Transcript Osteoarthritis

Osteoarthritis and Related
Conditions
Brian J. Keroack, MD
Clinical Features of Osteoarthritis
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Onset as young as mid 30’s (usually>40)
Early OA (1-2 years):
 Inflammatory symptoms prominent: Morning stiffness
(<1hr). “If I just keep going I’m OK.”
 Red, prominent PIP, DIP joints
 Normal Radiographs
Later:
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AM stiffness <30 min.
‘Mechanical’ symptoms: Worse with use. “I really pay for
what I do.” “I just don’t have the strength I use to.” (e.g.
jars, doors)
Joint abnormalities preclude normal use
Clinical Features of Late OA: continued
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Little Evidence of Inflammation
Deformities more prominent (angulation, bony proliferation)
Radiographs abnormal
Some patients actually get LESS symptomatic in non-weight
bearing joints. You will see many patients with hand
deformities that are asymptomatic
“My hands really don’t bother me like the use to.” “Once
they deformed, they stopped hurting.”
Weight bearing joint symptoms usually progress.
Risk Factors for Osteoarthritis
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Weight
Trauma
Genetics?—Amino acid substitutions in Type II
Collagen.
Secondary Osteoarthritis (later)
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Consequences of OA:
Spinal Stenosis
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Erosive Osteoarthritis
 More aggressive
 Destructive
 Persistent symptoms
 Inflammatory findings on
exam
Secondary Osteoarthritis
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Trauma
Congenital deformity
Endocrinopathies
Neuropathic Arthropathy
Avascular Necrosis
Padget’s Disease
Diffuse Idiopathic Skeletal Hyperostosis (DISH)
Hemophilia
Crystals (CPPD, Hydroxyapetite)
Illnesses Associated with Neuropathic
Arthropathy (Charcot Joint)
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Diabetes
Alcoholism
Tabes Dorsalis
Syrinx (meningomyelocele—cord compression)
Therapy
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Joint Conservation
Exercise
Weight Loss (Wt Bearing Joints)
NSAIDS (Cough medicine analogy: not disease modifying)
 Not benign: Ulcers 4%, greater with risk factors (age>60,
coumadin, past ulcer, prednisone use). Hypertension,
ACE+Diuretic+NSAID=trouble (e.g. CHF, Renal
failure)
COX-2: Safer for those at risk for ulcer (>65, coumadin,
prednisone, previous ulcer) similar renal effects.
Cardiovascular effects? 2.5 X increase in MI or CVA.
Mechanisms—1. Increase Thromboxane A2 (platelets
stickier).---2. Vascular remodeling (18 months)-Hypertension
Therapy: Continued
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??DMARDS—not yet
The problem: Sclerosis of subchondral bone in mid thirties,
apoptosis of chondrocytes in late thirties
If DMARDS are to succeed they will have to be studied a decade
before symptoms start
Remind me not to volunteer for a medicine that might work that I
will have for take for 10 years without knowing the long term
effects
Joint Replacement/Fusion
Medical vs Surgical Disease?
 Bone on Bone (X-rays never told me about symptoms)
 Night Pain
 “As soon as I step on the knee it hurts and it is all down hill
from there.”