PRINSIP GANGGUAN

MUSCULOSKELETAL
Inflamasi, ,acute and chronic
arthritis, , osteoporosis
 Inflammatory Reactions

• A nonspecific response to any agent that

causes cell injury
• Agents may be
– Physical (heat or cold)
– Chemical (concentrated acid)
– Microbiologic (bacterium or virus)
 Local and Systemic Effects of
Inflammation
• Local effects
– Capillary dilatation
• Increased blood flow, increased warmth and
redness
– Increased capillary permeability, leading to
extravasation of fluid, leading to swelling
– Attraction of leukocytes
• Migrate to site of injury
• Adhere to endothelium of small blood vessels
• Systemic effects: fever, leukocytes
Local and Systemic Effects of Inflammation
 Characteristic Signs of
Inflammation
• Heat and redness
– Dilated blood vessels and slowing of blood
through vessels
• Swelling
– Accumulation of fluid and exudate due to
extravasation of plasma
• Tenderness and pain
– Irritation of nerve endings
 Inflammatory Process
• Acute inflammatory process
– Polymorphonuclear leukocyte cell
• Most important cell in acute inflammatory response; actively
phagocytic cell
• Mononuclear cells (monocytes, macrophages) follow later to
clean up tissue debris
• Severe inflammatory process
– Systemic effects become evident (feeling ill, fever)
– Bone marrow accelerates production of leukocytes
resulting in ↑levels in bloodstream
– Liver produces acute phase proteins such as C-reactive
protein
• Mild inflammatory process
– Self-limiting, subsides with tissue resolution
 Outcome of Inflammation
• Depends on amount of tissue damage
– Severe inflammatory process
• Tissue damage → replacement of damage cells →
heal with scarring
– Mild inflammatory process
• Self-limiting, subsides with tissue resolution
• Outcomes
– Resolution
– Repair
– Areas of destruction replaced by scar tissue
– Mediators intensify inflammatory process
– Mediators generate more mediators
 Chemical Mediators of
Inflammation
• Chemical agents that intensify the inflammatory
process
• Cell-derived mediators
– Mast cells: specialized connective tissue cells with
granules filled with histamine, a vasodilator
– Histamine and serotonin: also in blood platelets
– Prostaglandins
– Leukotrienes: synthesized from arachidonic acid
• Mediators from blood plasma
– Bradykinin
– Complement
• Activated by antigen-antibody reaction
• Series of proteins that interact in a regular sequence
Chemical Mediators of Inflammation
 Acute Monoarthritis
Differential Diagnosis

• Infection
• Crystal-induced
• Hemarthrosis
• Tumor
• Intra-articular derangement
• Systemic rheumatic condition
 Risk Factors for Septic Arthritis

• Previous arthritis
• Trauma
• Diabetes Mellitus
• Immunosupression
• Bacteremia
• Sickle cell anemia
• Prosthetic joint
Pathogenesis of Septic Arthritis
• Bacteria enter joint and deposit in synovial
lining.
– Hematogenous spread or local invasion
– Acute inflammatory response
• Rapid entry into synovial fluid
– No basement membrane
 Septic arthritis
Clinical presentation

• Acute monoarthritis
– Cardinal signs of inflammation
• Rubror, tumor, calor, dolor
• +/- Fever
• +/- Leukocytosis

•Atypical presentations are not

uncommon
 Septic Arthritis
Joints Involved
60

50

40

30

20

10

0
Knee Hip Ankle Shoulder Wrist Elbow Other Polyart
 Polyarticular Septic Arthritis
• More likely to be over 60 years
• Average of 4 joints
– Knee, elbow, shoulder and hip predominate
• High prevalence of RA
• Often without fever and leukocytosis
• Blood cultures + 75%
• Synovial fluid culture + 90%
• Staph and Strep most common
• POOR PROGNOSIS
– 32%mortality (compared to 4% with monoarticular
disease)
Synovial fluid analysis
is essential in the
diagnosis of infectious
arthritis
 Synovial Fluid Analysis in Septic
Arthritis

• Cell count: >50,000 wbcs/mm3

• Differential: >75% PMNs
• Glucose: Low
• Gram stain : relatively insensitive test
• Culture: postive
Always use a wide bore needle when you suspect
infection, as pus may be very viscous and difficult to
aspirate
 When to order special cultures
• History of TB exposure
• Trauma
• Animal bite
• Live in or travel to endemic sites for Fungi
or Borrelia
• Immunocompromised host
• Unresponsive to conventional therapy
 Special Populations

• Prosthetic joints
• Patients on TNF inhibitors
• Sickle cell anemia
• HIV disease
• Transplant setting
 Management
• Joint aspiration
– Daily or more frequently as needed.
• Antibiotic therapy
– Based on gram stain/culture and clinical factors
– Duration is variable and depends on organism and
host factors
• Surgical intervention
– Only necessary if pt is not responding after 48 hrs of
appropriate therapy
Empiric Therapy for Septic Arthritis

• You must cover Staph and Strep

– Oxacillin
– Vanco if PCN-allergic or if concern for MRSA
• If infection is hospital acquired or
prosthetic joint- cover gram negatives
– 3rd generation cephalosporin
• Empiric coverage for GC is recommended
because of the high prevalence rate
 Septic arthritis

• Radiographs
– Minimal diagnostic utility
– Document any existing joint damage
– Evaluate for possible osteomyelitis
Septic hip-early disease Late disease
 Prosthetic joint infections
• Stage I within 3 months of surgery
– Usually transmitted at the time of surgery
– Staph and other gram positives most common
– Pain, wound drainage, erythema, induration
• Stage II 3-24 months
• Stage III >2 years post-surgery
– Usually caused by hematogenous spread to
abnormal joint surfaces
– Joint pain predominates
 Prosthetic joint infections

• Synovial fluid analysis

• May require biopsy
• If cultures are positive
– Remove prosthesis
– Treat with parenteral antibiotic until sterile
• Usually 6 weeks +
– Reoperate
• Revision is at high risk for recurrent infection
 Tuberculous arthritis

• History of exposure is helpful

• PPD may be negative
• Synovial fluid stain usually negative
• Culture may take 6-8 weeks to grow
• Best yield is probably synovial biopsy
 Acute Rheumatic Fever
JONES CRITERIA
Evidence of preceding strep infxn plus 2 major criteria or 1
major and 2 minor
MAJOR
Carditis
Migratory polyarthritis
Syndenham chorea
Erythema marginatum
Subcutaneous nodules
MINOR
Fever
Arthralgia
previous rheumatic fever or rheumatic heart disease
 Take Home Points
• Acute monoarthritis is septic until proven
otherwise
• Synovial fluid analysis must be performed
• Choose appropriate empiric abx
• Consider unusual pathogens in the setting of
immunocompromise
• Serial synovial fluid analyses should be
performed to document clearance of infection
• Consult ortho if not improving with aggressive
percutaneous drainage and abx
 ACUTE AND
CHRONIC
OSTEOMYELITIS
 DEFINITION

• Inflammation of the bone caused by

an infecting organism
 HISTORY

In the early 1900’s about 20% of

patients with osteomyelitis died and
patients who survived had significant
morbidity.
 Introduction
• The key to successful management is
early diagnosis and appropriate surgical
and antimicrobial treatment.
• A multi disciplinary approach is required,
involving an orthopaedic surgeon, an
infectious disease specialist, and a plastic
surgeon in complex cases with significant
soft tissue loss.
 Classification
1) The duration - acute, subacute and
chronic

2) Mechanism of infection – exogenous

or hematogenous

3) The type of host response to the

infection- pyogenic or non pyogenic
 Acute hematogenous
osteomyelitis
• Most common type of bone infection,
usually seen in children
• Decrease in incidence, could be due to
higher standard of living and improved
hygiene.
• Bimodal distribution- younger than 2
years, and 8-12 years
• More common in males
 Acute hematogenous osteomyelitis-
causes
• Caused by a bacteraemia

• Bacteriological seeding of bone

generally is associated with other
factors such as localized trauma,
chronic illness, malnutrition or an
inadequate immune system.
 Acute hematogenous osteomyelitis
pathophysiology

 In children the infection generally involves

the metaphyses of rapidly growing long
bones

 Bacterial seeding leads to an inflammatory

reaction which can cause local ischaemic
necrosis of bone and subsequent abscess
formation
 Acute hematogenous osteomyelitis
pathophysiology
• As the abscess enlarges, intramedullary
pressure increases causing cortical
ischaemia, which may allow purulent
material to escape through the cortex into
the subperoisteal space.
 Acute hematogenous osteomyelitis
pathophysiology

• A subperisoteal abscess then develops

• If left untreated this process eventually

results in extensive sequetra formation
and chronic osteomyelitis
 Acute hematogenous osteomyelitis
pathophysiology

• In children younger than 2 years, blood

vessels cross the physis, thus epiphysis
may be involved

• Limb shortening or angular deformity may

occur
 Acute hematogenous osteomyelitis
pathophysiology
• In children older than 2 years the physis
effectively acts as a barrier to the spread of a
metaphyseal abscess

• Metaphyseal cortex thicker, hence diaphysis

more at risk

• After physes are closed acute hematogenous

osteomyelitis is much less common
 Acute hematogenous osteomyelitis
pathophysiology
• After the physes are closed, infection can
extend directly from the metaphysis into
the epiphysis and involve the joint

• Septic arthritis resulting from acute

hematogenous osteomyelitis generally is
seen only in infants and adults.
 Acute hematogenous osteomyelitis
microbial pattern
• Staphylococcus aureus most common in older
children and adults
• Gram negative bacteria- increasing trend-
vertebral
• Pseudomonas most common in intravenous
drug abusers
• Salmonella in sicke cell
• Fungal infections in chronically ill patients on
long term intravenous therapy.
 Acute hematogenous osteomyelitis
microbial pattern
• Infants- staph aureus most common but group B
streptococcus and gram negative coliforms

• Prematures staph aureus andgram negative

organisms

• Hemophilus influenzae primarily in children 6

months to 4 years old, incidence decreased
dramatically by immunizations
 Acute hematogenous osteomyelitis
diagnosis
• History and physical examination
– Fever and malaise
– Pain and local tenderness
– Sweliing
– Compartment syndrome in children
 Acute hematogenous osteomyelitis
diagnosis
• Laboratory tests
– White blood cell count
– Erythrocyte sedimentation rate
– C-reactive protein
• checked very 2- 3 days post treatment
initiation
– Aspiration for suspected abscess
 Acute hematogenous osteomyelitis
diagnosis

• Plain radiographs

• Technetium-99m bone scan +/- MRI

 Radiographs
• Soft tissue swelling

• Periosteal reaction

• Bony destruction
(10-12 days)
 Bone scan

Can confirm
diagnosis
24-48 hrs after
onset
 Acute hematogenous osteomyelitis
Treatment

• Surgery and antibiotic treatment are

complementary, in some cases antibiotics
alone may cure the disease.

• Choice of antibiotics is based on the

highest bacteriocidal activity, the least
toxicity and the lowest cost
 Acute hematogenous osteomyelitis
Treatment
• Nade’s 5 principles of treatment
1. An appropriate antibiotic is effective
before pus formation

2. Antibiotics do not sterilize avascular

tissues or abscesses and such areas
require surgical removal
 Acute hematogenous osteomyelitis
Treatment- nades principles

3. If such removal is effective, antibiotics

should prevent their reformation and primary
wound closure should be safe

4. Surgery should not damage already

ischaemic bone and soft tissue

5. Antibiotics should be continued after surgery

 Acute hematogenous osteomyelitis
Treatment

• The two main indications for surgery in acute

hematogenous osteomyelitis are:
1. The presence of an abscess requiring
drainage
2. Failure of the patient to improve despite
appropriate intravenous antibiotic treatment
 Acute hematogenous osteomyelitis
Treatment- surgery
• The objective of surgery is to drain any abscess
cavity and remove all non viable or necrotic tissue
• Subperiosteal abscess in an infant-several small
holes drilled through the cortex into the medullary
canal
• If intramedullary pus is found, a small window of
bone is removed
• Skin is closed loosely over drains and the limb
splinted
 Acute hematogenous osteomyelitis
Treatment

• Generally a 6 week course of

intravenous antibiotics is given

• Orthopedic and infectious disease

followup is continued for at least 1
year
 SUBACUTE
HEMATOGENOUS
OSTEOMYELITIS

• More insidious onset and lacks

severity of symptoms

• Indolent course hence diagnosis

delayed for more than two weeks.
 SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
CLINICAL FEATURES
• The indolent course of subacute osteomyelitis is
due to:
– increased host resistance
– decreased bacterial virulence
– administration of antibiotics before the onset
of symptoms
• Systemic signs and symptoms are minimal
• Temperature is only mildly elevated
• Mild to moderate pain
 SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
INVESTIGATIONS
• White blood cell counts are generally normal

• ESR is elevated in only 50% of patients

• Blood cultures are usually negative

• Plain radiographs and bone scans generally

are positive
 SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
INVESTIGATIONS

• S. Aureus and Staphylococcus

epidermidis are the predominant
organisms identified in subacute
osteomyelitis
 SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
BRODIE ABSCESS
• Localized form of subacute osteomyelitis
occuring most commonly in the long bones
of the lower extremeties

• Intermittent pain of long duration is most

times the presenting compliant, along with
tenderness over the affected area
Brodie abscess
 SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
BRODIE ABSCESS
 On plain radiographs appears as a lytic lesion with
a rim of sclerotic bone

 S aureus is cultured in 50% of patients and in 20%

the culture is negative

 The condition requires open biopsy with curetage

to make the diagnosis

 The wound should be closed loosely over a drain

SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
Gledhill classification
 SUBACUTE HEMATOGENOUS
OSTEOMYELITIS
TREATMENT
• Biopsy and curettage followed by treatment
with appropriate antibiotics for all lesions
that seem to be aggressive

• For lesions that seem to be a simple

abscess in the epiphysis or metaphysis
biopsy is not recommended- IV antibiotics
for 48 hrs followed by a 6 week course of
oral antibiotics
 CHRONIC
OSTEOMYELITIS
• Hallmark is infected dead bone within a
compromised soft tissue envelope

• The infected foci within the bone are

surrounded by sclerotic, relatively
avascular bone covered by a thickened
periosteum and scarred muscle and
subcutaneous tissue
 com

• Sinus track cultures usually do not

corelate with cultures obtained at bone
biopsy
Classification of COM
Anatomical classification
 Diagnosis COM

• Based on
– Clinical
– laboratory and
– imaging studies
 Clinical evaluation COM

• Skin and soft tissue integrity

• Tenderness
• Bone stability
• Neurovascular status of limb
• Presence of sinus
 Laboratory COM
• Erythrocyte sedimentation rate
• C reactive protein
• WBC count only elevated in 35%
• Biopsy for histological and microbiological
evaluation
– Staphyloccocus species
– Anaerobes and gram negative bacilli
 Organisms in COM
• Girasi, 1981 found that the commonest
organisms found at the orthopaedic unit at
Kenyatta national hospital, then in kabete
was staphylococcus aureus which was
resistant to penicillin and ampicillin
 Imaging studies in COM
• Plain X rays
– Cortical destruction
– Periosteal reaction
– Sequestra
– Sinography
Sinography
 Imaging -

• Isotopic bone scanning more useful in

acute than in chronic osteomyelitis

• Gallium scans increased uptake in areas

where leucocytes and bacteria
accumulate. Normal scan excludes
osteomyelitis
 COM Imaging

• CT Scan
– Identifying sequestra
– Definition of cortical bone and
surrounding soft tissues
 COM Imaging
• MRI
– Shows margins of bone and soft tissue
oedema
– Evaluate recurrence of infection after 1 year
– Rim sign- well defined rim of high signal
intensity surrounding the focus of active
disease
– Sinus tracks and cellulitis
 Treatment of COM
• Surgical treatment mainstay
– Sequestrectomy
– Resection of scarred and infected bone
and soft tissue
– Radical debridement
– Resection margins >5mm
 Surgical treatment of COM
• Adequate debridement leaves a dead space that
needs to be managed to avoid recurrence, or
bony instability
– Skin grafts,
– Muscle and myocutaneous flaps
– Free bone transfer
– Papineau technique
– Hyperbaric oxygen therapy
– Vacuum dressing
 Treatment of COM
• Antibiotic duration is controversial
– 6 week is the traditional duration
– 1 week IV, 6 weeks of oral therapy
– Antibiotic polymethyl methacrylate (PMMA)
beads as a temporary filler of dead space
– Biodegradable antibiotic delivery system
Resection or excision for COM

• Resection of a segment of affected bone

may be necessary to control infection

• With techniques of bone and soft tissue

transport, massive resections can be
performed and reconstructed without
significant disability.
Resection or excision for COM
Amputation for osteomyelitis
• Amputation indications include
– Arterial insufficiency
– Major nerve paralysis
– Non functional limb-stiffness, contracture
– Malignant change
• Prevalence of maliganacy arising from COM
reported as 0.2 to 1.6% of cases.
• Most are squamous cell carcinoma, also
reticulum cell carcinoma,fibrosarcoma
 Sclerosing osteomyelitis of
garre’

• Bone is thickened and distended, but

abscesses and sequestra are absent.

• Cause unknown

• Thought to caused by a low grade,

possibly anaerobic bacterium
Sclerosing osteomyelitis
of garre’
 OSTEOPOROSIS
An overview of the condition and its treatment
 Definition

•Osteoporosis is a progressive systemic skeletal disease

characterised by low bone mass and micro-architectural
deterioration of bone tissue with a consequent increase in
bone fragility and susceptibility to fracture.
•World Health Organisation (1994)
•Osteoporosis is a chronic disease that has late clinical
consequences and has been referred to as a silent
epidemic because there are no associated signs or
symptoms before fracture.
 Bone
• 206 bones in the human skeleton
• Provide support, anchorage for muscles and protection for organs eg ribs
• Bone is a storage area for calcium and phosphorous salts and has an important role
in blood formation
• Before birth the skeleton is made of cartilage most of which is gradually replaced by
bone via a process called ossification.
• Bones of the human skeleton can be divided into long bone and flat bones
• Long bones are tubular and weight bearing and are made of a dense outer layer of
compact (cortical) bone and central region (medulla) made up of trabecular (spongy)
bone
• Trabecular bone makes up most of the short, flat and irregular shaped bones and the
epiphyses (ends) of the long bones
• It is much lighter than cortical bone and has a good strength to weight ratio
 Bone
• Trabecular bone is more susceptible to the effects of
osteoporosis

• Most osteoporotic fractures occur where there are high

levels of trabecular bone eg the vertebrae, the neck of
femur (hip) and the wrist
 Osteoporosis Pathogenesis
• Bone is constantly re-modelled and repaired due to
damage caused by daily use
• Osteoclasts “cut” into old bone (resorption) and
osteoblasts fill with organic matrix which becomes
mineralised (bone formation or ossification)
• In osteoporosis the net rate of bone resorption exceed
rate of bone formation- normally matched.
• Results in a decrease in bone mass and quality
 Bone tissue cells
• Basically three
• Osteoclasts- large multi-nuclear cells which release
enzymes and acids that digest protein and mineral
components of bone (resorption)
• Osteoblasts- bone builders, synthesize and secrete
collagen and other components to create a matrix which
is laid down in the bone. They initiate calcification of the
matrix and hence bone formation
• Osteocytes- mature bone cells (osteoblasts encased in
matrix secretions) responsible for exchange of waste
and nutrients.
Bone remodelling process
Normal v. Osteoporotic bone
 Osteoporosis Incidence

•UK incidence is 3 million (probably much more)

•Causes 310,000 fractures per year- including

60,000 hip, 50,000 wrist and 120,000 vertebral

•One in 3 women and one in 12 men over 50 will

sustain an osteoporotic fracture in their lifetime
 Risk factors for Osteoporosis
• Age- bone mineral density (BMD) decreases with age

• Hormones- lower levels of oestrogen after menopause accelerate

bone loss due to increased activity of osetoclasts.

• Premature menopause or hysterectomy causes earlier acceleration

of bone loss. Likewise surgical or chemical castration in men

• Gender- women are at increased risk of osteoporosis as they start

out with smaller bones and bone mass compared to men

• Genetic factors- family history of osteoporotic fracture, especially hip

fracture, increases risk
 Secondary causes of osteoporosis
• Long term corticosteroid use ie 5mg or more prednisolone
daily for 3 months or more
• Aromatase inhibitor treatment
• Hyperparathyroidism
• Hyperthyroidism
• Coeliac disease, malabsorption syndromes, inflammatory
bowel disease,IBS
• Anorexia
• Renal disease
• Rheumatoid arthritis
• Other drugs- PPI’S, SSRI’s, Anti-epileptics
 Modifiable risk factors
• Smoking- BMD lower in smokers

• Alcohol- BMD lower in alcoholics

• Weight- low BMI i.e. <19 is an indicator of low BMD

• Vitamin D and Calcium- vitamin D required for calcium absorption from

intestines, re-absorption from the kidneys and control of parathyroid
hormone

• Vitamin D levels and Calcium intake reduced in old age due to reduced
exposure to sunlight and changes in the epidermis and poor diet.

• Exercise- weight bearing exercise increases BMD and prolonged bed rest
decreases BMD
Bone Mass
 Diagnosis of osteoporosis
• Bone mineral density is main measure for diagnosis
• BMD measured by using Dual Energy X-ray Absorptiometry
(DEXA) scan
• Measurements usually made at lumbar spine and hip
• Usually reported as T scores and Z scores
• T score is the number of standard deviations from the peak bone
mass of young adults of the same sex
• Z score is the number of standard deviations from the average
bone mass of people of same age and sex
• T score between -1 and -2.5 indicates osteopenia
• T score -2.5 or less indicates osteoporosis
• T score -2.5 with a fracture is established osteoporosis
 Bone Mineral Density Values

• World Health Organization (WHO)

Osteoporosis Guidelines
DEXA scan results
 Criteria for referral for DEXA scan
(NHS Glasgow & Clyde)
• Over 50 yrs with a fragility fracture at any site (not
attributable to a RTA or a fall from above head height)
• Steroid exposure of at least 5mg prednisolone per day (or
equivalent) for at least 3 months
• Over 60 yrs and menopause under 45 yrs
• Over 60 yrs and acquired kyphosis
• Over 60 yrs and significant self-reported height loss
• Over 60 yrs and family history of 1 st degree relative with
fracture
• Over 60 yrs and family history of 1 st degree relative with
kyphosis
• Over 60 yrs and family history of 1 st degree relative with
DEXA confirmed osteoporosis
 Treatment of Osteoporosis
Bisphosphonates

• First line treatment for primary and secondary prevention of

osteoporotic fractures
• Reduce bone resorption by inhibiting action of osteoclasts
• Available orally as daily or weekly tablet, or as a yearly
injection
• Daily and weekly- alendronate, risedronate
• Yearly IV- zoledronate infusion
 Bisphosphonates cont.
• Oral bisphosphonates have complicated dosage regimes
and poor bioavailability
• Strong evidence to support their use
• Alendronate usually first choice due to cost
• GI Side effects are fairly common with oral
bisphosphonates
• Recent concerns regarding osteonecrosis of the jaw and
atypical stress fractures
 Treatment of Osteoporosis-
Strontium
• Claims to increase BMD by reducing bone resorption and
increasing bone formation by its action on osetoclasts and
osteoblasts

• Available as a powder for reconstitution and taken daily usually

bedtime

• Avoidance of food required 2 hours before and after administration

• GI side effects of nausea and diarrhoea but usually transient

• Possible slight increase in risk of venous thromboembolism (VTE)

 Treatment of Osteoporosis- others
• Raloxifene- selective oestrogen receptor modulator (SERM) which
selectively binds to oestrogen receptors on bone.
• Reduces incidence of vertebral fractures but no effect on non-
vertebral or hip fractures. Carries risk of VTE.
• Teriparatide- a fragment of recombinant human parathyroid
hormone. High levels of parathyroid hormone usually cause bone
resorption but pulsed doses cause formation. Daily injection.
Reduces vertebral and non-vertebral fractures but not hip.
Expensive and usually initiated by specialists.
• Calcitonin- hormone produced by thyroid gland. Given as a nasal
spray of synthetic calcitonin. Reduces risk of vertebral fracture only.
• Calcium and Vitamin D3- has an important role on bone formation
and remodelling. Calcium is required for bone mineralization and
vitamin D keeps parathyroid hormone secretion under control
 Newer Treatment
• Denosumab- a human monoclonal antibody
to the activator of receptors on osteoclasts
resulting in a reduction in their development
and activity and resultant increases in BMD
• Reduces risk of vertebral, non-vertebral and
hip fractures
• Given as a twice yearly s/c injection for 36
months
 Falls
• The most effective way to minimise osteoporotic fragility
fractures is to…….

• STOP PEOPLE FALLING!!!!

• If your Health Board has a Falls Prevention Programme

consider referral for your osteoporosis patients who have
suffered falls
Thank You