OA Flashcards
** OA physical exam findings **
-Crepitus
-Bony enlargement
-Mild swelling
-Joint instability
-Periarticular muscle atrophy
- Radiculopathy if facet hypertrophy causing neural foraminal compression
-Reduced ROM
-Facet OA worsens spinal stenosis w/ extension
** OA pathophysiology**
Repetitive trauma to articular cartilage → damage → DAMP release → activates innate immune system and adaptive (Th1>Th2; synovial fibroblasts secrete IL1/6/17, TNF cytokines causing less matrix synthesis and more apoptosis) *TNFb counters this and produces matrix and enhances chondrogenesis
-Chondrocytes increase proteoglycan synthesis but release more degradative enzymes → proteoglycan breakdown faster than it can be produced → articular cartilage thinning/softening → cracking/fissuring of cartilage → exposed underlying bone and synovial fluid forced into bone → subchondral cysts → remodelling/hypertrophy of subchondral bone → osteophyte and subchondral sclerosis
-Can occur under normal loads if underlying cartilage, bone, synovium, ligaments, muscles are abnormal from 2ndary cause
** How aging contributes to OA**
- – DECREASED chondrocytes
- – DECREASED proteoglycan synthesis – THINNER Collagen
- – SHORTENED GAGs → less H2O retention and elasticity
- – Increased “advanced glycation end products” accumulation (more rigid)
** Early Pathologic features of OA**
– Swelling of articular cartilage (Increased cartilage water content)
– Chondrocytes increase proteoglycan synthesis but release more degradative enzymes
– Loosening of collagen framework
** Late Pathologic features of OA**
– Degradative enzymes break proteoglycan faster than it can be produced by chondrocytes (less proteoglycan in cartilage)
– Articular cartilage thins and softens (joint space narrowing on XR)
– Fissuring/cracking of cartilage → underlying bone exposed → synovial fluid forced into bone by pressure of weight = subchondral cysts/geodes
– Remodeling/hypertrophy of subchondral bone → subchondral sclerosis and ostephyte (spur) formation
** Joint involved in primary idiopathic OA**
-CMC, PIP, DIP
-AC shoulder joint
-Hips, Knees, 1st MTPs
-Facet (apophyseal) joints of C/L spine
** Joints NOT involved in primary OA
AKA Joints in secondary OA**
Wrists, MCPs,
-Elbows, glenohumeral shoulder joint
-Ankles, 2nd-5th MTPs
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-**If see these, search for 2ndary causes of OA
OA synovial fluid
Normal viscosity w/ good string sign
-Clear and yellow colored
-WBC <1000-2000
-No crystals
-Negative Cx
** OA XR findings**
- Subchondral sclerosis/cysts
- Osteophytes
- NONuniform jointspace narrowing
- Deformities: Heberden, Bouchard, distal phalanx deviation (lateral/palmar)
- NONerosive (maybe gullwing in erosive OA)
- Vacuum sign in DDD (nitrogen in a degenerated disk space)
No ankylosis, calcification, nail or soft tissue changes
-Alignment can be abN
-Bone mineralization N
OA classification
Primary idiopathic
– Localized: DIP, PIP, 1st CMC, 1st MTP, hip, knee, spine
– Generalized (aka Kellgren’s syndrome)
-Secondary
Joint involved in Nodal OA
DIP, PIP, first CMC
Joints involved in erosive inflamm OA
DIP, PIP, first CMC
** Generalized and Localized OA Risk factors**
Generalized OA
-Age
-Heredity
-Sex (women >50)
-Smoking (contrib to DDD)
Localized OA
-Previous joint trauma
-AbN joint mechanics (varus, valgus, hip dysplasia)
-Obesity
- Hemarthrosis
- Metabolic/Inflammatory/Septic Arthritis
- Repetitive loading (job, sports eg boxers MCPs, ballet ankles, basketball knees/ankles, drill operator shoulder/elbows)
** How does obesity predispose OA predisposition?**
-Increased loads causes chondrocyte mechanoR to produce growth factor, cytokine, MMP
-Adipose = source of proinflamm cytokines (leptin, adiponectin, resistin, IL1/6, TNFa) even in non weight bearing joints
Erosive OA XR findings
Osteophytes
-Central erosions with GULL WING or inverted T appearance
-Joint ankylosis
Differentiating erosive OA from inflammatory arthritis
NO systemic symptoms
-NO involvement of MCPs, wrists, 2nd-5th MTPs
-NORMAL inflammatory markers
-Negative RF and ANA
Erosive OA pathophys
-Synovial hypertrophy w/ IL1 release causing MMP and central cartilage destruction/clearing
-Lymphocytic/neutrophilic infiltration
-**Erosion NOT from synovial pannus invasion
-Another hypothesis is role of hydroxyapatite and CPP crystals
Generalized OA
4+ sites symmetrically involved
DISH (diffuse idiopathic skeletal hyperostosis) clinical manifestations
- Most frequently T spine → stiffness & decreased ROM
-Pain is NOT significant
-Dysphagia if C spine involved
DISH radiologic findings
-Flowing ossification of anterior longitudinal ligament connecting at least 4 contiguous vertebral bodies
-Ossification separated from anterior vertebral body by thin radiolucent line (flowing candle wax)
-NORMAL disk spaces, apophyseal joints, and SI joints
** Secondary OA features**
Early age of onset
Atypical joints:
- MCP, Wrists,
- Elbows, Shoulders (GH NOT AC)
-Ankles, MTP2-5
** Causes of shoulder OA**
Chronic dislocation or hypermobility (EDS)
-Trauma
-Surgery
-AVN
-Inflammatory arthritis
-Rotator cuff tendinopahy/tear
-Crystal arthropathy (eg Milwaukee)
-Infection (septic joint)
** Secondary causes of OA **
Congenital
- Hip: Perthes disease, SCFE, FAI, congenital shallow acetabulum
- Dysplasia: epiphyseal or spondyloepiphyseal dysplasia
-Mechanical: hypermobility, leg length discrepancy, varus/valgus, scoliosis
-Trauma: ACL tear, fracture, meniscectomy
-Metabolic: hemochromatosis, gaucher’s, crystal deposition, hemoglobinopathy,Paget
-Endocrine: hyPOthyroid, hyPERPTH, acromegaly, DM
-Infectious: syphilis,septic
-Other: AVN, inflamm arthropathy, osteochondropathy 2/2 mycotoxin or selenium def
FAI clinical manifestations
-Groin pain w/ sitting/athletics
-Hip flexion limited to 90deg w/ painful internal rotation from impingement
-Click/snap w/ hip rotation 2/2 labral/chondral lesion
