Reactive Arthritis and Osteoarthritis

Question 1

What is reactive arthritis?

Answer 1

• sterile inflammation in joints following infection especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) infections
• Important extra-articular manifestations include: Enthesopathy, Skin inflammation, Eye inflammation
• Reactive arthritis may be first manifestation of HIV or hepatitis C infection
• Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)
• Symptoms follow 1-4 weeks after infection and this infection may be mild
• Reactive arthritis is distinct from infection in joints (septic arthritis)

Question 2

What are the musculoskeletal features of reactive arthritis?

Answer 2

Arthritis

• oligo
• asymmetrical
• lower limbs typically affected
• typically larger joints affected

ENTHESITIS

• Heel pain (Achilles tendonitis)
• Swollen fingers (dactylitis)
• Painful feet (metatarsalgia due to plantar fasciitis)

Spondylitis

• Sacroiliitis (inflammation of the sacro-iliac joints)
• Spondylitis (inflammation of the spine)

Question 3

Describe the extra-articular features of reactive arthritis?

Answer 3

Ocular
- sterile conjunctivitis

Genito-urinary
- sterile urethritis (will cause pain when passing urine)

Skin

• psoriasis-like rash on hands and feet (‘keratoderma blennorrhagicum’)
• Circinate balanitis (penis rash, looks painful)

Question 4

Reiter’s syndrome

Answer 4

Original description of Reactive arthritis = triad of arthritis, urethritis and conjunctivitis following infectious dysentery [Reiter’s syndrome]

Question 5

How do you distinguish reactive arthritis from RA?

Answer 5

• see slide 6 for more detail:

RA: polyarthritis, symmetrical, small joints, more common in females, RF+ (not always), no spondylitis

rA: oligoarthritis, larger joints, more common in males, RF, spondylitis

A patient with reactive arthritis will look better than a patient with RA.

Question 6

How is the diagnosis or reactive arthritis established?

Answer 6

• Clinical diagnosis
• Investigations to exclude other causes of arthritis e.g. septic arthritis
• Important investigations include:
  
  • Micorbiology (Microbial cultures – blood, throat, urine, stool, urethral, cervical; Serology e.g. HIV, hepatitis C); STI clinic for chlamydia testing
  • Immunology (RF, HLA-B27 -> genetic risk factor but not diagnostic because many people carry the gene)
  • Synovial fluid examination (Especially if only single joint affected -> no bugs on gram stain if it is rA, in sA you would have bugs there)

Question 7

Gonococcal arthritis

Answer 7

• Gonnorhoea and gonococcal arthritis is different from reactive arthrisis – this would affect multiple joints.
• It doesn’t tend to damage the joints as much as other septic arthritis due to e.g. staph aureus

Question 8

rA vs sA

Answer 8

• Synovial fluid culture: -ve in rA, +ve in sA
• Antibiotic therapy: not needed in rA, needed in sA
• Joint Lavage: yes for large joints in sA, no for rA

Patients with sA may be immunosuppressed e.g. HIV, SLE
- if one joint suddenly inflames don’t assume it is just a flare up of rheumatoid arthritis - investigate as it could also be septic which could cause major damage to joints.

Question 9

How is rA treated?

Answer 9

• in majority of patients complete resolution occurs within 2-6 months
• No role for antibiotics

articular:

• NSAIDs
• intra-articular corticosteroid therapy

extra-articular:

• typically self-limiting, hence symptomatic therapy
• e.g. topical steroids & keratolytic agents in keratoderma

Refractory disease:

• oral glucocorticoids
• steroid-sparing agents e.g. sulphasalazine

Question 10

Which joints are typically affected by osteoarthritis?

Answer 10

• Joints of the hand
  
  • Distal interphalangeal joints (DIP)
  • Proximal interphalangeal joints (PIP)
  • First carpometacarpal joint (CMC)
• Spine
• Weight-bearing joints of lower limbs
  - esp. knees and hips
  - First metatarsophalangeal joint (MTP) -> the big toe is a major weight bearing site.
• MCPJs are generally spared in OA

Question 11

Osteophytes in OA

Answer 11

• Osteophytes at the DIP joints are termed Heberden’s nodes
• Osteophytes at the PIP joints are termed Bouchard’s nodes

Osteophyte: a bony projection associated with the degeneration of cartilage at joints.

Question 12

What is OA associated with?

Answer 12

• Joint pain: worse with activity, better with rest
• Joint crepitus: creaking, cracking grinding sound on moving affected joint (joint noises aren’t always really something to be worry about?)
• palpable bone creaking
• Joint instability
• Joint enlargement: e.g. Heberden’s nodes, Bouchard’s nodes
• Joint stiffness after immobility (‘gelling’)
• Limitation of motion

Question 13

Radiographic features of OA

Answer 13

• Joint space narrowing
• Subchondral bony sclerosis
• Osteophytes
• Subchondral cysts

Question 14

Radiographic changes in Rheumatoid Arthritis vs. Osteoarthritis

Answer 14

• Joint space narrowing: + in both
• Subchondral sclerosis: - in RA; + in OA
• osteophytes: - in RA; + in OA.
• Osteopenia: + in RA; - in OA
• Bony erosions: + in RA; - in OA

See slide 17!!

Question 15

What causes OA?

Answer 15

• not AI
• not inflammatory
• wear and tear, due to degradation of the joints
  
  • due to excessive load bearing (e.g. construction workers)
  • due to abnormal joint components (cartilage fragments in synovial fluid, bony spurs)
• There is defective and irreversible articular cartilage and damage to underlying bone
• some degree of genetic predisposition
• hand OA is predominant in females, large joint not so much)
• mechanical factors are important: e.g. obesity, manual work, previos trauma (e.g. fracture)

Question 16

Management of OA

Answer 16

Management:

• Education
• Physical therapy – physiotherapy, hydrotherapy
• Occupational therapy
• Weight loss where appropriate (can be difficult due to pain in exercise)
• Exercise
• Analgesia
  - Paracetamol
  - Non-steroidal anti-inflammatory agents
  - Intra-articular corticosteroid injection (not too often because repeated injection may damage joint further)
• Joint replacement

Question 17

Mechanical properties of synovial joints

Answer 17

• hylauronic acid in synovial fluid
• aggrecan and Type II collagen in cartilage

=> water retenition, robust strength under pressure, stick absorption.

Question 18

Cartilage changes in OA

Answer 18

reduced proteoglycan
reduced collagen
chondrocyte changes e.g. apoptosis

Question 19

Bone changes in OA

Answer 19

Changes in denuded sub-articular bone

- Proliferation of superficial osteoblasts results in production of sclerotic bone e.g. subchondral sclerosis
 - Focal stress on sclerotic bone can result in focal superficial necrosis

new bone formation at the joint margins (termed osteophytes) -> attempt to heal, primary pathological feature

 - Sometimes you can detect osteophytes clinically (‘at the bedside’) and these have names
 - Osteophytes at the distal inter-phalangeal joints are called ‘Heberden’s nodes’
 - Osteophytes at the proximal inter-phalangeal joints are called ‘Bouchard’s nodes’

The correlation between the x-rays and symptoms are quite poor.

Question 20

Prognosis of OA

Answer 20

• benign prognosis
• reassure the patients that this is not RA
• the pain often resolves
• PT is one of the best interventions

Question 21

Treatment of OA

Answer 21

Therapeutic approaches not approved in UK!!!!!!

• the pain often resolves
• Glucosamine and chondroitin sulphate – commonly taken!
  • Dietary supplementation
  • Controversial – not recommended by NICE

Intra-articular injections of hyaluronic acid

• hyaluronic acid to increase lubrication (viscosupplementation)
• Only used in the knee joint and still experimental
• Not recommended by NICE (see above link)

Unlike RA no disease modifying osteoarthritis drug (DMOAD)
- ? Future therapies – stop matrix breakdown - ? aggrecanase inhibitors, cytokine inhibitors, stimulate repair of matrix…..