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Osteoarthritis

Definition
  • Slowly progressive degenerative disease characterised by the gradual loss of articular cartilage
Risk Factors
  • age >50 years
  • female gender
  • obesity
  • genetic factors
  • physical/manual occupation
  • knee malalignment
  • high BMD ?
Differential diagnosis
Epidemiology
  • About 8.5 million people in the UK have OA
  • OA is common in women and becomes more common with advancing age
    • 2% of women with a mean age of 71 develop radiographic knee OA every year, compared with 1.4% of men
    • 1% of women develop symptomatic knee OA every year, compared with 0.7% of men
  • The prevalence of currently recorded diagnosis of knee OA in patients >45 years old is 1.1%
  • The estimated prevalence of all those who had had knee OA diagnosed at some point was 5.5%
Aetiology
  • Exact aetiology for OA is unknown:
    • Age, hereditary predisposition, female gender, and obesity are associated with increased risk of OA
    • Articular congenital deformities or trauma to the joint also enhance the risk of developing OA
    • High BMD and low oestrogen status, such as in post-menopausal women, may be associated with higher risk of knee and hip OA
  • The above factors might lead to a joint environment that is susceptible to trauma and to external mechanical stressors that are exacerbated by certain physical activities
  • Local mechanical factors further facilitate the progression of the disease
    • Periarticular muscle weakness
    • Misalignment
    • Structural joint abnormality (i.e., meniscal tear)
Clinical features
  • Pain
  • Functional difficulties
  • Knee, hip, hand, or spine involvement
  • Bony deformities
  • Limited range of motion
  • Malalignment
  • Tenderness
  • Crepitus
  • Stiffness
  • Shoulder, elbows, wrists, or ankles involvement
  • Effusion
  • Antalgic gait
Pathophysiology
  • Failure in maintaining the homeostatic balance of the cartilage matrix synthesis and degradation, resulting from reduced formation or increased catabolism
  • Matrix metalloproteinases (i.e., collagenase; catalyse both collagen and proteoglycan degradation) are found in increased concentrations in osteoarthritis cartilage
    • Produced by chondrocytes
    • Synthesis can be stimulated by interleukin 1 (IL-1)
    • Blockage of these enzymes by doxycycline in animal models can reduce the severity of osteoarthritic lesions
  • IL-1 is one example of a catabolic cytokine that was found to be increased in the serum of patients with knee OA
  • The levels of anabolic cytokines, such as insulin-like growth factors (IGF-I), are decreased in OA
  • Nitric oxide might activate the metalloproteinases and play a role in cartilage degradation
  • In addition to the biological aspect, mechanical loading can contribute in harming the chondrocytes and cartilage.
  • The osteoarthritic process involves not only the cartilage but also other joint structures, resulting in bone remodelling and bone marrow lesions of the subchondral bone, synovial inflammation, capsular stretching and periarticular muscle weakness, and ligament laxity
  • The above elements, in addition to trauma, can lead to focal stress and eventual cartilage loss
    • This can further alter the joint anatomy
    • Predisposes it even more to the potential detrimental effects of mechanical factors and physical activities, by redistributing and increasing the focal loading in the joint
    • For example, in knee OA, genu varum (bow-legs) and genu valgum (knock-knees) are associated with increased risk of structural deterioration of the joint
  • These further worsen the joint's local environment and predispose it even more to external trauma and mechanical loading, resulting in a vicious circle culminating in joint failure


Investigations
  • Xray
    • new bone formation (osteophytes), joint space narrowing, and subchondral sclerosis and cysts
  • CRP and ESR
    • OA is a clinical diagnosis, but inflammatory markers should be ordered if inflammatory arthritis is a possible differential
    • For example, in an older patient who presents with a knee effusion.
  • MRI
    • MRI is not indicated for the diagnosis of simple OA in most joints. It is used to rule out other aetiologies for hip or knee pain, such as avascular necrosis.
    • => Cartilage loss, bone marrow lesions, and meniscal tears
Management

a) conservative
  • Approaches depend on site of OA and include patient education
  • Exercise programmes, physiotherapy and occupational therapy, quadriceps-strengthening exercises, knee braces, correct footwear, and patellar bracing or taping for patellofemoral pain
  • Proper use of a cane in the contralateral hand to the affected hip or knee can also reduce pain and improve function.
b) medical
  • Local analgesics should be used as first-line therapy
    • Capsaicin, methylsalicylate cream, or topical NSAIDs
  • Paracetamol should be added if local therapies alone fail to control symptoms.
  • Intra-articular corticosteroid injections
    • Suitable for acute exacerbation of symptoms
    • Especially effective for knee pain
    • The beneficial effect is temporary and usually lasts for a few weeks, but it varies among patients
  • Further NSAIDs / opioids
c) surgical
  • Replacement surgery is appropriate for OA of the hip and knee
  • Osteotomy is suitable for knee OA
  • Arthroplasty, osteotomy, and arthrodesis are options for thumb OA
Prognosis
  • OA is a chronic slowly progressive disease and is almost ubiquitous with advancing age
  • A combination of different modalities of treatment can provide adequate pain control and preserve function and quality of life for many patients
  • Despite treatment, most patients usually continue to have some degree of pain and functional limitation affecting their desired activities and quality of life
  • Complications of medication, particularly NSAIDs, are also problematic
  • In patients who fail to respond to medical and non-medical therapies, total joint replacement provides good long-term pain relief for most people
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