Osteoarthritis and joint deposition disorders

Question 1

Primary osteoarthritis

Answer 1

‘Degenrative joint disease’
• Insidious onset
• Age-related
• Oligoarticular (it may be generalised)

Question 2

Secondary osteoarthritis

Answer 2

• Young individuals (predisposing condition)
• Systemic diseases
• Congenital deformity

Question 3

Aetiology of osteoarthritis

Answer 3

1. Genetic factors
   • Multiple gene impact, although individually small summative effect
2. Environmental components
   • Age – exponential increase beyond the age of 50
   • Biochemical stress – influenced by obesity, muscle strength, joint stability, structure and alignment
   • ‘Knees and hands in women and hips in men’

Question 4

Pathophysiology of osteoarthritis

Answer 4

• Cartilage fibrillation (in two direction) matrix fracture
• Cartilaginous fragments may float into joint space
• Eburnation of subchondral bone
• Cystic formation of subchondral zone
• Formation of osteophytes
• Synovium membrane involvement (congestion, fibrosis, presence of chronic inflammatory cells)

Question 5

macroscopy of osteoarthritis

Answer 5

• Bone eburnation: exposed sub-chondral bone smoothed and polished as the new articular surface (polished ivory aspect)
• Concurrent strengthening and sclerosis of underlying cancellous bone
• Small fractures through sub-articular bone

Question 6

Osteoarthritis investigations

Answer 6

•	ESR: normal
•	Joint fluid: minimal change
•	X-ray: Radiographic images showing anklosing of the synovial joints and periarticular osteophytic formation 
o	Joint space narrowing
o	Subchondral bone sclerosis
o	Marginal osteophytes

Question 7

Herberden’s nodes

Answer 7

• Primary osteoarthritis
• Prominent nodes in DIP mostly painless (may ache)
• F>M

Question 8

Joint deposition diseases

Answer 8

1. Gout: monosodium urate deposition
2. Pseduogout: calcium pyrophosphate deposition
3. Alkaptonuria (ochronosis)

Question 9

Gout

Answer 9

•	Hyperuricaemia
•	Recurrent attacks of acute arthritis
•	Asymptomatic intervals
•	Progressive to chronic gouty arthritis
•	Renal involvement = gouty nephropathy
•	Tophus:
o	Inflamed monoarticular process
o	Sudden onset
o	Excruciatingly painful
o	75% first MTP joint
o	Resolution
o	40-50 yo

Question 10

Primary gout

Answer 10

Idiopathic
• 90% of cases
• Undefined enzyme defects: 95-98%
• Known enzymatic defects: rare

Question 11

Secondary gout

Answer 11

• 10% of cases
• Increased nucleic acid turnover (leukaemias)
• Specific enzyme defects (Lesch-Nyhan syndrome – complete lack of HGPRT)
• Chronic renal disease

Question 12

Patheogenesis of gout

Answer 12

• Deposition of monosodium urate crystals in articular cartilage
• Crystal shedding into synovial fluid
• Synovial fluid is poor solvent
• Periarticular tissues
• Stimulates inflammatory response

Question 13

Preciptating factors of gout

Answer 13

• Dietary
• Drugs (thiazides) and alcohol
• Emotional and physical stress
• Obesity

Question 14

Tophus

Answer 14

• Pathognomic hallmark of gout
• Deposits of masses of urate crystals in joint and other sites
• Surrounded by inflammatory reaction
• Chronic tophaceous gout

Question 15

Chronic gouty arthritis

Answer 15

• Chronic precipitation of urate in joint structures
• Follows repeated acute arthritic bouts
• Accumulated urate incites more vigorous inflammation

Question 16

Development of gouty nephropathy

Answer 16

• Deposition in medullary intersitium
• Intratubilar precipitation of urate crystals
Or
• Production of uric acid stones from free uric acid crystals

Question 17

Pseudogout

Answer 17

(aka chondrocalcinosis)
• Calcium pyrophosphate crystal deposition
• >50 yo: 6% of elderly
• Both sexes equally affected

Question 18

Classification of pseudogout

Answer 18

• Sporadic (idiopathic)
• Hereditary
• Secondary

Question 19

Pseudogout symptoms

Answer 19

• Usually asymptomatic

* May trigger acute, sub-acute or chronic arthritis

Question 20

Morphology of pseudogout

Answer 20

• Chalky white deposits in articular matrix, menisci, and inter-vertebral discs.

Question 21

Alkaptonuria

Answer 21

• Nowadays a rare autosomal recessive disorder, it was the first inborn error of metabolism to be discovered
• Its genesis relates to the lack of homogentisic oxidase and retention of homogentistic acid in the connective tissue and cartilage
• Tissue present a dark pigmentation (sclerae, tendons, nose, ears, zygomatic region) taking the name of Ochronosis (ochre colour).

Question 22

Pathogenesis of alkaptonuria

Answer 22

• Accumulation of homogentisic acid in the articular cartilage leads to brittleness and fibrillation
• The axial skeleton is primarily affected, with the process extending towards the large joints of the appendicular skeleton
• Small synovial joints are usually spared