Osteoarthritis Flashcards
Define osteoarthritis
Instead of being a pure cartilage disorder, OA is now considered as a partly inflammatory whole-joint disease that affects various anatomical structures in and around the joint capsule. These include muscle, ligaments, entheses, synovial tissue, and the sub-chondral bone.
Describe the features of osteoarthritis
- Quiet loss of structural integrity
- Slowly progressive
- Common
- Symptoms relatively late
- Major health care problem
Describe osteoarthritis as a mismatch disease
- at any given age prevalence is higher in modern environments, due to higher levels of obesity, chronic metainflammation, physical inactivity and diets of processed foods (high sugar, high saturated fat, low in fibre)
- other disease include hypertension, CHD etc.
Describe the epidemiology of osteoarthritis
- After age 50 women > men
- At age 55 plus 67% of women and 55% of men have radiographic OA in the hands
- At age 55 plus 53% of women and 33% of men have radiographic OA in the knee
- At age 55 plus about 25% have had knee pain on most days in a month in the past year
- Nearly half of patents with radiological features have no symptoms and vice versa ^[hence XR not part of diagnostic criteria]
- Knee, hip, and hand are most affected
- Highly variable natural history
- Association with CVD - related to physical inactivity
List risk factors associated with OA
Knee
- Age, gender, BMI, intense sport activity, occupational bending and lifting, previous knee injury, quadriceps strength deficit, bone density, previous injury, HRT (protective), low vitamin D, smoking, mal-alignment, genetics.
Hip
- Age, physical inactivity, BMI, previous injury, intense sport activity, high bone mass, occupations that require prolonged standing, lifting, or moving heavy objects, genetics.
Hand
- Age, grip strength, intense sport activity, genetics.
Genetics
- Heritability 20% (phenotypic variation due to genetic variation)
-
#### Mechanical factors:
- increased load
- loss of joint mechano-protection
- offloading: not used
Modifiables
- obesity
- impaired muscle function due to physical inactivity
- previous injury
- meta-analysis: NM and proprioception training reduces ACL injury rates by 50%
Describe the role of inflammation in OA
- Low grade inflammatory disease – in part induced by obesity, metabolic syndrome, innate immunity, and age-related inflammation.
- New concept metabolic syndrome associated OA- MetSOA
- Systemic inflammation is not the primary driver
- Mainly a secondary process induced by cartilage damage
note: adipokines, inflammatory mediators released from adipose tissue
Describe the role of obesity (and the importance of weight loss) in OA
Osteoarthritis – obesity as a risk factor
- Two meta-analyses found a dose-response relationship between increasing BMI and incidence of both knee and hip OA.
- Specifically, for each 5-unit increase in BMI, the risk of knee OA increased by 35%, and the risk of hip OA increased by 11%.
- More recent meta: OR of 1.98 and 2.66 for developing knee OA in o/weight and obese
Effect of weight loss
- Systematic review and meta-analysis of four RCTs including five intervention/control groups provided data from 454 patients.
- Pooled ES for pain and physical disability were 0.20 and 0.23 at a weight reduction of 6.1 kg (4.7 to 7.6 kg).
Obesity, visceral adiposity and inflammatory markers
- Cardiometabolic factors upregulate signalling molecules and key effector cells, resulting in damage to articular structures: intra-articular adipose, synovium, articular cartilage, subchondral and peri-articular bone
- Serum concentrations of CRP, TNF-α, and IL-6 (inflammatory markers) were significantly correlated with weight, BMI, waist circumference, hip circumference, and waist-hip ratio.
Describe the pathophysiology of OA
- Failure of the repair process of damaged cartilage due to biomechanical and biochemical changes in the joint
- Early response to damage - increased chondrocyte number and growth factors - failure
- Imbalance in favour of degradation - activated pro-inflammatory cytokines, GAGs down
- Increased synthesis of tissue-destructive proteinases (matrix metalloproteinses and aggrecanases).
- Apoptotic death of chondrocytes
- Inadequate synthesis of extracellular matrix
- Failure of cartilage to hold water
- Loss of function as shock absorber.
Mechanism of inflammation - synovitis
- In knee OA, synovitis is strongly associated with cartilage damage and bone marrow lesions.
- May be due to release of cartilage or subchondral bone breakdown products such as hyaluronan, cytokine expression by bone marrow macrophages or innate immunity activation by DAMPs
Role of synovitis
- Patchy chronic synovitis is due to cartilage debris and catabolic mediators entering the synovial fluid – leading to effusion and inflammatory pain.
- **Both synovitis and subchondral bone remodelling are actively involved in OA, often preceding cartilage damage
- **In OA, synovitis stimulates osteoclastogenesis, pannus formation and increases adherence of synovial tissue to cartilage
- **Chronic mechanical impairment in combination with metabolic dysregulation is a common trigger of subchondral bone changes and osteophytosis
- **Synovial tissue is highly vascularised and thus exposed to systemic influences such as hypercholesterolaemia, or low grade inflammation
Timeline – Cartilage Fissures -> Cartilage Gaps, Osteophyte formation and cartilage degradation
product into joint space –> Joint space narrowing and sclerosis (bone thickening)
Describe the clinical features of OA
- Pain. Worse with activity, relieved by rest.
- Stiffness. After rest < 30 mins.
- Loss of movement.
- Joint line tenderness
- Instability.
- Weakness.
- Swelling/deformity.
- Loss of function.
Describe sources of pain in OA
Intra-articular
- Not articular cartilage because not innervated
- Synovitis, subchondral bone changes, periosteal disruption (osteophytes), microfractures, ligament degeneration, capsular distension with effusions.
Extra-articular-peri-articular
- Inflammation of tendons, fascia, bursae, muscle spasm, nerve compression
Describe the NICE diagnostic criteria
Diagnose osteoarthritis clinically without imaging in people who:
- =>45
- have activity-related joint pain
- have either no morning joint-related stiffness OR morning stiffness not lasting longer than 30 minutes
DO NOT routinely use imaging to diagnose unless there are atypical features (night pain, fever, past history of tumour), or features that suggest an alternative or additional diagnosis.
Describe RA clinical features
- Onset – acute or insidious
- Typically a symmetrical arthritis affecting the wrists, and the metacarpophalangeal and proximal interphalangeal joints of the hands
- Involvement of MTPJs and PIPJs in the feet is not infrequent
- Almost any joint can be affected
- Inflammation of synovial tendon sheaths
- The number of swollen or tender joints at baseline is an indicator of progressive disease and future radiographic progression.
- Morning stiffness which can last up to an hour is a cardinal feature
- Systemic features include flu-like symptoms, fatigue, malaise, and weight loss
- Cervical spine involvement is common (30-50%)
- Better response to NSAIDs
Describe iOA features
- Inflammatory or erosive are terms used interchangeably to define a clinical subset of osteoarthritis of the hand (HOA).
- Targets inter-phalangeal joints and characterized by an abrupt onset, marked pain and functional impairment, inflammatory symptoms and signs, including stiffness, soft tissue swelling, erythema, and paraesthesiae.
- DIPJ>PIPJ, second and third fingers > fourth and fifth fingers.
- Mildly elevated C-reactive protein
- Worse outcome than non-erosive HOA.
- Frequent joint deformities – lateral subluxations, Heberden’s at DIPJ and Bouchard’s PIPJ nodes (hard, bony outgrowths), instability, and ankylosis.
- This subset is defined radiographically by subchondral erosion, cortical destruction, and subsequent reparative change, which may include bony ankylosis (fusion).
Describe the principles of management of OA
You must explain to the patient that:
- OA is diagnosed clinically and usually does not require imaging to confirm diagnosis
- management is guided by symptoms and physical function
- core treatments are therapeutic exercise and weight management, with information and support
Exercise
- offer therapuetic exercise tailored to their needs e.g. local muscle strengthening
- consider supervised sessions
- explain it may initially cause pain but will provide benefits in long-term to reduce pain and improve function
- an education program or behavioural changes should be considered along side therapeutic exercise, in a structured treatment package
Weight management
- if overeight or obese, advise that it will improve QOL, function, and reduce pain
- support them to choose a goal
- any loss is beneficial, but 10% is better than 5%
Information and support
- tailor info to patient needs and make it accessible
- advise on where to find info on condition, common misconceptions, exercise, management of symptoms, support, benefits and limitations of treatment
Describe principles of pharmacological management in OA
If needed, use drugs alongside non-pharmacological treatments, and to support therapeutic exercise.
Use the lowest effective dose for the shortest possible time.
Review with patient whether to continue, and review based on clinical need.
e.g.s topical NSAID for knee or other affected joints.
Consider oral NSAIDs if topicals are unsuitable, and offer a gastroprotective treatment in combination.
DO NOT OFFER paracetamol or weak opioids routinely ^[unless used infrequently in short term, or all other treatments ineffective or unsuitable], glucosamine, strong opioids or intra-articular hyaluronan injections.
CONSIDER intra-articular corticosteroids for short term relief if other drugs are ineffective or unsuitable, or to support therapeutic exercise.
