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
-
-**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
How does FAI cause OA
Flexion → abN contact between femoral head or prox femur (at head-neck jcn) with anterior rim of acetabulum → labral tears and early OA
-Due to deep acetabular socket or cam deformity
How does pes planus cause knee OA
-Rotation stress on medial knee from pronation
-Patella tracks laterally → patellofemoral OA
Why no ankle OA vs knee/hips
- Ankle = rolling joint w/ congruent surfaces at high load (vs knee=less congruent w/ sliding/rolling/rotation → more stress)
- Ankle cartilage thickness and composition makes it more resistant to catabolic cytokines
** OA nonpharm Tx**
ACR strong recommendation:
-Exercise
-Weight loss
-Tai Chi
-Cane, tibiofemoral knee brace, 1st CMC orthosis
-Conditional recommend:
-Heat/therapeutic cooling
-CBT
-Acupuncture
-Kinesiotaping
-Balance taping
-Patellofemoral knee brace, other hand orthoses
-Yoga
-Paraffin bath (hands)
-Radiofrequency ablation
** OA Tx - pharm**
-Tylenol
-Intermittent NSAIDs + PPI
If GI issues:
- Topical NSAIDs,
- Tramadol,
- Duloxetine
-IA steroids
-NO role for PO steroids
Erosive OA tx
Topical/PO NSAIDs
-IA steroids
-Varying success: HCQ, MTX, anti-TNF, IL1 ANT
** How does Glucosamine and chondroitin supplements work, do you support it **
Glucosamine and chondroitin are GAGs
-Can be incorporated into and increase chondrocyte production of proteoglycans
-Mild anti-inflamm fx
-Can block certain proteases
** 2020 guidelines recommend AGAINST given discrepancy between studies. VAS pain benefit in some trials
Glucosamine and chondroitin dosing
Glucosamine 1500mg daily
-Chondroitin 1200mg daily
Glucosamine and chondroitin side fx
Cause allergy in ppl w/ shellfish allergy
-May increase warfarin effect
How does hyaluronan work?
-Stimulates proteoclycan synthesis
-Antiinflammatory fx
-Antinociceptive fx
Hyaluronan side fx
Local injxn rxn
-Systemic allergic rxn (egg and feather component)
-Pseudoseptic rxn
** Indications for joint replacement in OA **
Severe pain unresponsive to medical therapy
- Consistent Night pain
- Unable to stand for >20-30 min
Loss of joint fcn
- Cannot walk 1+ block,
- Can’t put on shoes,
-Moved to aptment bc of inability to climb stairs
New therapies for OA
Autologous chondrocyte implantation or mesenchymal stem cell injxn
-Abrasion and microfracture surgery (micro drilling releases mesenchymal stem cells from marrow to repair cartilage)
-PRP (degranulated PLT releases TGFb, platelet derived GF, epidermal GF, insulin like GF that inhib inflamm, increases cartilage synthetic activity)
-Genicular nerve block (cooled radiofreq ablation of genicular nerve in knee)
** Name the 2 most frequent components of cartilage by dry weight?**
- Collagen (>90% type 2)
- Proteoglycan (glycosylated prot monomers)
** How does cartilage or chondrocytes get nourished? **
- Adult cartilage is avascular,
- Chondrocytes obtain nutrients through diffusion from synovial fluid (cartilage water squeezed out during weightbearing and sucked back when unloaded)
** Name the 3 constituents of normal cartilage and their relative proportions? **
Articular cartilage (wet weight) is more than 70% water, 15% collagen, 10% proteoglycans.
Chondrocytes constitute only 1% to 2% of its total volume.
** Describe the structure of the proteoglycans**
Proteoglycans are glycoproteins with 1+ glycosaminoglycan (GAG) chains made of either:
-Chondroitin sulfate/dermatan sulfate,
-Heparan sulfate/heparin,
-Keratan sulfate or
-Hyaluronic acid (usually the backbone)
** List 3 structural differences in proteoglycans in OA vs normal aging?**
Concentration: OA = early increase (not in aging), then decreases later (occurs in aging but not as much)
Molecular weight: decreased in both
Keratin sulfate [ ] : decreased in OA (INCREASED in aging)
Chondroitin sulfate [ ]: INCREASED in OA (decreased in aging)
Aggregation of proteoclycan: decreased in both (less in aging)
** Role of proteoglycan **
- Structural support to ECM
- Binds water to absorb high compressive loads
- Regulate cell adhesion, proliferation, migration, differentiation, survival, and death
** List the cell type most important in the cartilage degeneration in OA?**
Chondrocytes
- Increase proteoglycan synthesis but also release degradative enzymes (MMPs, ADAMTS-4) = more breakdown than production
- Damaged cartilage (chondrocytes) release DAMPs to activate innate immune system.
- The adaptive system, responds due to the DAMPS. T cells (Th1 > Th2) and synovial fibroblasts secrete IL-1, IL-6, IL-17, and TNF.
** List 1 family and 2 examples of substances that mediate degradation of cartilage in OA? List 2 molecules which inhibit the above 2 examples?**
MMP = cleave collagen & proteoglycans
- Collagenases,
- Gelatinases,
- Aggrecanases,
- Serine/cysteine proteases
Inhibitors of MMP
- Tissue inhibitor of MMP (TIMP) 1,2,3,4
- Synthetic zinc binding globulins (ZBG) or nonZBG
** What 3 enzymes or factors are important in OA? **
Anabolic factors:
- TGFb, IGF1,
- Bone morphogenic proteins (BMPs),
PGE2
Catabolic:
- IL1, IL6, TNFa
- MMP (collegenase, gelatinase, aggrecanase)
DISH Exam maneuvers
-Decreased spinal ROM of T spine, especially lateral flexion
- Nodules at enthesis (elbow, knee, Achilles)
** List 2 indications for intra-articular corticosteroid injection in OA of the knee? How long does an intra-articular injection last to the knee for OA?**
Pain
Failed other treatment options
Cohcrane review: up to 6 weeks relief
** List 3 potential complications of TKA or THA **
- Reaction to anesthetic or transfusions
- Vascular/nerve injury
- VTE
- Surgical site infection, PJI
- Periprosthetic fracture, dislocation, osteolysis
- Heterotopic ossification
- Patellofemoral disorders
- Wear and tear of prosthetic
- Aseptic loosening
** Indications for THA**
Same as for TKA, but includes:
- #
- AVN
- Periarticular pagets
- Hardware failure from previous replacement
**OA nonpharm recommended against **
AGAINST:
-TENS (transcutaneous electrical nerve stimulator)
-Massage, modified shoes, wedged insoles, vibration therapy, iontophoresis, Cspine collar, traction, distraction
Topical lidocaine, capsaicin (deplete Hydrotherapy
Not effective: pulsed electromagnetic fields, magnets
** Lumbar facet joint spinal stenosis:
List 2 activities which cause worsening of symptoms?
List 2 activities which cause improvement in symptoms?
List 4 findings on CT-Scan?**
Worsens
-Prolonged walking (esp downhill)
-Leaning backwards
-Spinal phalen’s (30s back extension)
Improves
- Leaning forward
- Sitting
CT findings (need <10mm AP diameter to consider it central stenosis)
- Oval spinal canal looks triangular
- Central disc bulge
- Facet hyperostosis
- Spondylosis (aka OA of the spine)
- Ligamentum flavum hypertrophy
