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Flashcards in Osteoarthritis Deck (10):

Osteoarthritis (OA)

-Degenerative joint disease of the elderly, characterized by progressive cartilage loss, subchondral bone thickening, and marginal osteophytes
-NO inflammation in OA
-After age 75 80% of people have OA


Normal articular cartilage

-Normal articular cartilage (type 2 collagen) provides an almost frictionless articulation and serves to absorb and dissipate load
-The cartilage is made by chondrocytes, which also secrete nzs to degrade the ECM
-Healthy collagen matrix is a balance btwn anabolic (production of collagen) and catabolic (destruction of collagen) processes


Pathogenesis of OA (!)

-A combination of things, mostly decreased articular cartilage matrix synthesis and increased matrix breakdown by the chondrocytes
-Biomechanical factors also contribute to loss of cartilage and matrix integrity
-Genetic and metabolic factors both play a role


Primary vs secondary OA

-Primary OA: no identifiable cause, often involves the spine, hip, and knee (weight bearing joints)
-Secondary OA: identifiable cause and can involve any joint
-Must consider secondary OA if arthritis is present in unusual locations or below age of 50



-Connective tissue manifestation of alkaptonuria (recessive metabolic d/o)
-Buildup of homogentisic acid in joints/tissues
-Results in pigmentation, calcification, and inflammation of joints and tissue
-Can be a cause of secondary OA



-Recurrent attacks of inflammatory arthritis
-Caused by elevated levels of uric acid in blood
-Uric acid crystallizes and the crystals (monosodium urate) are deposited into joints, tendons, tissue
-Can be a cause of secondary OA


Physical exam features of OA

-Bony enlargement: new bone formed due to worn down cartilage
-Effusions: swelling of the joints
-Heberden's and bouchard's nodes (OA of the hand)
-Heberden's: nodes of the DIPs (HeDIPs)
-Bouchard's: nodes of the PIPs (BoPIPs)
-Crepitus: crackling/popping sounds when the joint is passively moved


Strongest risk factors for OA

-Age and obesity
-Others: female, previous injury, genetics
-Previous injuries: old fractures, abnormalities of the meniscus, ligament tears
-Running is NOT a risk factor
-Gene that is associate w/ OA: type 2 collagen gene COL2A1


OA vs inflammatory arthritis

-OA is mechanically driven and not inflammatory
-Inflammatory arthritis can be due to autoimmune illness, crystalline arthropathy, infections, or malignancy
-Key differences: OA is always progressive (inflammatory can be acute or progressive), OA is mostly >50, morning stiffness lasts 30 min (1hr w/ IA), activity makes OA worse (makes IA better), rest makes OA better (makes IA worse), no heberden/bouchard nodes in IA, no osteophytes in IA


Rx of OA

-Mild-moderate pain: acetaminophen, topical agents
-Moderate-severe pain: joint aspirations if there are effusions, intra-articular injections of glucocorticoids and hyaluronan, COX-2 specific inhibitors, NSAIDs, tramadol, opioids
-If overweight, weight loss is key