2. Session Objectives:
By the end of the session the participant will be
able to :
Identify musculo- skeletal disorders ( Collagen ,
metabolic).
Describe the clinical picture of musculo-
skeletal disorders .
Discuss D.D. (differential diagnosis).
Management skills.

4. Osteoarthritis (OA)

5.  OA is the single most important cause of
locomotor disability.
 OA used to be considered as ‘wear and tear’
of the bone and cartilage of synovial joints
but is now recognized as a metabolically
active process involving the whole joint i.e.
cartilage, bone, synovium, capsule and
muscle.

6. The main reason for patients seeking medical
help is pain.
The level of pain and disability are greatly
influenced by the patients’ personality, level
of anxiety, depression and activity and often
do not correlate well with the clinical signs.

7. Risk Factors:
↑age (uncommon <45y.).
F > M.
↑ in black and Asian populations.
Genetic predisposition
Obesity.

8. Risk Factors:
Abnormal mechanical loading of
joint e.g. instability.
Poor muscle function.
Post-meniscectomy.
Certain occupations e.g. farming.

9. Symptoms and Signs
Joint pain ± stiffness, synovial thickening,
deformity, effusion, crepitus, muscle weakness
and wasting and ↓ function.
Most commonly affects hip, knee and base of
thumb.

10.  Typically exacerbations occur that may last
weeks to months.
 Nodal OA, with swelling of the distal
interphalangeal joints (Heberdens nodes) has a
familial tendency.

13. Investigations
X-rays may show ↓ joint space, cysts and
sclerosis in subchondral bone and
osteophytes.
Check FBC and ESR if inflammatory arthritis
is suspected (normal in OA).

14. Disc space containing:
-osteophytes (arrows)
-sclerosis of adjacent surfaces of vertebral
bodies

15. Cervical spondylosis:
-c5_c6 & c6_c7 disc spaces are
narrowed
-osteophytes (arrow)

16. Cervical spondylosis
Osteophytes (arrows) are narrowing
foramina

17. Management
Exclude other causes of pain:
sepsis, bursitis.
 Gout.
 Inflammatory arthritis and fibromyalgia.
 OA may be a coincidental finding and not the
cause of the patients’ pain.

18. Aim of treatment :
Patient education.
↓ pain.
Optimisation of function and minimization of
progression.

19.  Give information and advice and refer to
other members of the multidisciplinary
team as appropriate e.g. physiotherapist
for advice on exercises.
 Strapping and splints.

20.  OT for aids, chiropodist for foot care and
insoles.
 Social worker for advice on disability
benefits and housing and orthopaedic
surgeon for assessment for joint
replacement.

21. ↓ load on the joint: Weight reduction can ↓
symptoms and may ↓ progression in knee
OA.
Using a walking stick (opposite hand to
affected hip) and cushioned insoles or
shoes (e.g. trainers) can help.

22. Exercise and improving muscle strength ↓
pain and disability e.g. walking (for OA knee),
swimming (for OA back and hip but may make
neck worse), cycling (for OA knee but may
worsen patellofemoral OA).

23.  Refer to physiotherapy for advice on
exercises especially isometric exercises
for the less mobile.

24.  Pain control: Regular Paracetamol is
effective for many patients.
 NSAIDs are overused and there is no
evidence of additional benefit over simple
analgesics except in acute exacerbations.

25.  Topical NSAIDS have fewer side effects
than oral and may be helpful for superficial
joints, as may rubefacients and counter-
irritants (e.g. Capsaicin cream).
 Some patients find local heat or cold
soothing.

26.  Low dose antidepressants e.g.
Amitriptyline are a useful adjunct
especially for pain causing sleep
disturbance.

27.  Aspiration of joint effusions and Steroid
injections can help in exacerbations.
 There are ongoing trials of injections of
joint lubricants e.g. hyaline.

28.  Psychological factors have a major impact
on the disability from OA.
 Education about the disease and emphasis
that it is not progressive in most people is
important.
 Seek and treat depression and anxiety.

29.  Refer: To orthopaedics if diagnosis in
doubt (urgently if you suspect joint sepsis),
or if symptoms are severe for assessment
for joint washout, cartilage debridement or
joint replacement.

31. Gout

32. Gout:
Intermittent attacks of acute joint pain due
to deposition of uric acid crystals.
Prevalence: 3—8/1000.
↑ with age.
M:F ≈ 5:1.

33.  Predisposing factors: FH, obesity, excess
alcohol intake, high purine diet, diuretics,
acute infection, ketosis, surgery,
polycythemia, leukaemia, cytotoxics and renal
failure.

34. Associations:
Gout may be linked to ↑ risk of
hypertension and coronary heart
disease.

35. Acute Gout
Presentation:
Severely painful swollen joint (big toe
most common site).
Red skin which may peel.
May have fever.

36.  ↑ WCC.
 ↑ ESR.
 ↑ blood urate (but may be normal)
Resolves in <2wk.—often after 2—
7d. if treated.
 Exclude infection as cause of
symptoms.

37.  Microscopy of synovial fluid reveals sodium
monourate crystals.
 X-rays show soft tissue swelling only.
 These investigations are not routinely
required.

38. Treatment
Rest joint.
NSAIDs (e.g. Diclofenac or Indomethacin
50mg tds—caution if GI problems)
Or Colchicine (1mg then 500mcg 2—3hrly
until pain is relieved or side effects e.g.
nausea, vomiting or diarrhoea, max 6mg. do
not repeat within 3d).

39. Prevention
Lose weight.
Avoid excess alcohol.
Avoid purine rich foods (e.g. offal,
red meat, yeast extracts, pulses and
alcohol).
Avoid Thiazide diuretics and Aspirin.

40. Prophylactic medication:
Allopurinol 100—300mg daily
 wait until 1mo. after acute attack and co-
prescribe Colchicine (500mcg bd) or NSAID for
first l—3mo. to try and avoid precipitation of
another acute attack.
 Side effect—rash.
 Check serum urate level after 2mo.
 Aim for 4—7mg/dl.

41. Alternatively try an uricosuric e.g.
Probenecid 250—500mcg bd.

42. Chronic Gout
 Recurrent attacks, tophi (urate deposits)
in pinna, tendons and joints and joint
damage.
 Refer to a rheumatologist for on-going
treatment.

44. Gout: well defined erosion (arrow)at
metatarsophalangeal joint of big toe

45. Gout:
-tophi ; large soft tissue swellings e.g: around
proximal interphalangeal joint of the
index

46. Pseudogout And Calcium Pyrophosphate Deposition
Inflammatory arthritis due to
deposition of Pyrophosphate crystals.
Chondrocalcinosis seen on X-ray
(calcification of articular cartilage).
Knee, wrist and shoulder are most
commonly affected.

47.  Attacks are less severe than gout and
may be difficult to differentiate from OA.
Presence of joint crystals confirms
diagnosis.
 Chronic form also occurs—non-
erosive.
 Treat with analgesia and NSAIDs.

49. Osteoporosis

50. Osteoporosis
Bone mineral density (BMD) >2.5 standard
deviations (SD) below the young adult mean.
There is an ↑ relative risk of fracture x2—3 for
each SD ↓ in BMD.
Prevalence: 5%. F:M ≈ 4:1. ↑ risk with ↑ age.
1:2 women and 1:6 men will have an
osteoporotic fracture by the age of 90y.

51. Other Risk Factors:
 Menopause (particularly if <45y.) or
amenorrhoea during reproductive years.
 Prolonged steroid use or Cushing’s
disease
 Anorexia (and thin women generally)
 Mlabsorption.

52. Other Risk Factors:
• Prolonged bed rest/immobility.
• Family history.
• Thyrotoxicosis.
• Smoking.

53. Common fractures:
Wrist (Colles’).
Spine and hip (associated with 15% ↑
mortality).

54. Diagnosis
 Usually diagnosed after fracture occurs.
Osteoporotic vertebral collapse causes pain,
loss in height and kyphosis.
 Pain can take 3—6mo. to settle and requires
strong analgesia.
 Exclude other causes of pathological
fracture (e.g. malignancy).

55. Investigations:
 Ca2+, P04 and Alk Phos are normal.
Osteopoenia cannot be reliably diagnosed on
X-ray—though vertebral fractures may be
seen.
BMD measurement by DEXA (dual energy X-
ray absorpiometry) scan can quantify
osteoporosis.
Follow local referral guidelines.

57. Senile osteoprosis:
-decrease bone density
-well demarcated edge of
vertebral bodies
-partial collapse of vertebral bodies

58. BMD
T-SCORE:
Comparison of patient’s bone mass to
that of young normal subject
Z-SCORE:
Comparison of patient’s bone mass to
that of age and sex matched
subjects

59. T-SCORE:
T-SCORE > -1 normal
T-SCORE -1 : -2.5 osteopenia
T-SCORE < -2.5 osteoprosis

60. Treatment
 Treat those at high-risk and/or with history
of osteoporotic fracture without
investigations.
 BMD helps determine whether to start
preventative treatment in those with
borderline risk factors (treat if BMD >2.5 SD
below young adult mean).

61.  Address risk factors.
 Refer to start drug treatment with HRT or
Bisphosphonates—choice depends on
acceptability, tolerability and presence of
other indications or contraindications for
HRT.

62. Vitamin D (400—800 IU) combined with
Calcium supplements:
↓ fractures in the elderly.
Consider in housebound and institutionalized
patients.
Ca2+ supplements (≥l g elemental Ca2+/d.)
alone slow bone loss in postmenopausal
women but are less effective than
HRT/Bisphosphonates and there is no
evidence of ↓ fracture rate.

63. Calcitriol and Raloxifene
Role uncertain.
Use only on specialist advice.

64. Prevention:
Prevention is better than cure.
Aim to prevent fractures by targeting
high-risk patients.

65. Stop smoking:
• Stopping before the menopause ↓
later fracture rate by 25%.
Adequate dietary calcium intake:
• >800mg calcium (=1 pint milk) +
400-800Iu Vitamin D/d.

66. Regular exercise:
Weight-bearing activity >30min./d. ↓
fractures even in those >70y.
Hip protector pads:
For elderly likely to fall can ↓ fractures
but are poorly tolerated.

67. HRT:
Was the mainstay of osteoporosis
prevention in post-menopausal women and
is especially beneficial for women with pre-
mature menopause.
It postpones postmenopausal bone loss
and ↓ fractures.

68.  Optimum duration of use is uncertain (>5
—7y.) but benefit is limited to current or
recent users (no effect >5y. after stopping).
 Whether to start HRT straight after the
menopause or later is uncertain.

69. HRT use brings concerns regarding ↑ breast
cancer and venous thromboembolism.
Balance benefits and risks in each patient.
Long-term compliance with HRT is poor.

70. Prophylaxis for those on long term steroids:
>7.5mg Prednisolone/d. for >6mo. accelerates
bone loss and ↑ fracture risk.
Advise patients on risk, assess other risk
factors and ensure adequate calcium + vitamin
D intake.

71.  Prescribe concurrent prophylaxis (e.g.
HRT or Bisphosphonates) if >65y., >l5mg/d.
or strong risk factors without further
investigation.
 Otherwise assess BMD at baseline yearly
thereafter— treat if significant bone loss.

73. Rickets/Osteomalacia

74. Rickets/Osteomalacia
Vitamin D deficiency leads in children to
softening and deformity, particularly of the
long bones and in adults to fractures, bone
pain and proximal myopathy.

75. Characteristic features are: soft skull bones,
enlarged ends of ribs (rachitic rosary), bowed
legs or knock knees.
May also cause bone pain, pseudofractures
and short stature.

76. Causes:
 Dietary deficiency: Occurs particularly in
children with pigmented skin and in Northern
climates where there is less sunlight.
 2ry rickets: Vitamin D deficiency is due to
other disease e.g. malabsorption, liver
disease, renal tubular disorders or chronic
renal failure.

77. Vitamin D dependent rickets:
Rare autosomal recessive disorder resulting in
an enzyme deficit in the metabolism of vitamin
D.
Refer for specialist management.
Treatable with vitamin D and calcium.

78. Hyperphosphataemic rickets (vitamin D
resistant rickets):
X-linked dominant trait resulting in ↓
proximal renal tubular resorption of
phosphate.
Parathyroid hormone and vitamin D levels
are normal.

80. • Specialist management is
needed.

81. Osteomalacia
Asymptomatic
Diffuse skeletal pain
Proximal muscle weakness;waddling
gait and difficulties in climbing stairs
Pseudofracture
Treated by vit D and calcium

82. Osteomalacia: -looser’s zone (arrow)
-dec. bone density
-partial collapse of vertebral
bodies

84. Paget’s Disease Of Bone

85. Paget’s Disease Of Bone
Accelerated disorganized bone remodelling
due to abnormal osteoclast activity.
Affects up to 1:10 of the elderly but only 5%
are symptomatic.
M:F ≈ 3:1.

86.  Signs and symptoms: Pain—dull ache
aggravated by weight bearing.
 Deformity (bowing of weight bearing
bones especially tibia (sabre), femur and
forearm—usually asymmetrical), frontal
bossing of forehead.

91. Diagnosis:
Clinical X-ray (distinctive changes).
↑ bone specific Alkaline phosphatase
(normal Ca2+, PO4, PTH).

92. Management
↓ pain and long term complications with
Bisphosponates (e.g. Alendronate 40mg/d
for 6mo.) and analgesia.

93. Thank You