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