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Name = Osteoporosis |
  
Name = Osteoporosis |

Latest revision as of 01:27, 1 February 2012

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Osteoporosis
Classification and external resources
ICD-10 M80-M82
ICD-9 733.0
OMIM 166710
DiseasesDB 9385
MedlinePlus 000360
eMedicine med/1693 ped/1683 pmr/94 pmr/95
MeSH D010024

Osteoporosis is a disease of bone that leads to an increased risk of fracture. In osteoporosis the bone mineral density (BMD) is reduced, bone microarchitecture is disrupted, and the amount and variety of proteins in bone is altered. Osteoporosis is defined by the World Health Organization (WHO) in women as a bone mineral density 2.5 standard deviations below peak bone mass (20-year-old healthy female average) as measured by DXA; the term "established osteoporosis" includes the presence of a fragility fracture.[1] Osteoporosis is most common in women after menopause, when it is called postmenopausal osteoporosis, but may also develop in men, and may occur in anyone in the presence of particular hormonal disorders and other chronic diseases or as a result of medications, specifically glucocorticoids, when the disease is called steroid- or glucocorticoid-induced osteoporosis (SIOP or GIOP). Given its influence in the risk of fragility fracture, osteoporosis may significantly affect life expectancy and quality of life.

Osteoporosis can be prevented with lifestyle changes and sometimes medication; in people with osteoporosis, treatment may involve both. Lifestyle change includes exercise and preventing falls; medication includes calcium, vitamin D, bisphosphonates and several others. Fall-prevention advice includes exercise to tone deambulatory muscles, proprioception-improvement exercises; equilibrium therapies may be included. Exercise with its anabolic effect, may at the same time stop or reverse osteoporosis. Osteoporosis is a component of the frailty syndrome.

Pathogenesis

File:Osteoclast.jpg

Osteoclast displaying many nuclei within its "foamy" cytoplasm

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.[2] Bone is resorbed by osteoclast cells (which derive from the bone marrow), after which new bone is deposited by osteoblast cells.[3]

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.[3] 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.[3] 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.[3]

File:Active osteoblasts.jpg

Osteoblasts, several displaying a prominent Golgi apparatus, actively synthesizing osteoid containing two osteocytes.

The activation of osteoclasts is regulated by various molecular signals, of which RANKL (receptor activator for nuclear factor κB ligand) is one of best studied. This molecule is produced by osteoblasts and other cells (e.g. lymphocytes), and stimulates RANK (receptor activator of nuclear factor κB). Osteoprotegerin (OPG) binds RANKL before it has an opportunity to bind to RANK, and hence suppresses its ability to increase bone resorption. RANKL, RANK and OPG are closely related to tumor necrosis factor and its receptors. The role of the wnt signalling pathway is recognized but less well understood. Local production of eicosanoids and interleukins is thought to participate in the regulation of bone turnover, and excess or reduced production of these mediators may underlie the development of osteoporosis.[3]

Trabecular bone is the sponge-like bone in the ends of long bones and vertebrae. Cortical bone is the hard outer shell of bones and the middle of long bones. Because osteoblasts and osteoclasts inhabit the surface of bones, trabecular bone is more active, more subject to bone turnover, to remodeling. Not only is bone density decreased, but the microarchitecture of bone is disrupted. The weaker spicules of trabecular bone break ("microcracks"), and are replaced by weaker bone. Common osteoporotic fracture sites, the wrist, the hip and the spine, have a relatively high trabecular bone to cortical bone ratio. These areas rely on trabecular bone for strength, and therefore the intense remodeling causes these areas to degenerate most when the remodeling is imbalanced.[citation needed]

Signs and symptoms

Osteoporosis itself has no specific symptoms; its main consequence is the increased risk of bone fractures. Osteoporotic fractures are those that occur in situations where healthy people would not normally break a bone; they are therefore regarded as fragility fractures. Typical fragility fractures occur in the vertebral column, rib, hip and wrist.

Fractures

The symptoms of a vertebral collapse ("compression fracture") are sudden back pain, often with radiculopathic pain (shooting pain due to nerve root compression) and rarely with spinal cord compression or cauda equina syndrome. Multiple vertebral fractures lead to a stooped posture, loss of height, and chronic pain with resultant reduction in mobility.[4]

Fractures of the long bones acutely impair mobility and may require surgery. Hip fracture, in particular, usually requires prompt surgery, as there are serious risks associated with a hip fracture, such as deep vein thrombosis and a pulmonary embolism, and increased mortality.

Fracture Risk Calculators assess the risk of fracture based upon several criteria, including BMD, age, smoking, alcohol usage, weight, and gender. Recognised calculators include FRAX[5] and Dubbo.

Falls risk

The increased risk of falling associated with aging leads to fractures of the wrist, spine and hip. The risk of falling, in turn, is increased by impaired eyesight due to any cause (e.g. glaucoma, macular degeneration), balance disorder, movement disorders (e.g. Parkinson's disease), dementia, and sarcopenia (age-related loss of skeletal muscle). Collapse (transient loss of postural tone with or without loss of consciousness) leads to a significant risk of falls; causes of syncope are manifold but may include cardiac arrhythmias (irregular heart beat), vasovagal syncope, orthostatic hypotension (abnormal drop in blood pressure on standing up) and seizures. Removal of obstacles and loose carpets in the living environment may substantially reduce falls. Those with previous falls, as well as those with a gait or balance disorder, are most at risk.[6]

Risk factors

Risk factors for osteoporotic fracture can be split between non-modifiable and (potentially) modifiable. In addition, there are specific diseases and disorders in which osteoporosis is a recognized complication. Medication use is theoretically modifiable, although in many cases the use of medication that increases osteoporosis risk is unavoidable.

Nonmodifiable

The most important risk factors for osteoporosis are advanced age (in both men and women) and female sex; estrogen deficiency following menopause is correlated with a rapid reduction in bone mineral density, while in men a decrease in testosterone levels has a comparable (but less pronounced) effect. While osteoporosis occurs in people from all ethnic groups, European or Asian ancestry predisposes for osteoporosis.[7] Those with a family history of fracture or osteoporosis are at an increased risk; the heritability of the fracture as well as low bone mineral density are relatively high, ranging from 25 to 80 percent. There are at least 30 genes associated with the development of osteoporosis.[3] Those who have already had a fracture are at least twice as likely to have another fracture compared to someone of the same age and sex.[8]

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 3 units/day),[9] especially at a younger age, increases risk significantly.[10]
  • Vitamin D deficiency[11] - low circulating Vitamin D is common among the elderly worldwide.[12] Mild vitamin D insufficiency is associated with increased Parathyroid Hormone (PTH) production.[12] PTH increases bone resorption, 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.[12]
  • Tobacco smoking - tobacco smoking inhibits the activity of osteoblasts, and is an independent risk factor for osteoporosis.[9][13] Smoking also results in increased breakdown of exogenous estrogen, lower body weight and earlier menopause, all of which contribute to lower bone mineral density.[12]
  • Malnutrition - nutrition has an important and complex role in maintenance of good bone. Identified risk factors include low dietary calcium and/or phosphorus, magnesium, zinc, boron, iron, fluoride, copper, vitamins A, K, E and C (and D where skin exposure to sunlight provides an inadequate supply). Excess sodium is a risk factor. High blood acidity may be diet-related, and is a known antagonist of bone.[14] Some have identified low protein intake as associated with lower peak bone mass during adolescence and lower bone mineral density in elderly populations.[12] Conversely, some have identified low protein intake as a positive factor, protein is among the causes of dietary acidity. Imbalance of omega 6 to omega 3 polyunsaturated fats is yet another identified risk factor.[1]
  • Underweight/inactive - bone remodeling occurs in response to physical stress, and weight bearing exercise can increase peak bone mass achieved in adolescence.[12] 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.[12](Incidence of osteoporosis is lower in overweight people.)[15]
  • 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. In women, heavy exercise can lead to decreased estrogen levels, which predisposes to osteoporosis. In addition, intensive training without proper compensatory increased nutrition increases the risk.
  • 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).[16]
  • Soft drinks - some studies indicate that soft drinks (many of which contain phosphoric acid) may increase risk of osteoporosis;[17] Others suggest soft drinks may displace calcium-containing drinks from the diet rather than directly causing osteoporosis.[18]
  • Caffeine – contrary to popular belief, there is no evidence linking caffeine to osteoporosis.[19]

Diseases and disorders

Many diseases and disorders have been associated with osteoporosis.[20] For some, the underlying mechanism influencing the bone metabolism is straight-forward, whereas for others the causes are multiple or unknown.

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.[23] Alternate day use may not prevent this complication.[24]
  • Barbiturates, phenytoin and some other enzyme-inducing antiepileptics - these probably accelerate the metabolism of vitamin D.[25]
  • L-Thyroxine over-replacement may contribute to osteoporosis, in a similar fashion as thyrotoxicosis does.[20] 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,[26] and warfarin (and related coumarins) have been linked with an increased risk in osteoporotic fracture in long-term use.[27]
  • Proton pump inhibitors - these drugs inhibit the production of stomach acid; it is thought that this interferes with calcium absorption.[28] Chronic phosphate binding may also occur with aluminium-containing antacids.[20]
  • Thiazolidinediones (used for diabetes) - rosiglitazone and possibly pioglitazone, inhibitors of PPARγ, have been linked with an increased risk of osteoporosis and fracture.[29]
  • Chronic lithium therapy has been associated with osteoporosis.[20]

Diagnosis

File:Bone density scanner.jpg

A scanner used to measure bone density with dual energy X-ray absorptiometry.

The diagnosis of osteoporosis is made on measuring the bone mineral density (BMD). The most popular method is dual energy X-ray absorptiometry (DXA or DEXA). In addition to the detection of abnormal BMD, the diagnosis of osteoporosis requires investigations into potentially modifiable underlying causes; this may be done with blood tests and X-rays. Depending on the likelihood of an underlying problem, investigations for cancer with metastasis to the bone, multiple myeloma, Cushing's disease and other above mentioned causes may be performed.

Clinical decision rule

A number of clinical decision rules have been created to predict the risk of osteoporotic fractures. The QFracture score was developed in 2009 and is based on age, BMI, smoking status, alcohol use, rheumatoid arthritis, cardiovascular disease, type 2 diabetes, asthma, use of tricyclic antidepressants or corticosteroids, liver disease, and a history of falls in men. In women hormone replacement therapy, parental history of osteoporosis, gastrointestinal malabsorption, and menopausal symptoms are also taken into account.[30] A website is available to help apply this score.[31]

Dual energy X-ray absorptiometry

Dual energy X-ray absorptiometry (DXA, formerly DEXA) is considered the gold standard for the diagnosis of osteoporosis. Osteoporosis is diagnosed when the bone mineral density is less than or equal to 2.5 standard deviations below that of a young adult reference population. This is translated as a T-score. The World Health Organization has established the following diagnostic guidelines:[1][12]

  • T-score -1.0 or greater is "normal"
  • T-score between -1.0 and -2.5 is "low bone mass" (or "osteopenia")
  • T-score -2.5 or below is osteoporosis

When there has also been an osteoporotic fracture (also termed "low trauma-fracture" or "fragility fracture"), defined as one that occurs as a result of a fall from a standing height, the term "severe or established" osteoporosis is used.[1]

The International Society for Clinical Densitometry takes the position that a diagnosis of osteoporosis in men under 50 years of age should not be made on the basis of densitometric criteria alone. It also states that for pre-menopausal women, Z-scores (comparison with age group rather than peak bone mass) rather than T-scores should be used, and that the diagnosis of osteoporosis in such women also should not be made on the basis of densitometric criteria alone.[32]

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.[33] 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 less evidence for 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[34]

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".[35] Also cost-effective is the screening of adult men from middle age on to detect any significant decrease in testosterone levels, say, below 300.

Treatment

There are several medications used to treat osteoporosis, depending on gender. Medications themselves can be classified as antiresorptive or bone anabolic agents. Antiresorptive agents work primarily by reducing bone resorption, while bone anabolic agents build bone rather than inhibit resorption. Lifestyle changes are also an aspect of treatment.

Antiresorptive agents

  • Bisphosphanates
Bisphosphonates are the main pharmacological measures for treatment. However, newer drugs have appeared in the 1990s, such as teriparatide and strontium ranelate.
In confirmed osteoporosis, bisphosphonate drugs are the first-line treatment in women. The most often prescribed bisphosphonates are presentlyTemplate:Dated maintenance category sodium alendronate (Fosamax) 10 mg a day or 70 mg once a week, risedronate (Actonel) 5 mg a day or 35 mg once a week and or ibandronate (Boniva) once a month.
A 2007 manufacturer-supported study suggested that in patients who had suffered a low-impact hip fracture, annual infusion of 5 mg zoledronic acid reduced risk of any fracture by 35% (from 13.9 to 8.6%), vertebral fracture risk from 3.8% to 1.7% and non-vertebral fracture risk from 10.7% to 7.6%. This study also found a mortality benefit: after 1.9 years, 9.6% of the study group (as opposed to 13.3% of the control group) had died of any cause, indicating a mortality benefit of 28%.[36]
Oral bisphosphonates are relatively poorly absorbed, and must therefore be taken on an empty stomach, with no food or drink to follow for the next 30 minutes. They are associated with inflammation of the esophagus (esophagitis) and are therefore sometimes poorly tolerated; weekly or monthly administration (depending on the preparation) decreases likelihood of esophagitis, and is now standard. Although intermittent dosing with the intravenous formulations such as zolendronate (zoledronic acid) avoids oral tolerance problems, these agents are implicated at higher rates in a rare but unpleasant mouth disease called osteonecrosis of the jaw.[37] For this reason, oral bisphosphonate therapy is probably to be preferred, and doctors now recommend that any needed remedial dental work be done before treatment begins.[38]
  • Estrogen analogs
Estrogen replacement therapy remains a good treatment for prevention of osteoporosis but, at this time, is not recommended unless there are other indications for its use as well. There is uncertainty and controversy about whether estrogen should be recommended in women in the first decade after the menopause.
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.[22]
  • Raloxifene
Selective Estrogen Receptor Modulators (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, act on the bone by slowing bone resorption by the osteoclasts.[39] SERMs have been proved as effective in clinical trials.[40]
  • Calcitonin
Calcitonin works by directly inhibiting osteoclast activity via the calcitonin receptor.

Bone anabolic agents

  • Teriparatide
Recently, teriparatide (Forteo, recombinant parathyroid hormone residues 1–34) has been shown to be effective in osteoporosis. It acts like parathyroid hormone and stimulates osteoblasts, thus increasing their activity. It is used mostly for patients with established osteoporosis (who have already fractured), have particularly low BMD or several risk factors for fracture or cannot tolerate the oral bisphosphonates. It is given as a daily injection with the use of a pen-type injection device. In some countries, Teriparatide is licensed to be used for treatment only if bisphosphonates have failed or are contraindicated. (In the U.S., this restriction has not been imposed by the FDA.) Patients with previous radiation therapy, or Paget's disease, or young patients, should avoid this medication.
  • Calcium salts
Calcium salts come as water insoluble and soluble formulations. Calcium carbonate is the primary water insoluble drug, while calcium citrate, lactate, and gluconate are water soluble. Calcium carbonate's absorption is improved in acidic conditions, while the water soluble salts are relatively unaffected by acidic conditions.
  • Sodium fluoride
This agent has been shown to increase bone density in the vertebrae.

Other agents

  • RANKL inhibitors
Denosumab is a fully human monoclonal antibody that mimics the activity of osteoprotegerin. It binds to RANKL, thereby preventing RANKL from interacting with RANK and reducing it's bone resorption. It is currently (as of 11/2009) pending approval.
  • Strontium ranelate
Oral strontium ranelate is an alternative oral treatment, belonging to a class of drugs called "dual action bone agents" (DABAs) by its manufacturer. It has proven efficacy, especially in the prevention of vertebral fracture.[41] In laboratory experiments, strontium ranelate was noted to stimulate the proliferation of osteoblasts, as well as inhibiting the proliferation of osteoclasts.
Strontium ranelate is taken as a 2 g oral suspension daily, and is licenced for the treatment of osteoporosis to prevent vertebral and hip fracture. Strontium ranelate has side effect benefits over the bisphosphonates, as it does not cause any form of upper GI side effect, which is the most common cause for medication withdrawal in osteoporosis. In studies a small increase in the risk of venous thromboembolism was noted,[42] the cause for which has not been determined. This suggests it may be less suitable in patients at risk for thrombosis for different reasons. The uptake of (heavier) strontium in place of calcium into bone matrix results in a substantial and disproportionate increase in bone mineral density as measured on DXA scanning[43], making further followup of bone density by this method harder to interpret for strontium treated patients. A correction algorithm has been devised.[44]
Although strontium ranelate is effective, it is not approved for use in the United States yet. However, strontium citrate is available in the U.S. from several well-known vitamin manufacturers. Most researchers believe that strontium is safe and effective no matter what form it is used. The ranelate form is simply a device invented by the Servier company of France so that they could patent their version of strontium.[citation needed]
Strontium, no matter what the form, must be water-soluble and ionized in the stomach acid. Strontium is then protein-bound for transport from the intestinal tract into the blood stream. Unlike drugs like sodium alendronate (Fosamax), strontium doesn't inhibit bone recycling and, in fact, may produce stronger bones. Studies have shown that after five years alendronate may even cause bone loss, while strontium continues to build bone during lifetime use.[citation needed]
Strontium must not be taken with food or calcium-containing preparations as calcium competes with strontium during uptake. However, it is essential that calcium, magnesium, and vitamin D in therapeutic amounts must be taken daily, but not at the same time as strontium. Strontium should be taken on an empty stomach at night.[citation needed]

Nutrition

  • Calcium
Calcium is required to support bone growth, bone healing and maintain bone strength and is one aspect of treatment for osteoporosis. Recommendations for calcium intake vary depending country and age; for individuals at higher risk of osteoporosis (after fifty years of age) the amount recommended by US health agencies is 1,200 mg per day. Calcium supplements can be used to increase dietary intake, and absorption is optimized through taking in several small (500 mg or less) doses throughout the day.[45] 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.[46] In the report of WHO (World Health Organization) in 2007, because calcium is consumed by an acid load with food, it influences osteoporosis.[47][48].
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).[49] The meta-analysis, along with another study, also supported much better outcomes for patients with high compliance to the treatment protocol.[50] In contrast, despite earlier reports in improved high density lipoprotein (HDL, "good cholesterol") in calcium supplementation, a possible increase in the rate of myocardial infarction (heart attack) was found in a study in New Zealand in which 1471 women participated. If confirmed, this would indicate that calcium supplementation in women otherwise at low risk of fracture may cause more harm than good.[51]
  • Vitamin D
Several studies have shown that a high intake of vitamin D reduces fractures in the elderly,[49][52] The Women's Health Initiative found that though calcium plus vitamin D did increase bone density by 1% but it did not affect hip fracture. It did increase formation of kidney stones by 17%.[53]. This study has been criticised for using an inadequate dose of vitamin D (400 U) and for allowing the control arm to take supplemental vitamin D.

Exercise

Multiple studies have shown that aerobics, weight bearing, and resistance exercises can all maintain or increase BMD in postmenopausal women.[54] 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. The BEST (Bone-Estrogen Strength Training) Project at the University of Arizona identified six specific weight training exercises that yielded the largest improvements in BMD; this project suggests squat, military press, lat pulldown, leg press, back extension, and seated row, with three weight training sessions a week of two sets of each exercise, alternating between moderate (6-8 reps at 70% of 1-rep max) and heavy (4-6 reps at 80% of 1-rep max).[55] One year of regular jumping exercises appears to increase the BMD and moment of inertia of the proximal tibia[56] 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.[57][58][59] Strength training elicited improvements specifically in distal radius and hip BMD.[60] Exercise combined with other pharmacological treatments such as hormone replacement therapy (HRT) has been shown to increases BMD more than HRT alone.[61]
Additional benefits for osteoporotic patients other than BMD increase include improvements in balance, gait, and a reduction in risk of falls.[62]

Prognosis

Hip fractures per 1000 patient-years[63]
WHO category Age 50-64 Age > 64 Overall
Normal 5.3 9.4 6.6
Osteopenia 11.4 19.6 15.7
Osteoporosis 22.4 46.6 40.6

Although osteoporosis patients have an increased mortality rate due to the complications of fracture, most patients die with the disease rather than of it.

Hip fractures can lead to decreased mobility and an additional risk of numerous complications (such as deep venous thrombosis and/or pulmonary embolism, pneumonia). The 6-month mortality rate following hip fracture is approximately 13.5%, and a substantial proportion (almost 13%) of people who have suffered a hip fracture need total assistance to mobilize after a hip fracture.[64]

Vertebral fractures, while having a smaller impact on mortality, can lead to severe chronic pain of neurogenic origin, which can be hard to control, as well as deformity. Though rare, multiple vertebral fractures can lead to such severe hunch back (kyphosis) that the resulting pressure on internal organs can impair one's ability to breathe.

Apart from risk of death and other complications, osteoporotic fractures are associated with a reduced health-related quality of life.[65]

Epidemiology

File:L1 2 vertebral fracture.jpg

Lateral thoraco-lumbar spine X-ray demonstrating multiple wedge fractures

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.

Hip fractures

Main article: hip fractures

Hip fractures are responsible for the most serious consequences of osteoporosis. In the United States, more than 250,000 hip fractures annually are attributible to osteoporosis.[66] 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.[67]

Vertebral fractures

Between 35-50% of all women over 50 had at least one vertebral fracture. In the United States, 700,000 vertebral fractures occur annually, but only about a third are recognized. In a series of 9704 of women aged 68.8 on average studied for 15 years, 324 had already suffered a vertebral fracture at entry into the study; 18.2% developed a vertebral fracture, but that risk rose to 41.4% in women who had a previous vertebral fracture.[68]

Wrist

In the United States, 250,000 wrist fractures annually are attributable to osteoporosis.[66] 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.[67]

Rib Fractures

Fragility fractures of the ribs are common in men as young as age thirty-five on. These are often overlooked as signs of osteoporosis as these men are often physically active and suffer the fracture in the course of physical activity. An example would be as a result of falling while water skiing or jet skiing. However, a quick test of the individual's testosterone level following the diagnosis of the fracture will readily reveal whether that individual might be at risk.

Prevention

Methods to prevent osteoporosis include changes of lifestyle. However, there are medications that can be used for prevention as well. As a different concept there are osteoporosis ortheses which help to prevent spine fractures and support the building up of muscles. Fall prevention can help prevent osteoporosis complications.

Lifestyle

Lifestyle prevention of osteoporosis is in many aspects inversions from potentially modifiable risk factors. As tobacco smoking and unsafe alcohol intake have been linked with osteoporosis, smoking cessation and moderation of alcohol intake are commonly recommended in the prevention of osteoporosis.[citation needed]

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.[69]

Nutrition

Proper nutrition includes a diet sufficient in calcium and vitamin D. Patients at risk for osteoporosis (e.g. steroid use) are generally treated with vitamin D and calcium supplements and often with bisphosphonates. In renal disease, more active forms of Vitamin D such as paracalcitol or (1,25-dihydroxycholecalciferol or calcitriol which is the main biologically active form of vitamin D) is used, as the kidney cannot adequately generate calcitriol from calcidiol (25-hydroxycholecalciferol) which is the storage form of vitamin D.

High dietary protein intake increases calcium excretion in urine and has been linked to increased risk of fractures in research studies.[70] Other investigations have shown that protein is required for calcium absorption, but that excessive protein consumption inhibits this process. No interventional trials have been performed on dietary protein in the prevention and treatment of osteoporosis.[71]

Medication

Just as for treatment, bisphosphonate can be used in cases of very high risk. Other medicines prescribed for prevention of osteoporosis include raloxifene, a selective estrogen receptor modulator (SERM).

Estrogen replacement therapy remains a good treatment for prevention of osteoporosis but, at this time, is not recommended unless there are other indications for its use as well. There is uncertainty and controversy about whether estrogen should be recommended in women in the first decade after the menopause.

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.[22]

History

The link between age-related reductions in bone density and fracture risk goes back at least to Astley Cooper, and the term "osteoporosis" and recognition of its pathological appearance is generally attributed to the French pathologist Jean Lobstein.[72] The American endocrinologist Fuller Albright linked osteoporosis with the postmenopausal state.[73] Bisphosponates, which revolutionized the treatment of osteoporosis, were discovered in the 1960s.[74]

Organizations

The National Osteoporosis Society, established in 1986, is a United Kingdom charity dedicated to improving the diagnosis, prevention and treatment of osteoporosis.[75][76]

The National Osteoporosis Foundation (headquartered in Washington, D.C., USA) seeks to prevent osteoporosis and related fractures, to promote lifelong bone health, to help improve the lives of those affected by osteoporosis and to find a cure through programs of awareness, advocacy, public and health professional education and research. [2]

The International Osteoporosis Foundation (IOF) (headquartered in Nyon, Switzerland) functions as a global alliance of patient, medical and research societies, scientists, health care professionals, and international companies concerned about bone health. [3]

The Orthopaedic Research Society (headquartered in Rosemont, IL, USA) is a research and professional development society that has emphasized osteoporosis research, treatment and prevention for many years. [4]

See also

  • Back pain
  • Bone seeker
  • Hip protector
  • Dental X-ray
  • Osteopetrosis
  • Osteoimmunology
  • Ovariectomized rat model for osteoporosis research
  • Spaceflight osteopenia

References

  1. ↑ 1.0 1.1 1.2 WHO (1994). Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Report of a WHO Study Group. World Health Organization technical report series 843: 1–129.
  2. ↑ Frost HM, Thomas CC. Bone Remodeling Dynamics. Springfield, IL: 1963.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Raisz L (2005). Pathogenesis of osteoporosis: concepts, conflicts, and prospects.. J Clin Invest 115 (12): 3318–25.
  4. ↑ Kim DH, Vaccaro AR (2006). Osteoporotic compression fractures of the spine; current options and considerations for treatment. The spine journal : official journal of the North American Spine Society 6 (5): 479–87.
  5. ↑ Susan Ott. Fracture Risk Calculator. URL accessed on 2009-11-03.
  6. ↑ Ganz DA, Bao Y, Shekelle PG, Rubenstein LZ (2007). Will my patient fall?. JAMA 297 (1): 77–86.
  7. ↑ Melton LJ (2003). Epidemiology worldwide. Endocrinol. Metab. Clin. North Am. 32 (1): 1–13, v.
  8. ↑ Ojo F, Al Snih S, Ray LA, Raji MA, Markides KS (2007). History of fractures as predictor of subsequent hip and nonhip fractures among older Mexican Americans. Journal of the National Medical Association 99 (4): 412–8.
  9. ↑ 9.0 9.1 Poole KE, Compston JE (December 2006). Osteoporosis and its management. BMJ 333 (7581): 1251–6.
  10. ↑ Berg KM, Kunins HV, Jackson JL et al. (2008). Association between alcohol consumption and both osteoporotic fracture and bone density. Am J Med 121 (5): 406–18.
  11. ↑ Nieves JW (1 May 2005). Osteoporosis: the role of micronutrients.. Am J Clin Nutr 81 (5): 1232S–1239S.
  12. ↑ 12.00 12.01 12.02 12.03 12.04 12.05 12.06 12.07 12.08 12.09 12.10 12.11 12.12 12.13 WHO Scientific Group on the Prevention and Management of Osteoporosis (2000 : Geneva, Switzerland) (2003). Prevention and management of osteoporosis : report of a WHO scientific group. (pdf) URL accessed on 2007-05-31.
  13. ↑ Wong PK, Christie JJ, Wark JD (2007). The effects of smoking on bone health. Clin. Sci. 113 (5): 233–41.
  14. ↑ Jasminka Z. Ilich, PhD, RD and Jane E. Kerstetter, PhD, RD (2000). Nutrition in Bone Health Revisited: A Story Beyond Calcium. Journal of the American College of Nutrition 19 (6): 715–737.
  15. ↑ Shapses SA, Riedt CS (1 June 2006). Bone, body weight, and weight reduction: what are the concerns?. J. Nutr. 136 (6): 1453–6.
  16. ↑ Staessen J, Roels H, Emelianov D, Kuznetsova T, Thijs L, Vangronsveld J, Fagard R (Apr 3 1999). Environmental exposure to cadmium, forearm bone density, and risk of fractures: prospective population study. Public Health and Environmental Exposure to Cadmium (PheeCad) Study Group.. Lancet 353 (9159): 1140–4.
  17. ↑ Tucker KL, Morita K, Qiao N, Hannan MT, Cupples LA, Kiel DP (2006). Colas, but not other carbonated beverages, are associated with low bone mineral density in older women: The Framingham Osteoporosis Study. Am. J. Clin. Nutr. 84 (4): 936–42.
  18. ↑ (2004) Soft drinks in schools. Pediatrics 113 (1 Pt 1): 152–4.
  19. ↑ Waugh EJ, Lam M-A, Hawker GA, et al. (2009). Risk factors for low bone mass in healthy 40–60 year old women: A systematic review of the literature. Osteoporosis International 20: 1–21.
  20. ↑ 20.0 20.1 20.2 20.3 20.4 Simonelli, C et al. (2006). ICSI Health Care Guideline: Diagnosis and Treatment of Osteoporosis, 5th edition. (PDF) Institute for Clinical Systems Improvement. URL accessed on 2008-04-08.
  21. ↑ 21.00 21.01 21.02 21.03 21.04 21.05 21.06 21.07 21.08 21.09 21.10 21.11 Kohlmeier, Lynn Kohlmeier (1998). Osteoporosis - Risk Factors, Screening, and Treatment. Medscape Portals. URL accessed on 2008-05-11.
  22. ↑ 22.0 22.1 22.2 22.3 Ebeling PR (2008). Clinical practice. Osteoporosis in men. N Engl J Med 358 (14): 1474–82.
  23. ↑ Bone and Tooth Society of Great Britain, National Osteoporosis Society, Royal College of Physicians (2003). Glucocorticoid-induced Osteoporosis, London, UK: Royal College of Physicians of London.
  24. ↑ Gourlay M, Franceschini N, Sheyn Y (2007). Prevention and treatment strategies for glucocorticoid-induced osteoporotic fractures. Clin Rheumatol 26 (2): 144–53.
  25. ↑ Petty SJ, O'Brien TJ, Wark JD (2007). Anti-epileptic medication and bone health. Osteoporosis international 18 (2): 129–42.
  26. ↑ Ruiz-Irastorza G, Khamashta MA, Hughes GR (2002). Heparin and osteoporosis during pregnancy: 2002 update. Lupus 11 (10): 680–2.
  27. ↑ Gage BF, Birman-Deych E, Radford MJ, Nilasena DS, Binder EF (2006). Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch. Intern. Med. 166 (2): 241–6.
  28. ↑ Yang YX, Lewis JD, Epstein S, Metz DC (2006). Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA 296: 2947–53.
  29. ↑ Murphy CE, Rodgers PT (2007). Effects of thiazolidinediones on bone loss and fracture. Ann Pharmacother 41 (12): 2014–8.
  30. ↑ Predicting risk of osteoporotic fracture in men and women in England and Wales: prospective derivation and validation of QFractureScores -- Hippisley-Cox and Coupland 339: b4229 -- BMJ.
  31. ↑ www.qfracture.org.
  32. ↑ Leib ES, Lewiecki EM, Binkley N, Hamdy RC (2004). Official positions of the International Society for Clinical Densitometry. J Clin Densitom 7 (1). quoted in: "Diagnosis of osteoporosis in men, premenopausal women, and children"
  33. ↑ U.S. Preventive Services Task Force (2002). Screening for osteoporosis in postmenopausal women: recommendations and rationale. Ann. Intern. Med. 137 (6): 526–8.
  34. ↑ Martínez-Aguilà D, Gómez-Vaquero C, Rozadilla A, Romera M, Narváez J, Nolla JM (2007). Decision rules for selecting women for bone mineral density testing: application in postmenopausal women referred to a bone densitometry unit. J. Rheumatol. 34 (6): 1307–12.
  35. ↑ Schousboe JT, Taylor BC, Fink HA, et al. (2007). Cost-effectiveness of bone densitometry followed by treatment of osteoporosis in older men. JAMA 298 (6): 629–37.
  36. ↑ Lyles KW, Colón-Emeric CS, Magaziner JS, et al. (2007). Zoledronic acid and clinical fractures and mortality after hip fracture. N Engl J Med 357.
  37. ↑ Purcell, P. Boyd, I (2005). Bisphosphonates and osteonecrosis of the jaw. Medical Journal of Australia 182 (8): 417–418.
  38. ↑ (September 2007) "6.6.2 Bisphosphonates" British National Formulary, 54, British Medical Association and Royal Pharmaceutical Society of Great Britain.
  39. ↑ Taranta A, Brama M, Teti A, et al. (February 2002). The selective estrogen receptor modulator raloxifene regulates osteoclast and osteoblast activity in vitro. Bone 30 (2): 368–76.
  40. ↑ Meunier PJ, Vignot E, Garnero P, et al. (1999). Treatment of postmenopausal women with osteoporosis or low bone density with raloxifene. Raloxifene Study Group. Osteoporos Int 10 (4): 330–6.
  41. ↑ Meunier PJ, Roux C, Seeman E, et al. (2004). The effects of strontium ranelate on the risk of vertebral fracture in women with postmenopausal osteoporosis. N. Engl. J. Med. 350 (5): 459–68.
  42. ↑ O'Donnell S, Cranney A, Wells GA, Adachi JD, Reginster JY (2006). Strontium ranelate for preventing and treating postmenopausal osteoporosis. Cochrane database of systematic reviews (Online) (4): CD005326.
  43. ↑ Reginster JY, Seeman E, De Vernejoul MC, et al. (2005). Strontium ranelate reduces the risk of nonvertebral fractures in postmenopausal women with osteoporosis: treatment of peripheral osteoporosis (TROPOS) study.. J Clin Endorinol Metab 90: 2816–22.
  44. ↑ Blake GM, Fogelman I (2007). The correction of BMD measurements for bone strontium content. J Clin Densitom 10 (3): 259–65.
  45. ↑ Nutrition and Bone Health. NIAMS. URL accessed on 2008-01-28.
  46. ↑ (2007). Calcium & Milk. Harvard School of Public Health. URL accessed on 2008-01-28.
  47. ↑ Report of a Joint WHO/FAO/UNU Expert Consultation(2007) Protein and amino acid requirements in human nutrition, pp224-226. ISBN 978-92-4-120935-9
  48. ↑ Report of a Joint WHO/FAO/UNU Expert Consultation(2002), Human Vitamin and Mineral Requirements, pp166-167.
  49. ↑ 49.0 49.1 Tang BM, Eslick GD, Nowson C, Smith C, Bensoussan A (2007). Use of calcium or calcium in combination with vitamin D supplementation to prevent fractures and bone loss in people aged 50 years and older: a meta-analysis. Lancet 370 (9588): 657–66.
  50. ↑ Prince RL, Devine A, Dhaliwal SS, Dick IM (2006). Effects of calcium supplementation on clinical fracture and bone structure: results of a 5-year, double-blind, placebo-controlled trial in elderly women. Arch. Intern. Med. 166 (8): 869–75.
  51. ↑ Bolland MJ, Barber PA, Doughty RN, et al. (2008). Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. BMJ 336.
  52. ↑ Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B (2005). Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials. JAMA 293 (18): 2257–64.
  53. ↑ Jackson RD, LaCroix AZ, Gass M, et al. (2006). Calcium plus vitamin D supplementation and the risk of fractures. N. Engl. J. Med. 354 (7): 669–83.
  54. ↑ Bonaiuti D, Shea B, Iovine R, et al. (2002). Exercise for preventing and treating osteoporosis in postmenopausal women. Cochrane database of systematic reviews (Online) (3): CD000333.
  55. ↑ Houtkooper, L.B., Stanford, V.A., Metcalfe, L.L., Lohman, T.G., and Going, S.B. (2007). Preventing osteoporosis the Bone Estrogen Strength Training way. journal=ACSM's Health & Fitness Journal 11 (1): 21–27.
  56. ↑ Cheng S, Sipilä S, Taaffe DR, Puolakka J, Suominen H (2002). Change in bone mass distribution induced by hormone replacement therapy and high-impact physical exercise in post-menopausal women. Bone 31 (1): 126–35.
  57. ↑ Chien MY, Wu YT, Hsu AT, Yang RS, Lai JS (2000). Efficacy of a 24-week aerobic exercise program for osteopenic postmenopausal women. Calcif. Tissue Int. 67 (6): 443–8.
  58. ↑ Iwamoto J, Takeda T, Ichimura S (2001). Effect of exercise training and detraining on bone mineral density in postmenopausal women with osteoporosis. Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association 6 (2): 128–32.
  59. ↑ Kemmler W, Engelke K, Weineck J, Hensen J, Kalender WA (2003). The Erlangen Fitness Osteoporosis Prevention Study: a controlled exercise trial in early postmenopausal women with low bone density-first-year results. Archives of physical medicine and rehabilitation 84 (5): 673–82.
  60. ↑ Kerr D, Morton A, Dick I, Prince R (1996). Exercise effects on bone mass in postmenopausal women are site-specific and load-dependent. J. Bone Miner. Res. 11 (2): 218–25.
  61. ↑ Villareal DT, Binder EF, Yarasheski KE, et al. (2003). Effects of exercise training added to ongoing hormone replacement therapy on bone mineral density in frail elderly women. J Am Geriatr Soc 51 (7): 985–90.
  62. ↑ Sinaki M, Brey RH, Hughes CA, Larson DR, Kaufman KR (2005). Significant reduction in risk of falls and back pain in osteoporotic-kyphotic women through a Spinal Proprioceptive Extension Exercise Dynamic (SPEED) program. Mayo Clin Proc 80 (7): 849–55.
  63. ↑ Cranney A, Jamal SA, Tsang JF, Josse RG, Leslie WD (2007). Low bone mineral density and fracture burden in postmenopausal women. CMAJ 177 (6): 575–80.
  64. ↑ Hannan EL, Magaziner J, Wang JJ, et al. (2001). Mortality and locomotion 6 months after hospitalization for hip fracture: risk factors and risk-adjusted hospital outcomes. JAMA 285 (21): 2736–42.
  65. ↑ Brenneman SK, Barrett-Connor E, Sajjan S, Markson LE, Siris ES (2006). Impact of recent fracture on health-related quality of life in postmenopausal women. J. Bone Miner. Res. 21 (6): 809–16.
  66. ↑ 66.0 66.1 Riggs, B.L.; Melton, Lj 3.r.d. (2005). The worldwide problem of osteoporosis: insights afforded by epidemiology.. Bone.
  67. ↑ 67.0 67.1 MerckMedicus Modules: Osteoporosis - Epidemiology. Merck & Co., Inc. URL accessed on 2008-06-13.
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  69. ↑ Dalsky GP, Stocke KS, Ehsani AA, Slatopolsky E, Lee WC, Birge SJ (1988). Weight-bearing exercise training and lumbar bone mineral content in postmenopausal women. Ann. Intern. Med. 108 (6): 824–8.
  70. ↑ Feskanich D, Willett WC, Stampfer MJ, Colditz GA (1996). Protein consumption and bone fractures in women. Am. J. Epidemiol. 143 (5): 472–9.
  71. ↑ Kerstetter JE, O'Brien KO, Insogna KL (2003). Dietary protein, calcium metabolism, and skeletal homeostasis revisited. Am. J. Clin. Nutr. 78 (3 Suppl): 584S–592S.
  72. ↑ Lobstein JGCFM. Lehrbuch der pathologischen Anatomie. Stuttgart: Bd II, 1835.
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  74. ↑ Patlak M (2001). Bone builders: the discoveries behind preventing and treating osteoporosis. Faseb J. 15 (10): 1677E–E.
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