Osteoarthritis Flashcards
what is the definition of osteoarthritis?
Osteoarthritis (OA) is the result of mechanical and biological events that destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix, and subchondral bone. It involves the entire joint, including the articular cartilage, subchondral bone, pericapsular muscles, capsule, and synovium.
inflammation of articular and periarticular structure and alteration in cartilage structure
what is the epidemiology of osteoarthritis?
Most common arthritis
More common in women
Over 50 yrs, levels off at 70yrs
what is the aetiology of osteoarthritis?
Exact aetiology unknown
High bone mineral density and low oestrogen status, such as in post-menopausal women, may be associated with higher risk of knee and hip OA.
The preceding 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, such as periarticular muscle weakness, misalignment, and structural joint abnormality (e.g., meniscal tear), further facilitate the progression of the disease. The internal and external factors combined lead eventually to a failed joint.
Age, hereditary predisposition, female sex, and obesity are associated with increased risk of OA.
Articular congenital deformities or trauma to the joint also increase the risk of developing OA
what are the risk factors for OA?
Over 50 Female Obesity Genetics - COL2A1 collagen type 2 gene plays a role Knee malalignment Increased physical demand Post trauma High bone mineral density
what is the pathophysiology of OA?
loss of cartilage and disordered bone repair
Slow over time
Weight bearing big joints and hands
Matrix metalloproteinases (e.gcollagenase), enzymes that catalyse both collagen and proteoglycan degradation, are found in increased concentrations in OA cartilage.
Nitric oxide may activate metalloproteinases, thereby playing a role in cartilage degradation.
Inflammatory mediators play a role as potential drivers of joint tissue destruction. The number of pro-inflammatory mediators reported in the synovial fluid and tissue affected by OA is increasing.
Anabolic cytokine levels, such as those of insulin-like growth factors (IGF-I), are decreased in OA.
Aberrant chondrocyte metabolism is a response to changes in the inflammatory microenvironment and may play a key role in cartilage degeneration and OA progression. Under conditions of environmental stress, chondrocytes shift from oxidative phosphorylation to glycolysis, a process regulated by the AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) pathways.
what are the key presentations of OA?
Risk factors Pain Functional difficulties Knee, hip, hand and spine involvement Bony deformities Limited range of motion Malalignment less than 30 minutes of morning stiffness DIP, first metatarsophalangeal joint, hips, vertibrae, knees
what are the signs of OA?
Risk factors Knee, hip, hand and spine involvement Bony deformities Effusion Antalgic gait Heberden's nodes = DIP swelling Bouchard's nodes = PIP swellings
what are the symptoms of OA?
Pain Limited motion Tenderness Crepitus (creaking joints) Stiffness
what are the first line and gold standard investigations for OA?
X-ray of affected joints - osteophytes, joint narrowing, subchondral sclerosis and cysts
Serum CRP - normal or slightly elevated
ESR - normal
RF and ANA - negative
what is the differential diagnoses for OA?
Bursitis
Gout
Pseudogout
RA
how is OA managed?
Pain management:
Topical analgesia (capsaicin topical), physio, intra-articular corticosteroid injections, paracetamol before NSAIDs, gastroprotection (omeprazole), intra-articular hyaluronic acid, opioids (dihydrocodeine)
Ongoing:
Surgery (arthroscopy, arthoplasty, osteotomy, fusion), duloxetine
how is OA monitored?
Patients are monitored for progression of disease and response to treatment, as well as any adverse effects. They are asked about their pain response to treatment, function, and limitation in their activities due to their disease.
Patients are examined for declining range of motion in the affected joint, and for other signs reflecting advanced disease.
If the patient is taking a non-steroidal anti-inflammatory drug (NSAID) or a cyclo-oxygenase-2 (COX-2) inhibitor, tests for renal function and full blood count are obtained every 3 to 6 months.
what are the complications of OA?
Functional decline Spinal stenosis in cervical and lumbar OA NSAID related GI bleeding Effusion NSAID related renal dysfunction
what is the prognosis of OA?
Despite treatment, most patients continue to have some degree of pain and functional limitation affecting their desired activities and quality of life.
Complications of medication, particularly non-steroidal anti-inflammatory drugs (NSAIDs), are problematic.
