11.

OSTEOARTHRITIS

DEFINITION

Osteoarthritis (OA) is a multidimensional disease that affects all anatomical

structures in the joints, especially the cartilage and subchondral bone, producing
progressive functional deterioration.
Synonims for OA:
 Hypertrophic arthritis
 Degenerative joint disease
 Degenerative disc disease
 Generelized osteoarthritis (Kellgren’s syndrome)

EPIDEMIOLOGY

 the most common osteoarticular disease

 prevalence increases with age
Primary OA
 Women > Men
 Increased age
 Symptomatic OA 2-3% overall population
 Symptomatic knee OA – 11% (> 65 years old)
 Symptomatic hip OA – 5% (> 65 years old)
 Radiographic evidence: 50-80% > 65 years old
Secondary OA
 Known etiologic factor
 Different joint distribution

PATHOGENESIS

OA risk factors include mechanical, genetic and biochemical factors.

Risk factors for primary OA
 age
  gender – females are more affected than males
 high bone mass – pts. with osteoporosis are less likely to develop OA
 obesity - the effect of excess weight on overloading joints (knee, hip)
during weight-bearing activities, will cause cartilage breakdown and
damage to ligaments and other structures
 overused joint/mechanical factors – joints exposed to repetitive use
 genetic – mutations in genes encoding for matrix proteins lead to
premature OA
Risk factors for secondary OA
 hemarthrosis – secondary to trauma, diseases with defect coagulation.
Persistent and recurrent blood in the synovial fluid will lead to cartilage
destruction.
 metabolic diseases – acromegaly, Paget’s disease, Cushing’s syndrome,
crystalline arthropaties, amyloidosis.
 damaged joints
 neuropathic joints – diabetes – foot, ankle and spine are involved,
syringomyelia involves the elbows and shoulders, the knees are involved
in tabes dorsalis.

Pathogenesis involves all joint tissues including cartilage, bone, synovium,

ligamentous capsular structures, and surrounding muscle. It is characterized
structurally by active bone remodeling, degradation of articular cartilage, and
synovial inflammation resulting in loss of joint function and angular deformity or
malalignment. OA is thought to be also a cytokine-driven disease. (see figure
below)

Small proteins mediators

Cytokines
 Chemical signaling or
“cross-talk” among involved tissues

Inflammation – synovium
Remodeling subchondral bone
Enzyme activation
Extracellular matrix degradation
(articular cartilage)

CLINICAL MANIFESTATIONS

 Joint pain
 Crepitus
 Stiffness after immobility
 Limitation of motion
 Deformity
 Chronic disability

LABORATORY FINDINGS

 Erythrocyte sedimentation rate (ESR) - normal limits.

 Rheumatoid Factor is negative.
 Antinuclear antibodies (ANA) are not present.
 Synovial fluid:
 High viscosity with good string sign
 Color is clear and yellow
 White blood cells typically < 1000-2000/mm3
 No crystals and negative cultures
IMAGISTIC FINDINGS

Xray changes – ABCDES

A – no ankylosis, alignment may be abnormal
B – bone mineralization is normal, bony subchondral sclerosis, bony spurs
(osteophytes)
C – no calcifications in cartilage, irregular cartilage space narrowing
D – deformities of Heberden’s/Bouchard’s nodes, distribution: typical joints
involvement
E – no erosions (erosive arthritis – “Gull wing” sign)
S – slow progression over years, vacuum sign, no specific nail or soft tissue
abnormalities

CLASSIFICATION CRITERIA

Primary or idiopathic:
 localized form – one or two joint group involved - hands (erosive,
inflammatory; DIP, PIP, 1st CMC joints); feet (1st MTP joint), hip, knee,
spine
 generalized form – three or more joint groups involved associated
with Heberden’s or Bouchard’s nodes - Kellgren’s syndrome
Secondary - involves atypical joints such as: metacarpophalangeal joints, wrists,
ankles, shoulders, elbows.
Erosive or inflammatory OA affects the DIP and PIP joints of the hand with
negative RF or anti-CCP antibodies.

American College of Rheumatology (ACR) radiologic and clinical criteria for

HAND osteoarthritis (OA)
Clinical
1. Hand pain, aching or stiffness for most days or prior months
2. Hard tissue enlargement of two or more of 10 selected joints*
3. Metacarpophalangeal joints swelling in two or more joints
4. Hard tissue enlargement of two or more distal interphalangeal joints
5. Deformity of two or more of 10 selected hand joints*
OA if the items 1, 2, 3, 4 or 1, 2, 3, 5 are present.
* Ten selected joints include bilateral second and third interphalangeal proximal
joints, second and third proximal interphalangeal joints, and first
carpometacarpal joint.

American College of Rheumatology (ACR) radiologic and clinical criteria for

knee osteoarthritis (OA)
Clinical
1. Knee pain for most days or prior months
2. Crepitus on active joint motion
3. Morning stiffness lasting 30 minutes or less
4. Age 38 years or older
5. Bony enlargement of the knee on examination
OA if the items 1, 2, 3, 4 or 1, 2, 5 or 1, 4, 5 are present.
Clinical and radiographic
1. Knee pain for most days or prior months
2. Osteophytes at joint margins on radiographs
3. Synovial fluid typical of OA (laboratory)
4. Age 40 years or older
5. Crepitus on active joint motion
6. Morning stiffness lasting 30 minutes or less
OA if the items 1, 2 or 1, 3, 5, 6 or 1, 4, 5, 6 are present.

American College of Rheumatology (ACR) radiologic and clinical criteria for

hip osteoarthritis (OA)
1. Hip pain for most days or prior months
2. ESR of less than 20 mm at the 1st hour
3. Femoral or acetabular osteophytes on radiographs
4. Hip joint space narrowing on radiographs
OA if the items 1, 2, 3 or 1, 2 ,4 or 1, 3, 4 are present.
TREATMENT

OA’s treatment is multimodal – a combination of non pharmacological

procedures combined with drug therapy.

Objectives:

 patient education and information access

 pain relief

 optimization of function

 beneficial modification of the OA process

NON-PHARMACOLOGICAL MANAGEMENT
 Weight loss
 Patient education
 Rest of affected joints
 Exercise for muscle strengthening and aerobic conditions:
 Improvement of pain and joint function
 A state of psychological well-being
 No weight-bearing exercise – affects the articular cartilage and
subchondral bone
 Swimming
 Shock-absorbing insoles
 Hydrotherapy
 Superficial heat and cold
 Paraffin baths for hands
 Splinting (knee sleeves, CMC splints)
 Ambulatory aids (canes, crutches, walkers)
 Heel wedges, knee wedges to un weight medical compartment of knee
 Cervical collar
  Cervical traction or distraction
 Transcutaneous electrical nerve stimulator (TENS)
 Total joint replacement (hip, knee) – indications:
1. Severe pain unresponsive to medical therapy
2. Loss of joint function
Predictive factors for physical therapy success:
 1 joint affected (pain)
 Age ≤ 58 years old
 VAS (pain) ≥ 6/10
 40 m SPWT ≤ 25.9 sec.
 Onset ≤ 1 year

PHARMACOLOGICAL TREATMENT
 Acetaminophen
 NSAIDs
 Opiods
 Corticosteroids injections
 Hyaluronic acid injections

OA – FUTURE THERAPIES
 Metalloproteinase inhibitors – tetracycline's derivates (the inhibition of
collagenase, stromelysin – can slow the progression of osteoarthritis)
 Cartilage growth factors
 In vitro grown cartilage – repair of cartilage
 Erosive arthritis – MTX (in use)

TAKE HOME MESSAGES

OA is not an old person’s disease.

Risk factors for OA can be modified.

References:
1. Stone JH, A Clinician’s Pearls and Myths in Rheumatology, Springer 2009,
493: 23-26, ISBN: 978-1-84800-933-2
2.