1. Osteoarthritis
(Degenerative
arthritis/osteoarthrosis/hypertrophic
arthritis)

2. Osteoarthritis
 Osteoarthritis is a non-inflammatory,
degenerative condition of joints
Characterized by degeneration of articular
cartilage and formation of new bone i.e.
osteophytes.

4.  Common in weight-bearing joints such as
hip and knee.
 Also seen in spine and hands.
 Both male and females are affected.
 But more common in older women i.e.
above 50 yrs,particularly in
postmenopausal age.

5. Risk factors
 Obesity esp OA knee
 Abnormal mechanical loading
eg.meniscectomy, instability
 Inherited type II collagen defects in
premature polyarticular OA
 Inheritance in nodal OA
 Occupation eg farmers
 Infection:Non-gonococcal septic arthritis
Hereditary

6. Ageing process in joint cartilage
Defective lubricating mechanism
Incompletely treated congenital
dislocation of hip

7. Classification of OA
OA
Primary OA Secondary OA

8. Primary OA
 More common than secondary OA
 Cause –Unknown
 Common-in elders where there is no
previous pathology.
 Its mainly due to wear and tear changes
occuring in old ages mainly in weight
bearing joints.

9. Secondary OA
 Due to a predisposing cause such as:
1.Injury to the joint
2.Previous infection
3.RA
4.CDH
5.Deformity
6.Obesity
7.hyperthyriodism

10. Types of OA
 Nodal Generalised OA
 • Crystal Associated OA
 • OA of Premature Onset

11. Nodal Generalised OA
• • Heberden’s nodes
• • Bouchard’s nodes
• • CMC of thumb
• • Hallux
• valgus/rigidus
• • Knees & hips
• • Apophyseal joints

12. Crystal Associated OA
• Calcium pyrophosphate
• dihydrate occurs
• mainly in elderly
• women, and principally
• affects the knee

13. OA of Premature Onset
• • Previous meniscectomy
• • Haemochromatosis

15. Pathology
 OA is a degenerative condition primarily
affecting the articular cartilage.
1.articular cartilage
2.Bone
3.Synovial membrane
4.capsule
5.Ligament
6.muscle

16. Articular Cartilage
 Cartilage is the 1st structure to be affected.
 Erosion occurs,often central & frequently in wt.
bearing areas.
 Fibrillation,which causes softening,splitting and
fragmentation of the cartilage,occur in both wt.
bearing & non-wt. bearing areas.
 Collagen fibres split and there is disorganisation
of the proteoglycon collagen relationship such
as H2O is attracted into cartilage, which causes
futher softening and flaking.these flakes of
cartilage break off and may be impacted b/w the
jt.surfaces causing locking and inflammation.

17. Right: Early OA with
area of cartilage loss in
the center.
Left: More advanced
changes with extensive
cartilage loss and
exposed underlying
bone

18. Arthroscopic appearances
in OA of the knee joint:
fibrillated surface of the
cartilage on the medial
femoral condyle

19. Bone(Eburnation)
 Bone surface become hard & polished as
there is loss of protection from the
cartilage.
 Cystic cavities form in the subchondral
bone because eburnated bone is brittle
and microfractures occur.
 Venous congestion in the subchondral
bone.

20. Gross superior view of a
femoral head from a
patient with radiographic
stage I OA. This shows an
area of complete cartilage
loss, with polishing or
eburnation of the
underlying bone.

21.  Osteophytes form at the margin of the
articular surface,which may get projected
into the jt. Or into capsule & ligament,bone
of the wt.-bearing jt.
 There is alteration in the shape of the
femoral head which becomes flat and
mushroom shaped.
 Tibial condyles become flatened.

22. Osteophyte at margin of articular
surface

23. Synovial Membrane
 Synovial membrane undergo hypertrophy and
become oedematous (which can lead to ‘cold’
effusions).
 Reduction of synovial fluid secretion results in
loss of nutrition and lubricating action of articular
cartilage.
Capsule
It undergoes fibrous degeneration and there are
low-grade chronic inflammatory changes

25. Ligament
 Undergoes fibrous degernation
 There is low grade chronic inflammatory
changes and acc.to the aspect joint
become contracted or elongated.
Muscles
Undergoes atrophy,as pt. is not able to use
the jt. Because of pain which further limits
movts. and function.

28. Clinical features of OA
 Pain
 Stiffness
 Muscle spasm
 Restricted movement
 Deformity
 Muscle weakness or wasting
 Joint enlargement and instability
 Crepitus
• Joint Effusion

29. Clinical features 1
• Pain and tenderness
– Usually slow onset of discomfort, with
gradual and intermittent increase
– Pain is more on wt. bearing due to stress
on the synovial membrane & later on due
to bone surface,which r rich in nerve
endings coming in contact.
-initially relieved by rest but later on disturb
sleep.
-Diffuse/ sharp and stabbing local pain

31. Clinical features
• Pain and tenderness (cont)
– Types of pain
• Mechanical: increases with use of the joint
• Inflammatory phases
• Rest pain later on in 50%
• Night pain in 30% later on

32. Clinical features 2
• Movement abnormalities
– ‘Gelling’: stiffness after periods of inactivity,
passes over within minutes (approx
15min.) of using joint again
– Coarse crepitus: palpate/hear (due to
flaked cartilage & eburnated bone ends)
– Reduced ROM: capsular thickening and
bony changes in joint,ms. Spasm or soft
tissue contracture.

33. Clinical features 3
• Deformities
– Soft tissue swelling:
• mild synovitis
• small effusions
– Osteophytes
– Joint laxity
– Asymmetrical joint destruction leading to
angulation

34. Osteoarthritis of the DIP
joints. This patient has
the typical clinical
findings of advanced
OA of the DIP joints,
including large firm
swellings (Heberden’s
nodes), some of which
are tender and red due
to associated
inflammation of the
periarticular tissues as
well as the joint.

35. Knee joint effusion

36. A patient with
typical OA of the
knees. In the normal
standing posture
there is a mild varus
angulation of the
knee joints due to
symmetrical OA of
the medial
tibiofemoral
compartments.

37. Pseudolaxity due to
cartilage loss. The
joint is not loaded in
the first photograph

38. Unstable distal
interphalangeal
joints in OA. The
examiner is able to
push the joint from
side to side due to
gross instability, a
common finding in
late interphalangeal
joint OA.

39. Radiographic Classification
Stage 1 Bony spur only
Stage 2 Narrowing of jt.
Space,less than half of
the normal jt. space
Stage 3 Narrowing of jt.
Space,more than half
of the normal jt. space
Stage 4 Obliteration of jt. space
Stage 5 Subluxation or
sec.lateral arthrosis

40. Distribution of OA of the
hip joint. OA can
maximally affect the
superior pole, inferior
pole, posterior part or
other segments of the
hip joint. Superior pole
involvement, with a
tendency for the head
of the femur to sublux
superolaterally, is the
commonest pattern.
Involvement of the
whole joint (concentric
OA) is relatively
uncommon.

42. Special Investigations
• Blood tests: Normal
• Radiological features:
– Cartilage loss
– Subchondral sclerosis
– Cysts
– Osteophytes

44. Management

46. Treatment Principles
• Education
• Physiotherapy
– Exercise program
– Pain relief modalities
• Aids and appliances
• Medical Treatment
• Surgical Treatment

47. Education
• Nonsystemic nature of disease
• Prevent overloading of joint. Obesity!!
• Appropriate use of treatment modalities
– Importance of exercise program
– Aids, apliances, braces
– Medial treatments
– Surgical treatments

49. Exercise
• Will not ‘wear the joint out’
• Important for cartilage nutrition
• Some evidence that lack of exercise leads
to progression of OA

50. Exercise
• Encourage full range low impact
movements eg swimming, cycling
• Avoid
– Prolonged loading
– Activities that cause pain
– Contact sports
– High impact sports eg running

51. Quadriceps exercises
for knee OA.
Quadriceps exercises
are of proven value for
pain relief and
improving function, and
everyone with knee OA
should be taught the
correct techniques and
encouraged to make
these exercises a
lifetime habit. There is a
weight on the ankle.

52. Use of transcutaneous
nerve stimulation
(TENS) as an adjunct to
other therapy for pain
relief at the knee joint.
The use of
acupuncture, TENS and
other local techniques
to aid pain relief in
difficult cases of OA is
often worthwhile.

53. Aids and appliances
• Braces / splints
• Special shoes/insoles
• Mobility aids
• Aids: dressing, reaching, tap openers,
kitchen aids
• Taping of patella in patello femoral OA

54. Use of a cane, stick or other walking aid. This patient,
who has hip OA, has found that she can reduce the
pain in her damaged left hip by leaning on the stick in
the right hand as she walks. The reduction in loading
can be huge, and the effect on symptoms and
confidence with walking very beneficial.

55. The use of shoes and
insoles to reduce
impact loading on lower
limb joints. Modern
sports shoes (‘trainers’)
often have appropriate
insoles. Alternatively,
special heel or shoe
insoles of sorbithane or
viscoelastic materials
can be used. They may
help relieve pain as well
as reducing the peak
impact load on the
joints during walking.

56. Medical Treatment
• Simple analgesics: paracetamol, low dose
ibuprofen
• NSAID’s/Coxibs PRN regular
• Intra-articular corticosteroids
• Topical treatment eg NSAID creams,
capsaicin
• ‘Chondroprotective agents’

57. A patient with OA of the
carpometacarpal joint of
the left thumb
undergoing
arthrocentesis for
injection of a depot
corticosteroid
preparation. The
operator is distracting
the patient’s thumb to
open up the joint space.

59. Joint replacement surgery
• Indications: pain affecting work, sleep,
walking and leisure activities
• Complications
– sepsis
– loosening
– lifespan of materials (mechanical failure)