Osteoporosis resident survival guide
For details about osteoporosis click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]
| Osteoporosis Resident Survival Guide Microchapters |
|---|
| Overview |
| Classification |
| Causes |
| FIRE |
| Diagnosis |
| Treatment |
| Do's |
| Don'ts |
Overview
Osteoporosis was first discovered by John Hunter, British surgeon, in 1800's. Osteoporosis may be classified as primary or secondary, based on etiology; while, it is divided in to osteopenia, osteoporosis, and severe osteoporosis, based on disease severity. Osteoporosis occurs as result of an imbalance between bone resorption and bone formation. Major contributing factors to the development of osteoporosis include estrogen deficiency and aging. These factors might lead to osteoporosis by reactive oxygen species (ROS) mediated damage to osteocytes. Decrease in the capability of autophagy in osteocytes is another important factor which makes them vulnerable to oxidative stress. Genes involved in the pathogenesis of osteoporosis can be categorized in four main groups which include the osteoblast regulatory genes, osteoclast regulatory genes, bone matrix elements genes, and hormone/receptor genes. Osteoporosis must be differentiated from other diseases associated with a decrease in bone mineral density (BMD) such as idiopathic transient osteoporosis of hip, osteomalacia, scurvy, osteogenesis imperfecta, multiple myeloma, homocystinuria, and hypermetabolic resorptive osteoporosis. Osteoporosis is a major health problem involving 43.9% (43.4 million) of male and female population in the United States. Risk of osteoporosis increases with age. Osteoporosis usually involves individuals of age 80 years and older. White females and African-American males have the highest incidence among other races. Risk factors for osteoporosis are of two types, non-modifiable and modifiable factors. Non-modifiable risk factors include age, sex, menopause, and family history. Modifiable risk factors include smoking, alcohol consumption, immobility, glucocorticoid abuse, and use of proton pump inhibitor (PPI). Risk of fracture due to osteoporosis threatens every second postmenopausal women and every fifth old man. The 10-year risk for any osteoporosis-related fracture in 65-year-old white woman with no other risk factor is 9.3%. According to USPSTF guidelines, all women ≥ 65 years along with women < 65 years old with high risk of fracture must be screened for osteoporosis. There is no recommendation to screen men for osteoporosis. Screening for osteoporosis can be done by dual energy x-ray absorptiometry (DXA) of both hips and lumbar spine, and quantitative ultrasonography of the calcaneus. If left untreated, most of the patients with osteoporosis may develop fractures. With appropriate and timely usage of medications along with calcium and/or vitamin D supplementation, the outcome of osteoporosis is usually good. Apart from risk of death and other complications, osteoporotic fractures are associated with a decreased quality of life secondary to immobility and emotional disturbances. The impact of osteoporosis and osteoporotic fractures on human life becomes intense with aging. There are various lifestyle modifications that can prevent the development of osteoporosis, these include calcium and vitamin D supplementation, diet, exercise, smoking cessation, minimizing alcohol consumption, and fall prevention. The mainstay of treatment in primary osteoporosis is lifestyle modifications. High risk patients and patients with past history of osteoporotic fracture, require medical therapy. Bisphosphonates are the first line treatment for osteoporosis. Raloxifene is the second line treatment for osteoporosis in postmenopausal women and is also used for prevention. Denosumab is a human monoclonal antibody designed to inhibit RANKL (RANK ligand), a protein that acts as the primary signal for bone removal. Denosumab is used to treat osteoporosis in elder men and postmenopausal women. Teriparatide and abaloparatide are human recombinant parathyroid hormones used to treat postmenopausal woman with osteoporosis at high risk of fracture or to increase bone mass in men with osteoporosis.
Classification
Osteoporosis may be classified into several subtypes based on disease origin, and disease severity. Osteoporosis may be classified into several subtypes based on disease origin, and disease severity.
| Osteoporosis classifications | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Based on Severity | Based on Etiology | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Children and Adolescents | Adults | Children, Adolescents, and Adults | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Z-score measurement | T-score measurement | Bone loss due to other diseases? | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Z-score > -2.0 without fracture history | Z-score < -2.0 and significant fracture history (2 or more long bone fractures before 10 years of age or 3 or more long bone fractures before 19 years of age) OR One or more vertebral fractures occurring in the absence of local disease or high-energy trauma | -1 > T-score > -2.5 | T-score ≤ -2.5 | T-score ≤ -2.5 plus history of fracture | No | Yes | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Normal | Osteoporosis | Osteopenia | Osteoporosis | Severe osteoporosis | Primary osteoporosis | Secondary osteoporosis | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Juvenile Osteoporosis (JO)
Osteoporosis in children and adolescents is rare, usually is due to some comorbidities or medications, secondary osteoporosis. Surprisingly, no significant causes have been found for rare cases, idiopathic osteoporosis.
No matter what causes it, juvenile osteoporosis can be a significant problem because it occurs during the child’s prime bone-building years. From birth through young adulthood, children steadily accumulate bone mass, which peaks sometime before age 30. The greater their peak bone mass, the lower their risk for osteoporosis later in life. After people reach their mid thirties, bone mass typically begins to decline—very slowly at first but increasing in their fifties and sixties. Both heredity and lifestyle choices—especially the amount of calcium in the diet and the level of physical activity influence the development of peak bone mass and the rate at which bone is lost later in life.
Secondary Osteoporosis
As the primary condition, juvenile idiopathic arthritis (also known as juvenile rheumatoid arthritis) provides a good illustration of the possible causes of secondary osteoporosis. In some cases, the disease process itself can cause osteoporosis. In other cases, medication used to treat the primary disorder may reduce bone mass. For example, drugs such as prednisone, used to treat severe cases of juvenile idiopathic arthritis, negatively affect bone mass. Finally, some behaviors associated with the primary disorder may lead to bone loss or reduction in bone formation. For example, a child with juvenile idiopathic arthritis may avoid physical activity, which is necessary for building and maintaining bone mass, because it may aggravate his or her condition or cause pain.[1]
Idiopathic Juvenile Osteoporosis
Idiopathic juvenile osteoporosis (IJO) is a primary condition with no known cause. It is diagnosed after other causes of juvenile osteoporosis have been excluded. This rare form of osteoporosis typically occurs just before the onset of puberty in previously healthy children. The average age at onset is 7 years, with a range of 1 to 13 years. Most children experience complete recovery of bone.
Causes
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of osteoporosis, however complications resulting from untreated osteoporosis are common.
Common and Less Common Causes
FIRE: Focused Initial Rapid Evaluation
Osteoporosis; prevention, diagnosis, and management[14][15][16][17][18]
| Lifestyle modifications | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Exercise | Calcium Supplementation | Vitamin D supplementation | Smoking cessation | Reduced alcohol consumption | Hip protectors | Fall protection | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| • Balance, strength and functional training exercises | Women • 9-18 yrs: 1,300 mg • 19-50 yrs: 1,000 mg • 51-70 yrs: 1,200 mg • 71 and more yrs: 1,200 mg Men • 50-70 yrs: 1,000 mg • 71 and more yrs: 1,200 mg | Women • 9-18 yrs: 600 IU • 19-50 yrs: 600 IU • 51-70 yrs: 600 IU • 71 and more yrs: 800 IU Men • More than 50 yrs: 800-1,000 IU • Serum vitamin D level of 20 ng per mL (50 nmol per L) is recommended for good bone health | • Stop-smoking program and nicotine patch | Limit to: • One drink/day for women • Two drinks/day for men • Moderate alcohol may associated with slightly higher BMD and lower fracture risk in postmenopausal women | • Hard and soft hip protectors, upon preference | Multifactorial interventions: • Individual risk assessment • Tai Chi Chuan and other exercise programs • Home safety assessment and modification by an occupational therapist • Gradual withdrawal of psychotropic medication • Visual impairment correction • Improve mobility | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Chronic glucocorticoid (GC) use | Children and adolescent | Adults | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Children | < 40 yrs | ≥ 40 yrs | Men | Women | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Clinical fracture risk assessment: • Within 6 months of the start of GC treatment • Every 12 months during GC treatment • No need to bone mineral density measurement | As soon as possible but at least within 6 months of the initiation of GC treatment if: • High fracture risk • Significant osteoporotic risk factors (malnutrition, significant weight loss or low body weight, hypogonadism, secondary hyperparathyroidism, thyroid disease, family history of hip fracture, smoking, alcohol use) Every 2-3 yrs of GC treatment if: • Moderate-to-high fracture risk •• History of previous fracture •• BMD Z score < -3 •• Received very high-dose prednisone [≥30 mg/day and cumulative dose >5 gm] •• Risks for poor medication adherence or absorption •• Multiple osteoporotic risk factors | As soon as possible but at least within 6 months of the initiation of GC treatment: • FRAX with glucocorticoid dose correction Every 1-3 yrs of GC treatment if: • Continued GC treatment and are not treated with an osteoporosis medication beyond calcium and vitamin D • Receiving very high doses of GCs (initial prednisone dose ≥30 mg/day, cumulative dose > 5 gm in the previous year) • Positive history of osteoporotic fracture Every 2-3 yrs of GC treatment if: • Continued GC treatment and are currently treated with an osteoporosis medication in addition to calcium and vitamin D • Receiving very high doses of GCs (initial prednisone dose ≥ 30 mg/day, cumulative dose > 5 gm in the previous year) • Positive history of osteoporotic fracture occurring after ≥ 18 months of treatment with antifracture medication (other than calcium and vitamin D) • Risks for poor medication adherence or absorption • Other significant osteoporotic risk factors | • 18 yrs of age or 2 yrs after chemotherapy • Severe diseases • Low body weight • Chronic corticosteroid use • Delayed puberty • Gonadal failure • History of low-impact fracture | • Young Hypogonadal • More than 70 yrs • Less than 70 yrs with: ••Low body weight ••Prior fracture ••High risk medication use ••Disease or condition associated with bone loss | • More than 65 yrs • Postmenopausal women younger than 65 yrs with: ••History of fragility fracture •• Weigh less than 127 lb (58 kg) ••Medications or diseases that cause bone loss •• Parental history of hip fracture •• smoking •• Alcoholism •• Rheumatoid arthritis. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Dual energy X-ray absorptiometry (DEXA) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Under glucocorticoid therapy | No glucocorticoid therapy | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Calcium and vitamin D and life style modification | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Low risk | Moderate/High risk | Children | Adults | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| No further treatment Monitor with yearly fracture risk assessment with BMD testing every 2-3 years depending on risk factors | Age < 40 years 1. History of osteoporotic fracture, OR 2. Z score < -3 at hip or spine and prednisolone ≥ 7.5 mg/d, OR 3. >10%/year loss of BMD at hip or spine and prednisolone ≥ 7.5 mg/d, OR 4. Very high dose glucocorticoid and > 10 years | Age ≥ 40 years 1. History of osteoporotic fracture, OR 2. Men > 50 years and postmenopausal women with a BMD T-score ≤ -2.5, OR 3. FRAX 10-year risk for major osteoporotic fracture > 10%, OR 4. FRAX 10-year risk for hip osteoporotic fracture > 1%, OR 5. Very high dose of glucocorticoid | BMD T-score is not used for children until 20 yrs of age Osteoporosis defined as: • One or more vertebral fractures occurring in the absence of local disease or high-energy trauma • low bone density (BMD Z-scores < –2.0) and a significant fracture history (2 or more long bone fractures before 10 years of age or 3 or more long bone fractures before 19 years of age) | BMD<-2.5 OR -2.5 < BMD < -1 with 10-year risk of major osteoporotic fracture of at least 20% or a risk of hip fracture of at least 3% | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| • Treat with an oral bisphosphonate • Second-line therapy: teriparatide • Other suggested therapies (in order of preference) for high risk woman for whom the previous drugs are not appropriate: IV bisphosphonate Denosumab | • Treat with an oral bisphosphonate • Other suggested therapies (in order of preference): IV bisphosphonate Teriparatide Denosumab Raloxifene for postmenopausal women if no other therapy is available | Calcium daily intake: • 500 mg for children 1 to 3 years of age • 800 mg for children 4 to 8 years of age • 1300 mg for children and adolescents 9 to 18 years of age Weight-bearing activity and Short periods of high-intensity exercise • Jumping 10 minutes/day, 3 times/week Inflammatory bowel disease (IBD) • Anti tumor necrosis factor alpha (TNF-α) Moderate to severe osteogenesis imperfecta (2 or more fractures in a year or vertebral compression fractures) • Bisphosphonate | • Treat with an oral bisphosphonate Alendronate Risedronate • If patient has GI problem IV bisphosphonate Zoledronic acid • If patient not tolerate bisphosphonate Teriparatide Denosumab | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Pharmacotherapy efficacy
| Pharmacotherapy efficacy
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Diagnosis
- Osteoporosis has not any symptoms, until the patient encounters an osteoporotic fracture. The main symptom of osteoporotic fracture is bone pain.
- Due to the pathophysiology of the disease, neither physical examination nor laboratory studies are not diagnostic in osteoporosis. The main route of diagnosis is through measuring bone mineral density (BMD) by means of imaging studies.
- The most important modality for measuring bone mineral density (BMD), that every osteoporosis diagnostic and therapeutic decision are based on, is dual energy X-ray absorptiometry (DEXA).[19] DEXA is a 2-dimensional image of a 3-demensional subject, mainly depends on size of the bone which is studied; therefore, it would explain the variety of BMD upon sex, body weight, and also ethnicity.[20]
- Upon the world health organization (WHO) report in 1994, using T-score (standard deviations (SD) below or above the average of young Caucasian women), BMD measures are divided into three groups, include:
- T-score greater than -1.0 SD assumed as normal BMD
- T-score between -1.0 and -2.5 SD assumed as osteopenia
- T-score less than -2.5 SD assumed as osteoporosis[21]
- Z-score is same as the T-score, but the target population is matched for age, sex, race, and also in some studies, weight.
- Upon the world health organization (WHO) report in 1994, using T-score (standard deviations (SD) below or above the average of young Caucasian women), BMD measures are divided into three groups, include:
- The preferred skeletal sites for DXA measurements in children are lumbar spine (L1–4) and total body, not including the head. The cranium should be excluded from the total body scan analysis, because the head constitutes a large portion of the total body bone mass but changes little with growth, activity, or disease; inclusion of the skull potentially masks gains or losses at other skeletal sites.
- There are many other imaging modalities that are more precise than DXA, but used only in specific situations upon various disadvantages. They are including:
- Plain X-ray radiography
- Volumetric quantitative CT scan (vQCT)
- High resolution CT scan (hrCT)
- Micro CT scan (μCT)
- Magnetic resonance imaging (MRI)
- Quantitative ultrasound of olecranon
- Finite element modelling (FEM)
Treatment
Lifestyle modifications
| Intervention | Effect on outcomes[16] | ||
|---|---|---|---|
| Bone mineral density (BMD) | Spine fracture | Hip fracture | |
| Exercise | Highly effective | Moderately effective | Moderately effective |
| Calcium (± vitamin D) supplements | Highly effective | Moderately effective | Moderately effective |
| Dietary calcium | Moderately effective | Moderately effective | Moderately effective |
| Smoking cessation | Moderately effective | Moderately effective | Moderately effective |
| Reduced alcohol consumption | Mildly effective | Mildly effective | Moderately effective |
| Fall prevention programmes | - | Mildly effective | Mildly effective |
| Hip protectors | - | - | Moderately effective |
Pharmacotherapy
| Group[18] | Drug (brand) | Dosage | Route | Usage | Interval | Contraindications |
|---|---|---|---|---|---|---|
| Bisphosphonate | Alendronate (Fosamax) | 35 mg (7×5 gm) | Per oral (PO) | Prevention | Weekly (7×daily) |
|
| 70 mg (7×10 mg) | PO | Treatment | Weekly (7×daily) | |||
| Alendronate/cholecalciferol
(Fosamax Plus D) |
70 mg plus 2,800 IU
70 mg plus 5,600 IU |
PO | Treatment | Weekly | ||
| Risedronate (Atelvia) | 35 mg (delayed release) | PO | Treatment | Weekly | ||
| Risedronate (Actonel) | 35 mg | PO | Prevention and treatment | Weekly | ||
| 150 mg | PO | Monthly | ||||
| Risedronate/calcium carbonate (Actonel with calcium) | 35 mg per week (day 1) plus 1,250 mg calcium for no-risedronate days (days 2 through 7 of seven day treatment cycle) | PO | Prevention and treatment | Weekly | ||
| Ibandronate (Boniva) | 150 mg | PO | Prevention and treatment | Monthly | ||
| 3 mg | IV | Treatment | Every 3 months | |||
| Zoledronic acid (Reclast) | 5 mg | IV | Prevention | Every 2 years |
| |
| 5 mg | IV | Treatment | Annually | |||
| Selective estrogen receptor modulator (SERM) | Raloxifene (Evista) | 60 mg | PO | Prevention and treatment | Daily |
|
| Human monoclonal anti RANKL antibody | Denosumab (Prolia) | 60 mg | Subcutaneous (SC) | Treatment | Every 6 months | |
| Human monoclonal anti sclerostin antibody | Romosozumab | 210 mg | SC | Treatment | Monthly | - |
| Parathormone recombinant | Teriparatide (Forteo) | 20 mcg | SC | Treatment | Daily (approved for less than 2 years use) |
|
| Abaloparatide (Tymlos) | 80 mcg | SC | Treatment | Daily (approved for less than 2 years use) | - | |
| Hormonal | Calcitonin (Miacalcin) | 100 units | SC | Treatment (in women more than five years past menopause) | Daily | |
| 200 units | Intranasal | Daily |
Do's
Lifestyle modification for preventing osteoporosis
To reduce the risk of bone loss and osteoporotic fractures, women with osteoporosis or who are at risk of osteoporosis should be counseled about lifestyle changes, including:
- Weight-bearing exercise
- Smoking cessation
- Reducing alcohol intake
- Fall prevention
- Hip protector
Medications for preventing osteoporosis in postmenopausal women
Estrogen
- Conjugated estrogens (Premarin)
- Estropipate
- Estradiol
- Estrace: Oral tablet
- Climara, Menostar: Weekly transdermal patch
- Alora, Vivelle Dot: Biweekly transdermal patch
Estrogen/progestin
- Conjugated estrogens/medroxyprogesterone acetate
- Premphase: Continuous-cyclic
- Prempro: Continuous-combined
- Ethinyl estradiol/norethindrone acetate (Femhrt)
- Estradiol/norethindrone acetate (Activella)
- Estradiol/norgestimate (intermittent-combined; Prefest)
- Estradiol/levonorgestrel (continuous-combined; Climara Pro)
Follow up
In women older than 65 years with low bone mass, as indicated by bone mineral density reports, the World Health Organization’s Fracture Risk Assessment Tool (FRAX; available at http://www.shef.ac.uk/FRAX/index.aspx) should be used to establish if a woman is at increased risk of fracture.
Among those not at increased risk of fracture, screening should be performed:
- Every 15 years for women older than 65 years with a normal bone mineral density or a T-score of -1.5 or greater
- Every five years for women with a T-score of -1.5 to -1.99
- Every year for women with a T-score of -2.0 to -2.49
Dont's
- Don't use T-score for interpreting children BMD score; therapeutic option has to be decided based on Z-score in children, which is matched by age, sex, and race.
- Avoid certain drugs that can decrease bone mass in high risk patients, as much as possible. These include proton pump inhibitors, corticosteroids, and some of the newer antidepressants.
- Don't consider any pharmacological therapy indefinite in duration. After the initial treatment period, which depends on the pharmacological agent, a comprehensive risk assessment should be performed.
- There is no uniform recommendation that applies to all patients and duration decisions need to be individualized.[16]
- Don't utilize any procedure to measure bone density unless the results will influence the patient’s treatment decision.[22]
- Don't prescribe more than the safe upper limit for vitamin D intake for the general adult population, 4000 IU/day.[23]
- Don't prescribe bisphosphonates for patients with esophageal problems or inability to sit or stand upright.
References
- ↑ "Juvenile Osteoporosis".
- ↑ Krysiak R, Okopień B (2012). "[Pathogenesis and clinical presentation of andropause]". Pol. Merkur. Lekarski (in Polish). 32 (187): 70–3. PMID 22400185.
- ↑ Tanaka H (2005). "[Systemic bone diseases; clues for the pathogenetic mechanism of osteoporosis]". Clin Calcium. 15 (5): 776–82. PMID 15876739.
- ↑ Boente Mdel C, Asial RA, Winik BC (2006). "Geroderma osteodysplastica. Report of a new family". Pediatr Dermatol. 23 (5): 467–72. doi:10.1111/j.1525-1470.2006.00285.x. PMID 17014644.
- ↑ Hennekam RC (2006). "Hutchinson-Gilford progeria syndrome: review of the phenotype". Am. J. Med. Genet. A. 140 (23): 2603–24. doi:10.1002/ajmg.a.31346. PMID 16838330.
- ↑ Nojiri H, Saita Y, Morikawa D, Kobayashi K, Tsuda C, Miyazaki T, Saito M, Marumo K, Yonezawa I, Kaneko K, Shirasawa T, Shimizu T (2011). "Cytoplasmic superoxide causes bone fragility owing to low-turnover osteoporosis and impaired collagen cross-linking". J. Bone Miner. Res. 26 (11): 2682–94. doi:10.1002/jbmr.489. PMID 22025246.
- ↑ Lekva T, Ueland T, Bøyum H, Evang JA, Godang K, Bollerslev J (2012). "TXNIP is highly regulated in bone biopsies from patients with endogenous Cushing's syndrome and related to bone turnover". Eur. J. Endocrinol. 166 (6): 1039–48. doi:10.1530/EJE-11-1082. PMID 22450549.
- ↑ Ferlin A, Schipilliti M, Foresta C (2011). "Bone density and risk of osteoporosis in Klinefelter syndrome". Acta Paediatr. 100 (6): 878–84. doi:10.1111/j.1651-2227.2010.02138.x. PMID 21214887.
- ↑ Grasswick LJ, Bradford JM (2003). "Osteoporosis associated with the treatment of paraphilias: a clinical review of seven case reports". J. Forensic Sci. 48 (4): 849–55. PMID 12877306.
- ↑ Vasireddy S, Swinson DR (2001). "Male osteoporosis associated with longterm cyproterone treatment". J. Rheumatol. 28 (7): 1702–3. PMID 11469484.
- ↑ Gold DT, Solimeo S (2006). "Osteoporosis and depression: a historical perspective". Curr Osteoporos Rep. 4 (4): 134–9. PMID 17112423.
- ↑ Dytfeld J, Horst-Sikorska W (2012). "Pregnancy associated osteoporosis--a case report". Ginekol. Pol. 83 (5): 377–9. PMID 22708337.
- ↑ Elshal MF, Bernawi AE, Al-Ghamdy MA, Jalal JA (2012). "The association of bone mineral density and parathyroid hormone with serum magnesium in adult patients with sickle-cell anaemia". Arch Med Sci. 8 (2): 270–6. doi:10.5114/aoms.2012.28554. PMC 3361039. PMID 22662000.
- ↑ Buckley, Lenore; Guyatt, Gordon; Fink, Howard A.; Cannon, Michael; Grossman, Jennifer; Hansen, Karen E.; Humphrey, Mary Beth; Lane, Nancy E.; Magrey, Marina; Miller, Marc; Morrison, Lake; Rao, Madhumathi; Robinson, Angela Byun; Saha, Sumona; Wolver, Susan; Bannuru, Raveendhara R.; Vaysbrot, Elizaveta; Osani, Mikala; Turgunbaev, Marat; Miller, Amy S.; McAlindon, Timothy (2017). "2017 American College of Rheumatology Guideline for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis". Arthritis & Rheumatology. 69 (8): 1521–1537. doi:10.1002/art.40137. ISSN 2326-5191.
- ↑ Papaioannou A, Santesso N, Morin SN, Feldman S, Adachi JD, Crilly R; et al. (2015). "Recommendations for preventing fracture in long-term care". CMAJ. 187 (15): 1135–44, E450–61. doi:10.1503/cmaj.141331. PMC 4610837. PMID 26370055.
- ↑ 16.0 16.1 16.2 Cosman F, de Beur SJ, LeBoff MS, Lewiecki EM, Tanner B, Randall S; et al. (2014). "Clinician's Guide to Prevention and Treatment of Osteoporosis". Osteoporos Int. 25 (10): 2359–81. doi:10.1007/s00198-014-2794-2. PMC 4176573. PMID 25182228.
- ↑ Bachrach, L. K.; Gordon, C. M. (2016). "Bone Densitometry in Children and Adolescents". PEDIATRICS. 138 (4): e20162398–e20162398. doi:10.1542/peds.2016-2398. ISSN 0031-4005.
- ↑ 18.0 18.1 Hauk L (2013). "ACOG releases practice bulletin on osteoporosis". Am Fam Physician. 88 (4): 269–75. PMID 23944732.
- ↑ Messina C, Monaco CG, Ulivieri FM, Sardanelli F, Sconfienza LM (2016). "Dual-energy X-ray absorptiometry body composition in patients with secondary osteoporosis". Eur J Radiol. 85 (8): 1493–8. doi:10.1016/j.ejrad.2016.03.018. PMID 27048946.
- ↑ Seeman E (1998). "Growth in bone mass and size--are racial and gender differences in bone mineral density more apparent than real?". J. Clin. Endocrinol. Metab. 83 (5): 1414–9. doi:10.1210/jcem.83.5.4844. PMID 9589631.
- ↑ "WHO IRIS: Assessment of fracture risk and its application to screening for postmenopausal osteoporosis : report of a WHO study group [meeting held in Rome from 22 to 25 June 1992]".
- ↑ Nelson HD, Haney EM, Chou R, Dana T, Fu R, Bougatsos C. "Screening for Osteoporosis: Systematic Review to Update the 2002 U.S. Preventive Services Task Force Recommendation [Internet]". PMID 20722176.
- ↑ "Dietary Reference Intakes for Calcium and Vitamin D". 2011. doi:10.17226/13050.