Osteoarthritis

Osteoarthritis

·        Loss of articular cartilage in a synovial joint, and associated changes in underlying bone and other joint tissues

·        Is degenerative not inflammatory

·        Very common, although prevalence unknown due to variations in diagnosis

·        Risk facts:

o   Age: 75% of over 70 year olds and 90% of 80 year olds

o   Previous injury

o   Female and obesity (especially hip and knee) are debated

·        Non-specific symptoms: 

o   Pain: initially with/after exercise or at the end of the day, later also at rest and related to other factors. Pain with sleeping on hip at night

o   Stiffness: not as prominent as in inflammatory arthritis 

o   Swelling: due to ­synovial fluid (may contain a few mononucleocytes) and bony thickening

o   Loss of function (common to all arthritis)

o  Signs: joint instability, crepitus, joint tenderness, derangement, ¯ range of movement, effusion, fixed deformity 

·        Distribution:

o  Primary osteoarthritis:

§  Often – but not always - symmetrical 

§  Fingers: DIP and PIP, MCP joint of thumb but not of fingers. Can lead to Heberden‟s Nodes: marginal osteophytes at the base of the distal phalanx. Bouchard‟s Nodes on proximal IP joints 

§  Weight bearing joints: Hips, knees

§  Less Common:

·        Acromioclavicular joints

·        Lower cervical and lumbar spine

·        MTP joints of big toes 

o  Secondary Osteoarthritis (secondary to joint disease or injury – consider especially if it doesn‟t fit the joint distribution of primary):

§  Asymmetrical

§  Trauma (eg intra-articular fracture, dislocation, etc)

§  Infection

§  Metabolic: haemophilia, gout (or pseudogout if bigger joints), haemochromatosis

§  Avascular necrosis

§  Congenital (eg DDH)

§  Inflammatory (reactive or primary)

§  Neoplasia (eg prostate ® femoral head)

·        Pathology:

o  Cartilage = collagen proteoglycans + water (70%).  Made by chrondrocytes 

o  ¯Elasticity of cartilage ® mechanical stress causes deformation and stress on underlying bone. Fissuring and flaking of cartilage. Roughened cartilage surface. Blood vessels invade cartilage. ?Inflammatory cytokines mediate cartilage destruction 

o  Micro: villus fronds in cartilage 

o  Gross: Shiny, subchondral bone (eburnisation), subchondral cysts, osteophytes (extra-articular overgrowth of bone ® attempt to ­ weight bearing area)

·        Investigations:

o  X-ray

o  Lab tests usually normal (check for normal ESR, CRP, RF, ANAs, joint aspirate)

·        Management:

o  Conservative:

§  Inform, education

§  Do nothing, or 

§  Pharmacology (analgesics, NSAIDs): Paracetamol. NSAIDs have little evidence of further improvement, and cause renal impairment and GI bleeds. Potential for COX-2 inhibitors. Also glucosamine (from health food shop, 1500 mg/day) 

§  Steroid injection if secondary inflammatory component

§  Physiotherapy: 

·        Obtain and maintain full range of motion (¯range of motion ® ­loading on a smaller area of cartilage ® wears out faster) 

·        Exercise: eg quad exercises for osteoarthritis of the knee

§  Orthotics and other devices:

·        Weight loss and devices to reduce weight bearing across affected joints

·        Raising bed and chairs to reduce strain, walking sticks, handrails, etc

§  Aspiration of joint fluid

o  Surgery, especially for knee and hip (determined on functional/pain criteria):

§  Arthroscopic debridement (buys time) 

§  Osteotomy: take out a wedge of bone above or below the joint – realigns stress through the joint ® more even wear 

§  Arthroplasty: a prosthesis (considerable variety). Main indication is pain. Surgery to correct fixed flexion deformity is less successful. NB don‟t forget DVT prophylaxis

§  Arthrodesis: joint fusion