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Joint pathology

Joint pathology. Normal anatomy. Joints provide movement and support . Classification: Solid (nonsynovial) also known as synarthroses ; lack a joint space allow minimal movement Cavitated (synovial): have a joint space allow for a wide range of motion. Synovial joint. Joint space.

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Joint pathology

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  1. Joint pathology

  2. Normal anatomy • Joints provide movement and support. • Classification: • Solid (nonsynovial) • also known as synarthroses ; lack a joint space • allow minimal movement • Cavitated (synovial): • have a joint space • allow for a wide range of motion.

  3. Synovial joint

  4. Joint space • Boundary formed by synovial membrane. • Lined by synoviocytes. • Synovial fluid (SF): • Pale yellow to clear, viscous • Rich in hyaluronic acid: acts as lubricant • provides nutrition for articular cartilage. • Arthrocentesis: needle aspiration of SF

  5. Synovial fluid analysis • Routine studies of SF: • Gross appearance: normally pale yellow • WBC count and differential count : • normally <200 cells mm3, • neutrophils <25% of total count. • Culture & Gram stain :if infection is suspected • Crystal analysis

  6. Crystal analysis • Monosodium urate (MSU) : found in gout • needle shaped (monoclinic) • Special polarization shows negative birefringence • Calcium pyrophosphate dehydrate (CPPD) crystals: found in pseudogout. • Monoclinic or triclinic (rhomboid) • Special polarization shows weakly positive birefringence

  7. Monosodium urate crystal Negatively birefringent Calcium Pyrophosphate Positively birefringent crystal

  8. Classification of joint diseases • Osteoarthritis • Neuropathic- Charcot’s joint • Rheumatoid arthritis • Gout • Pseudogout • SLE • Ankylosing spondylitis • Reiter’s disease • Psoriatic arthritis • Infections • Trauma

  9. Osteoarthritis (OA) • Most common type of joint disease and joint disability in the US • A degenerative joint disease and is characterized by: • Progressive erosion of articular cartilage and • Associated reactive changes at the margin of the joints and in the subchondral bone. • Not primarily an inflammatory disease

  10. More common in women than men Primarily targets weight bearing joints Hips, knees cervical and lumbosacral spine Other joints: Distal interphalangeal joint (DIP) and proximal interphalangeal joint (PIP) of the hands Osteoarthritis

  11. Osteoarthritis con’t Causes: A combination of genetic and environmental factors. • Primary: as a result of aging phenomenon; • seen in older individuals • Secondary: develops as a result of a predisposing condition • seen in younger individuals • Trauma to joint • Obesity • Ochronosis - (alkaptonuria: accumulation of homogentisic acid) • Hemochromatosis

  12. Osteoarthritis con’t Pathogenesis: • Exact etiology of OA osteoarthritis is unknown • Most important factor that predisposes to development of OA is • effect of abnormal load (mechanical trauma) on a weight bearing joint

  13. Thinning of articular cartilage • Development of cracks

  14. Erosion and loss of cartilage

  15. Formation of : • Loose body/joint mice • Subchondral cyst

  16. Eburnation • Sclerosis • Narrowing of joint space • Loose body • Osteophyte

  17. Osteoarthritis • Joint findings: • Erosions and clefts in articular cartilage • Clefts penetrate into underlying subchondral bone • Fragmentation of cartilage and subchondral bone result in formation of loose bodies • Bone rubs on bone  polished ivory like appearance called eburnation • Subchondral bone cysts (visible on X rays) develop beneath the articular surface • Reactive bone formation at the margins of joints produce osteophytes (bony spurs).

  18. Bouchard’s nodes (PIP) Heberden’s nodes (DIP)

  19. Osteoarthritis Clinical findings: • Pain worse with activity • Morning stiffness : lasts less than half hour • Joint stiffness: with limitation of movement • Heberden’s nodes develop in the DIP joints and • Bouchard’s nodes in the PIP joints of the hand

  20. Osteoarthritis • Lab studies: • No specific laboratory abnormality. • Synovial fluid analysis : normal • Diagnosis: xray findings • Presence of osteophyte at joint margins • Joint space narrowing • Subchondral bone cysts

  21. Joint-space narrowing in the knee with osteophyte formation

  22. Neuropathic arthropathy (Charcot’s joint) • It is a non-inflammatory joint disease • Secondary to a neurologic disease. • Joint destruction is due to insensitivity to pain • Causes: • Diabetes mellitus (Most common cause) (tarsometatarsal joint) • Syringomyelia (shoulder, elbow, wrist joints) • Tabes dorsalis (hip, knee and ankle joint)

  23. Neuropathic arthropathy (Charcot’s joint) • Pathogenesis: • loss of proprioception and deep sensation leads to recurrent trauma  • progressive destruction, and disorganization of the joint

  24. Marked joint destructionis the hallmarks of a neuropathic joint

  25. Rheumatoid arthritis (RA) • It is a chronic systemic, inflammatory disease • Genetics, enviromental factor and autoimmunity contributes to the etiology. • 30-50 years of age • Affects the peripheral joints in a symmetric manner producing proliferative synovitis that causes: • destruction of articular cartilage • ankylosis (fusion) of joint • joint deformity and disability

  26. Rheumatoid arthritis (RA) Clinical features: • Symmetric bilateral involvement; warm, tender and swollen joints • Small joints of hands and feet • MCP and PIP joints (not DIP) • Other joints include: • Ankles, knees, wrists, and cervical spine • Note: involvement of joints causes: • Joint stiffness especially in the morning, which lasts more than an hour and improves with activity.

  27. Subluxation and fusion of joints

  28. Synovial hypertrophy with lymphocytic infiltration.

  29. Rheumatoid arthritis Extra-articular manifestations: • Rheumatoid nodules • Vasculitis • Pulmonary: pleural effusion; interstitial fibrosis • Baker’s cyst increased articular pressure leads to outpouching of the synovium • Carpal tunnel syndrome median nerve entrapment • Hematologic: anemia of chronic disease; Felty’s syndrome( AI neutropenia/splenomegaly)

  30. Rheumatoid arthritis • Baker’s cyst (synovial cysts): • It is usually found in the in the posterior aspect of the knee • It may be confused with popliteal artery aneurysm

  31. Rheumatoid nodule- present on extesor surfaces

  32. Interstitial lung fibrosis

  33. Rheumatoid arthritis Lab findings con’t • Blood work: • Elevated ESR • Positive rheumatoid factor (80%) • Anticyclic -citrullinated peptide CCP(most specific marker) • Synovial Fluid: • WBC: 3,000 – 50,000 • Mostly PMNs (neutrophils) • X-ray: • Soft-tissue swelling • Erosions at articular surface • Narrow joint space (destruction of articular cartilage) • Fusion of joints (ankylosis) • Joint deformity

  34. Juvenile Rheumatoid arthritis (JRA) • Definition: JRA is characterized by a chronic synovial inflammation of unknown cause • It usually occurs in young girls < 16 years of age • RF is usually absent seronegative • Still’s disease • Polyarticular JRA • Pauciartucular JRA

  35. Still’s disease: Commonly presents as an “infectious disease” with fever, rash,generalized lymphadenopathy neutrophilic leukocytosis and polyarthritis Polyarticular JRA: Clinically disabling arthritis affecting many joints Other features include: low-grade fever growth retardation, adenopathy cervical spine involvement Juvenile Rheumatoid arthritis (JRA)

  36. Juvenile Rheumatoid arthritis (JRA) • Pauciarticular JRA: • Arthritis is present in a few joints • Inflammation of the anterior uveal tract  uveitis • May lead to visual loss and blindness

  37. Gout • Gout is a disorder of uric acid metabolism characterized by: • Hyperuricemia • Recurrent attacks of joint inflammation (gouty arthritis) and tissue deposition of uric acid crystals • It can lead to joint destruction if untreated • Gender: males> females

  38. Gout • Causes: • Primary gout (Idiopathic)is due to: • Under-excretion of uric acid in urine- most common • Overproduction of uric acid- less common

  39. Gout Causes : • Secondary gout: due to a secondary disorder. • the cause of hyperuricemia is known but gout is NOT the main or dominant clinical disorder. • Common causes include: • ↑nucleic acid turnover: leukemia, lymphoma • Drugs: diuretics, aspirin, ethanol • Chronic Renal failure • Lead intoxication(Saturnine Gout)

  40. Gout Acute arthritis: clinical features • The initial attack • It commonly involves 1stmetatarsophalangeal joint (big toe) inflammation of this 1st MTP joint is called podagra • The involved joint is red, hot and exquisitely tender

  41. Pathogenesis of gout

  42. Gout Chronic gout: It develops in uncontrolled or poorly controlled gout • It is characterized by presence of tophi • Tophi: deposits of MSU crystals in soft tissues: Pathognomonic lesion of gout found in the helix of the ear, fingers, toes • M/E: granulomatous reaction with foreign body type of giant cells surrounding amorphous MSU crystals

  43. Gout Complications: • Arthritis: • Asymmetric polyarthritis with • erosion of cartilage and subchondral bone due to crystal deposition • Renal Disease – gouty nephropathy • chronic medullary interstitial nephritis • Urolithiasis (renal stones) • Acute Renal failure – MSU deposition in collecting tubules

  44. Gout • Synovial fluid: • Demonstration of MSU crystals in synovial fluid is diagnostic • Intracellular, needle-shaped, negatively birefringent crystals • CBC: Absolute neutrophilicleukocytosis • Serum uric acid levels: • Hyperuricemia is usually but not always present. • Only 5-20% patients with hyperuricemia develop gout • 10% patients with gout have normal uric acid levels

  45. Pseudogout ( chondrocalcinosis) • It is associated with deposition of CPPD crystals in joints i.e knee • It is a disease of the elderly • Pathogenesis: • Normal aging process  biochemical change in cartilage  ↑ level of pyrophosphate pyrophosphate combines with Ca++ crystals deposited in the articular cartilage • Release of CPDD crystals in the joint causes inflammatory reaction

  46. Pseudogout • Clinical findings • Asymptomatic (chondrocalcinosis) • Acute attack (pseudogout): • Oligoarthritis resembling gout • Chronic form: • Polyarthritis resembling RA

  47. Pseudogout • Clinical findings con’t • Synovial fluid analysis: • Blue staining rhomboid crystals. • Positive birefringence • Xray - calcification of articular cartilage

  48. Seronegativespondyloarthropathies • A group of related disorders. • Develop in genetically predisposed individuals • when they come in contact with certain environmental factors ( triggering agents) • Characteristics include: • Lack Rheumatoid factor (RF negative) • Individuals HLA-B27 positive • Male dominant • Involve sacroiliac joint ( sacroilitis) with or without peripheral arthritis

  49. Seronegativespondyloarthropathies • Types of spondyloarthropathy: • Ankylosing spondylitis (AS) • Reiter’s syndrome • Arthritis associated with • ulcerative colitis • shigellosis • psoriasis

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