Osteoarthritis, OA

Notes
  • Osteoarthritis (OA), the most common joint disorder, is also known as Degenerative Joint Disease or Osteoarthrosis or Hypertrophic Osteoarthritis.
  • The disease involves disruption and potential loss of joint cartilage as well as other joint pathology such as bone hypertrophy.
  • OA is classified into Primary OA and Secondary OA. The cause of Primary OA is mainly idiopathic while Secondary OA is caused by known factors such as;

_Chondrocalcinosis

_Congenital joint abnormalities

_Endocrine disorder

_Gout

_Infections that cause postinfectious arthritis

_Metabolic defects such as hemochromatosis, and Wilson disease)

_Neuropathic diseases

_Rheumatic Arthritis

_Trauma

  • Statistics: About 10% of the world population who are 60 years or older have symptomatic problems that can be attributed to OA. Knee OA is the most common form of OA and affects females more than males (4.9% of women at least 26 years of age as compared with 4.6% of men of the same age). In Kenyatta National Hospital distribution of OA was found to be as follows: 77% of knee OA, 15% of  hip OA, 3%  of hand OA, and 5% combined knee and hip OA (obese participants comprised 41.2% and overweight were 32.3%)
  1. Pathogenesis
  • The tissue damage, from various sources, stimulates chondrocytes as part of the repair process.
  • Proteoglycans and collagen production is increased.
  • However, there is a marked elevation of synthesis of enzymes that degrade cartilage and production of inflammatory cytokines.
  • This leads to the break down of the cartilage and death of chondrocytes through apoptosis resulting in eburnated and sclerotic bones as well as stiffening and infarction of subchondral bone.
  • The synovium also is inflamed and thickened. Besides, there is reduced quantity and viscousity of synovial fluid.
  • There is also tendinitis and contractures as periarticular tendons and ligaments are also affected.
  • Adjacent muscles become thinner and less supportive due to reduced usage.
Symptoms
  • Asymptomatic in some cases
  • Acute-on-chronic flares of symptoms
  • Joint pains that worsen with activity and towards the end of the day.
  • Joint / bony swelling
  • “Cracking” of joints
  • Flexion contracture (as the disease progress)
  • Tenderness on palpation
  • Deformity and subluxations
  • Myelopathy or radiculopathy (in cases where the spinal cord is affected)
  • Infarction of the spinal cord
Diagnosis
  • X-ray of joints noting loss of joint space, marginal osteophytes, high density of the subchondral bone, formation subchondral cyst, and joint effusion
  • Arthroscopy
  • Hemogram (that includes ESR)
  • MRI
Differential
  • Avascular necrosis
  • Bursitis
  • Gout
  • Internal derangements such as meniscal tears
  • Pseudogout
  • Psoriatic arthritis
  • Rheumatoid arthritis
Management
  • Lifestyle changes and supportive treatment

_Resting of joints e.g. using crutches when required.

_Weight reduction

_Physiotherapy and rehabilitation (to be started early)

_Proper balance between exercise and rest

  • Analgesics;

Either;

_Tabs Paracetamol 1gm QID

Or;

_Tabs Ibuprofen 400mg TID

(Other NSAIDs, including COX-2 can be used).

In case of more serious pain;

_Tabs Tramadol 50-100mg every 6 hrs (max. 400mg daily) – For those over 14 yrs.

  • In some patients intra-articular depot corticosteroids may support the relieve pain and enhanced joint flexibility. However, oral corticosteroids is not useful. Dose is repeated after 4-5wks

Either;

_Methyl prednisolone acetate intra-articular depo:

*large joint (knee, ankle, shoulder): 20-80mg;

*medium joint (elbow, wrist), 10-40mg;

*small joint (metacarpophalangeal, interphalangeal, sternoclavicular, acromioclavicular), 4-10mg.

Or;

Triamcinolone acetonide:

*smaller joints ; 2.5-5mg

*larger joints 5-15mg

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