Osteoarthritis Flashcards
What’s the most common arthropathy? What does the primary path involve? Inflammatory or non-inflamm process?
Osteoarthritis - most common arthropathy
¨Primary pathology involves cartilage, subchondral bone, and synovium
Non – inflammatory joint fluid, Involves active cytokines
¨Multi - factorial etiology
What is the progression of OA?
Progressive deterioration & loss of articular cartilage, leading to loss of normal joint structure & function
What causes primary OA? What joints are affected?
- Aging or Idiopathic.
- Hands: DIP, PIP, first CMC.
What causes secondary OA? What is it frequently comorbid with?
- Due to disorders* that damage articular cartilage, subchondral bone, or synovium.
- May have had congenital or developmental defects of the hips.
Name some causes of OA.
¨Vascular
¨Infectious, Inflammatory, or Infiltrative
¨Neoplastic/Neuromuscular
¨Degenerative, Deficiency
¨Idiopathic, Intoxication (Drugs)
¨Congenital
¨Autoimmune, Allergic
¨Traumatic
¨Endocrine/metabolic, Environmental
¨Depression (Anxiety)
What are some vascular causes of OA?
¨Vascular (sickle Cell, thalassemia, avascular necrosis)
What are some infectious, inflamm, and infiltrative causes of OA?
¨Infectious (Staph), Inflammatory (RA) Infiltrative (sarcoid, hemophilia)
What are some neoplastic or neuromuscular causes of OA?
¨Neoplastic (acromegaly, Pagets)/Neuromuscular (muscle weakness, tabes, diabetes/Charcot joint)
What are some congenital causes of OA?
(hip dislocation, slipped femoral epiphysis; genetics - differentially methylated genes; BMP and WNT signaling pathways)
What are some endocrine/metabolic causes of OA?
(obesity, alcaptonuria, gout, pseudogout, hemochromatosis, Wilsons)
What are some path characteristics of OA?
- Altered chondrocyte function
- Loss of cartilage - thinning
- Subchondral bone thickening - sclerosis
- Remodeling of bone
- Marginal spurs - osteophytes
- Cystic changes in subchondral bone
- Mild reactive synovitis
Describe the pathophysiology of OA.
external events and forces alter the synovium, articular cartilage, and/or subchondral bone resulting in cytokines (especially IL 17) and metalloproteases being released into the joint
Cartilage matrix degeneration follows.
This results in synovial cell stimulation and chondrocyte cloning in an attempt to repair the cartilage by increased proteoglycan (hyaluronic acid) production.
In turn, the cartilage swells. (IL1 is also a key mediator of cartilage damage and is produced in response to calcium and UA crystals that often accompany OA.
Eventually proteoglycans become exhausted and as a result numerous vertical slits occur in the articular surface cartilage. This change in the cartilage is known as flaking or “fibrillation” with cartilage thinning, and eosinophilia of the remaining cartilage.
What is ‘flaking’ in the context of OA?
exhausted proteoglycan stores leading to flaking on articular cartilage surface
What does loss of cartilage in OA lead to?
leads to narrowed joint spaces and further trauma from adjoining bone with more destruction in the high load areas.
As subchondral bone is subjected to vascular invasion with cellular proliferation, eburnation, and spur formation occur
What are bone spurs?
Vascularization with osseous metaplasia eventually produces ossifying cartilagenous protrusion referred to as spurs or osteophytes.
What leads to subchondral cysts?
Chronic impaction and intrusion of synovial fluid leads to subchondral cysts and osseous necrosis.
What are some common sites of OA presentations?
Cervical spine
Lumbar spine
1st CMC
PIP
DIP
Hip
Knee
1st MTP
What are some uncommon sites of OA?
Shoulder
Thoracic spine
Elbow
Wrist
MCP
Ankle
Subtalar
What are the sxs of OA?
¨Insidious onset
¨Deep, achy joint pain associated with movement*
¨Minimal stiffness – usually lasting < 30 minutes
Subchondral vascular congestion, osteophytic periosteal elevation, muscle fatigue, synovitis, effusion, stretched capsule, etc.
What are the physical signs of OA?
¨Limited ROM and crepitus
¨Joint line tenderness
¨Cool effusions
¨Spasm or atrophy of adjacent muscles
What are the diagnostic test appropriate for OA?
No specific diagnostic tests
•Synovial Fluid - class 1
(non-inflammatory – clear, yellow, WBC < 2000; < 25% neutrophils)
Does have citrullinated protein but no antibodies
What will xrays show of OA?
- cartilage loss/joint space narrowing
- osteophytes at joint margins
- subchondral sclerosis
- subchondral cysts
What are the subsets of OA?
¨Nodal O.A.
¨Erosive (inflammatory) O.A.
¨Generalized O.A.
¨Secondary Osteoarthritis – knees, hips and spine
¨Chondromalacia patellae
¨Spondylosis
What is another name for OA?
DJD - degenerative joint disease
What are some pathognomonic signs for DJD on the hands?
Heberden’s nodes - DIP
Bouchard’s nodes - PIP
1st CMC Joint: base of thumb
What are some deformities on xray that are pathognomic for erosive OA?
saw tooth (PIP) and gull wing deformity (DIP)
What are some clinical correlations and relative cytokine levels associated with erosive OA?
DRB1*011,
increased IL2,
increased sIL4/decreased IL4/decreased IL1 and TNF alpha.
Increased obesity/adiponectin.
What is needed for a Dx of erosive OA? What should or should not be present?
Central* subshondral erosions in 2 IP joints with 1 a DIP.
No psoriasis.
No gout or pseudogout.
Normal sed rate, C-RP, RF, and Anti-CCP.
No MCP or wrist involvement.
Subluxations and ankyloses*.
Abrupt onset in women.
How do erosions seen in erosive OA differ from erosions in RA?
Erosive OA: Central subchondral erosions in 2 IP joints with 1 a DIP
RA erosions are marginal and have no ankylosis
What should normal synovial fluid have/look like as far as:
clarity,
color,
WBCs/mL
PMNs %
RBCs
Glucose diff
Normal synovial fluid:
clarity - transparent
color - clear to pale yellow
WBCs/mL - 0-150
PMNs % - <25
RBCs - No
Glucose diff - 0-10
What should Group I noninflammatory synovial fluid have/look like as far as:
clarity,
color,
WBCs/mL
PMNs %
RBCs
Glucose diff
Group I noninflammatory synovial fluid
clarity - transparent
color - xanthrochromic
WBCs/mL - < 3000
PMNs % - <30
RBCs - No
Glucose diff - 0-10
What should Group II inflammatory synovial fluid have/look like as far as:
clarity,
color,
WBCs/mL
PMNs %
RBCs
Glucose diff
Group II inflammatory synovial fluid:
clarity - transparent/opaque
color - xanthrochromic to white/bloody
WBCs/mL - 3-75k
PMNs % - >50%
RBCs - no
Glucose diff - 0-40
What should Group III infectious synovial fluid have/look like as far as:
clarity,
color,
WBCs/mL
PMNs %
RBCs
Glucose diff
Group III infectious synovial fluid:
clarity - opaque
color - white
WBCs/mL - 50-200k
PMNs % - >90
RBCs - yes
Glucose diff - 20-100
What should Group IV hemorrhagic synovial fluid have/look like as far as:
clarity,
color,
WBCs/mL
PMNs %
RBCs
Glucose diff
Group IV hemorrhagic synovial fluid:
clarity - opaque
color - red brown or xanthrochromic
WBCs/mL - 50-10,000
PMNs % - <50%
RBCs - yes
Glucose diff - 0-20
What joints are involved with generalized OA? What are the locations within the joints?
Knees
•Most common location, 3 Compartments (med/lat/pat-fem.)
Hips
Spine (spondylosis) involves disc degeneration & facet involvement
- Cervical
- Thoracic*
- Lumbar
- Spinal Canal Stenosis
Feet - 1st MTP
What is involved in chondromalacia of the patella?
can be part of tibiofemeral osteoartritis
or
an isolated patellofemoral arthritis - abnormal patellar tracking, increased q-angle
What are the SSXs of isolated patellofemoral arthritis?
anterior knee pain that worsens with stair climbing or when rising from a seated position.
As it worsens from osteomalacia to advanced osteoarthritis, it interferes with walking and running
Describe the motion of the patella normally.
The patella is a sesamoid bone.
During flexion, the patella moves within a groove in the femur, the trochlea.
The patella is thought to travel in a J-shaped pattern, moving laterally with knee extension.
How common is patellofemoral arthritis in knee OA? What is the etiology?
Approximately 5% of patients with osteoarthritis of the knee have symptomatic patellofemoral arthritis in the absence of tibiofemoral arthritis.
The etiology of the arthritis is divided equally among patellar dislocation, fracture, and primary osteoarthritis.
What happens in spondylosis and disc disease?
common in cervical and lumbar spine
Neuroforaminal encroachment - pinched nerve, disc herniation, bone spurs, narrow disk
What happens in spondylolisthesis?
pars interarticularis fracture leading to spondylosis,
then spondylolisthesis
What are the SSXs of lumbar spinal stenosis? What causes it?
Lumbar spinal stenosis from facet joint osteoarthritis:
- Over age 70.
- Neurogenic claudication – worse with prolonged standing or walking; relieved by
sitting or lumbar flexion; Simian gate.
- Radicular pain – one or both buttocks or legs.
- Simian gate, and abnormal Romberg
When does OA of the elbow occur?
Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.
How is OA managed?
¨Education
¨Weight Reduction
¨Conditioning
¨Physical Therapy
¨Occupational Therapy
¨Topical Agents (capsaicin, diclofenac gel)
¨Acetaminophine
¨Salsalate
¨NSAIDs
¨Intra-articular Steroids
¨Tramadol
¨Duloxetine (Cymbalta)
¨Venlafaxine (Effexor)
¨Viscosupplementation hyaluronic acid
¨Surgery
¨Hydroxychloroquine (esp in erosive OA)
¨Colchicine
¨MTX
How is colchicine used for OA?
refractile inflammatory OA
calcium pyrophosphate deposition with joint degeneration
hooked osteophytes of calcium pyrophosphate deposition
gout
What are the SSXs of DISH?
Diffuse Idiopathic Skeletal Hyperostosis - DISH/Forestier’s disease
·Over 50 yoa, M > F. Usually asymptomatic and found accidentally on x-ray.
·Exuberant osteophytosis of thoracic* spine – 4 contiguous vertebrae.
·Preservation of joint and disc spaces.
·Ligamentous and entheseal calcification – “Whiskering” of pelvic brim, ischial tuberosities, and greater trochanters.
·Associated with metabolic syndrome (DM, HTN, dyslipidemia, hyperuricemia, and obesity).
·Anterior cervical osteophytes – dysphagia.
·Posterior spinal ligament calcification in the C-spine with hyperextension may produce a fracture with spinal cord injury (rare and mostly in Japanese).
What is DISH related to and why?
Related to metabolic syndrome and its logical extension (hyperinsulinemia/IGF-1).
IGF-1 causes differentiation of progenitor cells into osteoblast, and promotes angiogenesis into the articular cartilage with resultant ossification of ligaments and entheseal areas
What is the candle wax pattern seen in DISH?
Flowing ossification of the anterior lateral T-spine
Candle wax pattern.
No facet joint* ankylosis.
Normal IV discs.
What are some additional skeletal findings associated with DISH?
Candle wax pattern.
No facet joint* ankylosis.
Normal IV discs.
Right lateral involvement more than left
No sacroiliac sclerosis.
Acetabular entheseal calcification
What are the cervical SSXs seen in DISH?
Cervical involvement (rare) in DISH
Rare posterior ligament calcification - potential to produce cord compression
May develop mild dysphagia
What is the difference between osteophyte vs syndesmophyte?
Note clear space between ossified ligament and vertebral body.
Spinal calcification in AS directly abuts the vertebral body and disc and leads to ankylosis.
What are the DISH characteristics of the entheses?
Hypertrophic ossification at atypical sites (shoulder, metacarpalphalangeal, or elbow) suggest DISH.
Isolated bony spurs in the calcaneous, patella, and olecranon, especially if symmetrical, can lead to early diagnosis of DISH.
What is a sign of DISH seen on the pelvis?
Ligamentous calcification of the iliolumbar, sacrotuberous, and acetabular ligaments suggest DISH.
whiskering calcification on xray
What are the 3 MSK complications of DM?
Dupuytren’s contracture, shoulder periarthritis, and DISH
