OSTEOARTHRITIS

Epidemiology
 prevalence of OA at all joint sites progressively increases with age. OA affects 25-
30% of persons aged 45-64 years, OA affects 60% of persons older than 65 years,
and OA affects more than 80% of persons older than 75 years.
 Females have a higher prevalence of OA of the knees and hands, whereas males
have higher prevalence of OA of the hips

Pathogenesis
 Cartilage destruction secondary to biomechanical and biochemical forces
 IL-1 and TNF activates matrix metalloproteinases (MMP1, 8, 13) involved in
proteolytic digestion of cartilage
 TGF-B and IGF-1 plays a role in cartilage repair
 End result
1. Asymmetric joint cartilage loss
2. Subchondral sclerosis (bone density increased)
3. Subchondral cysts
4. Marginal osteophytes

Stage 1
 Proteolytic breakdown of the cartilage matrix occurs.
 Chondrocyte metabolism is affected, leading to an increased production of
enzymes, which includes metalloproteinases (eg, collagenase, stromelysin) that
destroy the cartilage matrix.
 Chondrocytes also produce protease inhibitors, including tissue inhibitors of
metalloproteinases (TIMP) 1 and 2 but in amounts insufficient to counteract the
proteolytic effect.

Stage 2
 fibrillation and erosion of the cartilage surface, with a subsequent release of
proteoglycan and collagen fragments into the synovial fluid.

Stage 3
 The breakdown products of cartilage induce a chronic inflammatory response in
the synovium. Synovial macrophage production of cytokines, such as interleukin 1
(IL-1), tumour necrosis factor-alpha, and metalloproteinases, occurs.
 These can diffuse back into the cartilage and directly destroy tissue or stimulate
chondrocytes to produce more metalloproteinases.
 pro-inflammatory molecules (eg, nitric oxide [NO], an inorganic free radical) also
may be a factor.
 compensatory bone overgrowth occurs in an attempt to stabilize the joint.
 At non-pressure areas along the articular margin, vascularisation of subchondral
marrow, osseous metaplasia of synovial connective tissue, and ossifying
cartilaginous protrusions lead to irregular outgrowth of new bone (osteophytes).
 Fragmentation of these osteophytes or of the articular cartilage itself results in
intra-articular loose bodies (joint mice).
 As the joint architecture is changed and further mechanical and inflammatory
stress occurs on the articular surfaces, the disease progresses unchecked.

Classification

Primary OA
 most common type of OA and has no identifiable underlying aetiology or
predisposing cause.
 More common in load bearing joints
 Associated with obesity

Secondary OA (other conditions that damage cartilage)

1. Metabolic
 Gout
 Inherited diseases of iron, copper, calcium storage
 Hemochromatosis (iron)
 Spoon nails (koilonychia)
 Associated with OA of knees and of 2nd/3rd MCPJ
 Hyperparathyroidism
 Wilson’s disease (copper)

2. Anatomic
 Congenital disorders causing abnormal joint loading
 Hyperlaxity
 Leg length inequality
3. Traumatic
4. Inflammatory
 Ankylosing spondylitis, septic arthritis

Subtypes of Primary OA
 1. Primary generalised OA
a. characterized by familial and often premature development of
Heberden and Bouchard nodes, as well as the precocious
degeneration of the articular cartilage of multiple other joints,
including the first carpometacarpal joints, knee joints, hip joints, and
spine articulations
2. Erosive OA
a. secondary to an aggressive form of the disease and usually occurs in
middle-aged women.
b. usually associated with acute features of inflammation and subsides
over months to years, leaving joint deformity and ankylosis.
c. typically bilateral and symmetric, and it occurs most often in the
interphalangeal, particularly distal interphalangeal, joints of the hands.
1st CMC often involved with squared off appearance
d. MCP joints and wrists are usually spared in erosive osteoarthritis
e. Because it can present as an acute to subacute onset symmetric
inflammatory arthritis with morning stiffness, it is often initially
mistaken for rheumatoid or psoriatic arthritis.
f. Radiographically, the erosions are centrally located in contrast to the
marginal erosions in rheumatoid arthritis. Osteophytes are present;
consequently, interphalangeal joints may assume a gull-wing
configuration, with central erosions flanked by raised lips of bone.
Periarticular soft-tissue swelling is evident.

Clinical
 particular predilection for the distal interphalangeal joint of the hand, base of
the thumb, knee, hip, and intervertebral facet joints.
 Examine for joint tenderness, joint effusion, instability, crepitus, reduced ROM,
disuse atrophy
 Heberden nodes, which represent palpable osteophytes in the distal
interphalangeal joints, are characteristic in women but not me

Xray features
1. Narrowed joint space
2. Osteophytes
3. Subchondral sclerosis
4. Subchondral cysts

Primary osteoarthritis can be differentiated from rheumatoid arthritis by its lack of

marginal erosions, and uniformity in joint space narrowing at the small hand joints;
furthermore, RA rarely involves the DIP joints.
DIPJ
 Responsible for only 5% of the arc of rotation of the finger.
 Finger tip position critical for function.
 FDP provides over half the power required for PIPJ flexion.
 Pain usually the 1st Sx and improves with the later development of instability.
 When pain, instability or the cosmetic problem can no longer be namaged by
medical treatment, arthrodesis is indicated
 Ideally fixed in extension or only a few degrees of flexion.
 In the thumb IPJ, if the collateral ligaments are intact, arthroplasty can be done; if
they are not arthrodesis is indicated.

PIPJ
 Contributes 20% to the arc of rotation of the finger.
 Important for fine manipulation.
 20-60 of flexion is sufficient for most tasks.
 Treatment options include: arthrodesis, silicone arthroplasty and free transfers
from the toes.
 Arthrodesis of a single joint is always less than satisfactory: the finger tends to lie
in the palm, hyper-extend at the MCPJ and to get in the way. Arthrodesis of all
the PIPJs is far more satisfactory.
 To be considered for arthroplasty, the collateral ligaments should be
reconstructible and the flexor tendons should have adequate power.