osteoarthritis of knee

1. Osteoarthritis O
Knee

2. OA KNEE
• Chronic, Non inflammatory, degenerative
disease.
• characterised by loss of articular cartilage
and periarticular bone remodelling,
particularly large weight-bearing joints
• Common in older patients but can occur in
younger patients ( genetic mechanism ,
previous joint trauma )

3. Pathophysiology
• Degenerative alterations primarily begin in the
articular cartilage
• External forces accelerate the catabolic effects of the
chondrocytes and disrupt the cartilaginous matrix
• Enzymatic destruction increases cartilage
degradation ↓ proteoglycans and collagen
synthesis
• Decreased strength of the cartilage is compounded
by adverse alterations of the collagen
• Reduced contact area of the cartilage

4. Pathophysiology
• Loss of cartilage results in the loss of the joint
space
• Progressive erosion of the damaged cartilage
occurs until the underlying bone is exposed
• Subchondral bone responds with vascular
invasion and increased cellularity, at areas of
pressure

5. Pathophysiology
• The traumatized subchondral bone may
undergo cystic degeneration
• At nonpressure areas along the articular
margin → irregular outgrowth of new bone
(osteophytes)

7. • Normal joint
• hinge joint formed

8. • Surface layer of cartilage
break down and wears
away,causes the bones
under the cartilage to rub
together
• Pain, swelling, and loss of
motion result
• formation of bone spurs

9. Incidence
• Incidence increases with age
• USA approximately 80-90% of individuals
older than 65 years have evidence of primary
osteoarthritis
• After age 55 years, the prevalence increases in
women in comparison with men

10. Incidence
• Equivalent prevalence occurs in men and
women aged 45-55 years (↑dramatically after
the age of 50 years)
• Most adults older than 55 years show
radiographic evidence of osteoarthritis
• No significant correlation exists between
incidence of OA and race

11. Causes
Primary OA
• Idiopathic
• Defective gene

12. Causes
Secondary OA
– Obesity
– Repetitive use (ie, jobs requiring heavy labor and
bending)
– Previous trauma (ie, posttraumatic OA)
– Infection

13. Causes
– Crystal deposition
– Acromegaly
– Previous rheumatoid arthritis (ie, burnt-out
rheumatoid arthritis)
– Heritable metabolic causes (eg, alkaptonuria,
hemochromatosis, Wilson disease)

14. Causes
– Hemoglobinopathies (eg, sickle cell disease,
thalassemia)
– Underlying orthopedic disorders (eg, congenital
hip dislocation, slipped femoral capital epiphysis)
– Disorders of bone (eg, Paget disease, avascular
necrosis)

15. History
• Insidious throbbing arthralgias with activity
• Initially, resting relieves the pain
• Eventually, the pain occurs even at rest
• Morning stiffness ≥ 30 minutes
• Intermittent joint swelling

16. Symptoms
• Pain
• Stiffness
• Gelling
• Instability

17. Signs
• Pain
• Tenderness
• Swelling
• Effusion
• Crepitus
• Limitation of movement and muscle wasting

18. Physical
• Early
– Joints may appear normal
– Gait may be antalgic if weight-bearing joints are
involved

19. Physical
• Later
– Visible osteophytes may be noted
– Joints may be warm to palpation
– Palpable osteophytes frequently are noted
– Joint effusion frequently is evidenced in
superficial joints

20. Physical
– Range-of-motion limitations, because of bony
restrictions and/or soft tissue contractures, are
characteristic
– Crepitus with range of motion is not uncommon

21. classification
1. Ahlbäck classification system
2. Kellgren and Lawrence system

22. 1. Ahlbäck classification system
• This classification was proposed by Ahlback et al in
1968.
• grade 1: joint space narrowing (less than 3 mm)
• grade 2: joint space obliteration
• grade 3: minor bone attrition (0-5 mm)
• grade 4: moderate bone attrition (5-10 mm)
• grade 5: severe bone attrition (more than 10 mm)

23. 2. Kellgren and Lawrence system
• This classification was proposed by Kellgren et al. in 1957 2
and later accepted by WHO in 1961.
• grade 0: no radiographic features of OA are present
• grade 1: doubtful joint space narrowing (JSN) and possible
osteophytic lipping
• grade 2: definite osteophytes and possible JSN on
anteroposterior weight-bearing radiograph
• grade 3: multiple osteophytes, definite JSN, sclerosis, possible
bony deformity
• grade 4: large osteophytes, marked JSN, severe sclerosis and
definite bony deformity

24. Imaging
• Plain radiographs
• Bone scans may be helpful in early diagnosis
of OA of the hand

25. • The space between the
bones of the upper and
lower leg is smaller
• Bony spurs
(osteophytes)
• Increase bone density
at the margin of the
joint

26. x-ray findings
–Joint space narrowing
–Osteophytes
–Subchondral sclerosis : ↑ bone density,
frequently found adjacent to joint space
–Subchondral cysts : fluid-filled sacs which
extrude from the joint

27. Diagnosis
• On the basis of the initial history and
examination
• X-rays

28. PROGRESS
• Osteoarthritis begins when the joint
cartilage starts to become worn down →
decreases the ability of the cartilage to
work as a shock-absorber to reduce the
impact of stress on the joints
• The remaining cartilage wears down
faster→ bones to grind against one
another
• Bone spurs may form

29. Treatment

30. Goals of managing OA
• Controlling pain
• Maintaining and improving the range of
movement and stability of affected joints
• Limiting functional impairment

31. Treatment
• Education and behavioural intervention
- Aim is to provide patients with an
understanding of the disease process, its
prognosis and the rationale and implications
of managing their condition
• Weight loss
- Weight loss (< 5 kg) has significant short-term
and long-term reduction in symptoms of OA

32. Treatment
• Mechanical aids
- Wear shock-absorbing footwear with good
mediolateral support, adequate arch support and
calcaneal cushion
• Exercise
• Aim of exercise is to reduce pain and disability by
strengthening muscle, improving joint stability,
increasing the range of movement and improving
aerobic fitness

34. Treatment
• Medication
- Acetaminophen (Tylenol®) is a mild pain
reliever with few side effects
• Anti-inflammatory medication, such as
ibuprofen and aspirin
• COX-2 inhibitors
• Glucosamine and Chondroitin sulfate

35. Treatment
• Intra-articular injection
- Glucocorticoids injection
- Hyaluronic Acid (HA) and similar
hyaluronan preparations (eg, Synvisc)

36. Treatment
• Surgery
• Arthroscopy (including debridement,and
lavage/irrigation)
• Proximal Tibial Osteotomy
• Artificial Knee Replacement
• Osteotomy
• Arthroplasty or Joint Replacement