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JOINT PATHOLOGY

JOINT PATHOLOGY. FERDA ÖZKAN M.D. YEDITEPE UNIVERSITY MEDICAL FACULTY. OBJECTIVES. Review joint structure Explain inflammatory processes of Joints Describe types of arthritis. JOINTS. Nonsynovial- (solid)- synarhtoses: Lack joint space-fibrous synarthroses

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JOINT PATHOLOGY

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  1. JOINT PATHOLOGY FERDA ÖZKAN M.D. YEDITEPE UNIVERSITY MEDICAL FACULTY

  2. OBJECTIVES • Review joint structure • Explain inflammatory processes of Joints • Describe types of arthritis

  3. JOINTS • Nonsynovial- (solid)- synarhtoses: Lack joint space-fibrous synarthroses -synchondroses • Synovial- have joint space

  4. Synovial Joint

  5. Synovial Joints • The boundry of the joint space is formed by the synovial membrane • Two types of synovial cells Type A- (macrophage like) phagocytic and synthetize hyaluronic acid Type B- (fibroblast like) produce various proteins

  6. SYNOVIOCYTES

  7. ARTICULAR HYALINE CARTILAGE Articular hyaline cartilage is composed of type 2 collagen, water, proteoglycans and chonrocytes. The water and proteoglycans give hyaline cartilage its turgor and elasticity and limit friction.

  8. Chondrocytes synthetize the matrix as well as enzymatically digest it Matrix turnover is controlled as chondrocytes secrete the degenerative enzymes in an inactive form and enrich the matrix with enzyme inhibitors

  9. Cytokines such as IL-1 and TNF trigger degradative process • The source of cytokines include -Chondrocytes -Synoviocytes -Inflammatory cells

  10. CHRONIC INFLAMMATORY SYNOVITIS

  11. Arthritis - Introduction • Inflammation of joints - Common • Common site for autoimmune injury • Heart valves & Joints - damage – Exposure of hidden antigens. • Infections. • Degeneration – Age/Stress/life style • Use it or Loose it….!

  12. Arthritis – Clinical features: • Pain •  Inflammation - capsule, synovium, periosteum. • Swelling: •  inflammation, effusion, proliferation. • Restricted movement •  pain, fluid, synovial swelling, damage. • Deformity •  mal-alignment, erosion, ankylosis

  13. Arthritis Clinical Classification: • Monoarthritis: • Local, asymmetric, secondary. • Acute:Bacterial, Trauma, Crystal, Reactive • Chronic :Tuberculosis, Lyme, Fungal, Trauma, Tumors. • Polyarthritis: • Chronic, symmetric, systemic. • Autoimmune, degenerative, Crystal. • Rarely infective.

  14. Polyarthritis Classification: • Autoimmune: • Rheumatoid,Ankylosing spondilitis, Psoriatic , Reiter’s syndrome, enteropathic • Degenerative:Osteroarthritis • CrystalDeposition: • Gout – Monosodiumurate • CPPD -Pseudo Gout • Infective -Septic, TB, Lyme etc. rare.

  15. Rheumatoid Arthritis

  16. RHEUMATOID ARTHRITIS • Autoimmune chronic systemic inflammatory disorder • Attacks joints, causing a nonsuppurative proliferative inflammatory synovitis • Destruction of articular cartilage and ankylosis of the joints

  17. RHEUMATOID ARTHRITIS • Symmetric, small joints • Usually in hands metacarpophalangeal and proximal interphalangeal joints • Feet, wrists,ankles, elbows and knees • Joints swollen, warm, painful particulary in the morning or following inactivity

  18. Epidemiology of RA • Prevalence about 1-3% of population • Female : Male ratio = 3-5:1 • Concordance in identical twins 30%

  19. Its pathogenesis is complex and incompletely understood, involving both type III (antigen-antibody complex) and type IV (T helper lymphocyte / macrophage-mediated) hypersensitivity reactions.

  20. Pathogenesis • Inciting agent activates immune system  immunological reactions  immune complexes in synovial fluid activate complement  inflammatory response  joint destruction. • Earliest change is inflammation and edema of synovium with increased vascularity and increased production of synovial fluid • shows evidence of CD4+ T helper cells migrating into the joint.

  21. Next steps: • synovial villi hypertrophy, • synovial cells proliferation, • increased vascularisation (angiogenesis) • pannus form (granulation tissue that grows across surface of articular cartilage from adjacent synovium).

  22. Marked synovial hypertrophy with formation of villi.

  23. Subsynovial tissue containing a dense lymphoid aggregate

  24. Synovial angiogenesis Tissue section of rheumatoid synovial pannus showing prominent new blood vessel formation

  25. Hyperplastic synovium may spread over and erode into cartilage and bone. • This destructive proliferation of synovium is known as pannus. • Large numbers of inflammatory cells (T and B lymphocytes, plasma cells and macrophages) take up residence within the synovium. • These secrete inflammatory mediators (cytokines, prostaglandins etc.) into the synovial fluid.

  26. This figure demonstrates • destruction of articular cartilage (open arrow; osteoclastic cells) • by synovial pannus (solid arrow). • It is thought that the pannus destroys the cartilage by production of metalloproteinases.

  27. Pannus can also destroy bone by recruiting osteoclasts to resorb bone matrix (open arrow). • Osteoclasts are very sensitive to IL1 and TNF, resorbing bone in response to production of these cytokines by the inflammatory cells infiltrating the pannus (solid arrow).

  28. Production of metalloproteinases by synovial cells is induced by the inflammatory cytokines IL1 and TNF-a which are both produced by chronically inflamed synovium. • These cytokines also cause synovial cells to proliferate and are probably responsible for the development of pannus.

  29. The muscles waste around the joint • Hyperemia develops • The joint capsule is distended • Destruction of unprotected bone at joint margin and subchondral bone by pannus • Later leading to marked joint damage and capsular laxity • Leading to deformity and fibrous ankylosis • Eventually bony ankylosis of the joint.

  30. N.Synovium - - R.Arthritis:

  31. RA - Pannus: Hyperplastic inflammed synovium

  32. Skin RA Nodule:

  33. Skin RA Nodule:

  34. Rheumatoid Nodule (skin): Palisading Macrophages Central Fibrinoid Necrosis

  35. Subcutaneous rheumatoid nodule with an area of necrosis surrounded by a palisade of macrophages and scattered chronic inflammatory cells.

  36. Joint involvement in RA:

  37. Swan Neck Deformity in RA:

  38. Joint Destruction in RA: Swan Neck Deformity

  39. RA Joint destruction, ankylosis:

  40. Extraarticular manifestations • Weight loss, malaise and fever; • Lymphadenopathy • Skin (rheumatoid nodules– in 50%, at periarticular positions subject to high external pressure; inflammatory granulomatous lesions; vasculitis (leukocytoclastic vasculitis and palpable purpura) • Eye (keratoconjunctitis, scleritis, episcleritis) • Respiratory (pleurisy, pleural effusions, interstitial fibrosis, rheumatoid nodules, bronchiolitis) • Cardiac (pericardial effusion, pericarditis, myocarditis, endocarditis, valvular heart disease) • Peripheral nerves: nerve compression by synovitis or tenosynovitis, syndrome of mononeuritis multiplex.

  41. Gastrointestinal (adverse effects from drugs) • Renal (amyloidosis, drug induced nephropathy, renal tubular acidosis) • Neurologic (entrapment syndromes – especially carpal tunnel, peripheral neuropathy from vasculitis – sensory and motor, mononeuritis multiplex) • Hematologic (anemia, leucopenia, lymphoma, thrombocytosis) • Hand deformities (fusiform swelling  spindle shape to fingers) • Cervical spine involvement.

  42. Juvenile Rheumatoid Arthritis: • Before age 16 • Multisystem involement - Spleenomegaly, • Starts with systemic involvement unlike RA. • No serum RA Factor – Seronegative • Antinuclear Antibody (ANA) +ve  autoimmune.

  43. Juvenile Rheumatoid Arthritis • Still (1887) : rheumatoid arthritis in children • Common connective tissue disease in children age 15 or less, 65% male. • Either oligoarticular (<5 joints), polyarticular (5 or more joints) or systemic. • Compared to classic rheumatoid arthritis, oligoarthritis is more common; • systemic large joints are affected more than small joints, • no rheumatoid nodules are present, • no rheumatoid factor is present, • ANA positive.

  44. Associated with HLA-DRB1, infections by mycobacteria, bacteria, viruses. • 70% recover • 10% have residual severe joint deformities • Symptoms: systemic onset with fever, rash, hepatosplenomegaly, generalized lymphadenopathy, serositis; also warm and swollen joints; pericarditis, myocarditis, pulmonary fibrosis, glomerulonephritis, uveitis, growth retardation. • Sites: knees, wrists, elbows, ankles. • Micro: similar morphologic changes as rheumatoid arthritis.

  45. Seronegative spondyloarthropathy • Inflammatory joint diseases that all share a common pathology and strong association to the HLA-B27 antigen and are negative for rheumatoid factor (seronegative). • Used to be referred to as variants of rheumatoid arthritis as they share many pathologic and radiologic features with rheumatoid arthritis. • ‘Spondylos’ is Greek for vertebrae.

  46. Ankylosing Spondylitis (Marie-Strumpell’s disease) • Psoriatic Arthritis (PsA) • Reactive Arthritis (ReA) (Reiter’s syndrome) • Enteropathic Spondylitis (Enteropathic synovitis) • Undifferentiated spondylitis

  47. Ankylosing Spondylitis(Marie-Strumpell’s disease) • Chronic inflammatory disorder primarily affecting the axial skeleton • Affected joints tend to fibrosis and ankylosis. • Cause unknown, • Strongly associated with HLA-B27 histocompatibility antigen (90%) • Affects up to 1% of population • Affects teenage boys • Chronic synovitis destroys articular cartilage and causes bony ankylosis • Inflammation of tendinoligamentous insertion sites cause osteophytes. • Symptoms: low back pain that gets progressively.

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