Osteoarthritis Flashcards
What is it?
A non-inflammatory disorder of movable joints characterised by deterioration or articular cartilage and the formation of new bone at the joint surfaces and margins.
New definition:
Age-related, dynamic reaction pattern of a joint in response to insult or injury. All tissues of the joint are involved. Articular cartilage is the most damaged but there is also damage to the underlying bone.
Is the condition inflammatory or non-inflammatory?
Non-inflammatory
What is another name for osteoarthritis?
‘wear and tear arthritis’
degenerative joint disease
Prevalence?
Most common disease affecting synovial joint
Prevalence increases with age
By 40, 90% have OA in weight bearing joints
What is the relationship to sex?
<45 yrs more common in males
>55 yrs more common in females
What cytokines are involved?
IL-1
TNF-a
NO
(Little inflammation, driven by mechanical forces)
What are the main pathological features?
Loss of cartilage and disordered bone repair
Define primary and secondary OA?
Primary/idiopathic - No identifiable predisposing cause
Secondary - underlying cause is implicated
Risk factors for OA?
Increased age Family history - genetic component Female post-menopausal Caucasian Obesity Occupation - manual labour, sports Local trauma Inflammatory arthritis Neuropathic conditions Deformities - e.g. congenital, SUFE. Increased bone density
Symptoms and signs of OA?
Pain - worse on exertion Stiffness - worst after rest Swelling - bony and soft tissue (effusion/intermittent or continuous from capsular thickening) Functional impairment (typically after middle age) Morning stiffness
Alteration in gait Bony enlargement Synovitis Limited ROM Crepitus Tenderness Deformity Muscle wasting Joint instability - late onset
Key radiological features of OA? (5)
Joint space narrowing Osteophyte formation Subchondral scleosis Subchondral cysts Abnormalities of bone contour
What is the pathogenesis?
Articular cartilage failure
Chondrocytes are the most important cells responsible for osteoarthritis
Some involvement of proteases, cytokines, anabolic cytokines and inflammation.
What is one key difference between OA and inflammatory joint disease?
Not associated with systemic manifestations.
What joints are most commonly affected?
Knee Hip DIPJ + PIPJ (two end joints) 1st CMC Spine 1st MTPJ
Describe the nature of the pain experienced in OA?
Insidious onset - months to years
Aggravated by activity
Relieved by rest
May be referred pain
What is the origin of the pain experienced in OA?
Articular cartilage and synovium has no nerve supply. Pain due to capsular stretching and vascular congestion of bone.
What is the name of the stigmata present in the hands which are the palpable osteophytes in the joints?
Heberden’s nodes - DIPJ
Bouchard’s nodes - PIPJ
What are the differential diagnosis of OA?
Rheumatoid arthritis
Gout
Osteonecrosis
Neuropathic joint
What signs are characteristic?
Pain worse at night/ on use
Morning stiffness <30 mins, degenerative. >1hr, inflammatory
Herberden’s and Bouchard’s nodes
What investigations would you do in OA?
X-ray (Asymmetric loss of joint space, sclerosis, cysts, osteophytes)
Majority of cases
Rheumatoid factor and anti-CCP negative
CT (for joints not clearly visible on x-ray)
MRI (rarely used)
Isotope bone scan (‘hot’ due to increased vascularity and new bone formation)
Laboratory tests (blood and synovial fluid - would expect to be normal)
Diagnostic injection
Arthroscopy (can help to isolate affected joint)
What is the management option selected dependent on?
Joint involved Stage of disorder Severity of symptoms Age of patient Functional needs
What are the management options for OA?
Conservative / Non-surgical
Injection
Surgical
What might conservative management of OA include?
Decrease load on joint (weight loss and exercise) Analgesia (topical products, capsaicin or NSAIDS, paracetamol, NSAIDs, Cox-2 inhibitors (w/o GI side effects of NSAIDS) Promote movement (physiotherapy) Mobility aids (waking sticks, heel raises)
Do any exercises increase the risk of OA?
Neuroanatomically normal (NAN) joints are at increased risk of developing OA in the absence of adequate exercise.
NAN joints are not at increased risk upon exposure to repetitive, low-impact, exercise.
NA abnormal joints are at increased risk upon exposure to repetitive, low impact, exercise.
NAN joints are at increased risk upon exposure to repetitive, high-impact exercise.
So basically, running would be risky as high impact and could affect normal joint.
Something low impact like walking would only be bad if neuroanatomically abnormal joint.
