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what is a growth plate ?
What is a growth plate ?
We as experienced breeders know the answers but I would like for you all to understand this as it is important .
Growth plates, or physes, are composed of several merged layers that produce longitudinal growth of the long bones by the method of endochondral ossification. Physeal damage is not uncommon in the small animal and can result from trauma, genetic disorders, nutritional imbalances, or other medical disturbances. The physis can be either completely or partially damaged and injuries can vary in their subsequent extensiveness from total growth arrest to retardation. Common sequelae of physeal injury include shortened limbs, angular limb deformation, and adjacent joint subluxation. Angulations can occur in multiple planes depending on the location of the growth plate damage and whether the affected bone is anatomically paired with another long bone, as with the radius and ulna. Malalignment can be in the frontal plane, resulting in varus and/or valgus deformities, or in the sagittal plane, causing pro- or recurvatum and rotationally causing internal or external bone torsion. A thorough understanding of the resulting pathology from physeal injury necessitates a discussion of the anatomy and physiology of the growth plate.
Although the physiology of the individual layers of the growth plate is unique, the functional unit of the physis can be summarized as a column of chondrocytes that proliferate, hypertrophy, and synthesize matrix before ultimately undergoing apoptosis . These functions are intimately regulated intrinsically by growth factors and mechanical forces and extrinsically both hormonally and mechanically. The growth plate can be divided into its various layers both morphologically and functionally. As such, a standard set of descriptive terms for the layers does not exist and will vary widely depending on the author.
For purposes of this discussion, a functional scheme of evaluation is presented including the 1) germinal zone; 2) columnar zone with upper proliferating area and lower maturation area; 3) hypertrophic zone with an upper four fifths possessing nonmineralized matrix and lower one fifth with mineralized matrix; and 4) outer metaphysis The cells within the germinal zone are also frequently referred to as resting cells because they do not proliferate. The small, irregularly spaced cells in the germinal zone contain a high concentration of lipid within their vacuolar contents, suggesting their important role in nutrient storage .

The upper portion of the columnar zone represents the only aspect of the growth plate in which chondrocytes undergo division. The active division in this area results in the stacking of flattened cells into columns that are separated from each other by large conglomerations of type II collagen. This proliferating portion of the columnar zone is high in oxygen content and undergoes active glycogen storage by the chondrocytes. The high concentration of rough endoplasmic reticulum within chondrocytes in the lower half of the columnar zone dictates their role in extensive matrix synthesis.
The hypertrophic zone of the physis is the driving force of longitudinal bone growth through cell expansion. The chondrocytes of this zone increase their intracellular volume anywhere from 5- to 10-fold. Variation in the rate of chondrocyte hypertrophy is now thought to be the main reason for different anatomically located physes to grow at different rates . Like the lower half of the columnar zone, the cells of the hypertrophic zone also possess a highly active metabolism that is responsible for large quantities of matrix synthesis. In addition to abundant type II collagen, both type X collagen and vascular endothelial growth factor (VEGF) are produced in the hypertrophic zone. The production of these elements is a hallmark for cellular differentiation and the ceasing of cellular division. These processes occur in an environment that is lower in oxygen tension and in which glycogen is consumed by the chondrocytes until depleted . In the lower one fifth of this zone, the matrix is modified for calcification and vascularization. Whereas recruitment for vessel ingrowth is signaled by the release of VEGF, matrix mineralization is mediated by budding vesicles formed from the chondrocyte plasma membrane. The vesicles contain calcium and enzymes, including both alkaline phosphatase and matrix metalloproteinase (MMP). Newly deposited matrix then forms in longitudinal septa between the columns of chondrocytes and primarily consists of crystalline hydroxyapatite. The septa eventually become primary trabeculae as the upper two thirds are resorbed by chondroclasts and the distal third acts as a scaffolding for osteoid deposition from osteoblasts. Within the mineralized cartilage, matrix forms a transverse septum that is invaded by capillary loops from the metaphysis as they penetrate the distal hypertrophic chondrocyte lacunae. The differentiated chondrocytes then undergo caspase-mediated programmed apoptosis.
Finally, the zone of the outer metaphysis is the area where the endochondral ossification process yields true bone tissue through remodeling of the primary trabeculae into trabeculae of lamellar bone, or secondary trabeculae. This remodeling is mediated by a variety of cells, including undifferentiated mesenchymal cells, preosteoblasts, and osteoblasts in addition to the metaphyseal vascular system. The combined areas of the distal hypertrophic zone and proximal metaphysis are also often referred to as the zone of provisional calcification.
During the late embryonic phase of development, the epiphyseal cartilages of the long bones are well vascularized, with vessels frequently crossing the physes either partially or completely. Following birth, the transphyseal vascular bridging is eliminated resulting in the physeal vasculature arising from two separate sources. Epiphyseal vessels supply the germinating, proliferating, and upper hypertrophic zones through diffusion, and separate metaphyseal vessels permeate to the level of the distal hypertrophic zone. The epiphyseal and metaphyseal vessels normally only anastomose once the physis has closed, marking the onset of skeletal maturity. Premature vascular anastomosis across the physis results in pathologic closure of the growth plate. Alteration in this specific vascular pattern can result in aberrant long-bone development at the level of the physis. Disruption of the epiphyseal blood supply is the most devastating injury to the physeal growth plate vasculature. Epiphyseal vessel damage can cause avascular necrosis of both the germinal chondrocytes and secondary ossification center of the epiphysis, resulting in ossification of the growth plate and premature cessation of growth. To the contrary, injury of the metaphyseal vasculature can result in transitory increases in physeal growth 
Bacteria are capable of invading the metaphyseal portion of the growth plate causing microabcessation through vascular sinusoids. Although it is not clearly understood why these infections occur, theories include reduced blood velocity through the torturous vascular system, low oxygen tension, and deficiencies in the reticuloendothelial system . Likely to be more common in the horse and human, bacterial physitis has been reported to occur in the dog most frequently in the lumbar vertebra, where it causes lucent widening of the growth plate and loss of definition of the physeal margins . Although collapse of the physis and subsequent sclerosis typically ensues, secondary sequestration has been reported requiring sequestrectomy and long-term antimicrobial therapy. As previously described, the physes function under intimate guidance by the various components of the endocrine system. Endocrine diseases, therefore, can result in alteration of normal growth-plate physiology and secondary skeletal deformities. It is important to note that some features typical of endocrine disorders are often accepted as breed characteristics in the dog. Increases (gigantism) or decreases (dwarfism) in body size can be considered normal and classified as constitutional, as the result of complex genetic effects, or abnormal, as the result of endocrinopathies or other complex disorders. Each condition can exist either proportionately or disproportionately, depending on whether the appendicular and axial skeletal components are altered in synchrony.
The anterior pituitary gland, under the stimulation of the hypothalamus, releases growth hormone, which plays an important role in chondrocyte proliferation, physeal development, and bone growth. Alterations in available concentrations of growth hormone result in developmental skeletal disorders. Reduction in levels of growth hormone production by the anterior pituitary gland typically results in proportionate dwarfism, which is a rare but well documented disorder in the dog, most frequently affecting the German shepherd dog. Congenital or juvenile-onset hypothyroidism has been frequently documented in the dog. The skeletal manifestations of this disorder include delay in time of ossification of the epiphyseal centers (epiphyseal dysgenesis) and physeal closure, stunted growth, and disproportionate dwarfis. Familial congenital hypothyroidism has been documented in Scottish deerhounds, giant Schnauzers , boxers , and toy fox terriers . Some evidence suggests that, if a diagnosis can be made at an early age (<4 months), appropriate treatment can result in remission.
A close association exists between the sex steroids, estrogen and testosterone, and the onset of skeletal maturity. Whereas androgen alone does not affect growth-plate closure, estrogen accelerates physeal fusion and terminates linear growth . Androgens are converted to estrogens via aromatization in the male, such that estrogen mediates growth termination in both genders. Thus, prepubertal surgical gonadectomy can affect bone development. Salmeri et al determined that radial and ulnar growth-plate closure was delayed in dogs by 4 months if surgical gonadectomy was completed at 7 weeks of age, and by 3 months if gonadectomy was completed at 7 months of age . Although not examined in this study, it was suspected that animals neutered prior to skeletal maturity might be more susceptible to sustaining traumatic Salter-Harris fractures for a longer time . Subsequently, spontaneous, atraumatic fractures of the capital physis in male cats have now been shown to be linked with prepubertal gonadectomy . This population of cats still possessed open growth plates at a mean age of 94.5 weeks, suggesting that the diminished presence of androgens could have resulted in delayed growth-plate closure and thus posed a higher risk for fractures -hence we inform you not to spay or neuter early and your vet knows this !!!
Chondrodysplasia is a general term referring to any number of disturbances in the development of the cartilaginous growth plates, primarily of the long bones. It frequently results in achondroplasia, which is disproportionate dwarfism, where the long bones of the appendicular skeleton are shortened but the axial components, including skull and vertebral column, are of normal size. Many types of chondrodysplasia have been documented and are cited as specific entities particular to certain breeds. Again, these disorders are distinguished from constitutional dwarfism owing to chondrodystrophy, which is accepted as a nonpathologic breed standard in many types of dog (e.g., Basset hounds, Welsh corgis, and beagles the Havanese carries some lines with this in the UK and USA and EU… Specific chondrodysplasias have now been documented for several canine breeds. The condition is well documented in the Alaskan malamute, in which a disproportionate dwarfism with concurrent macrocytic hemolytic anemia results from the autosomal recessive disorder. Among other clinical sequelae, hallmarks of the disease include derangement of the proliferative zone of the physes and abnormal endochondral ossification that is radiographically most apparent as flattened distal ulnar physes and retarded ossification of cuboid bones detected between 4 and 12 weeks.
Many nutritional disorders can affect bone physiology, and with respect to the growth plate specifically, it is well documented that certain dietary alterations can cause pathologic changes to physeal architecture and development. Diets low in vitamin D and phosphorus can result in rickets, causing derangement of the normal chondrocyte columns within the physes, an inability to appropriately calcify the matrix surrounding the hypertrophied cells, and diminished vascular invasion from the metaphysis necessary for physeal closure Hypervitaminosis A has been reported to cause exuberant and premature calcification of growth-plate cartilage, resulting in early physeal closure.
D.B. Fox
University of Missouri–Columbia, Veterinary Medical Teaching Hospital, Columbia, MD, USA.

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