Osteoarthritis

Wikis > Rheumatology > Osteoarthritis

Common non-inflammatory clinical syndrome/abnormality of synovial/diarthrodial joints characterised by progressive softening, fragmentation and loss of articular cartilage with increased activity of the subchondral bone  remodelling and sclerosis of subchondral bone and the development of marginal osteophytes. It is the most common joint condition. Affects 80%+ of those aged over 65 years, but <5% under age of 25 years. 20% of adults have osteoarthritis in the foot .Aetiology: Multifactorial – the actual initiating factor is unclear. Predisposing factors: 1) Endogenous factors (normal forces and abnormal cartilage): • ageing (more common with increased age) • hereditary (a strong genetic component is thought to be present, especially involvement of DIPJ’s) • gender (appears to play a role in which joints are affected) • ethnicity (affects all ethnic groups, but pattern/joint distribution of disease is different in some groups) • articular cartilage damage (eg infection, metabolic disorders, inflammatory arthritis) 2) Exogenous factors (abnormal force and normal cartilage): trauma obesity (stronger relationship in women than men; obesity is an important risk factor, as it is modifiable; more associated with osteoarthritis in knee, but not hip) • changed congruity of joint surface (eg knee valgus; excessively pronated foot) • single event trauma (eg accident; old sports injury) • multiple event trauma (may be occupation related; may be related to prolonged weightbearing on hard surfaces) • hypermobility – eg Ehlers-Danlos syndrome, Marfan’s syndrome • incongruity of joint surfaces – eg post surgical; slipped femoral epiphysis • smoking may be a factor in degenerative disc diseaseClassification: 1. Primary – no specific cause. 2. Secondary – specific factor can be identified – eg post-traumatic (acute, chronic); pre-existing inflammatory disease (eg gout, rheumatoid arthritis); metabolic/endocrine diseases (eg haemochromatosis, ochronosis, acromegaly, hypothyroidism, Wilson’s disease, Gaucher’s disease); dysplasia’s (eg epiphyseal dysplasia); hip disorders (eg Legg-Calve-Perthes disease, congenital hip dislocation, slipped capital femoral epiphysis)Pathogenesis: Both biomechanical and biochemical factors are involved in the cartilage destruction. Pathophysiologicaly it is characterised by a progressive degradation of the components of the extracellular matrix of the articular cartilage – this includes the loss of aggrecan, damage to the collagen fibres, increase in water content and an increase in proteoglycan synthesisInitiation will be dependent on the balance between the articular cartilage resistance to injury and the degree of mechanical stress  damage occurs when the structures can no longer resist the forces. When cartilage catabolism exceeds cartilage synthesis  osteoarthritis.Four stages have been identified in the pathogenesis: 1) Initial repair – proliferation of chondrocytes and increased synthesis of extracellular matrix. 2) Early stage osteoarthritis – the increased synthesis of extracellular matrix is exceeded by its degradation and increased protease activity  loss of articular cartilage. 3) Intermediate stage osteoarthritis – lack of synthesis of extracellular matrix with activity of proteases still increased  further degradation and loss of articular cartilage. 4) Late stage osteoarthritis – content of extracellular matrix is further reduced  articular cartilage very thin or absentCartilage is not innervated  pain is due to irritation of the subchondral bone or from distension of innervated joint capsule.Clinical features: Usually over age of 40. Gradual development of pain/aching in involved joint(s) – worse on use of joint, worse at end of day and after activity, pain relieved by rest, stiffness following inactivity (‘gelling’ or ‘gel phenomena’ – usually <30mins), limited joint range of motion – both active and passive, crepitus, joint enlargement, periarticular muscle wasting Joints may be tender to palpation (especially if synovitis is present) Osteophyte formation may be palpable. Heberden’s nodes – bony nodules or ‘lumps’ on DIPJ; Bouchard’s nodes – ‘lumps’ on PIPJ’s – presence usually indicates that patient has primary osteoarthritis. Symptoms are poorly correlated with pathological changes in articular cartilage.Radiographic changes: Asymmetric joint space narrowing (from loss of articular cartilage); osteophyte formation (from periosteal and synovial membrane stimulation as well as capsular traction); subchondral sclerosis/cysts (from increased activity of subchondral bone); intra-articular loose bodies (from fragmentation of osteochondral surface). Can get minimal soft tissue swelling.Course: Several patterns of progression have been identified: 1) Slow progression 2) Little or no change with mild symptoms 3) Stepwise deterioration with periods of rapid progression 4) Intermittent exacerbations with no radiological changes.Erosive, inflammatory osteoarthritis/Crain’s disease: • small subset of primary osteoarthritis with some joint inflammation superimposed on the degenerative symptoms  have ‘flare ups’ • usually female >50yrs
• usually DIPJ’s and PIPJ’s and carpo-metacapal joints in hand and first metatarsophalangeal joint in foot
• do have central erosions on x-ray’s
• sometimes misdiagnosed as rheumatoid arthritis

Involvement of Foot Joints:

Ankle joint:
• relatively uncommon for ankle to be involved despite major weightbearing role  major problems with gait and mobility if affected
• usually secondary to previous trauma
• usually have – tenderness along joint margin with firm swelling; crepitus; restricted painful range of motion; painful anterior draw sign; painful while standing and walking; stiff after inactivity, especially in morning. May have antalgic gait.
• varus or valgus alignment of ankle is common
• treatment – symptomatic relief; may need ankle foot orthoses - patellar tendon bearing AFO’s can reduce weightbearing pressures; weight loss; improve muscle strength; physical therapy; SACH or rocker sole shoe; surgical

Subtalar joint:
• from abnormal stresses at joint – trauma common cause
• Ledoux & Hillstrom (2001), as a result of their study, suggest that STJ osteoarthritis may be initiated and/or perpetuated by excessive calcaneal acceleration at heel strike
often get a heel pain or ankle pain referred from the osteoarthritis of the subtalar joint
joint is painful to move and crepitus may be felt. Weightbearing is generally painful.
calcaneus is often very everted.
subtalar joint articular facet configuration is associated with a higher prevalence of subtalar joint osteoarthritis – specifically those with a long continuous facet and a medial facet only (both are two facet joints) are at greater risk
treatment – rest; anti-inflammatory medication; surgical fusion if pain is severe and persists or if significant deformity
• for STJ and/or midfoot osteoarthritis – consider using rigid orthoses as aim is to prevent movement – use orthoses to hold joint in least painful position – take negative cast of foot in this position – for most this will be maximally pronated (balance forefoot to hold it in this position) – use flat heel post to prevent/restrict motion. A UCBL type device may be needed to restrict motion.

Midfoot joints:
• often result of trauma (fracture or dislocation) – but can be due to chronic malignment/poor biomechanics or post-surgical (especially rearfoot arthrodesis)
• pain is usually activity related and localised to involved joint
• irritation from shoes over osteophytes is common
• motion of involved joint is restricted
• x-ray will show joint space narrowing, subchondral sclerosis and marginal osteophytes
• treatment – orthoses to reduce load on joints; accommodative padding for osteophytes to protect from shoes; anti-inflammatory medication
• surgical – osteophyte excision; arthrodesis

First metatarsophalangeal joint:
• see hallux rigidus in Orthopaedics & Musculoskeletal Medicine chapter
• earliest symptom is tenderness on dorsum of first MPJ with crepitus on dorsiflexion from a flexed position

Lessor metatarsophalangeal joints:
• usually from trauma; Freiberg’s disease; systemic disease
• treatment – anti-inflammatory medication; rigid sole or rocker sole shoe; surgical  arthroplasty, debridement, arthrodesis

Interphalangeal joint:
• usually result of trauma
• can cause deformity and pain
• nail changes with distal IPJ joint osteoarthritis have been reported .
• treatment – rest; anti-inflammatory medication; rigid sole shoes; surgical arthrodesis

Osteoarthritis of the Knee and Foot Function:
Laterally wedged insoles have been shown to help medial compartment osteoarthritis of the knee 18,19,20,21,22,23. Varus alignment of the knee increases risk for medial knee osteoarthritis progression and valgus alignment of knee increased progression of lateral osteoarthritis . This raises the possibility of the potential role of foot orthoses/wedges in slowing progression.

Management:
• Education and reassurance of patient and family  self-management. There is widespread ignorance and misconceptions (eg ‘its one of those things’; ‘inevitable’) about the nature of osteoarthritis that leads to negative attitudes that can inhibit management of the disease. Positive attitudes need to be encouraged. A meta-analysis has shown the effectiveness of patient education on joint pain .
• Rest of affected joint(s)
• Exercise – gentle to increase range of motion; advice to keep active, but avoid excessive load on affected joint.
• Weight loss is important
• Reduction of adverse mechanical factors (eg weight loss, change biomechanics)
• Assistive devices (eg shock absorbing footwear, braces, walking sticks)
• Physiotherapy – heat, aerobic exercise, hydrotherapy, strapping, muscle strengthening, TENS
• Occupational therapy – help adapt to any disabilities and develop activities to minimise stress on joints; also good means of social support and patient education
• Correction of any predisposing and/or exacerbating factors.

Generic management of foot OA:
• Loss of weight  important
• Joint protection  footwear advice; foot orthoses
• Pain control (eg NSAID’s)
• Possible surgery if persistent

Pharmacological:
• Topical - capsaicin cream (eg Zostrix®) – shown to reduce pain in some controlled studies; NSAID’s – a meta-analysis of topical NSAID’s showed that 65% responded compared to 30% of those on placebo (Moore et al, 1998).
• Viscosupplementation (hyaluronan) – intra-articular joint lubrication to restore physical properties (viscoelasticity) of synovial fluid. Has been shown in a number of studies to have greater pain relief compared to placebo.
• Symptom modifying OA drugs (SMOADS)
paracetamol, acetaminophen
NSAID’s (eg Celebrex®, rofecoxib)
• Glucosamine – nutritional supplement taken orally; physiological substrate for synthesis of proteoglycans and hyaluronic acid – also inhibits protein degradation; has mild anti-inflammatory effects’ has been shown to have greater pain relief compared to placebo; effects take 4-6 weeks to occur
• chondroitin sulfate – nutritional supplement derived from cartilage (eg shark, cow trachea). Has a mild anti-inflammatory effect and may stimulate cartilage synthesis and inhibit breakdown. Compared to placebos, it has been shown to have greater pain relief, improved range of motion and reduced swelling.
• Disease modifying OA drugs (DMOADS)
• pentosan polysulphate (eg Cartrophen®) – stimulates cartilage synthesis and inhibits degradation and anti-inflammatory.

‘Analgesic arthropathy’ – can develop from increased physical activity when taking analgesics  increased joint damage

Surgical:
Arthroscopic “wash out”; joint debridement; joint replacement; joint realignment; arthrodesis.
Joint replacement indicated if pain is severe, non-responsive to pharmacological agents, joint function is lost, cannot walk for >50m, pain awakens from sleep, difficult standing in one place due to pain.

Related Topics:
Knee Osteoarthritis

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