2. Osteoarthritis (OA)
OA is a nonerosive, noninflammatory progressive
disorder of the joints leading to deterioration of the
articular cartilage and new bone formation at the joint
surfaces and margins.
OA is a disease of the cartilage initially, not bone.
OA is a clinical diagnosis.
3. OA is a disease that involves degeneration in
various structures of the joint, including
cartilage, bone, synovium, muscles, and
ligaments.
This can result in stiffness, loss of mobility,
swelling, and pain.
4. PREVALENCE
Most common form of arthritis and the second most common form
of disability in the United States.
Prevalence increases with age: approximately 70% population > 65
years old has radiographic
Increase in occupations with repetitive trauma.
Male:female ratio is equal between ages 45 and 55. After the age of
55, it is more common in women.
Obesity ® OA of the knee is most common.
6. CLASSIFICATION OF
OA
Primary OA (idiopathic)
Knees, MTP, DIP, carpal metacarpal joint (CMC), hips, and spine primarily involved.
Secondary OA ® follows a recognizable underlying cause.
Elbows and shoulder involvement
Chronic or acute trauma, connective tissue disease (CTD), endocrine or metabolic,
infectious,
neuropathic and crystal deposition, bone dysplasias
Erosive inflammatory OA.
Diffuse idiopathic skeletal hyperostosis (DISH)
7. OA Affected Joints
Primary OA: Knees, MTP, DIP, carpal
metacarpal joint (CMC), hips, spine
Secondary OA: Elbows and shoulders
8. PATHOLOGY
Early ® Hypercellularity of chondrocytes.
Cartilage breakdown: Swelling and loosening
of collagen framework.
Increased proteoglycan synthesis.
Minimal inflammation.
9. PATHOLOGY
Later ® Cartilage fissuring, pitting, and destruction.
– Hypocellularity of chondrocytes.
– Inflammation secondary to synovitis.
– Osteophytes spur formation—seen at the joint margins.
– Subchondral bone sclerosis (eburnation).
– Cyst formation in the juxta-articular bone.
Loss of proteoglycans.
Increased water content of OA cartilage leads to damage of the collagen network
(increased chondrocytes, collagen, and enzymes).
14. Symptoms
Dull aching pain increased with activity, relieved by rest.
Later pain occurs at rest.
Joint stiffness for <30 minutes; becomes worse as the day goes on.
Joint giving away.
Articular gelling ® stiffness after immobility lasting short periods and
dissipating after brief period of movement.
Crepitus on ROM.
15. Signs
Mono- or pauciarticular; shows no obvious joint pattern.
Localized tenderness of joints.
Pain and crepitus of involved joints.
Enlargement of the joint ® changes in the cartilage and
bone secondary to proliferation of synovial fluid and
synovitis.
16.
17. SPECIFIC JOINT
INvOLvEMENT
Heberden’s nodes ® osteophytosis (bone spur formation) at the DIP joints
Bouchard’s nodes ® PIP
First CMC joint
Knee—narrowing of medial compartment
Hips—narrowing of superior lateral compartment, loss of ROM
Acromioclavicular joint
First MTP joint
Spine
– Spondylosis
– Involvement of the intervertebral fibrocartilaginous disc and vertebrae
– Diffuse idiopathic skeletal hyperostosis (Snider, 1997)
