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Osteoporosis
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In one pass The easiest thing to miss about osteoporosis is that, day to day, it causes almost no sensation.
Educational content, not medical advice — consult a clinician.
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Chapter 1
Bones thin without warning
Put plainly, osteoporosis means the minerals in bone are carried away year after year and the honeycomb-like support structure inside collapses bit by bit, so the bone becomes porous and brittle and breaks under little force.
The fall it is most feared for is the one that breaks a hip. Within a year of a hip fracture, 20–30% of older adults have died (part of that reflects serious illness they already had, not the fracture alone), and of those who survive, about 40–50% are left with a disability. That is why it counts among the main causes of disability in old age.
The thing most worth remembering is the window after menopause. When menopause arrives, estrogen falls, and bone is lost fastest in the first 5–10 years (roughly −2 to −5% a year). The bone reserve, meaning the highest bone mass of a lifetime, peaks at around age 30. Between 35 and 50 the job is to hold on to it, and at menopause to act early.
Clinical · Where bones break, who is at risk, diagnosis
It helps to recognize the places bones break most easily:Vertebral compression fractures: the most common kind. Some people get sudden back pain; others notice nothing until an X-ray finds it. Over time it can mean losing height and developing a stoop.The hip (around the neck of the thigh bone): the most dangerous site in older adults.The wrist: easily broken when you put out a hand to catch a fall, and often where a middle-aged woman first finds out there is a problem.
Who is at higher risk? Some factors cannot be changed: being female, getting older, a family history, early menopause, a small frame. More can be changed: too little calcium, vitamin D or protein, no exercise, smoking, heavy drinking, very low body weight, and long-term steroid medicines. Later chapters go through how to address them one by one.
How does a doctor decide? Mainly with a bone-density scan (, a low-dose X-ray test). It gives you a score called the T-score: how many standard deviations your sits below the average of young adults. A score of T ≤ −2.5 counts as osteoporosis. Alongside it comes an online tool called FRAX, which estimates your fracture risk over the next 10 years. How DXA and FRAX work together, and which line means a drug should be considered, is at the heart of a doctor's treatment decision.
Clinical · Using FRAX to decide on treatment
FRAX is not a single number but a decision tool. Yet many doctors and patients are not sure how to use it, so here it is step by step.What FRAX asks for (online tool at frax.shef.ac.uk):
Age (40–90)SexWeight and height (used to calculate body mass index, )Any previous fractureA parent who broke a hipCurrent smokingSteroid use (the equivalent of ≥ 5 mg of prednisone a day for ≥ 3 months)Rheumatoid arthritisA cause of secondary osteoporosis (type 1 diabetes, underactive sex glands, overactive parathyroid glands, early menopause and so on)Heavy drinking (≥ 3 units of alcohol a day)The femoral-neck T-score from (optional; it makes the estimate more accurate)
The two results it gives:
The 10-year probability of a major osteoporotic fracture (MOF: hip, spine, upper arm or wrist)The 10-year probability of a hip fracture
Treatment lines (NOF 2014, AACE 2020):
Situations where drug treatment should start without calculating FRAX:
A DXA T-score ≤ −2.5 (at any site: lumbar spine, total hip or femoral neck)Any fragility fracture (spine, hip, wrist or upper arm), even if the T-score is still in the low-bone-mass range
With a T-score between −1.0 and −2.5 (low bone mass, osteopenia), look at FRAX:
A 10-year hip-fracture probability ≥ 3%, orA 10-year major-fracture probability ≥ 20%If either is met, drug treatment is recommendedIf both are below the lines: lifestyle, nutrition and strength training first, no drug for now
Country calibration:
FRAX has calibrated models for more than 80 countries and regions (mainland China has its own models for men and women, and Hong Kong and Taiwan each have their own)The mainland China calibration is based on a 2003 cohort, so with an aging population it may underestimate today's riskSome clinicians look at both the Hong Kong calibration and the DXA T < −2.5 line together
What FRAX cannot include:
How often someone falls, their balance and their eyesightThe trabecular bone score (TBS, a score of the bone's inner structure estimated from the spine DXA image)The shape of the vertebrae and tiny fractures already presentSome secondary causes (chronic kidney disease, how high the steroid dose is)So clinical judgment beyond FRAX is needed: people who fall repeatedly, have a very strong family history or show abnormal spine imaging may be treated even when FRAX is low
Putting it together as one decision path:
Any fragility fracture (spine, hip, wrist or upper arm): treatment should start, and the T-score no longer decides.DXA T ≤ −2.5: treatment should start.DXA T between −1.0 and −2.5: calculate FRAX. Hip ≥ 3% or MOF ≥ 20% means treat; below both lines, nutrition and exercise first, with a repeat DXA every 2 years.DXA T > −1.0: nutrition, exercise and prevention; for people with normal , the gap before the next scan can be longer, set by the doctor according to risk.
Should you have a DXA scan? (NOF 2014):
Women ≥ 65 and men ≥ 70: routine screeningWomen under 65 and men under 70: usually only with at least 1 major risk factor (early menopause, steroid use, a family history of fragility fracture, BMI < 18.5, smoking)Not casually: screening young people without symptoms achieves little
Chapter 2
How bone is broken down and rebuilt
The orders come from the building side itself (including the osteocytes buried in the bone), which sends out two opposite signals:
One is , the order to start work: it docks on a receptor of the osteoclasts and wakes up the demolition crew.The other is OPG, a decoy receptor: it looks like that receptor and grabs RANKL first, so the order never reaches the osteoclasts.
Whether bone grows or shrinks depends on which signal wins. Estrogen normally keeps OPG up and RANKL down, so when it withdraws after menopause, the balance tips toward removal; long-term steroid use and chronic inflammation push the same way. Putting mechanical load on bone, meaning strength training and exercise with impact, adds weight to the side that preserves bone. Calcium, vitamin D and protein are the building materials, not the switches for these signals.
Mechanism · Menopause and the osteoclast's acid pit
This is exactly why the window after menopause is so fierce. In the first year after menopause, estrogen drops sharply, rises and OPG falls, and the ratio between them jumps to 2–3 times what it was; bone is lost fastest in the first 5–10 years (about −2 to −5% a year). So the time that most needs action is not after a bone-density scan at 65, but the first year of menopause, when assessment and training should begin.Look more closely at how an osteoclast actually takes bone apart. It clamps onto the bone surface like a suction cup, seals off a small pit and pumps acid into it until the pit reaches pH 4.5. The calcium salt of bone (hydroxyapatite) dissolves in acid that strong, calcium and phosphate are released, and dedicated enzymes then digest the remaining collagen. Remember this acid pit: the most commonly used class of osteoporosis drugs, the bisphosphonates, exploits it.
Mechanism · The four-step trap of bisphosphonates
Bisphosphonates, the classic class of drugs, work a four-step trap that turns the osteoclast's own job against it:1. Lie in wait on the bone surface: they bind extremely strongly to bone's calcium salt, and once attached they can stay for years, even more than a decade.
2. Stay silent: as long as no osteoclast comes to break down that patch of bone, the drug just lies there and does nothing.
3. Wait to be swallowed: when an osteoclast starts breaking down that patch, it swallows the drug along with the bone; once the acid pit dissolves the mineral, the drug is inside the cell.
4. Make the demolition worker self-destruct: inside the cell the drug cuts a key production line, the osteoclast's internal scaffolding can no longer hold, and after about 48–72 hours the cell dies by apoptosis. The demolition crew is trimmed back with precision.
Randomized trials back the effect, all in women with postmenopausal osteoporosis. Zoledronic acid (5 mg by intravenous drip once a year; Black 2007, NEJM, the HORIZON trial) reduced vertebral fractures by 70% and hip fractures by 41% in relative terms. Another drug works on the line: denosumab, an antibody against RANKL given as a 60 mg injection under the skin every six months (Cummings 2009, NEJM, the FREEDOM trial), reduced vertebral fractures by 68% and hip fractures by 40% in relative terms.
Safety · Stopping denosumab can rebound
Denosumab has a rebound trap you have to remember: once it is stopped, the signal that was being held down surges back within 6–12 months, and several vertebral fractures can happen at once. So it cannot simply be stopped; a bisphosphonate is usually used to take over and bridge the transition.And do not forget that drugs are not the finish line. Between 35 and 50, nutrition, strength training and a sensible body weight hold on to the bone reserve; at menopause, evaluate hormone therapy early (see Perimenopause), together with strength training and enough calcium and vitamin D. Drugs and exercise do not replace each other: drugs lower fractures, while training gives bone and muscle mechanical stimulus and reduces falls. For someone who already has osteoporosis or has had a fragility fracture, eating and training do not replace the drug either.
Chapter 3
How food and strength training help
The first three are materials. Calcium is the brick bone is built from; get it first from milk, yogurt, cheese, dark leafy greens, tofu set with calcium and small fish eaten with their bones. Vitamin D helps the gut absorb calcium. Protein is raw material shared by bone and muscle. The idea that older people should eat less meat is a harmful myth: without enough protein, muscle and bone decline together.
The fourth, strength training, is the only one of the four that sends bone a direct signal: the more load bone takes, the more bone-building cells are called in to reinforce it. Walking alone is not enough; you need resistance training (squats, deadlifts, presses, rows) plus movements with impact. But in adults, the gain in is limited, far smaller than with drugs, and much of its benefit for fractures comes from stronger muscles and better balance, which mean fewer falls. So alongside strength training, fall prevention has to be part of the plan.
Numbers · How much calcium, vitamin D and protein
Calcium: after 50, women need about 1200 mg a day and men 1000–1200 mg, preferably from food. If you do take a supplement, remember two things: no more than 500 mg at a time (split doses are absorbed better), taken with meals; and there is no need to push past 1200 mg, because there is no evidence that more protects bone better. The effect of calcium supplements on fractures is small to begin with: in Bolland 2015's BMJ systematic review, calcium supplements reduced total fractures by only about 11%. As for the old dispute over calcium harming the heart: it came from Bolland 2010's , and in 2016 the National Osteoporosis Foundation (NOF) and the American Society for Preventive Cardiology (ASPC) reviewed it and concluded that calcium within the tolerable upper intake level, from food or supplements, is neutral for cardiovascular health. Food first is still worth sticking to, but the reason is overall nutrition, not cardiovascular risk.Vitamin D: over 50, usually 800–1000 a day, more for people who are quite deficient. A blood of at least 20 ng/mL (50 nmol/L) is enough for most people, and there is no need to chase higher. Sun, food and supplements all play a part.
Protein: healthy older adults need 1.0–1.2 g/kg of body weight a day; people recovering from a fracture or living with a chronic illness need 1.2–1.5 g/kg. It also helps to spread 25–40 g of protein onto each meal, which makes it easier to switch on muscle building.
In practice · How much to train, how not to fall
Strength training 2–3 times a week, with both resistance and impact. How bone responds to impact has been measured most cleanly in children: 100 jumps off a 61 cm box, 3 times a week, and after 7 months the bone mineral content at the femoral neck had risen 4.5% more than in the control group (Fuchs 2001, a randomized trial in 89 children around the start of school age). The effect in adults is much smaller, but it points the same way. Do not stop after 70; switch to a low-impact version and keep going.Fall prevention matters as much as strength training, and the dose decides the benefit. Pooling every exercise program, the fall rate in older adults dropped by about 21%; programs that both challenged balance and ran more than 3 hours a week cut it by about 39% (Sherrington 2017, 88 trials, 19,478 people). No effect was seen in older adults living in care homes and similar residential settings. Tai chi and standing on one leg are the balance-challenging half; the other half is putting in enough hours. At home, add anti-slip mats, handrails and bright enough lighting; get glasses fitted, have your hearing checked, and cut down on sedatives that make you dizzy. Strength, balance and fall prevention are the three pillars of bone health in older age.
Safety · Other nutrients, and pitfalls to avoid
The rest are extras: add them only if you are short, and do not stack them up. Vitamin helps activate osteocalcin, a protein that helps calcium bind into the bone matrix (natto has the most; a common dose is at 90–180 µg a day). But whether taking K2 reduces fractures, or keeps calcium from depositing in artery walls, is still unsettled in trials (see Vitamin K2). Magnesium (about 320–420 mg a day), zinc, B12 and folate also take part in building bone, and a varied diet is usually enough.Finally, two pitfalls to avoid on purpose. The first is smoking and alcohol: smoking lowers estrogen and directly drags down bone building, and more than 30 g of alcohol a day both reduces bone formation and makes falls more likely. The second is that some long-term medicines also harm bone, such as the acid-suppressing proton pump inhibitors (, which affect calcium and magnesium absorption) and steroids (which drain bone especially fast). Do not stop them on your own, but talk to your doctor about the dose and how long you take them, and make sure your calcium and vitamin D are adequate at the same time.
Chapter 4
Men, and bone loss from other causes
Men first. About 1/4 of men will have a fracture from osteoporosis in their lifetime (1/2 of women). That sounds lower, but once a man breaks a hip, his death rate within 1 year is actually higher (30–40%), because the problem is often found late and he often has other illnesses too. Yet fewer than 20% of men get a bone-density test (about 50% of women), which leaves a large gap nobody is watching.
Many men lose time to the line men don't get osteoporosis: I can still walk, it can't be that bad. They shrug off the first fracture and miss the chance to prevent a second. So any man who breaks a bone from a minor knock, a fragility fracture, should have his checked soon and be checked for an underlying disease. Do not wait for the second fall.
Clinical · Causes of secondary osteoporosis
A good share of osteoporosis is a side effect of another disease or a medicine. In men these secondary causes account for about 60% of cases (about 30% in women), quite a bit higher; finding them often means the cause can be treated and bone mass can even recover. The common groups, so you have a map:Hormones: low testosterone in men is the most common, and most reversible, cause; an overactive thyroid, overactive parathyroid glands and Cushing's syndrome can also quietly drain bone.Medicines: long-term steroids (the equivalent of 5 mg of prednisone a day for 3 months or more) are the leading medicine-related cause; acid-suppressing proton pump inhibitors and some anti-seizure drugs also harm bone; androgen-deprivation therapy for prostate cancer (ADT, which pushes testosterone very low) drains bone especially hard, and bone protection has to run alongside it.Other diseases: chronic kidney disease, celiac disease (poor absorption) and multiple myeloma. If someone aged 50 or over has unexplained bone pain, or a pathological fracture from a minor knock, the doctor will look especially carefully for myeloma.Lifestyle: heavy drinking, smoking and vitamin D deficiency.
Clinical · How treatment changes once a cause is found
Once a specific cause is found, the plan changes with it. A few of these touch on safety and are worth remembering:Steroid-induced osteoporosis (GIOP): start a bisphosphonate early, with calcium and vitamin D; do not wait until has fallen a long way.Low testosterone plus osteoporosis in men: testosterone replacement therapy () can be considered, but if testosterone is only borderline low and the symptoms are unclear, do not start it lightly.Overactive parathyroid glands: after the adenoma is removed surgically, the osteoporosis often improves on its own.Chronic kidney disease: once kidney function is poor enough ( < 30), ordinary bisphosphonates cannot be used, and the usual switch is to denosumab or to conservative care first. Denosumab needs no dose change for kidney function, but people in this group have a higher risk of severe low blood calcium on it, so blood calcium and vitamin D should be corrected first and blood calcium checked after the injection.Celiac disease: a strict Gluten-Free diet plus replacing the missing nutrients often brings bone density clearly back up within 1–2 years.
Chapter 5
When to take drugs, and which
The first choice is the bisphosphonates: cheap, with the deepest evidence. They work by holding back the demolition crew: when osteoclasts break down bone they swallow the drug along with it, bone breakdown slows, and bone density rises. The usual form is an alendronate tablet once a week; people with esophageal trouble, or who keep forgetting their pills, can switch to a once-a-year intravenous drip of zoledronic acid.
Taking the tablets involves two steps that must be followed: swallow on an empty stomach with a large glass of water, and stay upright afterward rather than lying down, because a tablet stuck on the esophagus can burn an ulcer into it. With long-term use there are two rare but important problems, osteonecrosis of the jaw and atypical femur fractures, so after a few years doctors usually schedule a drug holiday, and only people at high risk keep taking it.
The other classes of drugs (denosumab, injected bone-building drugs, and estrogen-related drugs) each have their own patients and their own hard warnings.
Clinical · When to start a drug
Drug treatment is for people at high risk and people who have already had a fracture. If any one of the lines below is met, guidelines such as the Endocrine Society's 2020 guideline recommend starting:T ≤ −2.5 (at any site)A previous fragility fracture, with a T-score between −2.5 and −1.0 (low bone mass plus a fracture)A FRAX 10-year hip-fracture probability ≥ 3%, or a major-fracture probability ≥ 20%
Clinical · Bisphosphonate doses and how long to take them
Drugs and doses:Alendronate 70 mg once a week: the first choice among tablets, and cheap. Other drugs in the same class are risedronate and ibandronate.Zoledronic acid 5 mg by intravenous drip once a year (Black 2007, NEJM, the HORIZON trial): for people who cannot take tablets or find it hard to keep taking them; it reduced the risk of vertebral fractures by 70% in relative terms.
How to take it: take the tablets on an empty stomach with a large glass of water, then stand or sit upright for 30 minutes, so the tablet does not sit on the esophagus.
Side effects: the tablets irritate the esophagus; long-term use (≥ 5 years) carries rare risks of osteonecrosis of the jaw (ONJ) and atypical femur fracture (AFF).
How long: usually 3–5 years, followed by a drug holiday of 1–2 years; people at high risk continue.
Clinical · Denosumab and bone-building drugs
Denosumab is a monoclonal antibody against (Cummings 2009, NEJM, the FREEDOM trial). For the background on RANKL and OPG, see How bone is broken down and rebuilt.By blocking RANKL, it keeps osteoclasts from maturing.It is given as a 60 mg injection under the skin every 6 months.It is potent: vertebral fractures fell by 68% and hip fractures by 40% in relative terms.Key warning: after stopping, drops quickly and a rebound of multiple vertebral fractures can occur, so a bisphosphonate is usually used to take over; it must not simply be stopped.It suits people willing to stay on long-term treatment who cannot use bisphosphonates, for example people with very poor kidney function.
Teriparatide and abaloparatide (parathyroid-hormone analogues):
They stimulate osteoblasts and truly build bone, rather than only slowing its breakdown.They are injected under the skin, are expensive, and are used for severe osteoporosis with several fractures already.Treatment usually lasts about 2 years. In 2020 the US label for teriparatide dropped the hard lifetime limit of 2 years, but going beyond 2 years still calls for a doctor to reassess fracture risk first; the label for abaloparatide still advises against more than 2 years of cumulative use. Afterward, a drug that curbs bone breakdown (a bisphosphonate or denosumab) is used to lock in the bone gained.They are not suitable for people who have had osteosarcoma, whose bones have been irradiated, or who have high blood calcium.
Romosozumab (a monoclonal antibody against sclerostin):
It works in two directions: sclerostin normally holds back bone building, and blocking it means more bone is built and less is broken down.It is injected under the skin once a month for 12 months, then followed by a bisphosphonate.It is potent: in the ARCH trial it raised bone density more, and reduced fractures more, than alendronate. There is no head-to-head comparison with denosumab using fractures as the endpoint.Cardiovascular warning: serious cardiovascular events were slightly higher in the ARCH trial, and people who have had a heart attack or stroke in the past year should not use it.
Clinical · Hormone-based drugs and long-term care
Estrogen and selective estrogen receptor modulators (SERMs):Menopausal hormone therapy: the balance of benefit and risk is most favorable when it is started early in the menopausal transition, between the ages of 50 and 59, and used short term (see Perimenopause).Raloxifene (a SERM): prevents vertebral fractures and lowers the risk of breast cancer, but raises the risk of blood clots in the veins (VTE).Bazedoxifene combined with estrogen.
Osteoporosis in men:
Men, and bone loss from other causes covers the details. Bisphosphonates, calcium, vitamin D and strength training apply just the same.If testosterone is low: testosterone replacement can be evaluated, with strict criteria (see Andropause).
How long to treat, and long-term care:
Reassess after 3–5 years of treatment.During a drug holiday, repeat the scan and check markers of bone turnover: CTX (which reflects how fast bone is broken down) and P1NP (which reflects how fast bone is built).Care works best across several specialties: endocrinology, rheumatology, geriatrics, nutrition and rehabilitation.
In practice · A drug-choice table and a self-check
A drug-choice table:| Situation | First choice | Alternatives |
|---|---|---|
| Postmenopausal osteoporosis, no contraindications | Alendronate tablets | Risedronate, zoledronic acid by drip |
| Esophageal problems, trouble keeping up with tablets | Zoledronic acid once a year, denosumab | — |
| Chronic kidney disease (eGFR < 30) | Denosumab (no dose change for kidney function; guard against severe low calcium) | — |
| Severe osteoporosis, several vertebral fractures | Teriparatide or romosozumab, then a bisphosphonate | Denosumab |
| Cardiovascular disease | A bisphosphonate (avoid romosozumab after a heart attack or stroke in the past year) | Denosumab |
| Osteoporosis in men | Alendronate, zoledronic acid, denosumab | Add testosterone replacement if testosterone is low |
| Steroid-induced osteoporosis | Risedronate, zoledronic acid | Make sure calcium and vitamin D are adequate |
Abbreviation in the table: is the estimated glomerular filtration rate, a measure of kidney function.
Self-check:
If you are more than 4 cm shorter than when you were young, it may be a vertebral compression fracture; an X-ray is advisable.A stoop together with chronic back pain calls for imaging.Any fragility fracture (a bone broken in a minor fall) calls for a scan and a full assessment soon.
Related stories (see Calcium, Vitamin D, Vitamin K2, see Protein & Amino Acids, see Sarcopenia): calcium, vitamin D, and protein are the materials bone is built from, and muscle decides whether you fall. For how long-term acid-suppressing drugs affect calcium absorption, see the story on reflux (see GERD).
References · 8
- Compston, J. E., McClung, M. R., & Leslie, W. D. (2019). Osteoporosis. The Lancet, 393(10169), 364-376. 10.1016/S0140-6736(18)32112-3
- Wang, L., Yu, W., Yin, X., Cui, L., Tang, S., Jiang, N., et al. (2021). Prevalence of osteoporosis and fracture in China: the China Osteoporosis Prevalence Study. JAMA Network Open, 4(8), e2121106. n=20,416, fieldwork 2017-2018. Aged 40+: osteoporosis in 20.6% of women (95% CI 19.3-22.0) and 5.0% of men (4.2-5.8); vertebral fracture 10.5% of men and 9.7% of women — nearly identical between the sexes. Only 1.4% of women and 0.3% of men with osteoporosis or fracture were on treatment. 10.1001/jamanetworkopen.2021.21106
- Cummings, S. R., San Martin, J., McClung, M. R., Siris, E. S., Eastell, R., Reid, I. R., et al. (2009). Denosumab for prevention of fractures in postmenopausal women with osteoporosis. New England Journal of Medicine, 361(8), 756-765. 10.1056/NEJMoa0809493
- Black, D. M., Delmas, P. D., Eastell, R., Reid, I. R., Boonen, S., Cauley, J. A., et al. (2007). Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. New England Journal of Medicine, 356(18), 1809-1822. 10.1056/NEJMoa067312
- Fuchs, R. K., Bauer, J. J., & Snow, C. M. (2001). Jumping improves hip and lumbar spine bone mass in prepubescent children: a randomized controlled trial. Journal of Bone and Mineral Research, 16(1), 148-156. ⚠️ POPULATION: 89 PREPUBESCENT CHILDREN aged 5.9-9.8 years, 100 jumps from a 61 cm box, 3×/week for 7 months. It is not a study of women under 50, and the site used to present it as one. 10.1359/jbmr.2001.16.1.148
- Sherrington, C., Michaleff, Z. A., Fairhall, N., Paul, S. S., Tiedemann, A., Whitney, J., et al. (2017). Exercise to prevent falls in older adults: an updated systematic review and meta-analysis. British Journal of Sports Medicine, 51(24), 1750-1758. 99 comparisons from 88 trials, 19,478 participants. ⚠️ THE DOSE IS THE FINDING: exercise overall cut the fall RATE by 21% (RR 0.79, 95% CI 0.73-0.85); programmes that BOTH challenged balance AND ran more than 3 h/week cut it 39% (IRR 0.61, 0.53-0.72), and those two variables explained 76% of the between-trial heterogeneity. No effect was seen in residential care, stroke survivors, or people recently discharged from hospital. 10.1136/bjsports-2016-096547
- Bolland, M. J., Avenell, A., Baron, J. A., Grey, A., MacLennan, G. S., Gamble, G. D., & Reid, I. R. (2010). Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ, 341, c3691. 10.1136/bmj.c3691
- Cosman, F., de Beur, S. J., LeBoff, M. S., Lewiecki, E. M., Tanner, B., Randall, S., & Lindsay, R. (2014). Clinician's Guide to Prevention and Treatment of Osteoporosis. Osteoporosis International, 25(10), 2359-2381. 10.1007/s00198-014-2794-2