^[52][53][54] Strength training elicited improvements specifically in distal radius and hip BMD.^[55] Exercise combined with other pharmacological treatments such as hormone replacement therapy (HRT) has been shown to increases BMD more than HRT alone.^[56]

Additional benefits for osteoporotic patients other than BMD increase include improvements in balance, gait, and a reduction in risk of falls.^[57]

Epidemiology

It is estimated^{[citation needed]} that 1 in 3 women and 1 in 12 men over the age of 50 worldwide have osteoporosis. It is responsible for millions of fractures annually, mostly involving the lumbar vertebrae, hip, and wrist. Fragility fractures of ribs are also common in men.  It is estimated that a 50-year-old white woman has a 17.5% lifetime risk of fracture of the proximal femur. The incidence of hip fractures increases each decade from the sixth through the ninth for both women and men for all populations. The highest incidence is found among those men and women ages 80 or older.^[62]

In the United States, 250,000 wrist fractures annually are attributable to Osteoporosis.^[61] Wrist fractures are the third most common type of osteoporotic fractures. The lifetime risk of sustaining a Colles' fracture is about 16% for white women. By the time women reach age 70, about 20% have had at least one wrist fracture.^[62]

Exercise

Achieving a higher peak bone mass through exercise and proper nutrition during adolescence is important for the prevention of osteoporosis. Exercise and nutrition throughout the rest of the life delays bone degeneration. Jogging, walking, or stair climbing at 70-90% of maximum effort three times per week, along with 1,500 mg of calcium per day, increased bone density of the lumbar (lower) spine by 5% over 9 months. Individuals already diagnosed with osteopenia or osteoporosis should discuss their exercise program with their physician to avoid fractures.^[64]