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SYSTEMIC PATHOLOGY - 1 > 12 - Bone II > Flashcards

12 - Bone II Flashcards

1
Q

What are the 4 types of pathologic processes that bone is susceptible to? (similar to other tissues and organs)

A
  1. Alterations of growth
  2. Circulatory disorders
  3. Inflammation and repair
  4. Degeneration and necrosis
    *limited range of reactions to injury and mechanisms of repair
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2
Q

What are the different types of alterations of growth?

A
  • Aplasia
  • Hypoplasia
  • Atrophy
  • Hyperplasia
  • Neoplasia
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3
Q

What are the 2 types of circulatory disorders?

A
  • Hemorrhage
  • Ischemia
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4
Q

What are the 4 generalities about the reaction of bone to injury and disease?

A
  1. 2 processes: removal of damaged bone (lysis or resorption) AND production of new bone
  2. Injury to periosteum (and endosteum) will usually be followed by formation of periosteal (and endosteal) new bone
  3. Bone density will CHANGE in response to changes in use
  4. Bone is effected by any disease involving abnormal calcium and phosphorus metabolism
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5
Q

What is the definition of a fracture?

A
  • Break or rupture in bone
  • Common occurrence
  • PHYSICAL discontinuity in a bone resulting in instability and pain
    o May lead to impaired movement
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6
Q

What is the impaired movement ‘types’ that may occur due to a fracture?

A
  • Lameness
  • Immobility
  • Recumbency
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7
Q

Descriptive terms used in radiology and surgery

A
  • Incomplete (green stick, hairline) vs. comminuted
  • Spiral vs. transverse vs spiral vs. oblique
  • Compound: fractured bone being exposed to air! (possibility of infection)
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8
Q

When are 2 times that fractures occur? (EXAM!)

A
  1. Normal bone fractures due to excessive force=TRAUMATIC FRACTURE
  2. Abnormal bone fractures under normal force=PATHOLOGICAL FRACTURE
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9
Q

What is fractured repair?

A
  • Healing of fractured bone
  • Divided into 5 phases
  • Arbitrary (how we explain it)
  • OVERLAP and CONCURRENT
  • Summary of COMPLEX events
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10
Q

Fracture repair is divided into 5 phases

A
  1. Injury and inflammation
  2. Organization of the hematoma
  3. Callus formation: external and internal callus
  4. Callus remodeling
  5. Callus modeling
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11
Q

First phase of fracture repair: injury and inflammation, ‘3 events’ that occur

A
  • Tearing of periosteum and endosteum
  • Rupture of blood vessels of the bone
  • Surrounding soft tissue injury
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12
Q

What do the 3 ‘events’ of phase I of fracture repair result in?

A
  • Ischemic necrosis of bone at fracture lines and associated marrow
  • Formation of hematoma
  • Inflammation
  • *promote IMMEDIATE activation and recruitment of platelets, macrophages, and other leukocytes=all release growth factors
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13
Q

Second phase of fracture repair: organization of hematoma

A
  • Hematoma between bone fragments begins to organize within 24-48hrs
  • Activation of undifferentiated mesenchymal (stem) cells of periosteum, endosteum and bone marrow
    o Invade hemostoma
  • Endothelial cells proliferate to form new blood vessels =neovascularization
  • *’soft’ callus
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14
Q

What is a ‘callus’?

A
  • Mass of exudate and connective tissue that forms around a fracture during repair
  • *Internal and external
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15
Q

External callus

A
  • More substantial (easily noticed) with the periosteum making an important contribution
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16
Q

Third phase of fracture repair: callus formation, distant from fracture gap

A
  • Blood supply is adequate and oxygen tension is HIGH (favourable environment)
  • Undifferentiated mesenchymal cells become osteoblasts that produce woven bone
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17
Q

Third phase of fracture repair: callus formation, near the fracture gap

A
  • Blood supply is poor and oxygen tension is low (‘poor’ environment (low pH))
  • Undifferentiated mesenchymal cells become fibroblasts and chondroblasts
  • *Cartilage produced by chondroblasts is later REPLACED by woven bone via endochondral ossification
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18
Q

Internal callus

A
  • Produced by endosteum
  • Formed similar to external callus
  • Smaller
  • May temporarily occlude medullary space
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19
Q

Third phase of fracture repair: callus formation

A
  • May begin within 24 hours
  • Bone production begins within 36hrs
  • Radiographic evidence possible by 2 weeks
  • *under favorable conditions it takes 4-6 weeks for primary callus to be replaced by ‘bony callus’
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20
Q

Fourth phase of fracture repair: callus remodelling

A
  • Woven bone is replaced by lamellar bone
  • Compact bone formed in cortex
  • Cancellous bone is formed in the metaphysis and diaphysis
  • *resorption and formation are about equal=represents remodelling
  • *cutting cones performs osteoclastic tunneling (points towards the fracture)
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21
Q

Time for callus formation and remodelling varies with

A
  • Age
  • Health and nutrition
  • Fracture type and location
  • Other injuries or infection
  • Method and quality of fixation, if any (ex. internal or external fixation)
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22
Q

Fifth phase of fracture repair: callus modeling

A
  • Restoration of fractured bone to its original form and function
  • *reduction in size of callus
  • *sculpting of bone in response to stresses of weight bearing and muscle pull
  • Months to years!
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23
Q

What are the three common complications of fracture repair?

A
  1. Nonunion
  2. Delayed union
  3. Malunion
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24
Q

Nonunion fracture repair

A
  • Failure of fragments of a fractured bone to heal (to become fused with bone)
25
Q

What is nonunion fracture repair commonly caused by?

A
  • Inadequate blood supply
  • Instability
  • Infection
  • Fragments of necrotic bone or soft issue
  • Other underlying disease (pathological fracture!)
26
Q

Delayed union fracture repair

A
  • Fracture that takes LONGER than normal to heal
  • *time required to heal and criteria is VARIABLE
27
Q

It can be difficult to differentiate between non-union and delayed union. What are ‘2 criteria’ used to decide on a non-union?

A
  • Lack of progress for 3 months after you expect the bone to heal (radiographically)
  • Lack of healing after 6 months will likely remain unhealed
28
Q

Malunion fracture repair

A
  • Healing of fracture bone that results in abnormal alignment (DEFORMITY!)
29
Q

What can malunions result in? (3)

A
  • Shorter limb due to fusion of overriding fragments
  • Axial deformities (or crooked/bent limbs)
  • Rotational deformities (twisted limbs)
30
Q

What is the physis a site of?

A
  • Longitudinal growth in endochondral bones
    o Injury can affect longitudinal bone growth
  • *Temporary structure composed of hyaline cartilage
    o Weaker and more easily injured
31
Q

When is the physis the widest or narrowest?

A
  • Widest: when growth is most RAPID
  • Narrowest: when growth SLOWS
32
Q

When does growth at the physis stop?

A
  • When it is entirely replaced by bone
  • *closure of growth plate=MARKS SKELETAL MATRUITY
33
Q

What are some of the disorders associated with the physis (5)?

A
  1. Physeal/growth plate fractures
  2. Growth retardation lattices
  3. Growth arrest lines
  4. Premature closure
  5. Osteochondrosis/osteochondritis
34
Q

What can be used to classify growth plate injuries?

A
  • SALTER-Haris classification
  • 5 types
  • lower the number=better the prognosis
  • *useful to communicate the nature of injury and PREDICTING PROGNOSIS
35
Q

SALTER-Harris classification

A
  1. S: straight across (separated or slipped)
  2. A: above (or away from the joint)
  3. L: lower (into the joint)
  4. TE: through everything
  5. R: rammed (ruined or crushed)
36
Q

What is an example of a Salter-Harris type I fracture?

A
  • capital femoral physeal fractures in cats
37
Q

Capital femoral physeal fractures of cats

A
  • Fairly common
  • Trauma? But sometimes without trauma?
    o UNCERTAIN PATHOGENESIS
  • *histologically: fracture physis is thickened with irregularly arranged chondrocytes=physeal dysplasia
38
Q

Which cats are most affected with capital femoral physeal fractures?

A
  • Young (4-24 months), overweight, neutered males (delayed physeal closure times)
    o May lead to physeal dysplasia
    o Open longer than normal (ex. after 7-9 months)
    o 24-38% of affected cats develop BILATERAL disease
39
Q

What are growth retardation lattices (GRLs) typically detected in?

A
  • Aborted, still born or neonatal animals
40
Q

What are growth retardation lattices?

A
  • Thin to wide bands of increased bone density (osteosclerosis) in the metaphyses, PARALLEL to the physes (also within epiphyses)
41
Q

What do GRLs represent?

A
  • Areas of impaired osteoclastic activity leading to retention of LONGITUDINAL trabeculae of primary spongiosa
  • *FAILURE OF REMODELLING
42
Q

GRLs are a nonspecific change and can caused by a WIDE variety of insults. What are some examples?

A
  • utero infection of fetal calves with BVD
  • canine distemper virus infection in growing puppies
  • exposure to LEAD in any developing or growing animal
43
Q

Where are growth arrest lines (GALs) typically detected?

A
  • Young, growing animals
  • *debilitating disease OR general malnutrition can retard growth and produce GALs
44
Q

What are GALs?

A
  • Linear lesions of osteosclerosis in metaphysis parallel to the physis
    o Line is because they are at RIGHT ANGLES to normal bone
  • Represent TRANSVERSE (vs. longitudinal) trabeculae of bone
45
Q

What are GALs a result of?

A
  • Period of retarded or arrested longitudinal growth
  • *layers of transverse trabeculae are carried into the metaphysis if growth resumes
46
Q

What is the importance of recognizing GRLs and GALs?

A
  • Consequence of a CHRONIC, UNDERLYING DISEASE CONDITION
    o NOT scute or spontaneous change
  • No ‘direct significance’ to the animal
47
Q

Grossly what do GALs and GRLs look like?

A

*alternating patterns of increased and decreased bone lattices

48
Q

If the premature closure of the physis is focal, what will it result in?

A
  • Altered shape of growing bone
49
Q

If the premature closure of the physis is complete, what will it result in?

A
  • Abnormally SHORT bones
50
Q

What are some known causes of premature closure of growth plates?

A
  • Trauma
  • Vit A toxicity
  • Manganese deficiency
  • Radiation
  • *multiple and interrelated factors, may depend on species and location of lesion
51
Q

What else may cause localized physeal closure?

A
  • Damage to epiphyseal vessels nourishing the proliferative zone of the physis
  • Feeding moldy cereal straw to pregnant cows: congenital spinal stenosis in western Canada
52
Q

Osteochondrosis or osteochondritis (EXAM): definition

A
  • Focal or multifocal failure (or delay) of endochondral ossification resulting in LOCALIZED thickening of hyaline cartilage
53
Q

Where might osteochondrosis occur?

A
  • Physeal or articular areas of endochondral ossification
    o Articular-epiphyseal (AE) complex
54
Q

AE complex

A
  • At end of bone (epiphysis) there is still some growth
    o Should have endocardial ossification
    o When failed=chondrolysis
55
Q

What might result in osteochondrosis?

A
  • Pain and lameness
    o Retained cartilage is not as stable as bone=subject to injury
56
Q

What are osteochondrosis and osteochondritis used to identify clinically?

A
  • Variety of manifestations and sequelae of presence of thickened cartilage
57
Q

What is an example of osteochondrosis in dogs?

A
  • Ununited anconeal process
    o Failure of anconeal process (secondary center of ossification) to fuse with the ulna
58
Q

What is an example of osteochondrosis in pigs?

A
  • Relatively common, but now rare
  • GENERALIZED condition that is most common and easily diagnosed around joints
  • Ex. Toxic amounts of Vit A=full closure of growth plate in humerus
    o Ex. mixing error at feed supply, polar bear liver
59
Q

What is an example of osteochondrosis in horses?

A
  • Physitis
    o Inaccurate pathological diagnosis
    o Generalized disease of YOUNG horses characterized by thickening an dysplasia of physes of certain long bones

SYSTEMIC PATHOLOGY - 1 (24 decks)

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