medicine semester i assignment – osteoporosis · web view... scanning electron micrographs to...

Contents

Definition and Epidemiology........................................................................................................2

Aetiology...................................................................................................................................... 4

Pathophysiology........................................................................................................................... 5

Clinical signs and symptoms........................................................................................................6

Differential diagnosis and investigations.....................................................................................7

Osteomalacia............................................................................................................................ 7Paget’s Disease (Osteitis Deformans).......................................................................................8Malignant Tumours................................................................................................................... 8

Orthodox medical treatment........................................................................................................9

Avoiding and recovering from fractures....................................................................................9Drug treatments....................................................................................................................... 9Lifestyle changes....................................................................................................................10

Natural medicine........................................................................................................................ 10

Prognosis................................................................................................................................... 10

Resource list.............................................................................................................................. 11

References................................................................................................................................. 12

Bibliography............................................................................................................................... 12

Appendix A Tables from the World Health Organisation technical report, 1994........................13

Appendix B Case study..............................................................................................................15

Appendix C Table of orthodox treatments.................................................................................17

Emily Greenslade (Bristol), Medicine Semester I Assignment – Osteoporosis page 1 of 22

Definition and Epidemiology

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 consequent increase in fracture risk.’ The

WHO report published in 1994, says that a bone

mineral density of more than 2.5 standard

deviations less than young adult reference mean

is the defined value for osteoporosis. The young

adult reference takes into consideration the

ethnicity of the patient.

Figure 1 shows the bone tissue for a normal adult

female compared with bone tissue of a 70 year

old woman. These images show that the

trabecular bone structure of the older woman has

become thinner and more connections between

the structures are missing.

Figure 1 – scanning electron micrographs to show the structure of L3 vertebra in a 31 year old woman (top) and in a 70 year old woman (bottom). Copyright British Medical Journal (BMJ), 2006

Osteopenia is a low bone density value which is not low enough to be classified as

osteoporosis, although an osteopenic individual has a high risk of developing osteoporosis.

Based on the 1994 WHO definition, a value of between 1 and 2.5 standard deviations from the

young adult mean would be classed as osteopenia.

Established (or severe) osteoporosis is diagnosed osteoporosis with a fracture. This information

is summarised in Table 1.

Table 1 – summary of bone mass values Definition Value


Normal 0-1 standard deviation below young adult meanLow bone mass (osteopenia) 1-2.5 standard deviations below young adult meanOsteoporosis More than 2.5 standard deviations below young adult meanEstablished (severe) osteoporosis

Osteoporosis + 1 or more fragility fractures

Based on information from WHO (1994) report – see reference list

There is a strong female bias for the condition with the highest incidence in white post-

menopausal women, although it is possible for anyone to be affected by the condition,

including children (O’Connor and Perkins, 2005). Figure 2 compares the incidence of

osteoporotic fractures between men and women and shows that women are twice as likely to

sustain wrist or hip fractures after 60, and vertebral fractures after 70 years of age.

Race has also been shown to be a factor for osteoporosis: negro races are less likely than

Caucasians to have the disease because of higher initial skeletal mass (WHO, 1994).

Figure 2 – Epidemiology of osteoporotic fractures in men and women. Copyright Dennison, Cole and Cooper (2005), taken from BMJ, 2006.

As part of the aging process bone density

naturally decreases which means that older

people are more likely to have the condition. An

older person is more likely to sustain a fragility

fracture (a fracture caused by a minor trauma)

and at this point be diagnosed with osteoporosis

which partially explains the relationship

between age and incidence (WHO, 1994).

The condition is often asymptomatic until a

fragility fracture occurs which is why the

condition is sometimes described as the ‘silent

thief’ (WHO, 1994). In the UK, osteoporosis is

responsible for over 60,000 hip, 50,000 wrist

and 120,000 vertebral fractures each year

(National Osteoporosis Society [NOS], 2006).


Aetiology

Osteoporosis can be primary or secondary which means it can result from another condition

such as Cushing’s syndrome (Gould, 2006).

Figure 3 shows that bone mass naturally reduces after peak bone mass has been reached at

around 35 years of age. In the primary form of the disease, the rate at which it diminishes with

age is affected by many factors: genetic (vitamin D receptors, family history, ethnic origin,

skeletal mass), nutrition (calcium intake, alcohol consumption), lifestyle (weight-bearing

exercise, smoking). Secondary causes include diseases affecting hormone balance, drugs and

conditions such as anorexia nervosa (WHO, 1994).

Figure 3 – Age related changes in bone mass throughout life in women and men, copyright BMJ, 2006.

The sex hormones, oestrogen and

testosterone, play a significant part in the

rate of bone formation because they

stimulate osteoblast activity. During the

menopause, oestrogen levels are greatly

reduced which that bone mass is reduced. In

addition to hormonal changes, women are

more likely to have osteoporosis because

they have lower peak bone mass (Tortora and

Derrickson, 2006).

Details of the factors associated with osteoporotic fractures and causes of osteoporosis in

adults can be found in Appendix A.

Risk and predisposing factors are varied so that cause of the disease process in an individual is

often complex and not definitive. For example, Liz Larsson was diagnosed as osteopenic in

2006 at the age of 44 although her lifestyle and family history did not indicate she was


particularly at risk. The mostly likely reason for her condition was that she had started the

menopause approximately 18 months previously. However, there were other things which

could have contributed to her low bone density such as prolonged use of the contraceptive

injection depo-provera. There may also have been a genetic element as a younger sister has

subsequently been told that her bones are thinner than expected. See Appendix B for her case

study.

Pathophysiology

Normal bone tissue is constantly being broken down and then rebuilt. During childhood and

early adulthood, more bone is built than is broken down. After peak bone mass has been

reached, bone loss starts in the fourth or fifth decade of life (Poole and Compston, 2006).

The normal process for remodelling bone is described in Figure 4. In an osteoporotic patient,

osteoclasts are more active and / or osteoblasts are less active with the result that more of the

internal structure and therefore strength of bone tissue is reduced (see Figure 1, page 2)

Atrabecular bone surfaces are covered by resting osteoblasts (cells which create bone matrix)

Bosteoclasts (cells which break down bone matrix) migrate to a dormant bone surface

Costeoclasts excavate a resorption cavity

Dmononuclear cells smooth the cavity

Eosteoblasts are attracted to the site where they synthesize bone-like matrix

Fsynthesis of the new matrix continues

GNewly formed bone calcifies

HWhen the process is complete, lining cells overlie the trabecular surface

Figure 4 – Steps in the remodelling sequence of trabecular bone, adapted from 1994 WHO report


Bones consisting of proportionally higher cancellous (trabecular) bone are particularly likely to

be affected because this type of bone is relatively more hollow than compact or cortical bone.

It also regenerates quickly which means that there is more opportunity for problems with

remodelling to have an effect (Gould 2006) (Reister O’Connor and Perkins, 2005).

Figure 5 - A man aged 78 presented with an acute onset of thoracic kyphosis over a period of 10 weeks. The differential diagnosis on magnetic imaging included the possibility of a neoplasm, but further investigations confirmed osteoporotic collapse.

Copyright: Shergill, I and Wilson-Macdonald, J, Nuffield Orthopaedic Centre NHS Trust, Oxford OX3 7LD

The effect of these changes on the body is that the patient’s bones are more prone to fracture.

This results in pain for the patient either through fracture or pressure on nerves through

vertebral collapse. Spinal fractures may cause loss of height and spinal deformity such as

kyphosis (increased thoracic flexion, see Figure 5) or scoliosis (increased lateral curvature).

Spontaneous or fragility fractures occur most commonly in the hip, wrist or vertebrae (Gould,

2006).

Clinical signs and symptoms

Reister O’Connor and Perkins (2005) describe osteoporosis as ‘a silent disease’ which means

individuals are likely to be asymptomatic until a fragility fracture occurs. They suggest that any

fracture which happens from a very minor trauma should be investigated as a fragility fracture,

as should ‘multiple fractures, even with significant trauma’.

Given that the definition of established osteoporosis according to the WHO study group report

in 1994 includes a clinically apparent fracture, this type of break can be considered a


pathognomonic sign. Presentation of a fragility fracture, particularly if the patient history

includes risk factor or factors listed in Appendix A should be treated as a red flag and further

diagnostic tests carried out.

Vertebral compression fractures may present as ‘nagging’ back pain initially but as the disease

progresses a patient will show clinical signs such as loss of height and deformity of the spine

(Reister O’Connor and Perkins, 2005). Figure 5 shows an example of kyphosis caused by

osteoporotic vertebral fractures.

Osteoporosis is likely to cause fractures in specific areas because of the higher proportion of

cancellous bone particularly if it is under pressure from supporting the body (vertebrae, hip) or

from protecting against falls. A wrist or Colles’ fracture is a typical sign of osteoporotic fracture

which occurs in the distal radius, ulna or smaller wrist bones. It is often a protective injury

when an individual puts out a hand to break a fall and should be treated as a red flag (Reister

O’Connor and Perkins, 2005).

Differential diagnosis and investigations

Osteoporosis is often asymptomatic, particularly if vertebrae are affected where approximately

two thirds of patients do not present a clinically evident fracture. When a patient has spinal

deformity or sustains a fragility fracture further investigation is required to confirm a diagnosis

of osteoporosis (Poole and Compston, 2006).

The primary investigative tool often seen as a gold standard is a dual energy x-ray

absorptiometry (DXA) scan (Reister and Perkins, 2005). It measures bone density using two

sources of x-rays. The scan can be carried out at any site but most commonly the test is used

to measure the lumbar spine (L2-L4 or L1-L4) and hip. This technique is easy to use and has a

high level of precision (WHO, 1994). See Appendix A (table 7) for other investigative tools.


There are other causes of fragile bones and deformity which would need to be ruled out:

Osteomalacia Characterised by demineralisation related to vitamin D deficiency.

Weaker bones result in compression fractures especially in the vertebral body and

femoral neck (Thibodeau and Patton, 2007).

Signs including site of fracture, and symptoms are very similar to osteoporosis and the

two disorders can co-exist.

Diagnosed by x-rays – bone demineralisation will be seen in the spine, pelvis and lower

extremities. Fibrous lamellae and incomplete areas of demineralisation are apparent in

the cortex (Merck, 2008)

Paget’s Disease (Osteitis Deformans) Characterised by more osteoclasts and compensatory osteoblast activity.

Bones are remodelled in a disorganised way which can cause weakness in some areas of

bone and additional strength in other areas.

Commonly affects the skull, humerus, femur, vertebrae and pelvic bones. Weakness can

cause fragility fractures similar to osteoporosis (Thibodeau and Patton, 2007)

Diagnosis is confirmed through x-ray (Figure 6) which would show abnormal architecture

(cortical trabeculation or thickening) and serum levels of alkaline phosphate, calcium

and phosphate (Merck, 2008).

Figure 6 – X-rays of bones affected by Paget’s Disease. Copyright BMJ, 1996


Malignant Tumours Osteosarcoma (osteogenic sarcoma) is the most

common malignant bone tumour and most often in

the metaphysic of the tibia, femur (see Figure 7) and

humerus.

Presents as bone pain and sometimes pathological

fracture. This would need to be ruled out because it

can quickly metastasise to the lungs, although peak

incidence is between 10 and 25 years (Gould, 2006).

Diagnosed through bone biopsy (Merck, 2008).

Figure 7 - Osteosarcoma of the distal femur in a young patient treated with pre-operative chemotherapy and a limb-sparing surgical procedure. Copyright www.Radium.no, Cancer Research Norway

Orthodox medical treatment

Once the diagnosis of osteoporosis has been confirmed, the disease is managed according to

the specific requirements of the individual patient. The following strategies from Reister

O’Connor and Perkins, 2005 and National Osteoporosis Society leaflets might be used in a

management programme:

Avoiding and recovering from fracturesAn individual with osteoporosis is very likely to sustain a fracture from a fall and may even fall

due to a spontaneous fracture (stress fracture). Precautions such as installing grab bars and

hand rails in the home, sufficient lighting, taking extra care in snow/icy conditions as well as in

the home can reduce the number of falls.

Femoral fractures may require surgery and hip replacement. Vertebral compression fractures

can be left untreated if the fracture is stable. If the vertebra is unstable percutaneous

vertebroplasty (injecting acrylic cement into the vertebra) or kyphoplasty (injecting a small

balloon) may be used for pain relief. Colles’ fractures (wrist) are treated by realigning the

bones and then splinting to immobilise while the bone heals.


Drug treatmentsThere are many drug treatment options but the biosphosphonates are the most common

group. They are given in tablet form and work by inhibiting osteoclast activity which allows

osteoblasts to work more effectively. There are several licensed in the UK including

Alendronate, Cyclical Etidronate, Ibandronate and Risedronate.

Hormone replacement and hormone mimicking drugs are also available. These work by either

stimulating osteoblasts (parathyroid hormone treatment) or inhibiting osteoclasts (oestrogen

and testosterone replacement therapies, raloxifene). Stronium ranelate works by both

stimulating osteoblasts and inhibiting osteoclasts.

Dietary supplementation of calcium and vitamin D is often recommended in conjunction with

other medication and for elderly people.

Medication such as nonsteroidal anti-inflammatory drugs are prescribed or suggested for acute

or chronic pain associated with osteoporotic fracture. More information about drug treatments

can be found in Appendix C.

Lifestyle changesSmoking, excessive alcohol intake, unbalanced diet and a sedentary lifestyle can all contribute

to bone mass loss. Management of osteoporosis is likely to include keeping active but this will

depend on the severity of the condition.

Natural medicine

There are not many natural treatments recommended for this condition. Natural treatments for

pain management such as acupuncture or massage (although this is not recommended for


severely osteoporotic patients) could be considered to mediate nerve pain from any spinal

damage or other fractures (Reister O’Connor and Perkins, 2005).

Diet, lifestyle changes and vitamin supplementation are often prescribed as part of orthodox

management for the condition (see ‘Orthodox Medical Treatment’ above).

Prognosis

The first stages of the disease are asymptomatic so the condition is often untreated until the

patient has a fragility fracture. Once diagnosed, ‘drug treatments have been shown to reduce

the risk of fractures by up to 50%’ (NOS, 2006).

According to the NOS (2006) the likely outcomes of osteoporosis in the UK are:

significantly reduced quality of life with 60% of patients limited in class I (e.g. feeding,

dressing) and 80% limited in class II activities (e.g. shopping, gardening) 12 months

after a hip fracture

18% mortality in the first three months following hip fracture

55% of patients require assistance at home in the first 12 months following a hip

fracture

40% of patients with vertebral fractures will have constant pain

loss of height, kyphosis and severe back pain lead to a lack of mobility which can worsen

the osteoporosis

Reister O’Connor and Perkins (2005) include constipation, weight loss and possible lung

compression leading to lung disease as outcomes of spinal deformity following vertebral

compression.


Resource list

National Osteoporosis Society (NOS)Camerton, Bath, BA2 0PJtel: 01761 471771, helpline: 0845 450 0230website: www.nos.org.uk, email: [email protected]

NOS Regional Support Groups:Cardiff and District – www.osteoporosis-cardiff.btik.comBridgend and District – www.nos-bridgend.org.uk

Useful websites:British Orthopaedic Association – www.boa.ac.ukBritish Geriatric Society (Falls and Bone Health Special Interest Group) – www.bgs.org.ukBritish Medical Journal – www.bmj.comNational Institute for Clinical Excellence (NICE) – www.nice.org.ukNHS Direct - www.nhsdirect.nhs.uk

Word count: 2,495 This figure does not include contents page, section headings, appendices, reference list or bibliography.


ReferencesPage numbers in brackets refer to pages of this assignment.

Gould, B E (2006) Pathophysiology for the Health Professions, Third Edition, Saunders Elsevier, Pages: 657-659 (4, 6 & 9)

National Osteoporosis Society (January 2006) Osteoporosis Facts and Figures Version 1.1, Pages: 2-4 (6, 11)

Merck Online, accessed 13 March, 2008:Osteosarcoma: http://www.merck.com/mmpe/sec04/ch044/ch044c.htmlPaget’s disease: http://www.merck.com/mmpe/sec04/ch037/ch037a.htmlVitamin D deficiency (osteomalacia): http://www.merck.com/mmpe/sec01/ch004/ch004k.htmlOsteomalacia and osteoporosis: http://www.merck.com/mmpe/sec04/ch036/ch036a.html

Poole, K E S and Compston, J E (2006)Osteoporosis and its management, British Medical Journal Volume 333; Pages: 1251 (5),1252 (7)

Reister O’Connor, C and Perkins, S (2005) Osteoporosis for Dummies, First Edition, Wiley Publishing, Pages: 63-67 (3), 23, 107, 109 (6), 109-110, 114-115, 136-137 (7), 107-117, 145-160, 161-175, 180-186, 194-196 (9-10)

Thibodeau, G A and Patton, K T (2007) Anatomy and Physiology, Sixth Edition, Mosby Elsevier, Page: 248 (8)

Tortora, G J and Derrickson, B (2006) Principles of Anatomy and Physiology, Eleventh Edition, John Wiley & Sons, Inc., Pages: 189-190 (4)

WHO Study Group (1994) Assessment of Fracture Risk and its Application to Screening for Postmenopausal Osteoporosis, World Health Organisation Technical Series (843), Pages: 3, 5-6 (2), 7-8, 62 (3), 15, 59-61 (4), 19 (5), 5-6, 29-30 (7)

Bibliography

Compston, J (1999) British Medical Association - Family Doctor Guide to Osteoporosis, First Edition, Dorling Kindersley

Epstein, O et al (2004) Pocket Guide to Clinical Examination, Third Edition, Mosby Elsevier

Mosby (2006) Mosby’s Dictionary of Medicine, Nursing and Health Professions, Seventh Edition, Mosby Elsevier

Ralston, S H (1997)Science, medicine, and the future: osteoporosis, British Medical Journal Volume 315; pages 469-472


Waugh, A and Grant, A (2006) Ross and Wilson – Anatomy and Physiology in Health and Illness, Tenth Edition, Churchill Livingston Elsevier

Appendix ATables from the World Health Organisation technical report, 1994

Table 5 – Causes of generalized secondary osteoporosis in adultsEndocrine disease / metabolic causes Hypogonadism

HyperadrenocorticismThryotoxicosisAnorexia nervosaHyperprolactinaemiaSystemic mastocytosisPorphyriaAdult hyposphatasiaDiabetes mellitusThalassaemiaPregnancy

Nutritional causes Malabsorption syndromes / malnutritionChronic liver diseaseScurvyVitamin D deficiency? Calcium deficiencyAlcoholismGastric surgery

Drugs Chronic heparin administrationVitamin D toxicityAnticonvulsants

Inherited disorders of collagen metabolism

Osteogenesis imperfectaHomocystinuria due to cystathionine deficiencyEhlers-Danlos syndromeMarfan syndrome

Other Rheumatoid arthritisMyeloma and some cancersImmobilization / space flight

Table 7 - Advantages and disadvantages of various techniques to assess fracture riskTechnique Advantages DisadvantagesQuantitative computed tomography

Gives true density valuesDiscriminates completely trabecular from cortical boneHigh resolutionLow precision error (radius)

Comparatively high radiation doseHigh costHigh accuracy error (single energy)Precision errors (spine)

Dual-energy X-ray absorptiometry

No isotopesHigh precisionLow radiation doseMultiple sites of assessment including spine and hip

Uncertain accuracy errors in vivoRelatively high costInfluenced by osteoarthritis and aortic calcification at


lumbar sitesSingle-photon absorptiometry and Single-energy X-ray absorptiometry

Low radiationHigh accuracyHigh reproducibilityLow costPortability

Restricted to appendicular sitesIsotope half-life short for SPA


Table 22 – Factors that have been associated with reduced risk of osteoporotic fractureNegro raceMuscular strengthOsteoarthrosisLactationMultiparityHigh calcium intakeModerate exerciseObesityFluoridation of drinking waterSome drugs – oestrogen, thiazide diuretics & calcium supplements

Table 23 – Factors that have been associated with increased risk of osteoporotic fracture in womenAgePrimary amenorrhoea (e.g. in Turner syndrome)Secondary amenorrhoea (e.g. in athletes, anorexia nervosa, prolactinoma)Anovulatory menstrual cyclesPremature menopause Idiopathic

Surgical oophorectomyHysterectomy (with ovarian conservation)

NulliparityProlonged immobilization and inactivityRace Caucasian or AsianSmokingAlcohol abuseLack of physical exerciseNutritional factors (low calcium intake, high caffeine, protein, fibre or sodium intake)Some drugs Corticosteroids

AnticonvulsantsProlonged heparin infusionsThyroxine

Certain diseases For complete list see Table 5 [in this appendix]

Low body mass indexPositive family historyPrior fragility fractureShort stature and small bones


Appendix B Case study

Subject name:

Age:

Ethnicity:

Diagnosed condition:

Elizabeth (Liz) Larsson

46

British, White

Osteopenia

Background

Liz had worked in public relations for a local authority and as a consequence was aware that osteoporosis was a very serious condition which many people were not aware they were at risk from or even had until it was too late.

Later in her career she attended a health fair at the university where she worked. One of the exhibitors was selling wrist scans to check for osteoporosis and, although Liz was only 44 at this point, she decided to have the scan.

She was given the result immediately and it showed that her bone density was that of someone 10 years older than her. She was referred to her general practitioner (GP) at this point.

She would not have been considered a high risk (see below) and it is only by chance that she has been diagnosed and treated for low bone density. If she had not been tested it is likely that she would have continued to lose density and would have been at high risk of developing osteoporosis without knowing it.

Diagnosis and treatment

When she saw her GP, she was prescribed Calcichew which is a calcium supplement taken in lozenge form once a day. She stayed on Calcichew for a year and was then sent for a dual energy x-ray absorptiometry scan (DXA). The diagnosis of osteopenia, or low bone mineral density, was confirmed.

Her GP prescribed her ibandronate (Bonviva) which is taken in tablet form once a month. She question whether she needed to take the drug and was advised that if she did not her bone status would be compromised when she was 60 and she would be much more likely to sustain a fracture. She agreed to medication and has not experience any adverse affects.

She was also given the following advice: don’t go into the menopause underweight avoid alcohol although small amounts of red wine may be beneficial keep dietary intake of calcium high continue with weight bearing, medium impact exercise

She will continue to be monitored and have DXA scans every two years.

Although she has not been given a definitive cause for her condition, it is likely that it was caused by early onset menopause.


Patient history

Liz started her periods relatively late at 16 and began the menopause 18 months before her wrist scan and so benefited from the protective effects of oestrogen for less time than average. However, her menstrual cycle prior entering the menopause had been very regular so she was not at high risk because of this.

Liz was receiving the depo-provera contraceptive injection for seven years. Her doctor monitored her oestrogen levels during this time. For the first five years she was at the high end of normal levels and it then started to fall. Her GP advised her to stop the injection which she did. NICE guidance recognises that this injection can cause bone mineral loss but states that this should return to normal after the injection is stopped (see additional information).

Her mother had not been diagnosed or shown signs of osteoporosis and her maternal grandmother died at 60 from cerebrovascular accident. Her paternal grandmother died at 97 years of age and had not lost significant height nor did she have spinal deformity or clinically apparent fractures.

Liz has three sisters none of whom have been diagnosed with osteopenia or osteoporosis. However, one of her sisters who is two years younger, recently had a very minor accident and had persistent pain in her ankle. When she went for an x-ray she was told that her bones looked ‘thinner than expected’.

Diet and exercise

Liz has always been very active. Between the ages of 10 and 14 she was a gymnast and enjoyed running and swimming throughout her adolescence. She completed RAF officer training at the age of 28 and had ‘no more than a blister’.

She has maintained good levels of dietary calcium through daily intakes of cheese and yogurt which she now supplements with fortified soya milk.

She has never smoked and has always been a very moderate drinker. She has increased her alcohol intake over the last couple of years but even so she has rarely gone over 14 units a week.

Additional information

Liz has joined the National Osteoporosis Society and learnt more about her condition from the magazine and website. She feels very luck to have been diagnosed early. She feels that there will be many people in her situation and would like to see a screening programme put in place to help prevent the onset of osteoporosis.

Depo-provera and osteoporosis:

National Osteoporosis Society website – Conference paper from 2005http://nos.org.uk/dr_media/nos/Contraceptive_jab_in_bone_thinning_debate_14-Mar-08.pdf

NHS National Institute for Clinical excellence – Clinical Guideline 30: Long-acting reversible contraception (quick guide) October 2005http://www.nice.org.uk/nicemedia/pdf/cg030quickrefguide.pdf NICE guidance


Appendix CTable of orthodox treatmentsName Treatment

TypeDescription Indicated for Not indicated for

Alendronate (Fosamax, alendronic acid)

Drug, bisphosphonate

Inhibits osteoclasts. Daily or weekly tablet.

Post menopausal women. Men who are corticosteroid users.

People with moderate to severe renal impairment. Not tested with pregnant/breast feeding women. Anyone with gastrointestinal tract problems.

Calcitriol (Rocaltrol)

Drug, active vitamin D

Helps absorption of calcium. Capsule twice daily.

Post menopausal women. Men only under specialist care.

People with hypercalcaemia or pregnant/breast feeding women.

Calcium & vitamin D

Supplement Supplements given as a drug or as well as other medication.

As a drug – older people in residential nursing homes.

Not as treatment under 75.

Cyclical Etidronate (Didronel PMO)


Inhibits osteoclasts. Taken in tablet form in 90 day cycle with Cacit (proprietary calcium supplement)

Post menopausal women with established osteoporosis or osteopenia. Corticosteroid users. Male osteoporosis and pre-menopausal women under specialist care.

People with moderate to severe renal impairment. People with very high blood/urine calcium.

Hormone Replacement Therapy

Drug, HRT Increases oestrogen which protects bone tissue. Evidence that risk of colon cancer is reduced. Tablets, patches, implants, gels, vaginal ring and nasal spray.

Menopausal women up to the age of 50 and at lowest dose. Not often prescribed for treatment of osteoporosis.

Men, pre-menopausal women.

Ibandronate (Bonviva)


Inhibits osteoclasts. Monthly oral tablet or injection every three months.

Post menopausal women. Male osteoporosis and pre-menopausal women under specialist care.

People with renal impairment. Not tested on pregnant / breast feeding women.

Pamidronate Drug, bisphosphonate

Inhibits osteoclasts and some evidence that it reduced bone pain. Intravenous drip once every month to six months.

Drug for Paget’s disease and only used in specific circumstances for osteoporosis.

Not licensed for osteoporosis.

Percutaneous Vertebroplasty / Kyphoplasty

Surgical procedure

Injection of surgical cement (PV) or small balloon (KV) into the vertebrae for pain relief .

Recent spinal fractures with moderate to severe pain.

If bones are too porous and fragile (cement leaks out).

Raloxifene (Evista)

Drug, SERM* Mimics oestrogen on some organs. Daily tablet. Shown to reduce spinal fractures but not hip.

Post menopausal women for treatment of osteoporosis and prevention in some cases.

People with history of clots, immobile, taking breast cancer drug treatments. Has not been tested for men and pre-menopausal women.

Risedroante (Actonel)


Inhibits osteoclasts. Weekly or daily tablet.

Post menopausal women for treatment of osteoporosis or at risk due to corticosteroid use.

People with renal impairment. Not tested for pregnant / breast feeding women.


Stronium Ranelate (Protelos)

Drug Suppresses osteoclasts and stimulates osteoblasts. Powder mixed with water, daily.

Post menopausal women.

Men – drug effects not yet tested.

* selective estrogen receptor modulator

Collated from National Osteoporosis Society Information Sheets:Alendronate (Fosamax or Alendronic acid) (June 2006)Calcitriol (Rocaltrol) (December 2005)Cyclical Etidronate (Didronel PMO) (June 2006)Hormone Replacement Theraby and Osteoporosis (January 2007) Ibandronate (Bonviva) (June 2006)Pamidronate (December 2005)Percuatneous Vertebroplasty (PV), Percutaneous Kyphoplasty (KP) and Osteoporosis (February 2007)Raloxifene (Evista) (October 2005)Risedronate (Actonel) (June 2006)Stronium Ranelate (Protelos) (August 2005)Supplements of Calcium and Vitamin D with Osteoporosis Treatments (January 2005)


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