6. Osteoarthritis and reactive arthritis Flashcards
What is reactive arthritis?
- Sterile inflammation in joints
* Following infection, especially urogenital (e.g. Chlamydia trachomatis) and GI (e.g. Shigella)
What are the important extra-articular manifestations of reactive arthritis?
- Enthesopathy (overlap between ReA and seronegative spondyloarthropathies)
- Skin inflammation e.g. circinate balanitis and psoriasis-like rash on hands and feet
- Eye inflammation e.g. sterile conjuctivitis
- Genti-urinary inflammation e.g. sterile urethritis
What serious infections can ReA be the first manifestation of?
HIV or hepatitis C
What people does ReA commonly affect?
- Young adults with genetic predisposition and environmental trigger
- e.g. HLA-B27 or salmonella infection
When do ReA symptoms appear following infection?
1-4 weeks after infection
Are the joints infected in ReA?
No, this is septic arthritis
Which MHC molecule is strongly associated with ankylosing spondylitis susceptibility and ReA?
Class I MHC - HLA-B27
Describe the musculoskeletal symptoms of ReA (arthritis, enthesitis and spondylitis)
Arthritis
• Asymmetrical
• Oligoarthritis (<5 joints)
• Lower limbs typically affected
Enthesitis
• Heel pain (achilles tendonitis)
• Swollen fingers (dactylitis)
• Painful feet (metatarsalgia due to plantar fasciitis)
Spondylitis
• Spondylitis (inflammation of the spine)
• Sacroiliitis (inflammation of the sacro-iliac joints)
How is the diagnosis for ReA established?
Microbiological analysis
• Cultures - blood, throat etc.
• Serology e.g. HIV, hep C
Immunological tests
• Rheumatoid factor should be negative
• HLA-B7 (only 9% are positive though, so not very useful)
Synovial fluid examination
• Especially if only single joint affected
• Fluid culture should be sterile (antibiotic therapy not necessary)
How is ReA treated?
- Articular - NSAIDs, intra-articular corticosteroid therapy
- Extra-articular - symptomatic therapy e.g. topical steroids + keratolytic agents
- Refractory (stubborn) disease - oral glucocorticoids, steroid-sparing agents
What is osteoarthritis?
- Chronic slowly progressive disorder
- Primarily due to failure of articular cartilage
- Typically affects the joints of the hand, spine and weight-bearing joints (hips and knees)
Which joints of the hand does OA affect?
- Distal interphalangeal joints (DIP)
- Proximal interphalangeal joints (PIP)
- First carpometacarpal joint (CMC)
Which joint in the feet does OA mainly affect?
First metatarsophalangeal joint
Which joints affected in OA are normally spared in RA?
DIP joints
What are Heberden’s nodes and Bouchard’s nodes?
- Heberden’s nodes - bony, prominent swelling around the DIP joints
- Bouchard’s nodes - bony swellings around the PIP joints
(both types of osteophytes)
How does joint pain in OA change with activity and rest?
- Worse with activity
* Better with rest
What is joint crepitus?
Creaking, cracking, grinding sound on moving affected joint
How is stability, size and mobility of joints affected in OA?
- Joint instability
- Joint englargement
- Joint stiffness - limitation of motion
Describe the radiographic features of osteoarthritis
- Joint space narrowing (loss of cartilage)
- Subchondral bony sclerosis (underlying bone reacting to damaged cartilage)
- Osteophytes
- Subchondral cysts
If the defective damage to the articular cartilage in OA reversible?
No
Is articular cartilage vascular or neural?
No - it is an avascular and aneural structure
What side chains does aggrecan contain and how does it attract water?
- Glycosaminoglycan side chains e.g. chondroitin sulphate, keratin sulphate
- Negative charge attracts water, keeping it hydrated
What are proteoglycans?
Glycoproteins containing one or more sulphated glycosaminoglycan (GAG) chains
What are glycosaminoglycans (GAGs)?
Repeating polymers of disaccharides
What is the only non-sulphated GAG?
Hyaluronic acid
Describe the cartilage changes in OA
- Reduced proteoglycan (aggrecan is the major one)
- Reduce collagen (type II)
- Chondrocyte changes e.g. apoptosis
Describe the bone changes in OA
- Proliferation of superficial osteoblasts => production of sclerotic bone
- Focal stress on sclerotic bone => focal superficial necrosis
What therapeutic approaches to OA are not approved/recommended in the UK?
- Glycosamine and chondroitin sulphate - dietary supplementation (no clear evidence)
- Intra-articular injections of hyaluronic acid - not recommended by NICE but still practised in private medicine
What disease modifying osteoarthritis drugs (DMOAD) can be used for OA?
There are none - maybe aggrecanase/cytokine inhibitors in the future?
