Guidelines for Management of Osteoporosis

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Review of management of Osteoporosis
Review_Osteoporosis_SVUH_MedEl_2008
Disease definition
The World Health Organisation (WHO) defines osteoporosis as a disease characterised by low bone mass and
microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture
risk.12 Thus, diagnosis is based on an individual’s bone mineral density (BMD), with reference to the number of standard
deviations from the BMD in an average 25-year-old woman (T-score).3 See Table 1.
Table 1. Bone Mineral Density & osteoporosis
T score
Normal
Osteopeania
Osteoporosis
Established osteoporosis
> -1 SD
-1 to -2.5 SD
< -2.5 SD
<-2.5 SD & one associated fragility fracture
This definition applies only to women. Recent reviews have suggested that applying the same definition to men, based on a
male normative range, has the same utility.4
Osteoporosis is best viewed as a chronic disease. It’s importance lies in the increased fracture risk it infers to those
individuals at risk of falling.5 Fragility fracture is defined as a fracture occurring after a fall from standing height or less. 1
Osteoporotic fragility fractures occur most commonly in the vertebrae, hips and wrists, and are frequently associated with
substantial disability, pain and reduced quality of life. In the absence of fracture, the condition is asymptomatic and often
remains undiagnosed.3
Historical Perspective6
Osteoporosis is known to have affected women for thousands of years. Egyptian mummies from 4,000 years ago have been
found with spinal kyphosis. The bone remodelling process was first observed by English surgeon John Hunter in the 18 th
century; but the term osteoporosis, meaning porous bone, was first described in the 1830’s by Jean Georges Lobstein. In the
1930’s Fuller Albright began treating post-menopausal women with oestrogen therapy. Densitometers, devices sensitive to
the detection of bone loss, were developed in the 1960s. In the 1980’s health institutions worldwide began to express
concerns with regard to the impact of osteoporosis on society, and calcium supplementation, good nutrition and exercise
were promoted as protective factors. In the 80’s and 90’s researchers discovered cytokines that influence the development
and activity of osteoclasts. Despite the long history of this disease and significant advances in its treatment and prevention,
osteoporosis remains a formidable challenge to medicine and currently creates a huge burden on society as well as on health
economics.
Disease Burden on Society
Osteoporosis affects both men and women and its prevalence increases with age, being especially common in
postmenopausal women. One in three women and one in twelve men over the age of 50 will suffer an osteoporotic fracture.
Hip fracture carries a mortality of 20% at 6 months, as well as significant morbidity- in terms of pain, deformity and loss of
independence. Institutionalisation is common with 50% of post-hip fracture patients losing their ability to live independently.1
Health Economics
Health costs of osteoporotic fractures are high. In 2000, the estimated cost of osteoporosis related fractures in the United
Kingdom was approximately £2 billion.1,7,8 Patients who have hip fractures use almost 20% of acute orthopaedic bed days.1
Osteoporosis is under-diagnosed and under-treated with the secondary prevention of fractures being widely neglected.5 A
recent 2005 audit undertaken in a UK primary care setting suggested that among women with a past history of fracture5,9
only 5% had had a DXA (dual x-ray absorptiometry) scan and less than10% were receiving treatment for secondary
prevention of fracture.
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Future Disease Trends
Osteoporosis is the most common disease of bone. Its incidence is rising rapidly with increasingly sedentary lifestyles and an
ageing population. Currently in the UK, approximately 300,000 patients present with osteoporotic fractures each year,
around a quarter of which are fractures of the hip. Hip fracture incidence in the UK increased by 2% per annum between
1999 and 2006.5,10 Projecting forward, this suggests that hip fracture numbers will double by 2050.5
Pathophysiology
Bone is composed of trabecular bone, which is metabolically active and cortical bone, which is less active. Bone remodelling
is tightly organised, consisting of simultaneous bone formation and resorption. The majority of adult bone mass is laid down
in adolescence and reaches its peak mass density in the fourth decade. Ageing alters the tight coupling between bone
resorption and formation leading to increased osteoclastic resorption and reduced osteoblastic activity. Hence, with age,
bone mass declines in both men and women. Lower levels of estrogen accelerate this decline in post-menopausal women.11
Features on History and Exam
Falls
Clinical risk factors related to physical function and falls are not risk factors for osteoporosis but are powerful predictors of
fracture risk.1,12
All older people presenting with a fall, reporting recurrent falls, or demonstrating abnormalities of gait and/or balance should
be offered a multifactorial falls risk assessment and be considered for individualised multifactorial intervention. 13 This is
regardless of whether or not they have fractured in the past. This assessment should include:
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Identification of falls history
Assessment of osteoporosis risk
Medication review
Gait, balance and mobility, and muscle weakness
Patient’s perceived functional ability & fear related to falling
Visual impairment
Cognitive impairment and neurological deficit
Urinary incontinence
Home hazards
Cardiovascular examination
History of previous fracture
Sustaining a fragility fracture at least doubles the risk of future fracture. An existing vertebral fracture increases the risk of
further vertebral fracture by a factor of 4 and doubles the risk of a subsequent hip fracture.1,14
Hip Fracture Prediction
Annual hip fracture risk can be estimated from age, sex and femoral neck BMD.1,15,16,17,18
A useful tool in the assessment of fracture risk is FRAX at
http://www.shef.ac.uk/FRAX/index.htm
For example, a 66-year-old lady with a BMI of 21.4 and a T-score of -2.3, who has no previous history of fracture
but whose mother had fractured her hip, has a 10-year probability of 18% for major osteoporotic fracture and of
2.1% for hip fracture. If she had a T-score of -2.6, her 10-year probability would increase to 20% and 4.1%
respectively. If, as well as a lower T-score, she had previously sustained a fracture, her 10-year risk would climb
to 32% and 6.7% respectively.
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Risk Factors for Osteoporosis
Table 2. summarizes the principal risk factors for osteoporosis
Non-modifiable
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Age - there is a progressive decrease in BMD with increasing age.1,19,20
Sex - women are at greater risk as they have smaller bones and hence lower total bone mass, lose bone more
quickly following the menopause, and typically live longer. Secondary causes of osteoporosis are more common in
men however, affecting approximately 40% of cases.1,21,22
Ethnicity – risk of osteoporosis is 2.5-fold greater in Caucasian than Afro-Caribbean women.1,19
Hormonal Factors - low BMD is associated with early menopause.1,23 This group of women should be considered
at high risk for osteoporosis.3 Current use of oestrogen replacement therapy is associated with a higher BMD.1,24
Family History – evidence from systematic reviews show that a positive family history of osteoporosis confers
increased risk to both women and men. This family history may include osteoporosis, kyphosis (“dowager’s hump”),
or low-trauma fracture after age 50 years as reported by the offspring.1,25
Modifiable
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Weight - weight loss or low body mass index (<19kg/m2) is an indicator of lower BMD.1,3,26
Smoking - BMD in smokers is lower than in non-smokers.1,21,27,28
Alcohol – excess alcohol consumption is believed to infer increased risk, despite limited study evidence. 1
Exercise – is protective against osteoporosis. A sedentary lifestyle during adolescence in particular has been linked
to an increased risk of low BMD.1,26,29,30,31
Diet - past dietary intake of milk in adult pre-menopausal women (45-49 years) has been positively associated with
BMD. Evidence of association between current calcium intake and low BMD is inconsistent. Vitamin D levels have
been shown to be positively correlated with BMD in independent living men and women aged >80 years in
Stockholm.1,32
Table 2 Principal risk factors for osteoporosis
Strongest Risk Factors
Fragility Fracture
Female Sex
Age > 60
Family History of Osteoporosis
Other Significant Risk Factors
Caucasian Origin
Early Menopause
Low BMI
Smoking
Sedentary Lifestyle
Long Term (> 3 months) corticosteroid use
Secondary causes of osteoporosis
The possibility of osteoporosis should be considered in patients with the following conditions:
Anorexia Nervosa/ Chronic Liver Disease/ Coeliac Disease/ Hyperparathyroidism/ Inflammatory Bowel Disease/ Male
Hypogonadism/ Renal Disease/ Rheumatoid Arthritis/ Long-term corticosteroid use/ Vitamin D deficiency/ Hypercortisolism/
Hyperthyroidism.
Pharmacologic agents11
The following agents are associated with low BMD:
Glucocorticoids/ Lithium/ Antacids (chronic use)/ Heparin/ GNRH agonists & antagonists/ Phenothiazines/ Cytotoxic drugs/
Anticonvulsants/ Tamoxifen (pre-menopausal)/ Vitamin A/ Methotrexate/ Warfarin/ Excessive thyroid supplementation/
Aluminium-containing medications/ Organ transplant therapy.
Investigations
Investigating the cause of a fall/recurrent falls13
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Separate to investigating the presence or otherwise of osteoporosis, all patients should be considered for appropriate
investigation of cause of falls. This should be guided by the clinical history and examination. Investigations may include
vision & hearing assessments, electrocardiography, brain imaging and assessment for orthostatic hypotension &
neurocardiovascular instability.
Dual X-ray Absorptiometry (DXA)
BMD is the major criterion used for the diagnosis and monitoring of osteoporosis. DXA scanning is the current standard
technique used to measure BMD, as shown by grade A evidence.1,33 BMD measurements should be taken at two sites to
improve diagnostic accuracy, preferably anteroposterior spine and hip. Hip BMD provides the best prediction of hip fracture
risk1,34 but does not exclude osteoporosis at the spine. The spine is the preferred site for monitoring treatment response.
DXA reports should include the annual hip fracture risk (or 10 year fracture risk). The measured BMD may be affected by
factors such as vertebral fracture or degenerative changes, so careful interpretation of the spine image and comparison of
the T-scores of individual vertebrae is necessary. DXA scanning is safe. Patients should be reassured that the radiation dose
from DXA is extremely small and typically corresponds to only a few days natural background radiation or a single
transatlantic flight.1
Plain Radiographs
Conventional radiographs should not be used for the diagnosis or exclusion of osteoporosis, as they are open to marked
observer variation and apparently normal density does not reliably exclude osteoporosis (grade A evidence).1,35 When plain
films are interpreted as “severe osteopaenia” it is appropriate to suggest referral for DXA. Grading of vertebral fractures and
the number of fractures should influence management.1,36
Peripheral Techniques1
Peripheral techniques (pQCT, peripheral quantitative computed tomography; pDXA, peripheral DXA; SXA, single-energy X-ray
absorptiometry; RA, radiographic absorptiometry; phalangeal ultrasound and peripheral radiographic fractal analysis) have
not been shown to have a role in the diagnosis of osteoporosis or in targeting therapy to reduce fracture risk as there is only
moderate correlation between forearm or heel BMD and axial BMD. The principal advantages compared to DXA are their
relatively modest cost and portability.
Quantitative Computer Tomography (QCT)1
QCT has been widely used to measure BMD, particularly in the spine. It can be performed with conventional CT scanners
with special software and can measure cortical and trabecular bone separately. Limiting factors on widespread introduction
include the high radiation dose and the cost of the scans.
Biochemical markers1
Studies have failed to demonstrate a consistent relationship between biochemical markers of bone turnover and bone
loss.1,33 Recent studies support the role that resorption markers measured in urine and serum can predict increased fracture
risk (OR~2) independently of BMD. Conclusive evidence demonstrating the value of one or more specific markers in fracture
risk prediction is still awaited.
Other laboratory tests
Renal, liver, bone & thyroid function tests, parathyroid hormone, protein electrophoresis and urine for bence jones proteins,
inflammatory markers, autoantibodies & cortisol may be useful if a secondary cause of osteoporosis or a different disease
process is suspected.
Differential Diagnosis
Low back pain
A wide differential exists including degenerative or inflammatory arthritis/ disc disease/ metastatic cancer/ multiple myeloma/
spinal stenosis/ other metabolic bone diseases.
Pathological fracture
A wide differential exists including metastatic cancer/ bone tumours or cysts/ radiotherapy/ infection/ certain inherited bone
disorders/ other metabolic bone diseases.
Treatment
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Symptomatic
The acute pain of fracture can vary widely and chronic pain is associated with significant physical dysfunction and decreased
quality of life.1
Acute Pain1
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General measures – RICE: rest, ice, compression, elevation
Specific measures - Splintage, reduction and plaster immobilisation or fracture fixation as appropriate.
Analgesic ladder
Analgesic Class
Rung 1
Rung 2
Rung 3
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Non-opioid
+/- adjuvant (eg NSAID)
Opioid for mild-moderate pain
+/- non-opioid
+/- adjuvant
Opioid for moderate-severe pain
+/- non-opioid
+/- adjuvant
Examples
Paracetamol
Ibuprofen
Dihydrocodeine
Morphine
The appropriate agents should be used regularly with the aim of pre-emptive pain control to promote comfort both
at rest and during active rehabilitation.5 Non-steroidal analgesics should be used with caution due to their high
incidence of gastrointestinal and renal toxicity. In difficult cases the involvement of the local Pain Service may be
beneficial.1
Ensure an adequate assessment of analgesia requirement is performed in cognitively impaired and acutely confused
patients. Non-verbal communications of pain include guarded posture, agitation, tachycardia, hypertension and
moaning.5
Intranasal calcitonin may be used off-license in cases with unremitting pain, unresponsive to other agents.1
Chronic Pain1
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Pharmacological measures – analgesic ladder as above, calcitonin & tetraparitide.
Non-pharmacological measures – include physiotherapy treatments,1,37,38 use of transcutaneous electrical nerve
stimulation (TENS), back strengthening exercises and acupuncture.
Disease modifying therapies3,5
Bisphosphonates3
Bisphosphonates are inhibitors of bone resorption and increase BMD by altering both osteoclast activation and function. Four
bisphosphonates, alendronate (Fosamax ®), etidronate (Didronel ®), risedronate (Actonel ®) and ibandronate (Bonviva ®,
Bondronat ®), are currently licensed in Ireland for the management of osteoporosis.
The largest study of alendronate, the Fracture Intervention Trial (FIT), comprised two placebo-controlled studies: one in
women with pre-existing fractures (established osteoporosis) and another in women without pre-existing fractures. The substudy in women with established osteoporosis found a relative risk (RR) of vertebral fracture of 0.53 (95% CI, 0.24 to 1.01)
and a RR of wrist fracture of 0.52 (95% CI, 0.33 to 0.92) for alendronate relative to placebo.
Pooled data from studies of etidronate have shown a RR for vertebral fracture of 0.43 (95% CI, 0.20 to 0.91) in favour of
those treated with etidronate versus placebo. Non-vertebral fracture studies have not shown a statistically significant
difference in RR in patients treated with etidronate when compared with untreated controls.
Studies of risedronate found a RR of vertebral fracture of 0.63 (95% CI, 0.51 to 0.78) compared to placebo, and an RR of
non-vertebral fracture of 0.67 (95% CI, 0.50 to 0.90).
All bisphosphonates are contraindicated when there is concomitant hypocalcaemia and etidronate and risedronate are
contraindicated in patients with severe renal impairment.
Bisphosphonates must be used cautiously in patients with active upper gastrointestinal problems due to their documented
potential adverse effect of oesophageal inflammation.
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Selective Oestrogen Receptor Modulators (SERMs)3
SERMS have selective activity in various organ systems, acting as weak oestrogen receptor agonists in some systems and as
oestrogen antagonists in others. The aim of treatment in osteoporosis is to maximise the beneficial effects of oestrogen on
bone and to minimise the adverse effects on the breast and endometrium.
Raloxifene (Evista ®) is the only SERM licensed for the treatment of osteoporosis in post-menopausal women. The MORE
(Multiple Outcomes of Raloxifene Evaluation) study included women with and without previous fracture. In women with
osteoporosis or established osteoporosis, a RR of vertebral fracture of 0.65 (95% CI, 0.53 to 0.79) at a dose of 60mg daily
and a RR of 0.54 (95% CI, 0.44 to 0.67) at a daily dose of 120mg was found. No significant difference was shown between
raloxifene and placebo for non-vertebral fractures.
Contraindications to use may include a history of venous thromboembolism, hepatic & renal impairment, undiagnosed
uterine bleeding and endometrial cancer. Raloxifene may be used for the treatment or prevention of osteoporosis in patients
with breast cancer, but only after their cancer therapy has been completed.
Raloxifene is associated with a 3-fold increased risk of venous thromboembolism, especially during the first 4 months of
treatment.
Parathyroid hormone (Teriparitide)3
Teriparitide (Forsteo ®) is a recombinant human parathyroid hormone and acts as an anabolic agent to stimulate new bone
formation. Teriparitide may also increase resistance by bone to fracture.
Teriparitide is administered by daily subcutaneous injection. Maximum suggested treatment duration is 18 months.
For vertebral fractures and grouped non-vertebral fractures in women with established osteoporosis, the main placebocontrolled RCT found RRs of 0.35 (95% CI, 0.22 to 0.55) and 0.65 (95% CI, 0.43 to 0.98) respectively in favour of
teriparitide. Teriparitide was also shown in this study to reduce the incidence of new or worsened back pain reported as an
adverse event. In a head-to-head study comparing teriparitide (40 mcg/day, twice the licensed dose) with alendronate
(10mg/day) a RR of non-vertebral fracture in women with osteoporosis of 0.30 (95% CI, 0.09 to 1.05) was found in favour
of the teriparitide group. The study did not look at non-vertebral fractures.
Contraindications to use of teriparitide may include pre-existing hypercalcaemia, severe renal impairment, metabolic bone
diseases other than primary osteoporosis, unexplained elevations of alkaline phosphatase and previous radiation therapy to
the skeleton. Osteosarcoma is a rare potential adverse effect of treatment.
Strontium Ranelate39
Strontium Ranelate (Protelos ®) is thought to have a dual effect on bone metabolism, increasing bone formation and
decreasing bone resorption.
The NICE Assessment Group reported the results of a published meta-analysis, which resulted in a RR for vertebral fracture
of 0.60 (95% CI 0.53 to 0.69, 2 RCTs, n = 6551); and an RR for all non-vertebral fractures (including wrist fracture) of 0.84
(95% CI 0.73 to 0.97, 2 RCTs, n = 6551). Hip fracture efficacy was established in one study. The RR for hip fracture in the
whole study population was 0.85 (95% CI 0.61 to 1.19, 1 RCT, n = 4932). In general, strontium ranelate was not associated
with an increased risk of adverse effects and for the most part adverse effects were mild and transient. Transient nausea,
diarrhoea and creatine kinase elevations were the most commonly reported clinical adverse effects.
One study published results on health-related quality of life. Strontium ranelate was said to benefit quality of life when
compared with placebo, as assessed by the QUALIOST osteoporosis-specific questionnaire and by the General Health
perception score of the SF-36 general scale.
Contraindications to use may include severe renal impairment. Strontium ahs been shown to have an increased risk of
venous thromboembolism (RR= 1.42).39 Therapy should be discontinued during treatment with oral tetracycline and
quinolone antibiotics.
Secondary Prevention of Fractures3,5
Fall prevention - most fractures result from a fall and half of fallers will have a further fall within the next twelve
months5,40. Interventions to reduce the risk of falls can be effective in preventing further events, yet currently less than half
of patients admitted to hospital with a fracture are offered a falls risk assessment.5.41
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Disease modifying therapies - between one half5,42,43,44 and two-thirds5,45 of hip fracture patients have experienced a
prior fracture. A comprehensive meta-analysis of the principal agents licensed for the treatment of osteoporosis suggests
that a 50% reduction in fracture incidence can be achieved during 3 years of pharmacotherapy. 5,46 NICE guidance3, see
Table 3, recommends bisphosphonates as first line treatment for post-menopausal women, with raloxifene recommended as
an alternative only if bisphosphonates are contraindicated, the patient is physically unable to take them, or if there has been
an unsatisfactory response to treatment. Due to its higher cost, teriparitide should be reserved for use by specialist centres.
At time of writing, NICE are updating their guidelines to include Strontium Ranelate.39
Patients should be Calcium and Vitamin D replete; all study subjects in bisphosphonate trials in osteoporosis to date have
been co-prescribed calcium and vitamin D supplements.
Other high-risk groups, to be considered for preventative strategies include housebound, frail, elderly patients and any
patient committed to 3 months or more of oral steroid therapy.
Table 3. NICE recommendations for bisphosphonate use in osteoporosis
NICE recommendations for bisphosphonate use in osteoporosis
Previous fragility fracture, aged 75 or over without the need for DXA
Aged 65-74 if osteoporosis is confirmed by DXA (T-score < -2.5)
Postmenopausal women <65 years if:
T-score -3.0 SD or below
T-score -2.5 SD plus one or more additional age-independent risk factors.
Age-independent risk factors include:
Low BMI (< 19 kg/m2)
Family history of maternal hip fracture before age 75
Untreated premature menopause
Conditions affecting bone metabolism (inflammatory conditions, hyperthyroidism, coeliac disease)
Conditions associated with prolonged immobility
Acute Hip fracture care5
Coordinated multidisciplinary fracture services (including orthopaedic surgeons, geriatricians, anaesthetists, nursing staff,
physiotherapists, occupational therapists, social workers and dieticians) for fragility fracture patients promote good quality of
care and reduce the costs of that care.5
Pre-operative assessment and care should focus on – diagnosis, which is usually apparent on radiograph but 10-15%
may be missed or delayed,5,47 assessment for other injuries and co-morbidities, prescription of adequate analgesia, supply of
pressure-relieving mattress, fluid resuscitation and brief cognitive assessment (Abbreviated Mental Test score). Patients
should be monitored for peri-operative confusion. Patients should be transferred to the orthopaedic ward without delay. For
patients on warfarin, surgery is best deferred until the INR is less than 1.5.
Prompt and safe surgery is essential to good hip fracture care and is ensured by good pre-operative assessment- using
protocols agreed by surgeon, anaesthetist & orthogeriatrician.
Post-operative care

Focuses on adequate analgesia to ensure patient comfort and early rehabilitation
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Pressure area care and venous thromboprophylaxis using TEDs (thrombo-embolic disorder stockings) and low
molecular weight heparin.

Nutrition - poor nutritional state is a powerful risk factor for hip fracture and hip fracture inpatients only achieve half
of their daily nutritional requirements.5,48 Oral multi-nutrient feed may reduce the risk of death or complications.5,49
Additional carers to assist in nutrition can be very effective when adherence is poor, and has been shown to reduce
mortality.5,50
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Early rehabilitation – early goals include sitting out on the first post-operative day. Progress is largely determined
thereafter by individual patient co-morbidities such as dementia and stroke disease.
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Delirium is a common complication and is best managed by collaboration with orthogeriatric services.
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Complex ethical issues regarding consent, resuscitation status, nutrition difficulties, and palliation of terminal illness
may arise in the care of frail or confused fragility fracture patients. Collaboration with orthogeriatric services is
beneficial.
Treatment follow-up and monitoring
Osteoporosis is best viewed as a chronic disease. Although fracture efficacy data for bisphosphonates only exists for up to 4
years of treatment, current recommendations are for treatment on a lifelong basis. Few data exist regarding BMD or fracture
risk after cessation of bisphosphonates. One study1,51 reported increases in markers of bone turnover, without changes in
BMD 2 years after stopping alendronate and this may indicate reactivation of processes that may ultimately result in bone
loss. Long-term management with bisphosphonates is currently advised until optimal treatment patterns have been clarified.
Future De Novo Investigations/ Treatment
There is evidence from recent studies that resorption markers measured in urine or more recently in serum can predict
increased fracture risk (OR~2) independently of BMD, but there is no conclusive evidence that has demonstrated the value
of one or more specific markers, in fracture risk prediction.1
Useful Information Sources/ Sites
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FRAX website  http://www.shef.ac.uk/FRAX/index.htm
Irish Osteoporosis Society http://www.irishosteoporosis.ie/
This site provides general information on osteoporosis in Ireland and details of its network of osteoporosis support
groups and the location of DEXA scanners in Ireland.
National Osteoporosis Society (UK) http://www.nos.org.uk
National Osteoporosis Foundation (USA) http://www.nof.org
National Institute of Clinical Excellence (UK) http://www.nice.org.uk
Areas of the site of particular interest include
o Clinical Guideline 21: The assessment and prevention of falls in older people
http://www.nice.org.uk/page.aspx?o=233391
o Osteoporosis - Secondary Prevention - Guidance http://www.nice.org.uk/TA087guidance
National Council on Ageing and Older People
http://www.ncaop.ie
This site is the home of the healthy ageing database, which provides information on over 300 research projects on
healthy ageing which have been carried out throughout the country.
Age & Opportunity http://www.olderinireland.ie
Useful Contacts
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SVUH Dept of Medicine for the Elderly, Ms. Lorraine Murray, Senior Administrator
Tel: 01-2214549
Fax: 01-2094609
SVUH Bone & Joint Unit
SVUH Pain Service
Carew House Day Hospital, SVUH
Tel: 01-2094122
Fax: 01-2094026
Irish Osteoporosis Society, 33 Pearse Street, Dublin 2.
Tel: 1890 252 751
Fax: +353 (0)1 6351698
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References
1
Scottish Intercollegiate Guidelines Network: management of osteoporosis. Edinburgh: SIGN; 2003. (SIGN
Publication No. 71)
2
Assessment of Fracture Risk and its Application to Screening for Post-menopausal Osteoporosis. Report of a
WHO Study Group. Geneva: WHO; 1994. (Technical Report Series 883)
3
National Institute for Health and Clinical Excellence. Bisphonates (alendronate, etidronate, risedronate).
Selective estrogen receptor modulators (raloxifene) and parathyroid hormone (teriparitide) for the secondary
prevention of osteoporotic fragility fractures in post-menopausal women. Technology Appraisal 87. January
2005. Available from: http://www.nice.org.uk/TA087guidance
4
Kanis JA, Johnell O, Oden A, De Laet C, Mellstrom D. Diagnosis of osteoporosis and fracture threshold in men.
Calcif Tissue Int 2001;69:218-21.
5
The Care of Patients with Fragility Fracture, British Orthopaedic Association, Sept 2007. Available from:
http://www.fractures.com/pdf/BOA-BGS_Blue_Book.pdf
6
http://www.medopedia.com/history-osteoporosis
7
Torgerson DJ, Bell-Syer SE. Hormone replacement therapy and prevention of nonvertebral fractures: a metaanalysis of randomized trials. JAMA 2001;285:2891-7.
8
The Economic Cost of Hip Fracture in the UK, The University of York, June 2000. Available from:
http://www.berr.gov.uk/files/file21463.pdf
Brankin E, Mitchell C, Munro R. Closing the osteoporosis management gap in primary care: a secondary
prevention of fracture programme. Curr Med Res Opin 2005;21:475-82.
9
Department of Health. Hospital Episode Statistics (England) 2006. Available from :
http://www.hesonline.org.uk/Ease/servlet/ContentServer?siteID=1937&categoryID=192
10
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Forciea MA, Schwab EP, Brady Raziano D, Lavizzo-Mourey R, eds. Geriatric Secrets. 3 ed. Philadelphia: Mosby;
2004.
12
Scottish Intercollegiate Guidelines Network: prevention and management of hip fracture in older people.
Edinburgh: SIGN; 2002. (SIGN Publication No. 56)
13
National Institute for Health and Clinical Excellence. Falls: The assessment and prevention of falls in older
people. Clinical Guideline 21, November 2001. Available from: http://www.nice.org.uk/Guidance/CG21
14
Klotzbuecher CM, Ross PD, Landsman PB, Abbott TA, 3rd, Berger M. Patients with prior fractures have an
increased risk of future fractures: a summary of the literature and statistical synthesis. J Bone Miner Res
2000;15:721-39.
15
De Laet CE, van Hout BA, Burger H, Hofman A, Pols HA. Bone density and risk of hip fracture in men and
women: cross sectional analysis. BMJ 1997;315:221-5.
11
16
De Laet CE, Van Hout BA, Burger H, Weel AE, Hofman A, Pols HA. Hip fracture prediction in elderly men and
women: validation in the Rotterdam study. J Bone Miner Res 1998;13:1587-93.
Doherty DA, Sanders KM, Kotowicz MA, Prince RL. Lifetime and five-year age-specific risks of first and
subsequent osteoporotic fractures in postmenopausal women. Osteoporos Int 2001;12:16-23.
18
Kanis JA, Oden A, Johnell O, Jonsson B, de Laet C, Dawson A. The burden of osteoporotic fractures: a method
for setting intervention thresholds. Osteoporos Int 2001;12:417-27.
17
19
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