Patterns of Disease: Bone Flashcards
-Main cell types. -The difference between traumatic and pathological fractures. -How to classify fractures. -The process of fracture repair- rigid, stable and unstable. -Possible complications of fracture repair. -Portals of entry of disease. -Specific examples of disease caused by direct entry of infection. -Structure of growth plates in young animals. -Why growth plates are so susceptible to infection. -Pathogenesis of embolic osteomyelitis. (37 cards)
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.
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.
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.
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.
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)
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.
FRACTURES
TRAUMATIC- Caused by excessive force.
PATHOLOGICAL- Abnormal bone is broken by minimal trauma or weight bearing. eg. Osteomyelitis, bone neoplasms, metabolic bone disease.
GROWTH PLATE FRACTURES
SALTER-HARRIS CLASSIFICATION
TYPES I-V.
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.
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.
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.
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.
GROWTH PLATE FRACTURE- SALTER-HARRIS TYPE V
Crushing of the growth plate. Compression fracture.
Complications can arise.
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.
THREE TYPES OF FRACTURE CLASSIFICATION
- Infraction
- Simple fracture
- Compound fracture
INFRACTION
Only cancellous/spongy bone is affected.
There is no cortical deformation.
Inflammation or necrosis predisposes to this kind of fracture.
SIMPLE FRACTURE
Involves cortical bone.
Skin is not broken- closed.
COMPOUND FRACTURE
Involves cortical bone.
Skin is broken, exposing bone to the environment- open.
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.
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.
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.
WOVEN BONE VS LAMELLAR BONE
Lamellar bone is organised and smooth.
Woven bone is disorganised new bone, with clumps of active osteoblasts visible.
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.
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.
