INFLAMMATORY/ AUTOIMMUNE AND DEGENERATIVE JOINT DISEASES. Wahinuddin Sulaiman Faculty of Medicine, UniKL Royal College of Medicine Perak
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1 INFLAMMATORY/ AUTOIMMUNE AND DEGENERATIVE JOINT DISEASES Wahinuddin Sulaiman Faculty of Medicine, UniKL Royal College of Medicine Perak
2 Outline Introduction Assessment / evaluation OA vs RA Treatment
3 JOINT PAIN
4 Introduction Arthritis = disorder of joints > 100 types of arthritis Various etiologies Global socio-economic burden Young - elderly
5
6 What is the social burden of MSK disorders in Malaysia? Based on data from National Institute of Health, Malaysia (Year 2000), 16,000 years of healthy life lost 15,200 years lost due to disability 1 out of 10 patients becomes disabled Malaysian Burden of Diseases and Injury Study. Institute for Public Health, National Institute of Health, Ministry of Health, Malaysia 2004
7 Assessment Articular or non articular Inflammatory or non inflammatory Acute or chronic Monoarticular or polyarticular Extra articular signs
8 ARTICULAR PERIARTICULAR Internal/deep joint pain Reduced ROM Effusion, synovial thickening, deformity Instabilitiy Crepitations, clicking, popping, or locking > Pain with active motion ROM preserved Inflammation away from joint No deformity
9 ARTHRITIS INFLAMMATORY Cardinal signs Systemic Sx Stiffness > 1 hr Laboratory : raised ESR/CRP NON-INFLAMMATORY No signs Stiffness < 1 hr Intermittent Triggers: trauma, repeated use Degenerative tumour
10 DEGENERATIVE AND INFLAMMATORY ARTHRITIS Degenerative Osteoarthritis (OA) Post-traumatic arthritis Arthritis following dysplasia Osteonecrosis Osteochondritis dissecans Inflammatory Rheumatoid arthritis (RA) SLE Spondyloarthritis Gout Pseudogout
11
12 HISTORY - Onset - progression - distribution of disease - stiffness - triggering, aggravating or relieving factor - diurnal variation - other systemic feature - functional disability General systematic medical history. Past medical and surgical history. Family history. Drug history.
13 Osteoarthritis - pathophysiology Disease of cartilage Primary vs Secondary Unknown triggering factor for Primary OA IL-1 : pro-inflammatory cytokine, inducing chondrocytes & synovial cells to synthesize MMPs degrade articular cartilage. IL-1 suppresses synthesis of type II collagen and proteoglycans and inhibits the transforming GF stimulated chondrocyte proliferation Leptin
14 The Abramson Lab, NYU School of Medicine, Department of Medicine, Division of Rheumatology
15 Yan et al. Medicine (2018) 97:14
16 RA Immunopathogenesis Unknown complex
17 Too CL, et al. Ann Rheum Dis 2016;75: doi: /annrheumdis Too et al. Arthritis Research & Therapy 2012, 14:R89 Familial Risks of Rheumatoid Arthritis: results from the Malaysian Epidemiological Investigation of Rheumatoid Arthritis case control study C. L. Too, L. K. Tan, A. F. Nurul Aain, S. Salsabil, H. Heselynn, S. Wahinuddin*, I. S. Lau, S. C. Gun, S. NorShuhaila, M. Eashwary, M. S. Mohd-Shahrir, M.-M. Ainon, R. Azmillah, O. Muhaini, C. Bengtsson, L. Padyukov, L. Alfredsson, L. Klareskog, M. Shahnaz, for MyEIRA study group Presented in EULAR Congress, Madrid 2017
18 McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011;365(23): See more at: 3#sthash.H4xgEihr.dpuf
19 Joint impact of osteoarthritis and rheumatoid arthritis Adapted from MedicineNet, Inc.
20 Characteristics OA Localized Asymmetric Large joints Older age Aggravated by activities No diagnostic test Radiologic imaging Symptomatic treatment RA Systemic Symmetric Small joints Younger age Morning stiffness Labs: RF, anti CCP, ESR/CRP Radiologic imaging Specific treatment
21 To be applied to patients: (1) who have 1 joint with definite synovitis, excluding the DIP joints, 1 st MTP joints, and CMC joints, and (2) in whom the synovitis cannot be explained by another disease.
22 OA PHYSICAL EXAM Inspection Palpation ROM
23 RA Clinical Picture Insidious onset /palindromic Morning stiffness Polyarthritis commonly small joint of the hands (exclude DIP) Subcutaneous nodules Labs
24 Radiologic Findings RHEUMATOID ARTHRITIS Periarticular osteoporosis Narrow Joint space Erosions Subluxations and deformities
25 Radiologic Findings : OA Cyst formation Osteophytes Loss of joint space Subchondral sclerosis
26
27 ARTHROCENTESIS
28 Treatment No curative treatment for both degenerative or non- inflammatory and inflammatory or autoimmune joint disorders. Early diagnosis and treatment of AIJD may halt the progression of the disease Gout, reactive arthritis are treatable is diagnosed early.
29 OA - TREATMENT Occupational & Physiotherapy NSAIDs and analgesics Intraarticular injections Arthrodesis Joint replacement Reconstructive surgery
30 RA - TREATMENT Pharmacological - NSAIDs/Analgesic - DMARDs (conventional or biologic) Non-pharmacological - physio/ot Surgery
31 Summary of diagnostic criteria differences between OA and RA Arthritis History P/E Tests OA Palpable body joint enlargement EMS < 30 min Pain RA Pain duration 6 wks EMS > 30 min Systemic symptoms (e.g. fatigue, anorexia) ROM Joint malalignment crepitus Synovitis Symmetrical Joint destruction X-tra articular Sx Radiologic Osteophytes Narrow joint space Lab Clear synovial fluid Radiologic Erosions on X-ray/MRI Synovitis (US/MRI) Serology ESR/CRP Anti CCP RF Singh JA, Furst DE, Bharat A, et al. Arthritis Care Res (Hoboken). 2012;64: Altman R, Asch E, Bloch D, et al. Arthritis and Rheumatism. 1986:29: Aletaha D, Neogi T, Silman AJ, et al. Arthritis & Rheumatism. 2010;62:
32 Characteristic CTD SpA Infectious Crystal arthritis arthritis RA SLE Vasculitis AS PsA ReA IBD Bacterial Viral Gout CPPD OA Symmetry Symmetric Asymmetric Inflammatory Noninflammator y Number Pauciarticular Polyarticular Joint involvement Spinecervical/ thoracic/ lumbar SI joint Small joints Wrists CMC MCP PIP DIP Ankle MTP Medium & Large joints Shoulders Elbows Hips/knees Systemic Fevers, uveitis, nodules, pneumonitis Malar rash, oral ulcers, pleurisy Rash, gangrene, CVA, headache, wrist drop, hemoptysis, GIT bleeding, proteinuria, h turia Uveitis, pneumonitis Psoriasis, Uveitis Uveitis, urethritis, enteritis CD, UC Fever Fever, rash Tophi, uric acid stones Preexisting OA, Wilson, ochronosis, hemochromatos is Laboratory tests RF, anti CCP ANA, dsdna, anti Sm, Urinalysis with proteinuria & hematuria, C3C4 ESR > 50, ANCA, temporal artery or other tissue Bx, urinalysis with proteinuria & hematuria HLA-B27 Test for Chlamydia. Gonorrhea, Salmonella, Shigella titres Tissue bx Lyme disease testing, joint/blood culture HBsAg, HCV, HIV, HPV-B19 SUA, MSU in synovial fluid CPPD crystal in synovial fluid, TSH, PTH, Fe, Mg, Phosphorus Radiologic Erosions No erosions Pulm infiltrates/nodules, angiography dilatation & stenosis Sacroilitis Erosions, Sacroilitis Effusions Erosions, overhanging edges Chondrocalcino sis Osteophyte s, narrow joint space GEORGE G.A. PUJALTE, Georgia SHIRLEY A. ALBANO-ALUQUIN. Differential Diagnosis of Polyarticular Arthritis. American Family Physician. 2015; 92(1):35-41
33 Conclusion Degenerative and autoimmune inflammatory joint disorders have distinctive clinical and laboratory features Detail history is important to support the clinical diagnosis Both conditions has underlying complex mechanistic pathogenesis and immunogenetic pathway play an important roles No curative treatment for both condition Early diagnosis and treatment especially for AIJD may halt the progression of the disease and systemic involvement AIJD should be referred to Rheumatologist due to its complexity in diagnosis, laborious and management.
34 THANK YOU The pain passes, but the beauty remains. ~ Pierre-Auguste Renoir ( )
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