Pathology of Joints

Mind Map by , created almost 6 years ago

Doctorate Pathology (Systems Pathology) Mind Map on Pathology of Joints, created by melian.yates on 12/02/2013.

Created by melian.yates almost 6 years ago
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Pathology of Joints
1 Types of Joints
1.1 Fibrous
1.2 Osseous
1.3 Cartilaginous
1.4 Synovial
1.4.1 Most clinically significant
1.4.2 Anatomy Composed of two bone ends bound together by a fibrous capsule & ligaments Inner surface of capsule is lined by synovial cells & the joint space contains synovial fluid
1.4.3 Functions Absorb force of impact (Cartilage & synovial fluid) Allow a variable degree of movement Articular cartilage Minimizes friction Transmits force to underlying bone (Distributes weight) Composition: Proteoglycan (PG) Collagen Cells Water Provides turgor & elasticity to articular cartilage Traps water (lubrication, flow of nutrients - joint flushing)
1.4.4 Causes of Injury: Trauma Joint instability Lubrication failure Infection Immune mediated
1.4.5 Response to Injury: 1st line of defense: Articular cartilage Limited response to injury Avascular, reinforced gel Little reparative capacity Chrondrocytes can't move very far Little remodeling occurs Few cells which can actually respond Only proteoglycan is continually turned over
2 Degenerative Joint Disease (DJD)
2.1 = Osteoarthritis
2.2 Destructive disease leading to loss of articular cartilage in one or multiple joints
2.3 Incorporates a variety of diseases with a common end stage
2.4 Initiating changes may be caused by: Trauma, Joint instability, synovial inflammation, ageing, etc.
2.5 Gross lesions identical: Cartilage breakdown & loss
2.6 Pathogenesis (Not entirely clear):
2.6.1 Primary event: Proteoglycan loss => Loss of lubrication => Collagen disruption Fibrillation of cartilage, Frays, clefts, Ulcers, Exposure of Bone, Eburnation, +/- Osteophytes & joint mice, brown/yellow discoloration, linear grooves, synovial hypertrophy & capsular fibrosis => Decrease in Tugor & Elasticity of Articular Cartilage
2.6.2 Failure of chrondrocytes to maintain balance b/w matrix break down & repair Degradative enzymes play a role: Matrix metalloproteinases (MMPs) Inhibitors normally control these enzymes Inhibitors are decreased in DJD => Activation Results in decreased proteoglycan => adverse effect on elastic properties of cartilage Release of cartilage breakdown products induces inflammation via local irritation Enzymes include: Gelatinases (digest type I & BM collagens) Collagenases (digest collagen) Stromelysins (digest non-collagenous proteins) Produced by chondrocytes, synoviocytes & inflammatory cells
3 Joint Inflammation
3.1 Arthritis
3.1.1 Classifications:
3.1.2 Infectious Farm animals & Horses (esp. young) Portals of entry include navel & GI tract => Bacteraemia Bacteria reach joints Haematogenously => Polyarthritis Multiple joints Other portals of entry: Traumatic inoculation Extension from bone or periarticular soft tissue (Dogs & Cats - One joint - trauma related) Acute Fibrinous Fibrinogen in blood vessels -> leaks -> fibrin Oedema, synovial villi thickened Early resolution is common, but fibrin may be converted to fibrous tissue (enlarged joint w/ restricted movement) Suppurative Fibrinosuppurative Outcomes: Infection cleared -> complete resolution Infection cleared -> healing by fibrosis Continued inflammation: Persistent, subclinical or intermittent Re-seeding of joint Failure to get rid of irritant bacterial products Chronic Lymphoplasmacytic Proliferative
3.1.3 Non-infectious Dogs & Cats Immune mediated disease Trauma Foreign material (urate crystals = gout (birds)) Often polyarthritis Two forms: 1) Erosive Immune process is JOINT centered Instability & luxation of multiple joints Ex. Rheumatoid arthritis: Small & toy breed Dogs (rare in Cats) Polyarthritis: Grey hounds Feline progressive polyarthritis Pathogenesis: Animal forms Abs against endogenous (unknown) Ag Abs IgG & IgM = Rheumatoid factor Complexes form & are depositied on articular surfaces Pannus formation (granulation tissue) => Cartilage erosion 2) Non-Erosive Joint NOT the primary target Immune complexes form elsewhere & settle in the joint Ex. Systemic lupus erythematosus (SLE) Dogs Anaemia, thrombocytopaenia, polymyositis, glomerulonephritis Chronic diseases (such as pyometra, otitis externa, IBD, endocarditis, UTI, fungal infections) can lead to immune complex deposition in joints No pannus & no villous hyperplasia of lining No cartilage destruction Idiopathic Drug associated Results from: Persistent antigenic material in the synovium Deposition of Ag/Ab complexes in the synovium
4 Developmental Disorders
4.1 Athrogryposis
4.1.1 Persistent congenital flexure of a joint in conjunction w/ muscle contraction
4.1.2 Causes: Inactivity or paralysis (in utero) Spinal dysraphism Intrauterine viral infections Toxic plants (poison hemlock)
4.2 Hip dysplasia
4.2.1 Common in Dogs (large/giant breeds)
4.2.2 Inherited disease in which joint laxity (instability) results in secondary degenerative joint disease (DJD)
4.2.3 Joint laxity -> Subluxation -> flattening of dorsal rim of acetabulum -> modeling of the acetabulum & femoral head
4.2.4 Contributing factors: Heredity, weight, over-exercise, low pelvic mass
4.2.5 Gross lesions: Articular cartilage (femoral head & acetabulum) Erosion &/or Ulceration Joint capsule/synovium Subchondral bone Shallow, wide acetabulum, Eburnation: Osteophyte formation Capsule stretched & thickened, w/ cartilage & bone formation w/in; round ligament may be ruptured
4.3 Osteochondrosis
4.3.1 A disorder of growth cartilage occurring in growing animals
4.3.2 Most species
4.3.3 Failure of Endochondral Ossification
4.3.4 Really a defect in cartilage growth (i.e. chrondrodysplasia)
4.3.5 Growth cartilage is not mineralized so is focally or multifocally retained An area of growth cartilage fails to undergo matrix calcification or vascular invasion, & therefore does not become converted to bone
4.3.6 Manifestations include thickened articular cartilage/cartilage flaps (osteochondritis dissecans or OCD), retained cartilage cores, bone cysts, angular limb deformity & DJD
4.3.7 Endochrondral ossification takes place at the: Physis Subarticular epiphyseal growth cartilage
4.3.8 Multifactorial: Trauma, genetic, rapid growth, ischaemia, nutritional
4.3.9 Idiopathic
4.3.10 Giant breeds: humoral head ( 4-8 months old) Horses: Distal tibia
4.3.11 Lesions bilateral in 70% of cases (But lameness often unilateral)
4.4 IVDD (Intervertebral Disk Disease)
4.4.1 Chrondrodystrophic Dogs: Predisposed to degenerative disk change from early age The nucleus pulpsus is replaced by chondroid tissue which mineralizes & fragments Annulus fibrosus secondarily degenerates
4.4.2 Non - Chondrodystrophic Dogs: Degeneration begins in the Annulus fibrosis Fibrosis of the nucleus (vs. chondroid degneration) Middle-aged Dogs affected & thoracolumbar area predisposed
4.4.3 Disk can herniate (if Annulus is intact - more common Non-chondrodystrophics) or Rupture through the Annulus (More likely in Chondrodystrophics) Extruded material is gritty. haemorrhagic or "cheesy"