Rheumatoid arthritis vs Osteoarthritis Katy Davidson and Hannah Brown

Osteoarthritis – key features A degenerative athropathy Most common type of arthritis Common in those over the age of 60 More common in women (M:F 1:3) Risk factors: Previous trauma of a specific joint Obesity Hypermobility of joints Occupation – i.e. manual labour Osteoporosis REDUCES risk of OA

Osteoarthritis – pathology Focal destruction of articular cartilage There is new and excess cartilage made but it isn’t perfect Focal erosions in this lead to rapid destruction of the cartilage and death of chondrocytes The surface becomes cracked with fibrilations The bone has lost its protection and is exposed The 2 bones in a joint rub against each other Microfractures and cyst formation Through attempts to regrow the bone forms osteophytes

Osteoarthritis - clinical features Clinical features Joint pain and stiffness Joint instability Loss of function Synovitis Causes joint swelling More common in RA Signs Joint line tenderness Limited ROM Joint crepitus Bony swelling Joint effusion Nodes Heberden’s nodes – DIP joints (outer Hebrides) Bouchard’s nodes – PIP joints Squaring of the hand – CMC joint

Osteoarthritis - investigations X – ray Often signs may be visible before symptoms develop Need a weight-bearing x-ray to assess joint space narrowing Blood tests – are normal ESR and CRP – negative RhF and antinuclear antibodies – usually negative but if positive are generally unhelpful MRI Show bone and cartilage changes Not widely used Athroscopy Good for looking at early cartilage changes ‘Joint mice’ – cartilage fragments

Osteoarthritis - treatment Treat the symptoms Physiotherapy and exercise Weight loss Pain relief – important to help function Paracetemol, codeine, NSAIDs Always remember gastro protection with long-term NSAIDs Steroids – local injections are often helpful Other treatments Joint replacement

Rheumatoid arthritis – key features An inflammatory arthropathy Women more affected (M:F 1:2) Before menopause risk is 3x higher for W but after it’s equal Genetic factors HLA-DR4 Environmental factors smoking, stress, infection Early morning stiffness & pain worse in the morning and after rest may last several hours Inflammatory markers – ESR and CRP – usually raised Anaemia of chronic disease – normochromic normocytic Symmetrical joints affected Extra-articular features are present

Rheumatoid arthritis - pathology Autoimmune reaction Triggers in susceptible individuals; external (infection), hormones (low oestrogen), immunological factors. T & B-cell activation leads to macrophage activation and chemo-attraction to joints leading to prolonged synovitis Rheumatoid factor (RhF) – anti-IgG Ab IgG and RhF form immune complexes that activate complement and cause the inflammation Only in 70% of all cases of RA Those without are called seronegative RA

Rheumatoid arthritis - pathology Pathological consequences Chronic inflammatory synovitis & synovocyte hyperplasia Progressive erosion of articular cartilage Pannus – the inflamed synovium Cytokine release – systemic disease Fatigue Atherosclerosis Increased bone turnover

Rheumatoid arthritis – clinical features Symptoms Early morning pain & stiffness >1hr – gets better with movement Symmetrical joints affected Often small joints of hands and feet Worse in the morning Signs Swollen MCP, PIP, wrist or MTP joints Ulnar deviation of fingers and dorsal wrist subluxation MCP inflammation, dislocation & tendons pull to ulnar side Boutonniere deformity PIP flexion & DIP hyperextension Swan neck deformities of fingers PIP extension and DIP flexion Atlanto-axial joint subluxation may threaten the spinal cord Z-thumb deformity Guttering on hands

Rheumatoid arthritis - investigations Bloods CRP & ESR FBC normocyctic normochromic anaemia LFT Raised Alkaline Phosphotase Rheumatoid Factor (RhF) -ve in ~30% RA patients. Only high values >100 indicate RA Non-specific – can be seen in other rheumatological conditions as well as hepatitis C & chronic infections Anti-cyclic citrullinated peptide (anti-CCP) +ve in 70% RA patients More specific especially in early disease! Often +ve when RF –ve Radiography: X-ray / MRI Erosions in joint margins Parts of bone not covered by articular cartilage Narrowing of joint space Pannus Fibrous Ankylosis Bony Ankylosis

Rheumatoid arthritis - treatment Mild – Moderate Disease 1 st line DMARD Azothioprine/Methotrexate / Sulfasalazine / Hydroxychlorquinine NOTE: LFTs, hepatitis B/C status needs to be check before commencement. Regular FBC/LFT/U&E monitoring required throughout treatment. Adjuncts Oral Corticosteroids Prednisolone IM Corticosteroid Dexamethasone NSAIDS Ibuprofen → Naproxen → Diclofenac NOTE: lowest effective dose should be given with PPI Higher Disease Activity Biological therapy TNFα InhibitorEtanercept / Infliximab B-cell (CD20) modulatorRituximab IL6 modulatorTocilizumab

Differences on x-ray

OsteoarthritisRheumatoid Arthritis Loss of joint space Osteophytes (marginal) Subchondrial cysts Subchondrial sclerosis Soft tissue swelling Juxta-articular osteopenia Decreased joint space Only in later disease Bony erosions Subluxation Complete carpal destruction

Osteoarthritis

RA Osteopenia

What’s this a feature of? Boutonniere deformity – extension DIP and flexion of PIP Rheumatoid arthritis

What’s this a feature of? Heberden nodes – DIP joints Osteoarthritis

What’s this a feature of? Bouchard nodes – PIP joints Osteoarthritis

What’s this a feature of? Swan neck deformity – DIP flexion and PIP hyperextension Rheumatoid arthritis

What extra- articular features may you have with RA?

Summary