Patterns of Disease- Bone Flashcards
Osteochondrosis latens
first lesion- necrosis of blood vessels in the epiphyseal cartilage of the articular epiphyseal complex (AEC)
At this stage, overlying cartilage and underlying subchondral bones aren’t affected–> microscopic lesion
Growing cartilage has blood vessels and at this stage, osteochondrosis in the AEC involves necrosis (this is the earliest lesion you can see histologically)
Osteochondrosis manifesta
When the ossification front reaches the area of blood vessel necrosis, there is a grossly visible area of necrotic epiphyseal cartilage.
osteochondrosis manifesta is the grossly visible area of necrotic epiphyseal cartilage.
this lesion is highly vulnerable to further damage– the cartilage hasn’t ossified!
Manifesta, though grossly visibile, is unlikely to be showing clinical signs.
Osteochondrosis dissecans
flaps of cartilage due to osteochondrosis
OCD: clefts can form in the osteochondrosis lesions of the AEC
overlying articular cartilage fractures can form and break off= “joint mouse”
can be pain due to bone and joint inflammation, joint effusion, non-specific synovitis
Bone cells
osteoblasts (on surface): cuboidal if active, flattened if non-active; form matrix, initiate bone mineralization and bone resorption.
Osteocytes (in matrix): detect changes in mechanical environment and signal to osteoblasts. Act like sensors; can detect changes in fluid flow within ECF
Osteoclasts: big multinucleate cells in lacunae- resorb bone.
Osteocytes and osteoblasts=a functional network separating ECF bathing the bone from the general ECF.
Changes caused by altered stress, strain and/or micro-cracks–>osteocytes detect and signal to osteoblasts to initiate bone formation or resorption.
Microdamage
stress fractures may be preceded by exercise-induced microdamage
e.g. dorsal metacarpal disease (DMD) in racehorses= reduced bone stiffness and periosteal (extra-bone) formation in dorsal cortex of the third metacarpal (canon) bone.
DMD: 24-70% of racehorses, 12% develop stress fractures
Not certain in microcracks predispose to fracture–> narrow margin between adapting to exercise and pathology (micro damage).
Complications of fracture repair
bony ends can move in a pocket of fibrous tissue to become a false joint (pseudo arthrosis)- worst case scenario
Other factors: malnutrition, bacterial osteomyelitis (particularly of compound fracture), interposition of large fragments of necrotic bone or soft tissue (including muscle).
Fractures
traumatic fracture= due to excessive force
pathological fracture= abnormal bone broken by minimal trauma or normal weight bearing e.g. osteomyelitis, bone neoplasms, metabolic bone disease
i.e. osteosarcoma- in dogs, usually start within marrow and erode their way out of the cortex
Fracture: growth plate
weak sites in young animals
from nearest epiphysis: resting zone (chondrocytes), proliferating zone (interstitial growth), hypertrophic zone (cartilage calcification), zone of resorption, zone of ossification (metaphysis).
Salter-Harris classification of growth plate fractures
Type I: transverse fracture through the growth plate (physis)
Type II: fracture through growth plate and metaphysis sparing epiphysis
Type III: fracture through growth plate and epiphysis, sparing metaphysis
Type IV: fracture through all elements- growth plate, metaphysis and epiphysis
Type V: compression fracture of the growth plate- growth plate is crushed.
Type I and II usually have few complications
Type III and IV: cross growth plate- i.e. from joint through cartilage
Type V: growth plate is crushed.
if you cross or crush the plate, resting cell layer can be damaged (growth stops) or the epiphyseal artery can be damaged.
Type III, IV or V–> premature growth plate closure- limb deformity.
Salter harris mnemonic
SALTR
I- S=Slip (separated or straight across): fracture of cartilage of physis
II-A=Above: fracture lies above physis, or AWAY from the joint
III-L= Lower: fracture is below the physis in the epiphysis
IV-T=Through: fracture is through metaphysis, physis and epiphysis
V-R=Rammed (crushed): physis has been crushed.
Fracture classification
trabecular bone only without cortical deformation=infractions
inflammation and necrosis predisposes bone to infractions- can see infractions with osteomyelitis
Simple fracture: fracture of cortical bone if skin unbroken
Compound: if skin broken and bone exposed to external environment
Comminuted: several small fragments
Avulsion: caused by pull of ligament (i.e. ligament pulls insertion site off)
Greenstick: one side of bone is broken, other side only bent
Transverse or spiral: refers to orientation of fracture line
Impaction: bone fractures and fractured piece gets rammed in
Compression fracture: bone’s sort of folded onto itself
Segmental fracture: fractured piece is mobile.
Stable fracture repair
Ideal: fracture ends get immobilized to give relative stability but not surgically fixed.
Immediate events: periosteum torn, fragments displaced, soft tissue traumatized, hematoma forms
At broken ends, can be necrosis of bone and marrow
Growth factors released by macrophages and platelets in the clot and from the dead bone helps stimulate proliferation of repair tissue–> very similar to wound healing in the skin.
Stable fracture: 24-48 hours
Proliferation of undifferentiated (stem or progenitor cells) mesenchymal cells and neovascularization: cells come in and penetrate blood clot (hematoma)
Formation of a loose collagenous tissue (just like any other tissue)
Mesenchymal cells= from persiosteum, endosteum; stem cells in medullary cavity
At 36 hours: first woven bone is visible
Callus=unorganized meshwork of bone that forms after a fracture
Primary callus of woven bone and possibly hyaline cartilage forms at 4-6 weeks (not nearly as fast as skin)
Bone is trying to make a callus- unorganized meshwork of bone that forms post fracture +/- cartilage.
Woven vs. lamellar bone
Woven is not as well organized as lamellar
in woven bone: active osteoblasts (plump cells); woven bone has irregular trabeculae
Lamellar bone: smooth and small osteocytes
Callus
=unorganized meshwork of bone that forms after a fracture
External (lateral side of bone)=formed by the periosteum
Internal (middle of bone)= between ends of fragments and in medullary cavity
Callus should bridge the gap, encircle the fracture site and stabilize the area.
Callus contains cartilage if the blood supply is less than optima. Because bone is weak, we need more blood–>low O2 encourages cartilage to form. It’s not a bad thing, as long as there IS bone present and it’s not ALL cartilage.
Cartilage of callus isn’t as strong, but eventually it undergoes endochondral ossification.
Over months to years, woven bone is replaced by strong lamellar bone= secondary callus
Callus can be reduced in size over a period of years by osteoclastic activity to restore normal shape of the bone.
how big callus is depends on how big fracture was to begin with.
Rigid fracture repair
surgical application of a device
ideally, there’s contact healing–> direct osteonal bridging with no callus
There can be a gap, but it has to be less than 1mm- bone cells migrate from ends and form lamellar bone at right angle to fracture line (remodels)
If gap is greater than 1mm, woven bone forms and must be modeled into osteonal (lamellar) bone.
Direct/contact healing
no gap, bu there’s a cutting cone
Cutting cone= osteoclasts cutting into the bone to allow direct bridging. Cone also has blood vessells most internally, then undifferentiated mesenchymal cells, then osteoblasts and at the bottom, doing the actual cutting, are osteoclasts.
Small gap healing (less than 1mm)
lamellar bone remodels and joins the gap together
Lamellar bone formed at a right angle to the fracture line. no intervening woven bone.
Complications of fracture repair
1st: inadequate blood supply- cartilage formation, can be necrosis (if there’s anoxia)
2nd complication: instability- excessive movement and tension favours developent of a fibrous tissue callus. fibrous tissue doesn’t stabilize the fracture, and unlike cartilage, doesn’t act as a template for bone formation.
Bone disease terminology
Osteitis=inflammation of bone
Periostitis= inflammation of the periosteum
Osteomyelitis=inflammation of the bone and medullary cavity
Sequestrum=fragment of dead bone isolated from the blood supply and surrounded by a pool of exudate
Portals of entry into bone
Direct or hematogenous
Direct
directly through periosteum and cortex
trauma that may or may not break the bone
direct extension: inflammation in an adjacent tissue e.g. from periodontitis or otitis media
ex: actinomyces bovis= lumpy jaw in cattle–> introduced into oral mucosa by penetrating injury e.g. wire. inflammation invades bone, severe suppurative and fibrosing osteomyelitis
On PM: see reactive, infected and inflamed bone. lots of new bone formation, but also lots of cavities.
In severe periodontitis, will see a huge bony reaction around the tooth roots
in severe otitis media, can see a hugely thickened tympanic bulla.
Hematogenous spread into bone
Blood gains access to the marrow cavity of the diaphysis and metaphysis via the nutrient foramen.
In young animals: epiphysis entered via epiphyseal artery and small branches of it cross the epiphysealcrotex. since the young bone has more blood vessels going into it, it’s more prone to hematogenous infection.
Hematogenous bacterial osteomyelitis is common in foals, neonatal ruminants and pigs.
Bacterial: purulent- exudate in the medullary cavity increases pressure and can compress vessels–> thrombosis–>infarction–>increased bone resorption.
How does bacteria get into body to being with? via perinatal umbilicus or oro-pharyngeal origin.
typically get into the bone at the zone of vascular invasion of the growth plate, either at the physis (metaphyseal growth plate) or articular epiphyseal complex.
Why do we get hematogenous entry into the articular-epiphyseal complex and the metaphyseal growth plate in particular?
Capillaries make sharp bends to join the medullary veins.
1) slow flow and turbulence of blood in larger descending limbs
2) lower phagocytic capacity
3) discontinuous endothelial cells
4) no anastomoses, so thrombosis results in infarction, which favors bacterial localization. If blood vessels get blocked, that’s it: the blood can’t go anywhere.
