Osteoarthritis

1. Osteoarthritis Fadi Hassan – Hull York Medical School

2. Overview Definition Epidemiology Aetiology Signs and symptoms Pathogenesis Clinical Subsets Investigations Treatment options

3. Definition “Disease of synovial joints marked by cartilage loss and peri -articular bone response. It usually affects the wrist, hip, knee and the ankle joint. It causes the bones to be exposed and damaged leading to pain and impaired movement”

4. Epidemiology OA is the most common type of arthritis as prevelance increases with age. Leading cause of chronic disability affecting 8 million people in the UK and 27 million in the US. Women over the age of 55 are affected more than men of a similar age. Associated with major socio-economic implications especially in developed countries.

5. Aetiology Can be classified as Primary Secondary Or as Hereditary Developmental Metabolic Mechanical

6. Primary OA Could be related to aging Reduced proteoglycan content leading to the joint being less resilient and more susceptible to degradation speeding up the process of degeneration. Genetic Twin studies shown that there is a greater prevalence of the disease in siblings and specifically identical twins (more than 60%)

7. Secondary OA Obesity Injury to joints/ligaments Ligamentous instability Congenital abnormalities Diabetes Septic arthritis Inflammatory diseases (gout, lyme disease) Alkaptonuria (black urine) Ehlers- Danlos syndrome (EDS) Hemochromatosis Wilson’s disease

8. Secondary OA - Alkaptonuria Inherited disorder of phenylalanine and tyrosine metabolism as a result of enzymatic defect leading to accumulation of alkapton ( homogentisic acid and its oxide) in blood/urine Excess homogentisic acid causes damage to cartilage tissue.

9. Secondary OA - EDS “Connective tissue disorder causing defects in the synthesis of collagen (I/II) that in normal situations help in resisting deformation and maintains the connective tissue elasticity”

10. Pathogenesis Collagen matrix degeneration is mediated by the action of Matrix MetalloProteinases like Collagenase (MMP1 and MMP13) by cleaving collagen Stromelysin (MMP3) which is active against fibronectin and laminin in the extracellular matrix. MMPs are secreted by chondrocytes in an inactive form which leads to degeneration of collagen and proteoglycan upon extracellular activation. The role of Tissue Inhibitors of Metalloproteinases TIMPs play a role in regulating MMP production and any disturbance in this pathway leads to cartilage degradation

11. Pathogenesis Deficiency of growth factors (IGF-1) and transforming growth factor (TGF-B) play a role in impairing matrix repair as a result of reduced collagen synthesis. Other mechanisms? Genetics: Mutations in the gene for type II collagen (COL2A1) have been associated with early OA Vitamin C and antioxidants deficiency

12. Synovial Inflammation As breakdown products from the cartilage are released into the synovial space, the cell lining the joint will try and remove them leading to an inflammatory response. Cytokines production regulates cartilage damage Interleukin-1 and tumour necrosis factor release stimulates metalloproteinase Interleukin-6 and Interleukin-8 may also be involved. NF-KB transcription factor mediates the production of cytokines and MMPs.

13. Clinical subsets Localized OA Nodal (joints of the hands – DIPs >PIPs)  Pain + swelling = functional impairment Hip: occurs most frequently at the superior pole of the hip where there is joint space narrowing and sclerosis affecting the upper surface of femoral head and acetabulum. Knee: medial compartment > lateral compartment Can be retropatellar Primary generalized: main characteristics are >1 joint, familial tendency, female predominance and autoimmune association Erosive: DIPs and PIPs  subchondral cysts developing into RA Crystal-associated (calcium pyrophosphate deposition ) Chondrocalcinosis characterized by patchy linear calcification on x-ray

14. Patchy linear calcification

15. Diagnosis and clinical features History Sharp aching pain and stiffness Burning sensation in the muscles or tendons Usually affects the hands, feet, spine, hip and knee Humid and cold weather usually exacerbates the symptoms Gets better with gentle use but worsens on excessive use Main principle that distinguishes OA from RA

16. Diagnosis and clinical features Examination It can cause crackling noise (crepitus) on moving the joint Associated locking Muscle atrophy Lax ligaments Joint effusion Heberden’s nodes (DIP) and/or Bouchard’s nodes (PIP) limiting movement of the joints OA of the toe leads to formation of bunions

17. Diagnosis and Clinical features Investigations X-ray: Joint space narrowing Subcondral sclerosis Osteophyte formation Subcondral cyst formation Blood tests Raised CRP (in some cases) Normal ESR Rheumatoid factor and antinuclear antibodies are negative MRI: early cartilage and subcondral bone changes, although it is not routinely used due to the cost Arthroscopy can reveal early fissuring and surface erosions

18. Imaging

19. Imaging

20. Treatment Lifestyle modification Weight loss Patient education Moderate exercise Manual therapy (manipulation of muscles and joints) Medications Surgical approach: Considered if non-surgical treatment lose their effectiveness in pain management Age, activity level and the condition of affected joints are all factors that should be considered Accupuncture Supplements (multivitamins, ginger, Omega-3-FA)

21. Treatment Medications Acetaminophen (COX inhibitor) is usually the first line of treatment and is recommended for mild-moderate symptoms NSAIDs like ibuprofen are more effective for severe symptoms. However, they’re associated with greater side effects like GI bleeding COX-2 selective inhibitors ( celecoxib ) is associated with less side effects but higher rates of CV diseases Topical NSAIDs like diclofenac could be used Opioid analgesics such as morphine improve pain but have greater side effects. Steroids (hydrocortisone) achieve short term pain relief but they have side effects Osteoporosis, weight gain, infections, HTN, diabetes, skin thinning, muscle weakness, mood and behavioural changes, cataracts and stomach ulcers

22. Treatment Surgical approach Arthroplasty (joint replacement) Parts of the bones are removed and artificial joint with metallic or plastic components are created Joint resurfacing ( metal-on-metal articulation) Placing a metal cap over the reshaped articular surfaces removing very little bone compared to arthroplasty Revision is easy with this option as the bone is preserved so other procedures can still be considered in the future (like arthroplasty ) Arthroscopy Arthroscope is used to remove bone spurs, cysts and damaged surfaces from the joint. Osteotomy Involves realignment of the long bones to ease off the pressure on the joints Joint fusion Fusion both ends of the bone together and holding them in place using pns , plates or screws while they heal. This procedure usually sacrifices the joint’s flexibility