Bone-Joint Pathology Review

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Bone-Joint Pathology Review
2010-12-05 09:28:41
Bone Pathology

VPTH 602 Bone Path Review
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  1. Endochondral Ossification involves
    Cartilage template
  2. In Endochondral Ossification, centers of ossification develop with:
  3. Major growth of long bones occurs at
    metaphyseal growth plates (Physes)
  4. Mineralization of cartilage matrix occurs so that:
    vascular ingrowth can occur, bringing in osteoclasts and developing osteoblasts
  5. primary trabeculae (spongiosa) on histo are
    thin seams of pink osteoid deposited on the mineralized cartilage spicules
  6. Woven Bone is:
    Primary spongiosa produced very rapidly
  7. Lamellar Bone is modelled
    deeper in the growth plate; produced from woven bone and inner cartilage spicules
  8. Lamellar Bone is more organized,
    less cellular and stronger than woven bone
  9. Where can woven bone be found
    Trabecular (cancellous) or Compact (osteonal) bone
  10. A "tide line" of mineralization anchors articular cartilage into the subchondral bone when
    the epiphyseal growth plate begins to close
  11. Loss of overlying cartilage due to DJD results in
    sclerosis (thickening) of Subchondral Bone
  12. Intramembranous ossification occurs without
    cartilage template
  13. Intramembranous bone formation occurs
    within a cellular mesenchyme from which osteoprogenitors and osteoblasts develop
  14. Compact Bone is predominantly found
    in the cortex of long bones and bears the brunt of forces on the diaphysis
  15. which type of bone surrounds a haversion canal
    well organized concentric lamellae of compact bone
  16. Trabecullar bone consists of
    interconnected struts that distribute forces
  17. Where is trabecular bone concentrated?
    within epiphysis and metaphyses
  18. Trabecular bone serves as reserve for
    Calcium and Phosphorus
  19. Which type of bone is preferentially resorbed when minerals are needed?
  20. Lamellar bone can be both
    Trabecular and Compact; characterized by nice alignment of well-mineralized collagen fibers; it is much stronger than woven bone
  21. After insult, what kind of bone is laid down first?
    woven bone is produced and can be present within both compact and trabecular bone. It will later be modeled (during “quiet, restful times”) to lamellar bone.
  22. Woven bone is
    Produced faster, inherently weaker, less organized/ more cellular, and present in compact bone and trabecular bone
  23. Defects in bone formation can have different consequences depending on
    location; I.e. Palatoschisis exposes nasal cavities and results in aspiration pneumonia
  24. Equine Wobbler's Syndrome
    disease results from malformations of the cervical vertebrae. These are irregular bones with multiple centers of ossification that involve both endochondral ossification (facets, vertebral bodies) and intramembranous bone formation (laminae, transverse processes, etc). Can compress spinal cord if severe enough
  25. Osteochondritis Dessicans (OCD)
    Dissecting cartilage flap, results in 1)Much more severe joint instability2)Much more inflammation (exposure to the well-vascularized subchondral bone -> blood/serum/fibrin, non-suppurative inflammatory cell exudation)3)More rapid and advanced DJD (degenerative osteoarthritis = degenerative joint disease)
  26. Osteochondrosis
    lesion characterized by roughened articular cartilage
  27. Joint Mouse
    OCD lesion can fragment away from the bone, leading to a free-floating osteochondral fragment
  28. Pathogenesis of OCD
    The defect in endochondral ossification will -> a FOCAL retained cartilage core-> results in a “weak point” in the articular epiphyseal complex and can result in cartilage degeneration and the formation of a fissure -> dissecting cartilage flap
  29. Difference b/w Osteochondrosis and osteochondritis dessicans
    with Osteochondritis dissecans, there is formation of a dissecting cartilage fissure/flap
  30. During Growth, Disorders of Bone resorption result in a
    Growth Retardation Lattice
  31. Growth Retardation Lattices
    an osteosclerotic bone dz that results in increased bone density
  32. Acquired Causes of Growth Retardation Lattices
    Defects in Osteoclast Resorption:Acquired:InfectiousBVD and CDV -> kills osteoclasts -> retained primary trabeculaeToxicLead -> kills osteoclast ->retained primary trabeculae, “lead line”
  33. Congenital causes of Growth Retardation Lattices
    Congenital:Osteopetrosis (autosomal recessive mutation in black angus cattle) -> defect in osteoclasts -> entire medullary cavity is filled with mineralized primary trabeculae
  34. Osteoporosis
    Caused by Calcium deficiency, Protein Calorie Deficiency, Disuse Atrophy, Chronic Glucocorticoid excess
  35. Osteopenia
    DECREASED BONE DENSITY OF MASS (structure of bone is normal, AMOUNT of bone is REDUCED)
  36. Osteoporosis Definition
    CLINICAL SYNDROME of REDUCED BONE MASS manifested by BONE PAIN and PATHOLOGIC FRACTURESResults in THINNING and INCREASED POROSITY of bone (Trabecular >> Osteonal bone).
  37. With Osteoporosis, what happens to osteoblasts and trabeculae
    Trabeculae are thin and sparse; osteoblasts are flattened rather than plump and polygonal in regions of new bone formation
  38. Important causes of Rickets and Osteomalacia
    Failure of mineralization due to Vit. D Deficiency, Phosphorous Deficiency
  39. Sites affected by Rickets and Osteomalacia In Young animals:
    1) Cartilage growth plates- sites of Endochondral Ossification2) Sites of bone turnover modeling: immature woven -> lamellar bone remodeling: normal continual physiologic turnover
  40. Sites affected by Rickets and Osteomalacia In mature animals
    Growth plates have closed, so only sites of bone turnover are affected; clinical signs of pain and pathologic fractures take longer to develop and manifest; exception= layer hens due to constant demand for Ca
  41. Because you cant mineralize cartilage growth plates or sites of new bone formation due to deficiencies, Rickets results in
  42. rickets and renal dz
    Vit D production is lost, thus young animals in renal failure can develop rickets and fibrous osteodystrophy
  43. Fibrous Osteodystrophy
    Persistent Elevation in PTH; Renal fail -> high phosphorous; Nutritional dietary excess -> high phosphorous; primary causes less common
  44. Pathogenesis of renal fibrous osteodystrophy
    Chronic Renal Failure -> Retained PO4 -> CaPO4 crystallization -> decreased iCa levels -> detected by PT glands -> production of PTH and bilateral PT hyperplasia -> stimulation of OCL bone resorption -> fibrous replacement due to decreased OB bone formation and differentiation of mesenchymal cells to fibroblasts (instead of OB)
  45. appearance of jaw with fibrous osteodystrophy
    thick and pliable with wiggly teeth- rubber jaw
  46. Other signs apparent FO
    accompanying signs of uremia; sublingual ulcers, uremic mineralization of pleura and endocardium, bilateral parathyroid gland hyperplasia, shrunken, firm, pitted kidneys
  47. Fracture repair Part 1
    Tearing of the periosteum & displacement of fracture ends with adjacent soft tissue trauma;Hemorrhage with hematoma & clot formation by fibrin polymerization
  48. Frature Repair Part 2
    1)Impaired blood flow -> Necrosis of fracture ends2)Release of cytokines & growth factors by platelets & macrophages within the blood clot (TGF-B, BMP, PDGF) & necrotic cells from damaged tissue 3) Proliferation of undifferentiated mesenchymal cells (stem cells) and granulation tissue (new capillaries embedded within a loose structural network of fibrous tissue)
  49. Fracture Repair Part 3 (within 3 days)
    Differentiation of mesenchymal stem cells into osteoblasts Metaplasia of granulation tissue to cartilage and boneFormation of woven bone and primary fracture callus Establishment of the primary fracture callus can take up to 4-6 weeks Consists of extensive periosteal and endosteal woven bone with periosteal vessels Low O2 tension will result in hyaline cartilage formation -> later undergoes endochondral ossification
  50. Articular fractures can heal with good return to fxn and minimal DJD with:
    minimally displaced fractures, with good sx anatomic reductions and healing
  51. What may occur from fractures that have poor vasculature, are infected, or are severely displaced with excessive motion
    Osteomyelitis and sequestra, fibrous non-union, and/or degenerative osteoarthritis
  52. what is a sequestrum
    dead bone fragment
  53. Osteomyelitis
    Inflamm. of bone most likely due to:Bacterial infxn: Coliforms, Salmonella, Strep zooepidemicus (neonates) Actinomyces bovis, Staphylococcus auereus, etc (adults)Fungal infxn: Coccidioides immitis, Blastomyces dermatitidis, Aspergillus, Candida
  54. Infections in bone can result in
    infection of joint (and vice versa)
  55. Most common routes of entry in neonates
    Umbilicus, Resp. Tract, GI Tract
  56. In Lg Animal Neonates, septic arthritis and osteomyelitis are:
    fairy common and typically occur within growth plates, easily entering joint
  57. Lumpy Jaw
    Caused by Actinomyces Bovis- Pyogranulomatous osteomyelitis with osteoproliferation and osteolysis; aggressive bone infxns can resemble neoplastic processes
  58. Diskospondylitis
    infection of the intervertebral disk and vertebral bodies; typically result from prostatitis and Brucella infection (dogs, pigs)
  59. Degenerative Osteoarthritis
    often final pathway for:infectious arthritis, Malarticulations from fractures or OCD, non-infectious inflamm. arthritis
  60. Imp't features of Chronic Degen. arthritis (from OCD lesion)
    Cartilage thinning, erosion, and ulceration -> EBURNATION (when there is bone on bone contact) and “polishing”Subchondral bone sclerosis and lippingPeriarticular osteophytosisSynovial membrane villous hyperplasiaJoint capsular fibrosis
  61. Canine Hip Dysplasia
    Genetic predisposition in German Shepherd (and some other large breeds of) dogsResults in increased coxofemoral joint laxity -> Degenerative osteoarthritis (DJD) and hindlimb lameness
  62. Cardinal Signs of DJD (coxofemoral joints)
    Loss of joint space from cartilage atrophy, erosion and ulcerationFlattening of the femoral head & shallow acetabular cupsSubchondral sclerosis and “lipping”Periarticular osteophytosis
  63. Ankylosis
    self-fusion of a joint; can occur from chronic, severe DJD
  64. **Osteosarcoma
    most common primary bone tumor in the appendicular skeleton of large and giant breed dogsAgressive neoplasm with rapid progression and met.
  65. Osteosarcoma characterized by:
    1)Osteolysis2)Osteoproliferation3)Production of mineralized or non-mineralized bone matrix (osteoid) by neoplastic osteoblasts 1 and 2 can be seen on X-ray; 3 requires histopath