Vet Path B 250-215 Bone Anatomy, Development Repair

Front 1

Back 1

Front 2

Back 2

Front 3

Osteoblast

Back 3

Bone cell that produces osteoid

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Label

Back 4

Front 5

Osteoid

Back 5

ECM matrix produced by osteoblasts

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Osteocytes

Back 6

Trapped osteoblasts

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Lacunae

Back 7

Spaces in calcified bone containing osteocytes

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Canaliculi

Back 8

Small canals linking lacunae with trapped osteocytes

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Haversian systems

Back 9

3D structure or concentric rings within compact bone

Front 10

Osteoclasts

Back 10

Cells (multinucleated) that remodel bone
- monocyte/macrophage lineage

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Periosteum

Back 11

Connective tissue membrane covering bone

Front 12

Compact bone (type of lamellar bone - mature)
- brief description

Back 12

Outer layer of cortex of all bones
- filled with densely packed Haversian systems

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Spongy or cancellous bone (type of lamellar bone - mature)

- what is it?
- where's it found?

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Spicules of bone arranged as a trabeculae meshwork or lattice
- form a network within the ends of long bones and core of short and flat bones
- medullary cavity (spaces filled with bone marrow)

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Bone & skeleton
- 3 main functions

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Strength: structure and support
Mobility: movement
Mineral reservoir

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Main components of cartilage

Back 15

Cells: chondrocytes
ECM (collagen proteoglycans )
water (80-90%)

***NO bvs, lymphatics, nerves***

Front 16

Main components of bone

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Cells: osteocytes, osteoblasts, osteoclasts
ECM (mineral, collagen, GAGs)

**Blood vessels, lymphatics, nerves**

Front 17

Collagen resists ? strain

Back 17

? resists tensile strain

Front 18

Proteoglycans resist ? strain

Back 18

? resists compressive strain

Front 19

2 main types of bone

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Woven (immature)
Lamellar (mature)

Front 20

2 types of lamellar bone

Back 20

Compact (cortical)
Cancellous (trabecular, spongy)

Front 21

Immature bone
- where found (3)?

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Confined to areas of rapid bone formation
- developing skeleton
- fracture callus
- bone diseases (eg hormonal, tumours)

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2 types of ossification

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Intramembranous ossification
Endochondral ossification

Front 23

2 sites of intramembranous ossification

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Bone development at;
- flat bones
- periosteal surfaces (is this repair?)

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Endochondral ossification
- 4 overall steps

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Chondrocyte proliferation and hypertrophy
Periosteal invasion bringing blood vessels and osteogenic cells
Woven (immature) bone deposited
Lamellar (mature) bone replaces woven bone

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Articular cartilage provides ? growth

Back 25

___ cartilage provides epiphyseal growth

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Growth plate cartilage provides ? and ? growth

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___ ___ cartilage provides metaphyseal and diaphyseal growth

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Articular epiphyseal complex = ____
Metaphyseal growth plate = ____

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___ = (epiphyseal) growth plate
___ = physis

Front 28

Define modelling
- what are the two types

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Modelling is the processes leading to changes in size and shape of bone
- primary remodelling
- secondary remodelling

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Define stress

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___ is the force exerted on bone

Front 30

Define strain

Back 30

__ is the effect of the stress on bone

Front 31

What are the two types of strain on bone?
- where do they act?
- which cell types are most active?

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Tensile strain:
- convex, osteoblastic
Compressive strain:
- concave, osteoclastic

Front 32

Primary remodelling
- occurs when?

Back 32

___ remodelling occurs during growth and is the replacement of young bone with adult bone

Front 33

Secondary remodelling
- occurs when?

Back 33

___ remodelling continues throughout life and is the replacement of old bone with new bone

Front 34

Molecules that allow osteoblasts and osteoclasts to communicate (coupling)?

Back 34

RANK-L and RANK-R

Front 35

Why does hypercalcaemia occur during some cancers?
- associated with what cancers in the dog?

Back 35

Some tumour cells secrete a soluble form of RANK-L triggering osteoclastic activity.


Some tumours secrete a PTH-like molecule triggering Incr. osteoclast activity
- commonly lymphoma & anal gland adenocarcinoma

Front 36

3 main molecules controlling bone composition

Back 36

VitD
PTH
Calcitonin

Front 37

Actions of VitD in two main sites

Back 37

Intestine
- incr. Ca and P absorption
Bone & cartilage
- incr mineralisation

Front 38

__ are the major sensors of variation in plasma calcium

Back 38

Parathyroid gland cells are the major sensors of plasma ___

Front 39

When plasma calcium falls, ___ synthesis and release is enhanced

Back 39

When ___ falls, PTH synthesis and release is enhanced

Front 40

Actions of PTH at 2 main sites

Back 40

Kidney
- incr tubular resorption of Ca and tubular excretion of P
- incr. VitD active form
Bone
- incr osteoclast numbers and activity

Front 41

___ is the physiologic antagonist of PTH
and is secreted by ___

Back 41

Calcitonin is the physiologic antagonist of ___
and is secreted by the parafollicular (C) cells of the thyroid

Front 42

Actions of calcitonin at 2 main sites

Back 42

Kidney
- decr. tubular resorption of Ca & P
Bone
- decr osteoclast activity

Front 43

When plasma calcium rises, ___ secretion is enhanced.

Back 43

When ___ rises, calcitonin secretion is enhanced

Front 44

Fractures repair by the process of __ __

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Fractures repair by the process of secondary intention (edges not in close apposition)

Front 45

List the stages of fracture repair
- include duration

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Reactive
- haematoma (immediate)
- granulation (within 48h)

Reparative
- primary callus (after 7d, max 3w)
- secondary callus (mo - y)

Remodelling (mo - y)

Front 46

Discuss organisation and granulation tissue formation in fracture healing

Back 46

Within 48h,
capillaries & fibroblasts enter haematoma
produce granulation tissue
- has potential to undergo metaplasia to cartilage and bone

Front 47

What comprises a primary callus in fracture healing

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Fibrous tissue, cartilage, woven bone

- osteoprogenitor cells in periosteum and endosteum produce external and internal calluses

- woven bone laid down in these calluses

- bridge forms between ends

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What comprises a secondary callus in fracture healing

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Endochondral ossification of cartilage
- woven bone is replaced by lamellar bone

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Factors (8) contributing to delayed union of bone fractures

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Movement (instability, mechanical stress)
Infection
High glucocorticoids
Poor blood supply
Displaced bone ends
Necrotic fragments in bone
Foreign body at fracture site
Underlying primary bone disease

Front 50

Factors (2) causing non-union of bone fractures

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Fracture ends united by scar tissue

Poorly differentiated fibrocartilage over bone ends

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Likely 2 fates of necrotic bone at a fracture site

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May be incorporated into the callus and repopulated by osteoblasts and osteocytes providing blood supply re-established. Eventual remodeling

Persist as necrotic sequestrum, cyst or abscess

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Pseudoarthrosis

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Can form after fracture repair with poorly differentiated fibrocartilage over bone ends and central cavity lined by synovial cells

Front 53

Effects on bone of increased mechanical stress in
- young
- adult

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Young: increases metaphyseal trabecular bone & thickness of cortices

Adult: Reduces remodelling, conserves bone present

Front 54

Effect of mechanical reduced stress on adult bone

When is this important?

Back 54

Increases resorption -> decreased bone strength

- imp when bone immobilised, weightless, prolonged disuse

Front 55

What is the weakest part of a long bone in the growing animal?

Back 55

The growth plate

Front 56

What is epiphyseolysis?

When can it occur?

What is the prognosis?

Back 56

Complete seaparation of epiphysis from metaphysis in growing animal
- dt horizontal shear forces

Prognosis is good if the proliferative zone and blood supply remain intact.

Front 57

Why can epiphyseolysis at the proximal femur result in avascular necrosis

Back 57

Greater risk of vascular damage as the nutrient vessels run along the neck of the femur

Front 58

How can an angular limb deformity result?

Back 58

Damage to blood supply and/or chondrocytes in the proliferation zone on one side only of a growth plate

Front 59

What are exotoses

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Localised outgrowth of new bone beneath the periosteum dt periosteal damage leading to activation & proliferation of osteoblasts