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Flashcards in Patterns of Disease: Bone Deck (37):
1

OSTEOCHONDROSIS LATENS

The first lesion seen in osteochondrosis.
Necrosis of blood vessels in the epiphyseal cartilage of the articular-epiphyseal complec (AE complex).
Overlying cartilage and subchondral bone are NOT yet affected.
Microscopic lesions only.

2

OSTEOCHONDROSIS MANIFESTA

When the ossification front reaches the area of necrosis caused by first lesions, there is a GROSSLY VISIBLE area of necrotic epiphyseal cartilage.
This lesion is highly vulnerable to further damage.

3

OSTEOCHONDROSIS DISSECANS

Clefts can form in the osteochondrosis lesion of the AE complex.
The overlying articular cartilage fractures, and a flap can form.
If the flap breaks off, it forms a 'joint mouse'.
Can cause pain, nonspecific synovitis, joint effusion.
Hyperaemic, hyperplastic synovium.

4

BONE CELLS

OSTEOBLASTS on surface form matrix and initiate bone mineralisation and resorption.
OSTEOCYTES in matrix detect changes in mechanical environment and signal to osteoblasts.
OSTEOCLASTS resorb bone.

Osteoclasts and osteocytes form a functional network sepearating the normal ECF from the bone ECF (Bone Tissue Fluid).
Osteocytes can detect changes in the fluid flow within the ECF.
Changes caused by altered stress and strain and/or microcracks (microfractures) are detected by osteocytes, which signal to osteoblasts to initiate bone formation or resorption.

5

MICRODAMAGE

'Stress' fractures may be preceded by excercise induced microdamage.
eg. Dorsal metacarpal disease (DMD) in racehorses seen due to reduced bone stiffness and periosteal bone formation in the dorsal cortex of the third metacarpal (cannon). 12% of animals will go one to develop stress fractures (though it is not sure if microcracks predispose to fractures)

6

BONE STRUCTURE

LONG BONE is comprised mostly of compact (cortical) bone, formed from osteons/Haversian systems.
These have a central/Haversian canal, with a blood vessel in that nourishes the bone.
Layers of compact bone surround the central canal as concentric lamellae, and osteocytes are contained within lacunae.
The blood vessels in the central canals are connected between osteons by Volkmann's canals, which run horizontally.
There is a central marrow cavity in the long bones, surrounded by cancellous (spongy) bone.

FLAT BONES are comprised of cancellous (spongy) bone, full of trabeculae, sandwiched between compact bone.
We see osteons in the compact bone, as above.

7

FRACTURES

TRAUMATIC- Caused by excessive force.
PATHOLOGICAL- Abnormal bone is broken by minimal trauma or weight bearing. eg. Osteomyelitis, bone neoplasms, metabolic bone disease.

8

GROWTH PLATE FRACTURES

SALTER-HARRIS CLASSIFICATION
TYPES I-V.

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GROWTH PLATE FRACTURE- SALTER-HARRIS TYPE I

Fracture is seen underneath the growth plate (on the long part of the bone- transverse physeal fracture).
The growth plate is not crossed.
Usually has few complications.

10

GROWTH PLATE FRACTURE- SALTER-HARRIS TYPE II

Fracture through the physis and metaphysis- like Type I but extending in to the long part of the bone.
The growth plate is not crossed.
Usually has few complications.

11

GROWTH PLATE FRACTURE- SALTER-HARRIS TYPE III

Fracture through the growth plate and epiphysis (end of the bone).
The growth plate is crossed, meaning complications are more likely to be seen.

12

GROWTH PLATE FRACTURE- SALTER-HARRIS TYPE IV

Epiphysis, growth plate and metaphysis are all fractured.
The growth plate is crossed, meaning complications are more likely to be seen.

13

GROWTH PLATE FRACTURE- SALTER-HARRIS TYPE V

Crushing of the growth plate. Compression fracture.
Complications can arise.

14

SALTER-HARRIS TYPES III-V

Complications are more likely to be seen with these types of fracture, as the growth plate is crossed/crushed.
This can damage the resting cell layer or the epiphyseal artery which nourishes the cells.
This can result in premature growth plate closure in young animals, and thus limb deformity.

15

THREE TYPES OF FRACTURE CLASSIFICATION

1. Infraction
2. Simple fracture
3. Compound fracture

16

INFRACTION

Only cancellous/spongy bone is affected.
There is no cortical deformation.
Inflammation or necrosis predisposes to this kind of fracture.

17

SIMPLE FRACTURE

Involves cortical bone.
Skin is not broken- closed.

18

COMPOUND FRACTURE

Involves cortical bone.
Skin is broken, exposing bone to the environment- open.

19

FRACTURE TYPES

TRANSVERSE- Fracture line is horizontally across bone.

OBLIQUE- Fracture line passes obliquely across bone.

SPIRAL- Caused by torsion, fracture line is 'spiral'.

COMMINUTED- Several small fragments of bone caused by fracture.

AVULSION- Caused by pull of ligament.

SEGMENTED- More than one fracture produces a segment of bone.

IMPACTED- Bone fractures then is pushed in to itself.

COMPRESSION- Bone is folded in on itself, causing bulging at the area of compression.

GREENSTICK- Only one side of the bone is broken. The other is bent.

20

STABLE FRACTURE

Fracture ends are immobilised, giving relative stability but no surgical fixture.
Immediate events of fracture- periosteum torn, fragments displaced, soft tissue trauma, haematoma formation.

21

STABLE FRACTURE REPAIR

Necrosis of bone and marrow can be seen at broken ends.
Growth factors are released by macrophages and platelets in the clot (in fracture site) and from dead bone.
These are important in stimulating proliferation of repair tissue.
STABILISES FRACTURE. Weak mechanical strength.

24-48 hours- proliferation of undifferentiated mesechymal cells and neovascularisation (angiogenesis)- cells and vessels penetrate the haematoma.
-Form a loose collagenous tissue.
-Mesenchymal cells come from the periosteum, endosteum and stem cells in the medullary cavity.
Weak mechanical strength.

At 36 hours, the first woven bone is visible. Weak mechanical strength.
Callus- unorganised meshwork of bone that forms after a fracture.
Primary callus of woven bone and possibly hyaline cartilage is seen after 4-6 weeks. This is moderately strong.

22

WOVEN BONE VS LAMELLAR BONE

Lamellar bone is organised and smooth.
Woven bone is disorganised new bone, with clumps of active osteoblasts visible.

23

CALLUS

EXTERNAL- formed by periosteum.
INTERNAL- formed between ends of fragments and in medullary cavity.

Should bridge the gap, encircle fracture site and stabilise area.
Develops to a large size to compensate for the fact that it is weaker than normal bone.
Will contain cartilage if blood supply is less than optimal; this means the callus is not as strong, but it will eventually undergo endochondral ossification.

24

SECONDARY CALLUS

Formed over months/years in stable fracture repair.
Woven bone is replaced with strong, smooth mature lamellar bone.
Callus can reduce in size over a period of years due to osteoclast action- this helps to restore the normal shape of the bone.
Mechanical strength returns to almost normal.

25

RIGID FRACTURE REPAIR

Involves surgical application of a device.
Ideally, there is CONTACT healing- direct osteonal bridging with no callus formation.
-If gap is less than 1mm, bone cells migrate from ends and form lamellar bone at a right angle to the fracture line (remodels). IDEAL.
-If gap is more than 1mm, woven bone forms and must be modelled in to lamellar bone. REALISTIC.

26

COMPLICATIONS OF FRACTURE REPAIR

-Inadequate blood supply can cause cartilage formation, or necrosis if there is anoxia (no bloody supply).
-Instability- excessive movement and tension predisposes to development of a fibrous tissue callus.
Fibrous tissue does not stabilise the fracture, and does not act as a template for bone formation (like cartilage does).
-Bony ends can move in a pocket of fibrous tissue to form a false joint- PSEUDOARTHROSIS.
-Other factors- bacterial infection, malnutrition, interposition of large fragments of necrotic bone or tissue (including muscle), age.

27

OSTEITIS

Inflammation of bone

28

PERIOSTITIS

Inflammation of periosteum

29

OSTEOMYELITIS

Involves the medullary cavity

30

SEQUESTRUM

Fragment of dead bone, isolated from blood supply and surrounded by a pool of exudate.

31

PORTALS OF ENTRY IN TO BONE

1. Direct.
2. Haematogenous.

32

DIRECT ENTRY IN TO BONE

Directly in through the periosteum and cortex.
Via trauma that may or may not break the bone.
Via direct extension eg. from periodontitis, otitis media- inflammation extends from soft tissue to bone.

33

DIRECT EXTENSION

"Entry in to the bone from a contagious focus of infection"
eg. Actinomyces bovis- causes lumpy jaw in cattle.
Introduced in to oral mucosa through penetrating injury.
Invades the bone (maxilla/mandible), causing severe suppurative and fibrosing myelitis.

34

HAEMATOGENOUS ENTRY IN TO BONE

Blood gains access to marrow cavity of diaphysis and metaphysis by nutrient foramen.
In young animals, access is gained through the physis/AE complex in the epiphyseal artery and it's small branches that cross the epiphyseal cortex.

35

BONE INFECTION

Via haematogenous spread.
Haematogenous bacterial osteomyelitis is common in foals, neonatal ruminants and pigs.
Bacterial- purulent/suppurative.
Exudate in the medullary cavity increases pressure and can compress vessels, causing thrombosis and infarction, with increased bone resorption (osteoclasts).
Perinataltransmission is of umbilical or oropharyngeal origin.
Typically at zone of vascular invasion of the growth plate, either at the physis OR the AE complex.

36

WHY DOES THE ARTICULAR EPIPHYSEAL COMPLEX CONTRIBUTE TO INFECTION AT GROWTH PLATES?

The AE complex is the point where articular and epiphyseal (growing) cartilage meet.
Capillaries make sharp bends/loops to join the medullary veins at the AE complex or metaphyseal growth plate.

FACTORS CONTRIBUTING TO INFECTION AT GROWTH PLATE:
-Slow flow and turbulence of blood in larger descending limbs.
-Lower phagocytic capacity.
-Discontinuous endothelial cells.
-No anastomoses, so thrombosis results in infarction, which favours bacterial localisation.

37

EMBOLIC OSTEOMYELITIS

Embolus lodges in capillary loop at metaphysis.
This causes inflammation and lysis of metaphyseal bone and growth plate cartilage.
This can cause mechanical instability; the periosteum responds by producing woven bone (reactive).
Exudate/pus from embolus/microabscess can lyse the cortex at it's thinnest point- METAPHYSEAL CUT BACK ZONE.
Exudate can then extend in to the periosteum, causing inflammation- periositis.
Exudate can also extend to joint surface (arthritis) and through sinus on to skin surface.