Patterns of Disease- Bone Flashcards Preview

Pathology > Patterns of Disease- Bone > Flashcards

Flashcards in Patterns of Disease- Bone Deck (25):

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. 




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). 



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 


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



=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 



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. 


Embolic osteomyelitis

embolus lodges in the capillary loop at the metaphysis

inflammation causes lysis of the metaphyseal bone and growth plate cartilage.

this can cause mechanical instability- the periosteum responds by producing reactive (woven) bone- this works to at least make the bone bigger. 

if the embolus (microabscess) gets REALLY big, the exudate can lyse the cortex of the bone at its thinnest point= metaphyseal cut back zone.

this exudate can extend into the periosteum=periostitis

exudates can also extended into the joint (arthritis) and onto the surface of the skin

Consequences of growth plate embolism? necrosis and inflammation.