Cartilage Pathology Flashcards
how does long bone growth occur
- endochondral ossification
- mesenchymal condensation
- differentation into hyaline cartilage
- calcification
- vascular invasion
- ossification centres
what are the structures shown
what are the zones shown of the metaphyseal growth plate cartilage
R = resting zone
P = proliferation zone
H = hypertrophic zone
C = front of cartilage calcification & ossification (primary spongiosa)
what is the blood supply to the physeal growth plate and why is it important
branches of the epiphyseal artery supply the resting zones of the growth plate
branches of the metaphyseal artery form capillary loops at the metaphyseal side where endochondrial ossification occurs
integrity of this vascular supply is critical to the process of endochondral ossification
what is the articular epiphyseal cartilage complex (AECC)
immature skeleton (young growing animal)
articular cartilage overlies the temporary growth cartilage of the epiphysis cartilage (EC)
what are the structures
articular cartilage (AC)
epiphyseal cartilage (EC)
the physeal growth plate EC undergoes endochondral ossification
where does articular cartilage lie
overlies the temporary growth cartilage of the epiphysis
what is epiphyseal cartilage
highly dependent on a network of blood vessels (running in the cartilage canals) from perichondrium & subchondral bone
contributes to growth/development of epiphysis
what is articular cartilage
smooth glistening and white to bluish grossly
thickest in young and at sites of maximal weight-bearing
in adult skeleton
how are nutrients obtained for articular cartilage
no blood vessels, lymphatics and nerves
nutrients obtained by diffusion from synovial fluid
what makes up articular cartilage
chondrocytes (5% of tissue)
95% matrix secreted by chondrocytes
proteoglycans (aggrecan –> chondroitin sulphate, keratin sulphate) bind to hyaluronic acid to form a large aggregate with negative charge –> water (70-80% of matrix)
collagen mainly type II and also type V, VI, IX, X and XI
what are the key components of synovial joints
SZ = superficial zone resists shearing forces
mid and deep zones (MZ and DZ) function in shock absorption
TM = tidemark –> boundary between uncalcified articular cartilage and calcified cartilage
CC = calcified cartilage attaches articular cartilage to bone by its irregular (interlocking) interfaces
what is synovial fossae
some joints of ruminants, horses, pigs
non-articulating depressions near midline of joints
aquired during joint modelling the first months of postnatal life
central depressions with distinct borders and a smooth, blue to pink surface, reflecting the proximity of the subchondral capillary bed
what is important to note about the synovial fossae
synovial fossae should not be mistaken for lesions in the articular cartilage or as indicators of collapsed subchondral bone
what structure is this
synovial fossae
what is articular cartilage response to a superficial injury
response varies with nature of the insult and depth of lesion
superficial lacerations not penetrating the tidemark (no hemorrhage/inflammation) –> chondrocytes adjacent to the lesion proliferate in small clusters (chondrones) –> may produce new matrix but do not migrate into lesion
what is a full thickness articular cartilage injury response
penetrating subchondral bone –> hemorrhage –> hematoma –> inflammation –> PDGF + TGFB from platelets –> inflammation + mesenchymal cell proliferation chondrocytes –> produce matrix rich in proteoglycans and collagen II
defect filled with fibrocartilage
attached to adjacent hyaline articular cartilage
what is fibrocartilage repair tissue
similar to fibrous scar in other organs
replacement of articular cartilage at sites of deep injury
but adequate performance when subjected to mechanical loading
–> new bone formation (at base of the lesion) –> restoring the subchondral bone plate
what are matrix metalloproteinases (MMPs)
enzymes capable of matrix digestion
normal constituents of the matrix, but present in an inactive form
what are the types of metalloproteinases (MMPs)
gelatinases –> degradation of type I & basement membrane collagen
collagenases –> degradation of various collagen types (including type II)
stromelysins –> degradation of non-collagenous proteins/aggrecan
how can MMPs be activated
degenerating/reactive chondrocytes
inflammatory cells –> MMPs also active in cartilage/bone remodelling in endochondral ossification
what are tissue inhibitors of metalloproteinases (TIMPs)
in the matrix
control mechanism counterbalancing the destructive effects of activated MMPs
what are aggrecanases
degredation of aggrecans
what occurs when proteoglycans are lost
altered hydraulic permeability of cartilage –> interfering with joint lubrication –> further mechanical injury –> disruption of collagen fibres on articular cartilage surface –> surfaces of affected cartilage yellow-brown with a dull roughened appearance
what occurs with progressive proteoglycan loss
collagen fibres condensation and clefting/fissuring (fibrillation) –> loss of surface cartilage (erosion/ulceration) –> exposure of subchondral bone with thickening (eburnation) –> polished appearance due to direct bone on bone contact
what is primary degenerative joint disease (DJD)
no apparent predisposing cause
common in older animals
what is secondary degenerative joint disease (DJD) and common examples
associated with underlying abnormalities of the joint or supporting structures
abnormal directional forces and/or joint instability
hip dysplasia
cruciate ligament rupture
what is occuring
loss of staining in the superficial articular cartilage stroma due to proteoglycan loss
pink cartilage –> indicating loss of proteoglycans
goes to fibrilation stage next slide
what is occuring here
superficial cartilage is necrotic and ragged
groups of chondrocytes (chondrones) within the remaining articular cartilage
fibrilation stage
what is occuring here
osteophytes (bony projection)
what is occuring here
eburnation
dense sclerotic subchondral bone
what is chondrodysplasias
hereditary development cartilage disorders –> abnormalities of skeletal growth –> disproportionate dwarfism
what is lethal bulldog type bovine chondrodysplasia
extremely short limbs usually rotated
short domed head with protruding mandible
short vertebral column
cleft palate
large ventral abdominal hernia
what is lethal bulldog type bovine chondrodysplasia caused bye
mutations in aggrecan (ACAN) gene
what is spider lamb syndrome and what causes it
autosomal recessive with incomplete penetrance
long limbs and neck
shallow body
scoliosis and/or kyphosis of thoracic spine
point mutation in FGFR3 gene
disorganized ossification centers resulting in variably sized and abnormally shaped and orientated vertebrae
what is texel sheep chondrodysplasia
autosomal recessive trait
reduced growth rate, short neck and legs
both articular and physeal cartilage –> disorganization of chondrocytes
foci of chondrolysis (loss of chondrocytes & matrix)
coalescing into clefts/cystic spaces
what is chondrodysplasia in the alaskan malamute
recessive
disproportionate, short legged dwarfism
hemolytic anemia
what is feline physeal dysplasia & slipped capital femoral epiphysis
most common in male & overweight cats
affected females often have affected male littermates
young cats (2-4) but older than the age of expected physeal closure
what is the pathology of feline physeal dysplasia & slipped capital femoral epiphysis
persistence of dysplastic growth plates –> disorganized chondrocyte clusters surrounded by abundant matrix
changes also present in other physeal growth plates –> only the proximal femoral physis fractures –> because of shear forces at that site
what is being shown here
unilateral slipped capital femoral epiphysis
what is shown here
fracture through the persistent dysplastic physis
what is shown here
persistent physis –> abnormal hypertrophic chondrocytes arranged in clusters instead of well organized columns
what is osetochondrosis
failure of endochondral ossification affecting articular-epiphyseal cartilage (AEEC) & physeal growth plate –> young growing animals
what are the 3 eitologies of osteochondrosis
- genetics: influence on body conformation –> contribution to lesion development
- trauma: promotes progression of osteochondrosis latens to more advanced lesions(many young pigs have early lesions but most resolve in –> pigs that get more exercise lesions are more likely to progress to advanced lesions)
- vascular factors: focal failure of vascular supply to growing cartilage –> localized ischemic necrosis –> initiation of early subclinical lesions
what are 3 forms/stages of osteochondrosis
- osteochondrosis latens
- osteochondrosis manifesta
- osteochondrosis dissecans (OCD)
what is osteochondrosis latens
focal ischemic necrosis of growth cartilage but not articular cartilage of the AECC (articular-epiphyseal cartilage)
cannot see nuclei just pink amorphous substance
damage to vessel canals –> ischemic damage
what is osteochondrosis manifesta
retention of necrotic cartilage –> failure of endochondral ossification
grossly or radiographically visible focus of cartilage necrosis in subchondral bone (may or may not show c/s, can resolve by gradual removal of necrotic cartilage focus)
what is osteochondrosis dissecans (OCD)
necrosis dissecting through articular cartilage with cleft formation often resulting in flaps of articular cartilage –> clinically relevant lesion, irreversible
complete separation and necrosis of the growth cartilage –> flaps of cartilage
what is shown here
ostechondrosis latens
what is shown here
osteochondrosis manifesta
persistent focus of necrotic cartilage (with necrotic cartilage canals*) incorporated into the epiphysis by the ossification front
what is shown here
medial and humeral condyle flaps of articular cartilage separated by fissures and clefts from the surrounding intact cartilage
what is shown here
dissecting band of necrosis and separation extending along the deep growth cartilage and communicating with the articular surface
what are the predilection sites of osteochondrosis in swine
distal femur (esp. medial femoral condyle)
humerus (condyles and head)
where are the prediliction sites of osteochondrosis
distal femur (medial condyle and both trochlear ridges)
distal tibia (cranial intermediate ridge and medial malleolus)
talus (trochlear ridges)
articular processes of the cervical vertebrae
what are the prediliction sites of osteochondrosis in dogs
humerus (head and medial condyle)
distal femur (both condyles)
talus (medial and lateral trochlear ridges)
what are the prediliction sites of osteochondrosis in cattle
talus (medial and lateral trochlear ridges)
distal femur (both trochlear ridges)
what are the predilection sites of osteochondrosis in general
sites of high dynamic load during movement/exercise
what is shown here
dog humerus head OCD
usually young males of large and giant breeds
grossly similar lesion common in middle-aged and older dogs as a result of cartilage erosion without pre-exisiting osteochondrosis
what is shown here
horse cervicle vertebral malformation-malarticulation
osteochondrosis of the articular facet joints can contribute to invertebral joint instability
could affect joint stability –> displacement and compression of spinal cord leading to cervical stenotic myelopathy (wobbler syndrome)
what is shown here
osteochondrosis dissecans
severe cleft and collapse
distal femur
extensive clefting and loss of articular cartilage on the lateral trochlear ridge
small cartilage nodules (attempts at local repair) –> produce matrix to fill the defect (ineffective because surface is disrupted)
what occurs after early lesions of articular osteochondrosis
lesions with cartilage canal necrosis and ischemic chondronecrosis in regions where cartilage canal vessels traverse the chondro-osseuous junction
subclinical ischemic chondronecrosis preceding and predisposing to OCD and subchondral bone cysts
process of traversing tissue junctions renders the canal vessels vulnerable to failure in the distal femur
what is occuring here
cartilage canal necrosis & ischemic chondronecrosis at the junction between AEEC and subchondral bone
what is occuring here
osteochondrosis manifesta
medial femoral condyle
cystic lesions in subchondral bone –> extensive errosion and cavities in the subchondral bone
what is the difference between these lesions
pseudocyst lesion –> unifromly radiolucent defect within bone
area of ischemic chondronecrosis surrounded by epiphyseal trabecular bone
what is a true cyst lesion
granulation tissue containing dilated blood vessel with a thin or thick wall
what occurs with osteochondrosis in physeal growth plate cartilage
lesions distinct from OC and AEEC
early lesions –> cone shaped foci of retained cartilage extending into the metaphysis
no necrotic cartilage
what is the possible pathogenesis of osteochondrosis in physeal growth plate cartilage
trabecular microfractures in primary spongiosa –> interference with vascular invasion of mineralized cartilage during endochondral ossification –> persistence of hypertrophic zone chondrocytes (retained wedges of hypertrophic cartilage in metaphysis)
what are proliferative lesions of cartilage
- tumours and tumour like lesions
chondroma
chondrosarcoma
osteochondroma
feline osteochondromatosis
- other
synovial chondromatosis
what is a chondroma
benign tumour of cartilage
rare in all species, most commonly reported in aged dogs & sheep
slow growth rate, with deformation of affected bones
generally painless swelling
phalanges, cervical spine, ribs
what is a chondrosarcoma
malignant tumour of cartilage
where is chondrosarcoma more frequently found
more in dogs mostly med/large breeds
also in cats
more common in flat bones, pelvis, ribs, nasal turbinates (long bones possible)
slow growth but with local invasion, possible recurrence following surgery metastatic spread less frequent and with longer latency compared with OSA
what are the signs of nasal, pelvic, long bone chondrosarcoma
nasal –> sneezing and epitaxis
pelvic –> masses possibly associated with constipation, tenesmus, hind limb lameness
long bones –> painful swelling, pathological fractures
what are extraskeletal chondrosarcomas
heart
arteries
retroperitoneum
bladder
omentum
lung
what is osteochondroma
cartilage capped osseous outgrowth arising from surface of a bone formed by endochondral ossification
what is monostotic and polyostotic osteochondroma
monostotic single bone affected –> solitary osteochondroma
polyostotic multiple bones affected –> osteochondromatosis
what are the clinical signs of osteochondromas
depend on size and location
disfigurement, lameness, pain, paresis, paralysis
–> typically enlarge in synchrony with physeal growth
–> growth ceases once the skeleton reaches maturity
–> continued growth after skeletal maturity suggests malignant transformation
what is occuring here
- tumour in spinal process of vertebrae –> compression of spinal cord
- lesion in lumen of trachea causing partial obstruction of airway
histological appearance: superficial cartilage layer and the presence of the islands of cartilage with associated lamellae of new formed bone (endochondral ossification)
what is feline osteochondromatosis
unlike osteochondromas in dogs and horses which are developmental disturbances that cease growth at skeletal maturity feline osteochondromatosis shows progressive growth
what does feline osteochondromatosis affect
typically affecting multiple bones (skull, ribs, vertebrae)
what causes feline osteochondromatosis
oncogenic retroviruses (FeLV, FeSV) detected in cases of osteochondromatosis
speculated viral-induced proliferation
what is primary synovial chondromatosis
idiopathic nodular cartilagineous metaplasia of the synovium mostly dogs (large and giant purebreds)
what is presentation of primary synovial chondromatosis and how is it diagnosed
lameness and painful swelling of single joint
cartilage nodules NOT visible with x-rays –> can be detected with echo, CT and contrast arthography
what is secondary synovial chondromatosis
associated with chronic degenerative joint disease (DJD)
nodules less numerous (compared with primary SC) and often mixed with other forms of synovial proliferation and metaplasia
erosive changes in the articular cartilage are more marked than the synovial proliferation
what is occuring here
primary synovial chondromatosis
very prominant nodules arising from synovial membrane
what is occuring here
secondary synovial chondromatosis
nodules and thickening of synovial membrane
pieces of articular cartilage that break free
metaplasia of the hyperplastic synovium into cartilage, which undergoes ossification to form bony nodules (osteophyte formation)
these lesions can detach and become free floating within the synovial fluid (joint tropi)
what does chondrodysplasia in Alaskin Malamute cause
Rx changes apparent as early as 7-10 d and more pronounced after 3 weeks
- bowing of radius and ulna
- lateral deviation and enlargement of carpus
- sclerotic and abnormally shaped metaphyses
–> disruption of the metaphyseal blood supply –> impaired vascular invasion of the developing growth plate
irregular thickening of growth plates in the limb bones
islands of hypertrophic cartilage extend into metaphysis –> close to healing trabecular microfractures
growth plate lesions similar to rickets
what is the difference between pseudocysts and true cysts in the subchondral bone of horse due to osteochondrosis
pseudocysts: result of ischemic necrosis of cartilage being incorperated at level of endochondral ossification resulting in radiolucent lesion in the trabecular bone and maybe even the metaphyseal growth plate
true cyst: focus of ischemic chondro-necrosis affecting blood vessels in the subchondral bone with dilation of the blood vessels, microfractures, formation of granulation tissue, and formation of cystic lesion –> can progress with collapse of the superficial articular cartilage
