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osteoarthritis
most common joint disease
leads to joint pain, swelling, stiffness
a result of the body’s failed attempt to repair damaged tissues
not just a case of wear and tear
prevalence of OA
more common in older age (42% of Canadian adults 65+ diagnosed with OA)
greater prevalence in women
Stats Canada 2023-2024
OA and death
OA does not result in death, however some data show a slight inc in mortality due to other causes (e.g. comorbidities)
OA commonality
OA is the most common chronic disease in Canada
1 in 5 Canadians have OA (most common form of arthritis) with numbers increasing to 1 in 4
close to 1 in 2 when only considering adults age 65+
OA impacts
OA has impacts on a societal level
$33 billion indirect and direct healthcare costs
loss of productivity
cartilage
made of chondrocytes which produce ECM (collagen fibers, elastin, proteoglycan)
poor blood supply and innervation
when damaged, cannot heal very well
allows for frictionless movement at joints and provides cushioning
OA risk factors
non-modifiable
genetics, age, sex
modifiable
weight (fat mass), injury, smoking, diet, repetitive movements or chronic strain on joints (e.g. certain professions like construction w/ prolonged bending/crouching)
knee OA
in a healthy knee:
smooth, thick articular cartilage covering bones
normal space visible on imaging, cushioning bones
osteoarthritic knee:
cartilage uneven, worn down, may have fissures, or even complete loss in areas
decreased joint space due to cartilage loss
types of OA
knee OA
hip OA
hand OA
spinal OA
spinal OA
bony spurs and narrowed disks compared to healthy spine
changes in posture, can create significant pain
mechanisms of OA
pressure on joints
overweight
injury
pressure on joints
mechanical stress activates mechanoreceptors, leading to the release of inflammatory cytokines and increased proteolytic enzyme activity
erosion of cartilage occurs (even more inflammation, viscous cycle)
overweight
weight can increase pressure on joints
adipose tissue also secretes inflammatory cytokines (Il-áşž, TNF-alpha, IL-6) activating catabolic enzymes
augments cartilage erosion
injury
high load/stress on specific joint compartments (e.g. medial tibio-femoral compartment after ACL tear)
PA and OA risk
moderate PA: no risk associated
intense, competitive sport/PA: inc risk due to inc injury risk and repeated trauma
PA generally does not inc risk in those already diagnosed with OA
why all the fuss
no cure: current treatments focus on symptom management
increased risk: increased risk (increased injury risk and increased repeated trauma) with intense competitive sport
cycle of chronic pain: significant impact on QoL, leading to decreased PA, increased sedentary behaviour, and potential depression
cycle of chronic pain
chronic pain and reduced QoL (Arthritis Society Toronto) ; OA often leads to a viscous cycle
Chronic joint pain
Reduced mobility and function
Avoidance of physical activity
Increased sedentary behaviour
Loss of strength and joint stability
Potential depression or anxiety related to pain and disability
OA treatment
treatment is mainly about managing symptoms of OA, not curing it
medication
physical modalities
exercise and movement
supportive devices
injections
surgical options
medication
Acetaminophen – helps reduce pain.
NSAIDs – reduce both pain and inflammation.
physical modalities
Ice – decreases swelling and numbs pain.
Weight loss – reduces joint load, especially in weight-bearing joints.
exercise and movement
Low-impact exercise (e.g., walking, cycling, swimming)
Proper joint alignment during physical activity
supportive devices
Braces – help improve alignment and reduce joint stress
injections
Hyaluronic acid injections – improve lubrication and reduce pain (variable effectiveness)
surgical options
Joint resurfacing surgery
Osteotomy – realigns bones to reduce abnormal joint loading
Joint replacement – for severe or end-stage OA
Biver et al 2019
investigated the relationship between gut microbiota and OA risk factors (e.g. obesity, metabolic syndrome, joint injury, inflammation)
modern life style factors (low PA and diets high in sugar, saturated fats, and low in fiber) contribute to low-grade inflammation and obesity
habits are associated with microbial dysbiosis
many of these risk factors are modifiable, suggesting potential pathways for OA prevention or improved management through changes in diet, physical activity, and interventions targeting gut health
dysbiosis
imbalance or disruption in the normal composition of the gut microbiota
harmful or pro-inflammatory bacteria may increase, while beneficial bacteria decrease
reducing post operative pain
post operation there may be pain
pharmacological approaches
interventional/procedural approaches
importance of anatomy
pharmacological approaches
Opioids – provide systemic pain relief after surgery.
interventional procedural approaches
Peripheral nerve block (PNB) – anesthetizes specific nerves to reduce pain locally.
Key point: Needle placement must be precise to target the correct nerve.
Radiofrequency (RF) ablation – uses heat to interrupt nerve signals and reduce chronic or post-surgical pain.
Key point: Electrode positioning is critical for effective ablation.
medical cannabis
studies suggest CBD/medical cannabis could be used for OA pain
Animal studies:
Cannabidiol (CBD), a component of medical cannabis, may reduce OA-related pain and inflammation (Philpott HT et al., 2017).
Pre-clinical evidence:
Medical cannabis shows potential in managing pain in OA and other chronic diseases (Ko GD et al., 2016)
OA and exercise
exercise can be performed without pain (low-impact activities and modifications to intensity and joint loading)
regular exercise can also improve pain and slow symptom progression
GLA:D
Good Life with Osteoarthritis in Denmark is an evidence-based program for OA management
Focuses on:
Patient education about OA
Supervised exercise targeting strength, balance, and joint stability
GLA:D effects
GLA:D shown to:
Reduce pain
Improve mobility and physical function
Support long-term self-management
Alkatan et al 2016
Purpose: Test if 12 weeks of swimming or cycling can reduce OA joint pain and stiffness and improve function and QoL.
Goal: Determine if low-impact aerobic exercise is a safe and effective way to manage OA symptoms and improve functional capacity
Alkatan et al methods
Design: Randomized controlled study, 12 weeks
Participants: 48 adults with mild-to-moderate OA
Groups: Swimming vs cycling
Exercise: 45 min/session, 3x/week, 60–70% HR reserve
Outcomes: WOMAC for pain, stiffness, function; handgrip, knee strength, 6-min walk test
Alkan et al results
Both groups: reduced pain and stiffness, improved function
Increased strength and 6-min walk distance (~15–30%)
No difference between swimming and cycling
Quality of life also improved
Alkan et al discussion
Both exercise groups (swimming and cycling) showed significant reductions in joint pain, stiffness, and physical limitations (all p < 0.05).
Both groups also had significant improvements in functional capacity: handgrip strength, isokinetic knee extension/flexion power increased by ~15‑30%, and distance covered in 6‑minute walk test increased.
There were no significant differences in the magnitude of improvement between the swimming and the cycling groups (i.e., both modes were similarly effective).
Additional benefit noted: improvements in quality of life accompanying pain/functional gains.
Alkan et al conclusion
The authors suggest that non–weight‑bearing aerobic exercise (like swimming or cycling) is feasible and effective for OA patients, especially those who may have difficulty with weight‑bearing activity due to pain or joint load
They highlight the buoyancy of water (in swimming) as particularly beneficial since it reduces joint loading; however, cycling (land‑based but non–weight bearing) produced similar improvements, suggesting the key aspect may be aerobic, low‑impact training rather than the environment per se.
They discuss concerns in OA that increased physical activity might increase “wear and tear” of joints, but their findings challenge that notion—showing improvements rather than deterioration.
Limitations: The study duration was 12 weeks (short‑term), participants had moderate OA (grade I–III) so generalizability to severe OA (end‑stage) is unclear; and adherence in longer term isn’t addressed.
Foucher et al 2021
Purpose:
Examine how walking energetics (i.e., the metabolic cost of walking) and hip abductor muscle strength are related to physical activity levels in older women who have hip osteoarthritis (OA).
Goal:
Determine whether inefficient walking (higher energy cost) and weaker hip abductors are key factors limiting physical activity in hip‑OA patients — which could inform targeted rehabilitation strategies
Foucher et al methods
Design: Cross‑sectional observational study. PMC+1
Participants: Older women with hip OA (exact number/sample details not given in the summary I found). ScienceDirect
Measures: Walking energetics (likely oxygen consumption or metabolic cost during walking), hip abductor muscle strength, and self‑reported or objectively measured physical activity level.
Analytical approach: Associations between walking cost, abductor strength and physical activity were tested.
Foucher et al results
Higher walking energy cost (less efficient walking) was significantly associated with lower physical activity in women with hip OA
Lower hip abductor strength was also linked to reduced physical activity
These two factors (energetics + abductor strength) together help explain why some hip OA patients might be less active
Foucher et al discussion
Authors propose that hip OA, biomechanical inefficiencies — such as weak hip abductors and altered gait requiring more energy — may reduce physical activity because walking becomes more “costly” (fatiguing or uncomfortable).
They suggest that rehabilitation programs for hip OA should target hip abductor strengthening and improve gait efficiency (perhaps via gait training, assistive devices, or targeted exercise) to increase activity participation.
They also discuss that increased physical activity is important for overall health and for slowing OA progression, so addressing these limiting factors could have broader benefits.
Limitations discussed include the cross‑sectional design (cannot infer causation), possible measurement limitations, and the fact the sample was older women only (so generalizability to men or younger patients may be limited)