Page 1070 - Adams and Stashak's Lameness in Horses, 7th Edition

1036 Chapter 10

inhibited in this zone by a morphogen produced in the which is an important process that contributes to the
resting zone. 1 final shape of the bone (Figure 10.4). 55
VetBooks.ir Hypertrophy Zone Vascularity of the Physis

After the chondrocytes finish cell division, they The blood supply to the growth plate originates from
continue to mature and hypertrophy in the columns the epiphyseal, metaphyseal, and perichondral circula­
4,38
established in the proliferating zone. Matrix vesicles tions. Transphyseal vessels (those crossing the growth
begin to form in this region. Matrix vesicles are micro­ plate) are present in large epiphyses and may serve as a
structures that form in the extracellular matrix from route for spread of infection from the metaphysis to the
the cytoplasmic membrane of the chondrocytes and epiphysis. The metaphyseal circulation forms a series of
contain products essential for calcification including loops that penetrate the longitudinal septa, enlarging as
alkaline phosphatase and calcium. Type X collagen is they return toward the diaphysis and forming a sinusoid.
49
also produced from the cells in this zone, which helps This produces a sluggish pattern of blood flow within
set up the matrix assembly for mineralization and the physis that predisposes this region to bacterial locali­
55
53
helps increase calcium influx into matrix vesicles. zation and osteomyelitis.
Within the zone, cells increase in size from the epiphy­ The integrity of the blood vessels within the zone of
seal to metaphyseal side of the physis (Figure 10.4) Ranvier is important for continued appositional growth
due to the presence of factors such as insulin‐like at the periphery of the epiphyseal growth plate.
60
growth factor. At the base of the hypertrophic zone, Disruption of the blood supply in this perichondral
the size of the chondrocytes can be five times larger region can potentially cause ischemia to the physis, con­
8
than those cells in the proliferative zone. This increase tributing to asynchronous growth and a subsequent
in cell volume is what increases the rate of longitudi­ angular limb deformity (ALD). In addition, lack of
7
nal growth of the physis. The hypertrophied chondro­ blood supply, particularly to the ossification zone, can
cytes closest to the metaphysis have less metabolic prevent proper bone formation and potentially contrib­
activity, ultimately leading to cell degeneration and ute to disruption of bone growth or osteochondrosis
11,40,41,66
death. Cell death triggers vascular invasion and calci­ (OC).
9
fication. 12,49 Because this zone is the transition zone
between the cellular and bony region of the physis, Biomechanical Aspects of the Physis
combined with the relative lack of matrix surrounding
the large chondrocytes, the zone of hypertrophy has Although the exact mechanism is not completely
been considered to be the structurally weak link of the understood, tension and compression on the physis are
physis. 4,39 essential for continued orderly bone development and
growth. Each growth plate has a biologic range of
55
both tension and compression within which it will
Zone of Calcification/Ossification respond. Within this range increasing tension or com­
pression will accelerate physeal growth, while reducing
The zone of calcification is an ill‐defined region that tension or compression will decrease physeal growth.
starts in the lowest region of the hypertrophic zone. The However, beyond the physiologic limits of tension or
matrix between the cells gradually becomes mineralized compression, physeal growth may be significantly
due to deposition of hydroxyapatite crystals (Figure 10.4). decreased or even stopped; this is referred to as the
This is thought to be initiated by the matrix vesicles, and Hueter–Volkmann law of physeal growth. 25,55 This law
it depends on several factors such as the availability of states that when mechanical compression is applied,
calcium and phosphate ions, cobalt and collagen, the pH, growth will be retarded but that tensile forces will stim­
and the enzyme alkaline phosphatase. 49 ulate growth. This has an important practical applica­
The zone of ossification is sometimes called the zone tion in the management of foals with ALDs. If we
of angiogenesis because the terminal ends of the capillary assume that a foal with an ALD of the carpus (carpus
sprouts impinge on the hypertrophic chondrocytes. Here valgus) exerts an asymmetric load on the distal radial
osteogenic buds, which consist of capillary sprouts and physis, then the physis will stimulate growth on the
osteoprogenitor cells, invade the columns of calcifying concave (tension) side of the physis and slow growth on
cartilage. 35,49 In the horse, there is approximately one the convex (compression) side of the physis, serving to
capillary sprout per column of cells. After the vessels straighten the limb without intervention. However,
49
come in, osteoblasts deposit osteoid, the organic part of unrestrained exercise may cause physeal compression
bone, on the matrix surrounding the columns of calcified that is greater than the physiologic range and therefore
cartilage. This forms longitudinally orientated bony prevent autocorrection of the ALD. In addition, foals
spicules (with a cartilaginous core inside) that make up with physitis or physeal dysplasia may have weaker
the region called the primary spongiosa. Eventually the metaphyseal bone than normal, which may be more
bone of the primary spongiosa is replaced by secondary susceptible to trauma. 4
spongiosa, which lacks remnants of the cartilage core.
55
As the bone elongates, bone at the diaphyseal end is Cessation of Physeal Growth
removed by osteoclasts at the same rate that new bone is
being formed on the epiphyseal side of the metaphysis. As bone growth ceases, the physis becomes progres­
Thus, there is a continuous sequence of events, with cell sively thinner, and finally the epiphysis and metaphysis
division at one end, bone formation, and bone destruction, fuse. 38,39 The cartilaginous growth plate is replaced with