Non-Inflammatory Arthritides: Osteoarthritis Neuropathic Arthropathy Acute Rheumatic Fever Ochronosis Secondary Pulmonary Hypertrophic Osteoarthropathy

Inflammatory Arthritides: Rheumatoid Arthritis Systemic Lupus Erythematosus Juvenile Rheumatoid Arthritis Relapsing Polychondritis Spondyloarthropathies Ankylosing Spondylitis Reiter’s Syndrome Psoriatic Arthritis Enteropathic Arthritis Crystal Deposition Disease Gout Chondrocalcinosis Calcium Hydroxyaptite Crystal Deposition Disease

Infectious Arthritides Pyogenic Arthritis Tuberculous Arthritis Fungal Arthritis Lyme Disease

Haemorrhagic Arthritides Haemophilic Arthropathy Sickle Cell Disease Pigmented Villonodular Synovitis

· 200 WBCs, 25% PMNLs

· Glucose and protein equal serum values

· Normal viscosity (high)

· Straw colour

· firm mucin clot

· 2000-75000 WBCs, 50% PMNLs

· Moderately decreased glucose (25mg/dl

lower than serum glucose)

· Low viscosity

· Yellow-green colour

· Friable mucin clot

· Synovial fluid complement is decreased

in RA and normal in ankylosing

spondylitis

· > 80000 WBCs, ³ 75% PMNLs

· Positive gram stain (and cultures)

· Low glucose (> 25mg/dl less than serum

values)

· Opaque fluid

· Increased synovial lactate

Non-inflammitory Arthritides 

Osteoarthritis (OA)

Osteoarthritis (OA) is a degenerative joint disease characterised by progressive loss of articular cartilage with associated new bone formation and capsular fibrosis. It is the most common form of arthritis. Nearly everyone who lives long enough will be affected by OA. Its prevalence increases steeply with age and there may be a genetic predisposition.

OA is classified as primary when it arises without an obvious cause, and secondary when it occurs following certain predisposing factors (such as previous trauma, congenital deformity, infection or a metabolic disorder).

Aetiology

On a cellular level, osteoarthritis may be due to failure of chondrocytes to repair damaged cartilage. Excessive stresses are applied to articular cartilage and there is an inadequate chondrocyte response, leading to degeneration of the articular cartilage. The disparity between the stress applied and the chondrocyte response may be due to:

• abnormal loads over a small area of cartilage
• weakening of the cartilage (not well understood)
• abnormal support by subchondral bone

Pathogenesis

Current concepts on the pathogenesis of OA are based on the assumption that whatever the provoking cause, there is a final common pathway of changes in articular cartilage. It has been suggested that the initiating event is fatigue fracture of the collagen meshwork, is followed by increased hydration of the articular cartilage and loss of proteoglycans from the matrix into the synovial fluid. There is some evidence of increased collagenolytic activity but collagen loss may also be due to mechanical causes.

Alternatively, it has been proposed that the initial lesions are microfractures of the subchondral bone following repetitive loading. Healing of these microfractures results in significant loss of resilience of the subchondral bone. A stress gradient develops in the adjacent articular cartilage. As the process evolves there is fibrillation of the cartilage, and deep clefts appear with reduplication and proliferation of chondrocytes within them. Proliferative changes also occur simultaneously at the joint margins with formation of osteophytes. Eventually articular cartilage is lost altogether in areas of maximum mechanical stress and the underlying bone becomes hardened and eburnated. There may be cyst formation.

Changes in osteoarthritic cartilage:

1. Increased water content (in contrast to decreased water content in normal ageing)
2. This occurs early, and suggests some weakening of type II collagen
3. Changes in proteoglycans
4. There are shorter chains and shifts in the concentration of proteoglycans. The chondroitin/keratin ratio is decreased.
5. Collagen abnormalities
6. Disruption is caused by an increase in collagenase and proteoglycan-degrading enzyme concentration.
7. Proteoglycan binding
8. Proteoglycans bind to hyaluronic acid. This results from the action of proteolytic enzymes, due to increased prostaglandin E and decreased numbers of link protein.
9. Rate of synthesis
10. Rate of synthesis of DNA, collagen, and proteoglycans are increased
11. Increased levels of:
12. Cathepsins B and D, metalloproteinases (collagenase, gelatinase, and stromelysin).
13. Interleukin-1
14. Enhances enzyme synthesis and has a catabolic effect (causing cartilage degeneration).
15. GAGs and polysulfuric acid

Clinical features

Patients usually present after 40-50 years. The knee joint is most commonly affected. Pain is of an insidious onset, and progresses over months or years. Stiffness and swelling occur in later stages of the disease. Range of movement is reduced and there may be associated crepitus.

Investigations and Diagnosis

Diagnosis is made largely clinically by the presence of gradual onset of pain after activity, pattern of joint involvement and lack of significant soft-tissue swelling. Radiology may be useful and joint fluid analysis helps rule out other causes of arthritis.

Radiology:

• osteophytes
• narrowing of joint space
• subarticular sclerosis and bone cysts

Joints that are commonly involved are the distal and proximal interphalangeal joints, and carpometacarpal joints of the hand. There is usually superolateral involvement of the hip joint and asymmetric involvement of the knee.

Microscopic changes:

• loss of superficial chondrocytes
• cloning of chondrocytes (more than one chondrocyte per lacunae)
• replication and breakdown of the tidemark
• fissuring
• cartilage destruction with eburnation of subchondral pagetoid bone

Treatment

• Protection of affected joints from overloading
• weight loss
• use of walking stick
• 
  
• Exercise of supporting muscles around joints to avoid wasting.
• Supportive measures such as pain relief by analgesics or NSAIDs.
• Surgical treatment is indicated for patients with persistent symptoms and pain and ranges from arthroscopy to arthroplasty.
• Realignment osteotomies may be done in younger patients to redistribute weight bearing load at the knee to prevent further damage.
• Total joint arthroplasties for older patients (over 60) in advanced cases that are resistant to conservative treatment.

Neuropathic Arthropathy

Neuropathic arthropathy, also known as Charcot joint, is a rapidly progressive form of osteoarthritis caused by a disturbance in the sensory (position sense and pain) innervation of a joint. In the upper limbs it is most commonly associated with syringomyelia, followed next by Hansen’s disease. 25% of patients with syringomyelia get a Charcot joint. In the lower limbs, common causes include tabes dorsalis, peripheral neuropathies especially diabetes, cauda equina lesions, and congenital insensitivity to pain.

Clinical features

Include an unstable, swollen, yet painless joint. Effusions may be seen. Patients are typically older, and may present with haemarthrosis. Radiological changes include advanced destruction on both sides of the joint, joint distension due to increased amount of fluid, irregular bits of bone embedded in fibrous tissue, and heterotopic ossification.

Treatment

Involves stabilising the affected joints by limitation of activity and use of appropriate splintage, such as callipers and casts. Total joint arthroplasty and use of other orthopaedic hardware are contraindicated.

Acute Rheumatic Fever

Acute rheumatic fever is sometimes included in the inflammatory group of arthritides. Although was the most common cause of childhood arthritis, its prevalence in developed countries has progressively declined since the advent of antibiotics.

Pathogenesis

Acute Rheumatic Fever is triggered by infection with specific streptococcus.