Transcript OA Knee

Osteoarthritis
• Typically affects the fingers, spine, hips
and knees
BY
INT. KAMOLWAN
OA KNEE
• Chronic, degenerative disorder of
multifactorial aetiology, 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 )
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
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
Pathophysiology
• The traumatized subchondral bone may
undergo cystic degeneration
• At nonpressure areas along the articular
margin → irregular outgrowth of new bone
(osteophytes)
• Normal joint
• hinge joint formed
• 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
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
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
Causes
Primary OA
• Idiopathic
• Defective gene
Causes
Secondary OA
– Obesity
– Repetitive use (ie, jobs requiring heavy labor
and bending)
– Previous trauma (ie, posttraumatic OA)
– Infection
Causes
– Crystal deposition
– Acromegaly
– Previous rheumatoid arthritis (ie, burnt-out
rheumatoid arthritis)
– Heritable metabolic causes (eg, alkaptonuria,
hemochromatosis, Wilson disease)
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)
History
• Insidious throbbing arthralgias with activity
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Initially, resting relieves the pain
Eventually, the pain occurs even at rest
Morning stiffness ≥ 30 minutes
Intermittent joint swelling
Symptoms
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Pain
Stiffness
Gelling
Instability
Signs
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Pain
Tenderness
Swelling
Effusion
Crepitus
Limitation of movement and muscle
wasting
Physical
• Early
– Joints may appear normal
– Gait may be antalgic if weight-bearing joints
are involved
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
Physical
– Range-of-motion limitations, because of bony
restrictions and/or soft tissue contractures,
are characteristic
– Crepitus with range of motion is not
uncommon
Imaging
• Plain radiographs
• Bone scans may be helpful in early
diagnosis of OA of the hand
• 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
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
Diagnosis
• On the basis of the initial history and
examination
• X-rays
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
Treatment
Goals of
managing OA
• Controlling pain
• Maintaining and improving the range of
movement and stability of affected joints
• Limiting functional impairment
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 shortterm and long-term reduction in symptoms
of OA
Treatment
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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
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
Treatment
• Intra-articular injection
- Glucocorticoids injection
- Hyaluronic Acid (HA) and similar
hyaluronan preparations (eg, Synvisc)
Treatment
• Surgery
- Arthroscopy (including debridement,and
lavage/irrigation)
- Proximal Tibial Osteotomy
- Artificial Knee Replacement
- Osteotomy
- Arthroplasty or Joint Replacement