Osteoarthritis and joint deposition disorders Flashcards
Primary osteoarthritis
‘Degenrative joint disease’
• Insidious onset
• Age-related
• Oligoarticular (it may be generalised)
Secondary osteoarthritis
- Young individuals (predisposing condition)
- Systemic diseases
- Congenital deformity
Aetiology of osteoarthritis
- Genetic factors
• Multiple gene impact, although individually small summative effect - 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’
Pathophysiology of osteoarthritis
- 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)
macroscopy of osteoarthritis
- 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
Osteoarthritis investigations
• 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
Herberden’s nodes
- Primary osteoarthritis
- Prominent nodes in DIP mostly painless (may ache)
- F>M
Joint deposition diseases
- Gout: monosodium urate deposition
- Pseduogout: calcium pyrophosphate deposition
- Alkaptonuria (ochronosis)
Gout
• 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
Primary gout
Idiopathic
• 90% of cases
• Undefined enzyme defects: 95-98%
• Known enzymatic defects: rare
Secondary gout
- 10% of cases
- Increased nucleic acid turnover (leukaemias)
- Specific enzyme defects (Lesch-Nyhan syndrome – complete lack of HGPRT)
- Chronic renal disease
Patheogenesis of gout
- Deposition of monosodium urate crystals in articular cartilage
- Crystal shedding into synovial fluid
- Synovial fluid is poor solvent
- Periarticular tissues
- Stimulates inflammatory response
Preciptating factors of gout
- Dietary
- Drugs (thiazides) and alcohol
- Emotional and physical stress
- Obesity
Tophus
- Pathognomic hallmark of gout
- Deposits of masses of urate crystals in joint and other sites
- Surrounded by inflammatory reaction
- Chronic tophaceous gout
Chronic gouty arthritis
- Chronic precipitation of urate in joint structures
- Follows repeated acute arthritic bouts
- Accumulated urate incites more vigorous inflammation
Development of gouty nephropathy
• Deposition in medullary intersitium
• Intratubilar precipitation of urate crystals
Or
• Production of uric acid stones from free uric acid crystals
Pseudogout
(aka chondrocalcinosis)
• Calcium pyrophosphate crystal deposition
• >50 yo: 6% of elderly
• Both sexes equally affected
Classification of pseudogout
- Sporadic (idiopathic)
- Hereditary
- Secondary
Pseudogout symptoms
- Usually asymptomatic
* May trigger acute, sub-acute or chronic arthritis
Morphology of pseudogout
• Chalky white deposits in articular matrix, menisci, and inter-vertebral discs.
Alkaptonuria
- 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).
Pathogenesis of alkaptonuria
- 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
