OA of the Knee & Spine Flashcards
What is RA?
- Group of inflammatory disorders, highly variable phenotype
- Local & systemic inflammation
- Results in connective tissue & internal organ damage
What are the risk factors for RA?
- 50% of risk (genetic factors)
- Different inflammatory cascades lead to common pathway
- 50% to 80% +ve (IgM & IgA = Rheumatoid factors)
What are the impairments in RA?
- Synovial inflammation
- Joint destruction
- Articular cartilage damage
- Bone erosion
- Internal organ damage
How are chronic diseases different from acute diseases in terms of feedback loops?
Acute diseases:
- Negative feedback loop
- Initiator»_space; immune inflammatory response»_space; inhibitory loop
Chronic diseases:
- Positive & negative feedback loops
- As above +
- Immune inflammatory response»_space; damage/apoptosis»_space; autoamplifying loop
What is the pathophysiology of RA?
- Over production of tumour necrosis factor (TNF)
- Overproduction of pro-inflammatory cytokines in synovium (synovitis)
- Fibroblast-like cells invade the cartilage in synovium, leads to joint destruction
- Osteoclast activation leads to joint destruction
What is significant about dendritic cells?
Most potent subset of antigen presenting cells.
What is the role of mast cells in RA?
Release histamines, inflammatory mediators & substances that promote angiogenesis and fibrosis
What are the two forms of RA?
+ve RA factor & +ve autoantibody
- More lymphocytes in synovial tissue
- More joint damage
- Fewer remission
+RA factor & -ve autoantibody
- More fibrosis & increased thickness of synovium
Which body systems can be affected by RA?
- Pulmonary: Nodules, PE, fibrosing alveolitis
- Ocular: Keratoconjunctivitis sicca, episcleritis, cleritis
- Vasculitis
- Nail fold
- Cardiac: Pericarditis, pericardial effusion, valvular heart disease
- Neurological: Nerve entrapment, cervical myelopathy, peripheral neuropathy, mononeuritis multiplex
- Cutaneous: Palmar erythema, pyoderma gangrenosum, vasculitic rashes, leg ulceration, amyloidosis
What are the symptoms of RA?
- Joint swelling
- Pain/stiffness (commonly AM >1 hr)
- Weakness
- Deformity
- Fatigue
- Malaise
- Fever
- Weight loss
- Depression
What are the articular characteristics of RA?
- Palpation tenderness
- Synovial thickening
- Effusion (early on)
- Erythema (early on)
- Decreased ROM (later on)
- Ankylosis (later on)
- Subluxation (later on)
What is the distribution of RA?
- Symmetrical (especially later on)
- Distal more commonly than proximal
- PIP, MCP/MTP, wrist/ankle more commonly than elbow/knee, shoulder/hip
What is OA?
- Failure of the recovery of articular cartilage from stress
- Caused by genetics, overload, instability, trauma
What are the risk factors for OA?
- Age
- Family history/genetics
- Obesity (in knees, load & inflammation)
- Sex (F)
- Occupation
- Abnormal joint shape
- Limb alignment (knee valgus/varus)
- Joint trauma (major or minor repeated)
Where does articular cartilage get its nutrients from?
Synovium
What are the systemic factors affecting joint vulnerability in OA?
- Increased age
- Female gender
- Racial/ethnic factors
- Genetic susceptibility
- Nutritional factors
What are the intrinsic factors affecting joint vulnerability in OA?
- Previous damage
- Bridging muscle weakness
- Increasing bone density
- Malalignment
- Proprioceptive deficiencies
What are the loading factors affecting joint vulnerability in OA?
- Obesity
- Injurious PA
What are the clinical features of OA?
- Joint pain/ache
- Morning stiffness <30mins
- Joint swelling
- ROM
+/- crepitus
+/- Joint line tenderness
+/- Joint deformity - Bony enlargement
- Weakness/atrophy
What are the imaging features of OA?
- Loss of joint space
- Subchondral bone sclerosis
- Para-articular cysts/spurs
- Bone scan: hot spots (bone inflammation)
What is the distribution of OA?
- Knee/Hip
- 1st MTP/ CMC
- Cx and Lx (less common Thx)
What is OA characterised by?
- Disorganisation of articular cartilage
- Oedema (of cartilage)
- Chondrocyte apoptosis
- Tide line undulation
- Cartilage loss
- Change in collagen type and reduction of aggrecan
What are the subchondral bone changes in OA?
- Thickening
- Osteoclast resorption & osteoblast bone formation
What is the effect of anti-resorptive drugs (e.g. biophosphonates) in OA?
Positive effect on cartilage & bone degeneration
What are the characteristics of each stage of OA?
- Very early: Superficial lays loss & structural changes
- Early: Internal structure changes & fibrillation
- Moderate: Loss of organisation & hypertrophy
- Late: Cartilage loss & denudation
- End: Sclerosis
What functional scores are used to assess OA of the knee?
- KOOS
- Oxford knee score
- LEFS
- TUG
What functional scores are used to assess OA of the hip?
- HOOS
- Oxford hip score
- LEFS
- TUG
What functional scores are used to assess OA of the ankle?
Foot and ankle score
- Symptoms
- Pain
- ADL
- Sport and rec
- QoL
What functional scores are used to assess OA of the spine?
- Not a clear set of PROM
- A pain score, a QoL score and pathology (e.g. ODI, Roland Morris) score
What performance scores are used to assess OA of the knee & hip?
- Stair climb
- 6 mwt
- Gait analysis (4 x 10mwt)
- Strength
- 30 second chair test
- TUG
What are the core treatments for knee OA according to the OARSI guidelines?
- Land-based exercise
- Weight management
- Strength training
- Water-based exercise
- Self management & education
What are the principles of physio treatment for OA?
- Unload affected site (weight management, SPS)
- Correct biomechanics (orthotics, gait retraining)
- Strengthen muscles
- Improve control & proprioception
- Pain relief
- Life style modification (Change of exercises, learn what aggs, coaching)
What treatments should not be given for OA?
- Electrotherapy
- Avocado soybean
- Chondroitin +/-
- Glucosamine
- Acupuncture
- Opioids (largely uncertain)
- Knee arthroscopies
What is spinal spondylosis?
- Diagnosed by XR
- 3 joint pathology (disc space narrowing, facet degeneration, osteophytes)
- Disc space narrowing appears to be initiator of spondylosis
What are examples of spondylosis being different from OA?
- Facet joint OA can be present without DSN
- Osteophytes can form without cartilage association
- DSN common in ageing
- Facet OA associated with knee & hand OA, but not DSN
What are the risk factors for spondylosis?
- Association between osteophytes or DSN & LBP is modest
- Osteophytes appear earlier than DSN and FOA - OA changes modest association with LBP
- DSN progression associated with hip/knee OA
What interventions should be used to treat OA in a 40yo?
- Keep weight down
- Strength, flexibility, protection
- Moderate exercise
- Avoid injury
- Avoid surgery
What interventions should be used to treat OA in a 70yo?
- ROM
- Stretching
- Proprioception and balance
- Falls prevention
- Strengthening for stabilisers
- Treatment of gait adaptations
- Education of how to manage
- Joint replacement
