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Inflammatory Joint Diseases

Inflammatory Joint Diseases. Prof. Dr. Ece AYDOĞ Physical Medicine and Rehabilitation. Learning objectives :. be able to describe epidemiology and etiopathogenesis of rheumatoid arthritis

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Inflammatory Joint Diseases

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  1. Inflammatory Joint Diseases Prof. Dr. Ece AYDOĞ PhysicalMedicineandRehabilitation

  2. Learning objectives: be able to describe epidemiology and etiopathogenesis of rheumatoid arthritis be able to describe clinical forms of rheumatoid arthritis according to initial patterns (insidious, acute, intermediate) be able to enumerate the old and new diagnostic criteria formed the League of American College of Rheumatism.

  3. be able to describe the laboratory findings, radiographic findings of early and late stage, articular (disease-specific deformities), and extra-articular signs of rheumatoid arthritis be able to enumerate pharmacological and non pharmacological treatment and poor prognostic criteria of rheumatoid arthritis. be able to describe the clinical signs of polimyalgiarheumatica and Sjögren's syndrome

  4. RHEUMATOID ARTHRITIS (RA)

  5. DEFINITION Systemic autoimmune inflammatory disorder of unknown etiology that primarily affects the synovial lining of the diarthrodial joints. This chronic, symmetric erosive synovitis develops in the joints and leads to destruction. These erosions are pathognomonic of RA.

  6. EPIDEMIOLOGY • Female to male ratio is 3:1 • Prevalence: approximately 1% of the population • Age range from 20 to 60 years, prevalence rises with age, peak incidence between 4th and 5th decade

  7. ETIOLOGY • Multiple and multifactorial • Genetic • Sex and sex hormones • İnfectious agents • Diet, trauma, stress, cigarette

  8. ETIOLOGY Genetic factors • Twin studies • Major Histocompatability Complex (MHC) on chromosome 6 • Class II MHC allele HLA-DR4 (HLA-DR4 haplotype) and DR1

  9. ETIOLOGY Two major theories: • 1. Infectious agents • 2. Immunogenetic→ Class II surface antigens-presenting cells

  10. Numerous Cellular Interactions Drive the RA Process Immune complexes Bacterial products IL-1, TNF-, etc Rheumatoid factors B cell IL-1 Soluble factors and direct cell–cell contact T cell HLA -DR Antigen- presenting cells Macrophage B cell or macrophage IL-1 and TNF- Synoviocytes Chondrocytes Pannus Articular cartilage Production of collagenase and otherneutral proteases Arend W. Semin Arthritis Rheum. 2001;30(suppl 2):1-6.

  11. Cytokines • synovial lining proliferation, pannus• endothelial activation, angiogenesis• fibroblast activation, fibrosis

  12. Pannus Formation is the Most Important Destructive Element in RA • Pannus: • Membrane of granulationtissuethatcoversthearticularcartilage at jointmargins • Fibroblast-likecellsinvadeanddestroytheperiarticular bone andcartilage at jointmargins • Vasculargranulationtissue is composed of: • Proliferatingfibroblasts • Numeroussmallbloodvessels • Variousnumber of inflammatorycellsmainly T lymphocytes (PolymorphicNeutrophil PMN are in fluid) • Occasionallycollagenfibersareseenwithinphagolysosomes of cells at theleadingedge of pannus • Jointankylosismayoccur in laterstages

  13. RA Is Characterised by Synovitis and Joint Destruction NORMAL RA Inflamed synovial membrane Synovial membrane • Major cell types • T lymphocytes • macrophages Pannus Cartilage • Minor cell types • fibroblasts • plasma cells • endothelium • dendritic cells Synovial fluid • Major cell type • neutrophils Capsule Cartilage thinning Adapted from Feldmann M, et al. Annu Rev Immunol. 1996;14:397-440.

  14. IL-1 and TNF- Have a Number of Overlapping Proinflammatory Effects Proinflammatory effects of IL-1 Proinflammatory effects of TNF- COX-2PGE2NOAdhesion moleculesChemokinesCollagenasesIL-6 TNF-Osteoclast activation Angiogenic factors IL-1 cell death COX-2 = cyclo-oxygenase type 2; PGE2 = prostaglandin-E2; NO = nitric oxide

  15. IL-1 Plays a Pivotal Role in the Inflammatory and Destructive Processes of RA IL-1 Activates monocytes/macrophages Induces fibroblast proliferation Activates chondrocytes Activates osteoclasts Inflammation Synovial pannus formation Cartilage breakdown Bone resorption

  16. PATTERN OF ONSET • Insidious → 50%–70% • Initial symptoms can be systemic or articular • Slow onset from weeks to months • Constitutional symptoms: fatigue, malaise • Diffuse musculoskeletal pain may be the first nonspecific complaint with joint involvement later • Most commonly symmetric involvement although asymmetric involvement may be seen early • Morning stiffness in the involved joints lasting one hour or more • Swelling, erythema • Muscle atrophy around the affected joints • Low grade fever without chills

  17. Acute Onset→ 10%–20% • Onset over several days • Less symmetric in presentation • Severe muscle pain • Intermediate Onset→ 20%–30% • Onset over several days to weeks • Systemic complaints more noticeable

  18. DIAGNOSIS OF RA 1988 American Rheumatologic Association (ARA) Criteria • Must satisfy 4–7 criteria • Criteria 1 through 4 must be present for at least six weeks ARA Criteria: • 1. Morning Stiffness • In and around the joint • Must last at least one hour before maximal improvement • 2. Arthritis of Three or More Joints • Three or more joint areas simultaneously affected with soft tissue swelling or fluid • Observed by a physician • 14 possible joint areas are bilateral proximal interphalangeal (PIP), metacarpal phalangeal (MCP), wrist, elbow, knee, ankle and metatarsal phalangeal (MTP)

  19. ARA Criteria • 3. Arthritis of the Hand Joints • At least one joint area swollen in the wrist, MCP and/or PIP • 4. Symmetric Arthritis • Simultaneous involvement at the same joint area on both sides of the body • Absolute symmetry is not needed • 5. Rheumatoid Nodules • Subcutaneous nodules over extensor surfaces, bony prominence or in juxta-articular regions • Observed by a physician • 6. Serum Rheumatoid Factor (RF [+]) • 7. Radiographic Changes (Hand and Wrist) • Erosions, bony decalcification, and symmetric joint-space narrowing

  20. The 2010 American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis Patients who: 1) have at least 1 joint with definite clinical synovitis (swelling) 2) with the synovitis not better explained by another disease Classification criteria for RA (score-based algorithm: add score of categories A–D;a score of ≥6/10 is needed for classification of a patient as having definite RA) A. Joint involvement: Score: 1 large joint0 2-10 large joints1 1-3 small joints (with or without involvement of large joints) 2 4-10 small joints (with or without involvement of large joints) 3 >10 joints (at least 1 small joint)5

  21. B. Serology (at least 1 test result is needed for classification)Score Negative RF and negative ACPA0 Low-positive RF or low-positive ACPA 2 High-positive RF or high-positive ACPA 3 C. Acute-phase reactants (at least 1 test result is needed for classification) Normal CRP and normal ESR0 Abnormal CRP or abnormal ESR 1 D. Duration of symptoms <6 weeks 0 ≥6 weeks 1

  22. Rheumatoid factor ESR and C-reactive protein Thrombocytosis, Hypochromic normocytic anemia, Eosinophilia Hypergammaglobulinemia Hypocomplementemia Synovial fluid analysis Low viscosity WBC → 1,000–75,000 mm3 > 70% PMNs Transparent - cloudy LABORATORY

  23. Rheumatoid Factor • 85% of the patients with RA have a (+) Rheumatoid Factor (RF [+]) • Associated with severe active disease with increased systemic manifestations (nodules) • Serial titers are of no value • Can still be RF (−) and have RA because (+) diagnosis needs four to seven diagnostic criteria • + RF can be seen in other diseases: Rheumatic (SLE, scleroderma, Sjögren’s), viral, parasitic, bacterial, neoplasms, hyperglobulinemic purpura

  24. RADIOGRAPHIC FINDINGS • Early findings • Soft tissue swelling • (+) Juxta-articularosteopenia (bone wash-out)

  25. Marginal bone erosions (near attachment of joint capsule)

  26. Erosion of theulnarstyloid

  27. Atlantoaxial subluxation (> 2.5–3 mm)

  28. Uniformjointspacenarrowingduetoloss of articularcartilage (hips, knees, etc.) • Axialmigration of thehip (ProtrusioAcetabulum) • Malalignmentandfusion of joints

  29. Hand and Wrist Deformities BoutonnièreDeformity • Hyperextension of the MCP • Flexion of the PIP • Hyperextension of the DIP

  30. SwanNeckDeformity • Flexioncontracture of the MCP • Hyperextension of the PIP • Flexion of the DIP

  31. UlnarDeviation of theFingers

  32. Tenosynovitis of theFlexorTendonSheath • One of themostcommonmanifestation of thehands in RA • Can be a majorcause of handweakness • Diffuseswelling of thevolarsurfaces of thephalangesbetweenthejointswithpalpablegrating of theflexortendonsheath • May be confusedwith de Quervain’sdisease

  33. CarpalBonesRotate in Zig-ZagPattern

  34. Cervical Spine • AtlantoaxialJointSubluxations→ MostCommonareAnteriorSubluxation • Instability • Odontoidor Atlas can erode • Withflexion, theAtlantoaxial (AA) spaceshould not increasesignificantly: anyspacelargerthan 2.5 or 3 mm is consideredabnormal • Tenosynovitis of thetransverseligament of C1 • Cervicalmyelopathy → erosion of theodontoidprocess, ligamentlaxityorrupture

  35. Foot • HammerToeDeformities • Hyperextension of the MTP and DIP withflexion of the PIP • ClawToeDeformities • Hyperextension at the MTP jointandflexion of the PIP and DIP joints • Pain on themetatarsalheads on weightbearing • HalluxValgusDeformity • LateralDeviation of theToes

  36. Ankle • Ligament weakness leading to pronation of the hindfoot • Tarsal tunnel syndrome • Synovial inflammation leads to compression of the posterior tibial nerve Hip Deformities • Symmetric involvement • Protrusio acetabulum: Inward bulging of the acetabulum into the pelvic cavity • Accompanied by arthritis of the hip joint, usually due to RA

  37. Shoulders • Glenohumeral arthritis • Effusions can occur; decreased range of motion (ROM) may lead to frozen shoulder • Rotator cuff injuries Elbow • Subcutaneous nodules • Olecranon bursitis • Loss of full elbow extension is an early problem and may lead to flexion deformities • Ulnar Neuropathies

  38. Knee Deformities • Common symmetric joint involvement • Loss of full knee extension which may lead to flexion contractures • Quadriceps atrophy leading to increased amount of force though the patella • Force leads to increased intra-articular pressure in the knee joint causing the synovial fluid to drip into the popliteal space called a popliteal (Baker’s) cyst

  39. EXTRA-ARTICULAR MANIFESTATIONS • Morecommon in patientsthatare: • RF (+) • Withrheumatoidnodules • Severe articulardisease • MHC class HLA DRB1 Alleles

  40. General Malaiseorfatigue • Skin • SubcutaneousNodules • Present in 50% of RA patients • Form subcutaneously, in bursae, andalongtendonsheaths • Typicallylocatedoverpressurepoints • Extensorsurface of theforearm • Can occursinglyoraggregate in clusters • Methotrexatemayenhancethedevelopmentoracceleratethedevelopment of rheumatoidnodules • VasculiticLesions • Leukocytoclasticvasculitisandpalpablepurpura

  41. Ocular • Keratoconjunctivitis sicca (dry-eye syndrome) • Episcleritis → benign, self-limited • Scleritis • Pulmonary • Interstitial lung disease • Interstitial fibrosis • Rheumatoid nodules • Pulmonary fibrosis • Pleurisy • Inflammation of the cricoarytenoid joint → dysphagia, dysphonia • Bronchiolitis obliterans

  42. Cardiac • Pericarditis • May lead to constrictive pericarditis with right-sided heart failure • Valvular heart disease • Gastrointestinal • Xerostomia—dryness of the mouth secondary to decreased salivary secretion • Gastritis and Peptic Ulcer Disease (PUD) associated with non-steroidal anti-inflammatory drugs (NSAIDs) (not directly linked to disease)

  43. Renal • Rare glomerular disease usually related to drug (gold) • May see renal involvement if amyloidosis develops • Hematologic • Hypochromic- normocytic anemia • Felty’s syndrome

  44. Neurologic • Cervical spine • Most common at C1-C2, destruction of the transverse ligament or the dens itself • Cervical myelopathy • Gradual onset of bilateral sensory paraesthesia of the hands and motor weakness • Neurologic exam findings may include → Babinski, Hoffman’s, hyperactive Deep Tendon Reflexes (DTRs) • Entrapment neuropathies • This is secondary to fluctuation in synovial inflammation and joint postures • Mononeuritis multiplex —inflammatory—not due to compression

  45. Felty’s Syndrome • “She felt her spleen” • Classic triad of RA,splenomegaly,leukopenia • Seen in seropositive RA, usually with nodules • Occurs in the fifth to seventh decades with RA > 10 years • Women comprise two-thirds of cases • Often associated with leg ulcers

  46. Caplan’s Syndrome • Intrapulmonary nodules—histologically similar to rheumatoid nodules • (+) rheumatoid factor • Associated with rheumatoid arthritis and pneumoconiosis in coal workers • Granulomatous response to silica dust

  47. TREATMENT • Education • Joint protection • Home exercise program • Relative Rest • Required for the acutely inflamed joint

  48. Exercise Acute disease: with severely inflamed joints, actual splinting to produce immobilizationwith twice daily full and slow passive range of motion to prevent soft tissue contracture Mild disease: (moderate synovitis) requires isometric program

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