Common Joint Disorders PDF

Common Joint Disorders Prof. Salim Bafakeer MD pathology  Common Joint disorders  Five major groups:  Arthritis caused by specific microorganisms, such as septic arthritis due to staphylococcal infection or Lyme disease caused by a spirochete; ...

Common Joint Disorders Prof. Salim Bafakeer MD pathology  Common Joint disorders  Five major groups:  Arthritis caused by specific microorganisms, such as septic arthritis due to staphylococcal infection or Lyme disease caused by a spirochete;  Arthritis of unknown etiology, such as rheumatoid arthritis (RA);  Degenerative joint disease/osteoarthritis (OA);  Metabolic arthritis, such as gout;  Arthritis resulting from trauma (or overuse).  Common Joint disorders Clinical features: Pain:  Inflammation - capsule, synovium, periosteum. Swelling:  inflammation, effusion, proliferation. Restricted movement:  pain, fluid, synovial swelling, damage. Deformity:  mal-alignment, erosion, ankylosis.  Osteoarthritis (OA): Degenerative Joint Disease  Osteoarthritis is the most common joint disorder.  Degenerative end result - (ageing); >80% in >65 y.  Large weight bearing joints.  Characterized by Progressive deterioration and loss of the articular cartilage Formation of bony outgrowths ("osteophytes") Thickening and sclerosis of the subchondral bone.  Classified as primary (idiopathic) or secondary.  Osteoarthritis (OA)  Primary osteoarthritis ( Idiopathic) The common "arthritis" which affects older people, due to "wear-and-tear No initiating cause  Secondary osteoarthritis About 5% in younger individuals Generally develop in a joint damaged by:  Trauma  Metabolic disorder (such as hemochromatosis or diabetes mellitus, marked obesity)  Deformity (such as congenital dislocation of the hip).  Osteoarthritis (OA)  Pathogenesis: an intrinsic disease of articular cartilage. Significant changes in both the composition and the mechanical properties of cartilage. Early; the degenerating cartilage contains increased water, decreased concentration of proteoglycans weakening of the collagen network, caused by decreased local synthesis of type II collagen and breakdown of preexisting collagen. Increased the level of IL-1, TNF and nitric oxide in osteoarthritic cartilage. Increased apoptosis  decrease in the number of functional Chondrocytes. Chondrocytes in deep layers proliferate to repair the damage, but the deterioration of cartilage eventually predominates.  Osteoarthritis (Morphology)  Initially the superficial layers of cartilage are degraded due to the biochemical changes.  At this stage the articular surface is granular and softer than normal.  Small tears called fibrillations occur at the articular surface.  Progressive fibrillation & erosion of articular cartilage  forms loose bodies " Joint mice"  Eventually full thickness portions of cartilage are sloughed off.  When cartilage is damaged the joint space narrows  Subchondral sclerosis of the bone, an ivory-like consistency (eburnation).  Synovial fluid is forced into subchondral regions to form fibrous walled cysts (Subchondral cyst).  Bone outgrowth at the margins of the joints (Osteophytes).  Osteoarthritis (OA) fibrillation of the articular cartilage  Osteoarthritis (OA); Clinical course  Often asymptomatic, but joint pain, Limitation in range of movement, crepitus (a crackling sensation when the joint is moved), are prominent symptoms in some patients, and later joint enlargement or deformity can occur.  Osteophytes can impinge on spinal foramina resulting in cervical and lumbar nerve root compression with radicular pain, muscle spasms, muscle atrophy ad neurological deficits  Herberden nodes, small osteophytes on the distal interphalangeal joints, common in female with primary OA.  Rheumatoid Arthritis (RA)  A chronic systemic inflammatory disorder primarily affecting joints producing a nonsuppurative proliferative synovitis that often progresses to destruction of the articular cartilage and ankylosis.  Is a very common condition, prevalence 1 %.  More common in women, 3:1.  Most cases arise in young or middle-aged adults.  Rheumatoid Arthritis (RA) Etiology  Genetic Susceptibility: – Strong association with HLA DR4. – HLA DR4 or DR1 in 65% to 80% cases.  Microbial inciting agent: – Epstein-Barr virus, Borrelia & Mycoplasma  Autoimmunity: – IGM anti IgG – RA Factor. – Helper T cell (CD4) cells produce cytokines.  Pathogenesis of Rheumatoid Arthritis (RA)  The disease initiated- in a genetically predisposed individual- by activation of T- helper cells responding to some arthritogenic agent, possibly microbial.  T helper cells produce cytokines activate the macrophages, B- cells and stimulate synovial cells and fibroblast proliferation.  Activated macrophages  cytokines  proliferation of fibroblasts, Chondrocytes and synovial cells  Enzymes  damage.  B cells  IgM (Rheumatoid factor), Autoantibodies directed against the Fc portion of IgG.  RFs are present in serum and synovial fluid in 80 % of patients.  RF factor complex  type III injury (immune complex)  inflammation damage.  Rheumatoid Arthritis (Morphology)  Joint:  Grossly: the synovium becomes edematous, thickened and hyperplastic.  Histologically: Chronic synovitis, characteristic by: 1) Synovial cell hyperplasia and proliferation. 2) Infiltration of synovial stroma by a dense perivascular inflammatory infiltrate composed of CD4+ T cells, plasma cells and macrophages. 3) Increased vascularity due to angiogenesis. 4) Aggregation of organized fibrin on the synovial surface and in the joint space (Rice bodies). 5) Accumulation of neutrophils in the synovial fluid and along the surface of synovium. 6) Increased osteoclast activity in the underling bone, allowing the synovium to penetrate into the bone, leading to bone erosion and osteoporosis. 7) Pannus formation, a fibrocellular mass of synovium and synovial stroma. Rheumatoid Arthritis (RA) RA - Pannus RA - Pannus Rheumatoid Arthritis (RA)  Rheumatoid Arthritis (RA)  The articular cartilage subjacent to the Pannus is eroded  destroyed.  Subarticular bone  erosion.  Pannus fills the joint space  fibrosis  calcification  permanent ankylosis.  Destruction of tendons, ligaments and joint capsule deformities.  Extra-Articular RA:  Rheumatoid Nodules  Vasculitis  Pleuritis  Pericarditis  Tendonitis. Rheumatoid subcutaneous nodules:  Occur in 25 % of patients.  Occur along the extensor surface of the forearm or areas subjected to mechanical pressures.  Firm, nontender, oval or round masses up to 2 cm.  Central focus of fibrinoid necrosis surrounded by a palisade of macrophages, rimmed by granulation tissue. Rheumatoid Nodule (skin)  Rheumatoid Arthritis (RA); Clinical Features:  The diagnosis clinically, based on the presence of four or more of these seven findings: Morning stiffness. Arthritis in 3 or more joint areas. Arthritis of small hand joints. Symmetric arthritis. Rheumatoid nodules. Serum rheumatoid factor. Typical radiographic changes.  Gout and Gouty arthritis  Gout is a disorder of purine metabolism which is characterized by  Long standing hyperuricemia;  Recurrent episodes of inflammatory arthritis (gouty arthritis).  Usually monoarticular in onset caused by precipitation of monosodium urate (MSU) crystals.  A Peak incidence in the fifth decade.  A family history of gout is often obtained in about 25% of cases.  Classified as primary (90%) and secondary forms (10%).  Primary Gout caused by either an overproduction of uric acid as a result of enzymatic defects (~10% of primary cases) or renal under-excretion of uric acid (~90% of primary cases); the basic renal defect in the majority of patients with primary gout is not established  Gout and Gouty arthritis  In patients with secondary hyperuricemia due to an overproduction is usually associated with an excessive breakdown of cells as in – Myeloproliferative disorders, – Leukemias, – Multiple myeloma, – Some carcinomas, – Hemolytic anemias, – Massive cell lysis produced by cytotoxic drug therapy.  Secondary hyperuricemia caused by renal under-excretion of uric acid may result from: – Chronic renal disease – Diuretic drug treatment (which interferes with the renal secretion of uric acid and causes blood volume contraction) – Salicylates – Ethanol  Pathogenesis of Gouty arthritis  Hyperuricemia is necessary, but not sufficient, for the development of gout  Only about 10% of patients with hyperuricemia develop gout.  Other factors that contribute to the development of symptomatic gout include:  Age of the individual and duration of the hyperuricemia. Gout usually appears after 20 to 30 years of Hyperuricemia  Genetic predisposition.  Alcohol consumption  Obesity  Drugs (e.g., thiazides) that reduce excretion of urate  Increased levels of uric acid in the blood and other body fluids  precipitation of monosodium urate crystals.  Macrophages in the synovium phagocytose the crystals, stimulating the production of mediators that recruit leukocytes  Also activate complement  generation of C3a and C5a  accumulation of neutrophils and macrophages in the joint and synovial membrane.  Phagocytic cells  release of toxic free radicals and inflammatory mediators; IL-1, IL-6, IL-8, Leukotrienes, and TNF  intensify the inflammatory response and activate synovial cells and cartilage cells to release proteases  tissue injury.  Gouty arthritis; Morphology  Acute arthritis:  Deposition of monosodium urate crystals in synovial tissues, appear as pale, elongated, needle-like structures, accompanied by neutrophilic inflammatory infiltrate, local congestion, and edema.  Chronic tophaceous arthritis:  Deposition of Tophi on the articular cartilage and adjacent joint capsule, Tophi may also form in other sites.  Tophi are large, irregular deposits of chalky white sodium urate.  Histologically: a mass of amorphous crystalline ureates surrounded by chronic granulomatous inflammatory reactions, composed of macrophages, lymphocytes, foreign body-type giant cells and fibroblasts.  Gout Tophi Microscipic: a mass of amorphous crystalline ureates surrounded by chronic granulomatous inflammatory reactions  Gout and Gouty arthritis  Gout is divisible into four phases:  Asymptomatic hyperuricemia,  Acute gouty arthritis, typically a monoarticular inflammatory arthritis which initially involves the metatarsophalangeal (MTP) joint of the big toe in 90 % or more of patients, characterized by  Sudden onset of joint pain  Tenderness  Swelling  Redness the appearance of which may be mistaken for a septic joint.  Intercritical gout; an asymptomatic interval.  Chronic tophaceous gout, develops on average about 10 years after the initial acute attack and is characterized by juxtaarticular bone erosion and loss of the joint space  Gouty nephropathy: occur in 10-25% of gouty subjects: Precipitation of uric acid crystals within renal tubules and interstitium. Uric acid stone. Obstructive uropathy and pyelonephritis. Big Toe in Gout  SUPPURATIVE ARTHRITIS ("septic arthritis")  Acute suppurative arthritis is caused by joint infection with pyogenic microorganisms.  The most common agents are, gram positive cocci (Staph, Strep), gonococcus, and gram negative rods (E. coli, H. 'flu, Pseudomonas; Salmonella in sickle cell disease).  Bacterial arthritis is usually monoarticular and involves large joints. (Gonococcal arthritis often involves a series of joints.)  Characterized by purulent inflammatory changes in the synovial membrane and synovial fluid, and, if not promptly recognized and appropriately treated, leads to destruction of the articular cartilage and joint.  The infection of a joint occurs most commonly by hematogenous spread, and less frequently by extension from a neighboring infection or by introduction through a penetrating wound or following surgery.  SUPPURATIVE ARTHRITIS (“Septic arthritis")  Risk factors: – Immune deficiencies, – severe illness, – joint trauma, – Chronic arthritis, – Intravenous drug abuse  Symptoms: – Sudden development of acutely painful and swollen joint with restricted range of motion, systemic findings.  When infection is suspected, joint effusions should be aspirated under sterile conditions, synovial fluid culture and gram stain performed.  Septic Arthritis ORGANISM PEAK AGE INCIDENCE GRAM STAIN Hemophilus Gram negative Children influenzae coccobacilli Neisseria Gram negative Young adults gonorrheae diplococci Salmonella young with Sickle Cell An. Gram negative rods Gram positive Staph. aureus Adults cocci in clusters Escherichia Adults Gram negative rods coli Pseudomonas Adults Gram negative rods Gonococcal Arthritis Thank you