Osteoarthritis and spondyloarthropathies Flashcards
what is osteoarthritis and what is the disease characterised by?
Osteoarthritis (OA) is the most common form of arthritis (~twice as common in women than men):
OA is the most common musculoskeletal condition: ~8.75 million people, have sought treatment for OA (in 2013; number is on the rise).
Used to be considered to be due to “wear and tear” but now is recognised as a metabolically active disease process affecting the whole joint (cartilage, bone, capsule, muscle).
OA is a ‘disease of synovial joints’, characterised by:
Progressive destruction/loss of articular cartilage.
Changes in subchondral bone: accompanying periarticular bone response i.e. hardening (sclerosis) and refashioning of underlying bone and formation of osteophytes (bony projections).
Synovial inflammation (more aggressive in rheumatoid arthritis, RA).
Changes in periarticular muscle.
Pain (and stiffness).
OA: disease progression
Initial Repair:
Proliferation of chondrocytes which synthesise the extracellular matrix (ECM) of bone (ECM major components: type II collagen and aggrecan).
Early stage OA:
Degradation of ECM exceeds chondrocyte activity resulting in net breakdown and loss of articular cartilage in joint.
Subchondral bone remodelling increases.
Intermediate stage OA:
Failure of ECM synthesis and increased breakdown of cartilage.
Late stage OA:
Extreme or complete loss of articular cartilage, joint space narrowing.
Bony outgrowths (new bone) appear at joint margins (osteophytes).
Bone remodelling decreases (is abnormal), subchondral bone sclerosis increases and there is also weakness of periarticular muscles.
Pain and reduced joint movement.
what is the diff between oa and ra
OA: Cartilage loss, eventually joint is ‘ground down’ due to injury/overuse.
RA: Overactive immune system, chronic inflammation (synovitis).
what are the risk factors of oa
Increasing age:
OA is uncommon in people <45 year olds (2%) but is common in people >65 year olds: prevalence is 68% in women and 58% in men.
Gender:
<45 years of age, more common in men.
55-70 years of age, more common in women.
Knee OA more common in women.
Ethnicity:
Hip OA is less common in Chinese, Afro-Caribbeans and Asians, rather than in Europeans.
Genetic predisposition (~20% of cases: currently no identified genes).
Obesity (~63% OA can be attributed to obesity, especially knee OA).
Physical (mechanical stress) and occupational factors (i.e. farmers).
Trauma (e.g. Joint injury; not giving enough time to heal).
Linked to other conditions (secondary arthritis).
what are the symptoms of oa
Joint pain (and stiffness):
Commonly affects weight-bearing joints (hip, knee, spine), or hands (base of thumb).
Asymmetry of joints affected is common.
Pain is worse with movement (activity-related joint pain), no pain at rest.
Morning stiffness in joint lasts for less than 30 minutes.
Synovial thickening (can lead to bone deformity).
Deformity of joint.
Bony swellings (~ 10x more common in women):
Heberden’s nodes: mostly occur on finger joints, near fingertip (also referred to as the distal interphalangeal joints).
Bouchard’s nodes: on lower joints (proximal interphalangeal joints).
Joint Effusion (fluid around joint).
Muscle weakening or wasting (osteophytes may contribute via nerve compression).
Crepitus (sound/sensation i.e. crackling).
Limited joint movement.
what is the diagnosis of oa
Diagnose OA clinically (without investigations), if person:
Is 45 or over.
Has activity-related joint pain.
Has either no morning joint-related stiffness, or has morning stiffness lasting no longer than 30 min.
If require further investigations (e.g. possible alternative diagnosis, like gout):
X-ray:
Narrowing of joint space.
Bony protrusions (osteophytes).
Bone sclerosis (abnormal bone density).
Magnetic Resonance Imaging (MRI):
Provides information about cartilage and peri-articular structures (tendons).
what are the treatment goals of oa
Reduce Pain (symptomatic):
In most cases, pain is due to damage to bone and cartilage (not inflammation) analgesia and joint protection often are all that is required.
Increase mobility:
Physical therapy, exercise regime, etc
Reduce disability
Minimise disease progression:
Joint protection.
OA management:core treatments
People with clinical OA, offer advice on following core treatments:
Access to appropriate information (education):
Increase understanding of OA and its management
Discuss footwear (if applicable).
Activity and exercise:
Discuss benefit of local muscle strengthening, general aerobic fitness (builds up muscle strength and improves range of joint movement).
Interventions to achieve weight loss (if overweight/obese):
Assess lifestyle, offer advice on how to implement changes (explore eating patterns/diet and physical activity levels; helps protect affected weight-bearing joints).
Investigate environmental, social and family factors (i.e. family history of overweight/obesity) and if there are any comorbidities.
OA management:non-pharmacological treatments
Many OA patients (~60%) report benefiting from non-drug treatments; these should be considered as an adjunct to core treatments:
Thermotherapy: use of local heat or cold.
Electrotherapy: use of TENS (transcutaneous electrical nerve stimulation) for pain relief.
Aids and devices (if required): bracing/joint supports/insoles; also, can consider walking sticks, tap turners.
Manual therapy: manipulation and stretching, particularly for OA of hip.
DO NOT OFFER:
Nutraceuticals:
glucosamine or chondroitin products:
Acupuncture.
OA management:pharmacological treatments
diagnosed oa
1st line
Analgesics (for pain relief): Topical NSAIDs in addition to core treatments should be considered ahead of oral NSAIDs* (topical: fewer side effects), COX-2 inhibitors, paracetamol or opioids- * Use oral NSAIDs/COX-2 inhibitors at lowest effective dose for the shortest period of time
(Topical capsaicin should be considered as adjunct to core treatments for knee or hand OA)
(Use standard NSAID or a COX-2 inhibitor (not etoricoxib 60 mg). Co-prescribe with proton pump inhibitor (PPI)
NSAIDs insufficient for pain relief
Addition of opioid analgesics should be considered: risk to benefit ratio should be
considered, esp. in older people
Intra-articular corticosteroid injections should be considered as adjunct to core treatments for relief of moderate to severe pain in people with OA
surgery
Do not offer rubefacients for treating OA
OA management:topical nsaids and rubefacients
use
examples
Most people with OA have symptoms for many years, likely involving treatment combinations: common scenario is a person taking different analgesics at same time (e.g. NSAIDs and opioids).
Topical preparations of ibuprofen, ketoprofen, felbinac, piroxicam are available:
Even if applied topically, systemic effects (hypersensitivity and can ‘set-off’ asthma) can result if large amounts of topical NSAIDs are used: discontinue use if rash develops.
Patients should avoid exposure of area to excessive sunlight (avoid possibility of photosensitivity).
Rubefacients can relieve pain in joints, tendons and/or muscles through mild counter-irritation of the skin:
Rubefacients cause redness, dilate capillaries, thus, increasing blood flow to area.
Example: Capsaicin (0.025%) is licensed for the symptomatic relief of OA.
Can take 1-2 weeks before pain relief is achieved. Transient burning sensation during initial treatment: if too much cream is applied or if used less than 3-4 times per day.
