Osteoarthritis - Clinical features , diagnosis , management

1. Osteoarthritis

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

3.  Common in weight-bearing joints such as hip and knee.
 Also seen in cervical , lumbosacral spine and in hands (DIP, PIP, base of thumb).
 Both male and females are affected.
 But more common in older women i.e. above 50 yrs,particularly in postmenopausal
age.

4. JOINT PROTECTIVE MECHANISMS
 SYNOVIAL FLUID
 JOINT CAPSULE AND LIGAMENTS
 MUSCLE
 SENSORY AFFERENTS
 UNDERLYING BONE

5. SYNOVIAL FLUID
 Reduces friction between articulating cartilage surfaces
 Hyaluronic acid + lubricin
 Concentration of the above – reduced in injury/ inflammation of synovium

6. LIGAMENTS, SKIN, TENDONS
 Contain mechanoceptor sensory afferent nerves
 Provide feedback via spinal cord to muscles + tendons

7. CARTILAGE
 Impact absorbing capacity along with synovium
 Earliest OA changes occur here
 Healthy cartilage – avascular due to angiogenesis inhibitors in cartilage
 Diseased cartilage – invasion of blood vessels into cartilage from bone and proliferation
in synovium
 VEGF synthesis in bone + cartilage is implicated
 OA cartilage – depletion of aggrecan, loss of type 2 collagen, unfurling of collagen
matrix

9. 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

10. Articular Cartilage
o Cartilage - 1st structure to be affected.
o Erosion occurs, often central & frequently in wt. bearing areas.
o Fibrillation - causes softening, splitting and fragmentation of cartilage,in both wt.
bearing & non-wt. bearing areas.
o Collagen fibres split , disorganisation of proteoglycan-collagen relationship
o Further softening and flaking.
o Flakes of cartilage break off, may be impacted b/w jt.surfaces  locking and
inflammation.

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

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

13. 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.

14. 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.

15.  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.

16. Osteophyte at margin of
articular surface

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

19. Ligament
Undergoes fibrous degeneration
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.

22. CLINICAL FEATURES
 JOINT PAIN – ACTIVITY RELATED
 IN EARLY DISEASE – Episodic, triggered by overuse of diseased joint
 Progressively, continuous pain, even disturbs sleep at night
 Stiffness of the joint.
 Morning stiffness – brief ( <30min)
 In knee- buckling, catching, locking
 Pain with activities requiring knee flexion ( climbing stairs, rising from a chair )

24. 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.

25. Knee joint
effusion

26. 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.

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

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

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

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

34. 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.

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