Epiphyseal Plate

This is called the epiphyseal plate and represents the mechanism that produces longitudinal growth of the bone.

From: The Human Body , 2019

Musculoskeletal System

Robert G. Carroll PhD , in Elsevier's Integrated Physiology, 2007

SKELETON

The adult body contains 206 bones, which together represent a tissue that is capable of growth, adaptation, and repair. Bone consists of an organic framework of proteins in collagen fibers. Hydroxyapatite crystals are embedded in this framework and provide a significant store that helps regulate plasma Ca++ levels (see Chapter 13).

Joints are articulations at the place of contact between two or more bones. Most of the joints in the body are synovial. They are freely movable, permitting position and motion changes. Ligaments and tendons reinforce the joint and help limit motion. Articular disks are located between the bones in some synovial joints and act to buffer forceful impact. Fibrous joints are articulations in which bones are held together by fibrous connective tissue. Cartilaginous joints are held together by cartilage, such as the ribs.

Bone marrow is the source of pluripotent blood cells (see Chapter 6). In adults, blood cells form in marrow cavities in the skull, vertebrae, ribs, sternum, shoulder, and pelvis. There are two types of bone marrow: yellow and red. Yellow marrow is composed mostly of fat cells and is found in the shafts of long bones. Yellow marrow does not normally produce blood cells. Red marrow has a hematopoietic function, manufacturing both red and white blood cells. It is located in the cancellous spaces of flat bones.

Bone contains three types of cells. Osteoblasts form bone by catalyzing the crystal formation of Ca++ and PO4 − in a collagen meshwork. Osteocytes are osteoblasts that are encased in the bone matrix. Osteoclasts resorb damaged or old bone cells during periods of growth or repair. They are also crucial in returning Ca++ from bone to the bloodstream.

ANATOMY

Epiphyseal Plate

In children and young adults, the epiphyses are separated from the diaphysis by epiphyseal cartilage or plates, where bone grows in length. Estrogen and testosterone release at puberty initiates closure of the epiphyseal plates. When bone growth is complete, the epiphyseal cartilage is replaced with bone, which joins it to the diaphysis. Fractures of the epiphyseal plates in children can lead to slow bone growth or limb shortening.

The coordinated activity of these bone cells allows bone to grow, repair itself, and change shape. Even mature bone constantly changes, with new cells being formed and old cells being destroyed. The process of bone turnover is called remodeling, and it is one of the major mechanisms for maintaining Ca++ balance in the body. As much as 15% of the total bone mass normally turns over each year. Rebuilding of bone requires normal plasma concentrations of Ca++ and PO4 − and is dependent on vitamin D.

Movement

Skeletal muscle contraction occurs when an α-motor neuron excites an individual muscle fiber. Outflow from the CNS motor cortex descends to the anterior horn of the spinal cord, where a synapse leads to activation of an α-motor neuron. The axon from the α-motor neuron transmits the action potential to the neuromuscular junction. ACh released at the neuromuscular junction binds to receptors on the muscle end plate, initiating an action potential in the muscle cell. The action potential spreads through the T tubules, causing release of Ca++ from the sarcoplasmic reticulum and contraction of the muscle.

Movement requires a shift of the position of the bones as they articulate across a joint. Skeletal muscle is attached to two different bones by fibrous tendons. Shortening of the skeletal muscle causes angles connecting the bones to decrease (for flexor muscles, i.e., biceps) or to increase (for extensor muscles, i.e., triceps). The musculoskeletal system functions as a unit to allow movement of the body.

Heat Production

The activity of skeletal muscle produces heat as a metabolic byproduct, which usually must be transmitted to the environment. Some of this heat can be used to maintain body temperature, as described in Chapter 1.

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Surgery of the Bovine Digit

Karl Nuss , in Food Animal Practice (Fifth Edition), 2009

Resection of Infected Epiphyseal Plates of the Phalanges or the Metacarpal/Metatarsal Bones

In fattening bulls, but also in heifers, the epiphyseal plates of the metacarpus/metatarsus and, rarely, those of the phalanges may become infected hematogenously. 35,36 Medical treatment consists of parenteral antibiotics and NSAIDs. A tourniquet is applied to the affected limb, and antibiotics such as cephalosporins or penicillin are administered intravenously. A bandage or splint is then applied to the leg. If medical treatment fails, surgical excision involving curettage of the affected parts of the physis can be attempted. Half-limb casts are indicated to stabilize the physis. In advanced cases it may be necessary to drill out the entire epiphyseal growth plate. 37 After radical surgery, a transfixation pin cast must be applied for limb stabilization (see Fig 53-8, B and C).

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The Skeleton

Bruce M. Carlson MD, PhD , in The Human Body, 2019

The Epiphyseal Plate and Growth in Length of a Bone

The power to increase the length of a bone is concentrated in the cartilaginous epiphyseal plates located near each end of the bone. These plates are situated between the shaft of the bone and the secondary ossification centers within the epiphyses. The general functional principle is expansion of the cartilage toward the epiphysis, with simultaneous removal of cartilage and its replacement by bone on the diaphyseal side, all while remaining at about the same thickness. In terms of absolute measurements, the epiphyseal plate moves away from the midpoint of the bone as the bone lengthens. A complex set of cellular phenomena, involving several zones of activity, is required to accomplish this.

Starting from the epiphyseal end of the plate and working inward toward the shaft, the first zone is a layer of resting cartilage (Fig. 4.14). Immediately beneath is a region of chondrocyte proliferation. The resulting daughter cells line up into columns of flattened cells, much like a stack of pancakes. These cells hypertrophy, changing the shape of the flattened cells to an almost cuboidal configuration. This change of shape expands the epiphyseal plate toward the end of the bone, thereby lengthening the bone. Then the hypertrophied chondrocytes secrete type X collagen into the cartilaginous matrix, and the matrix begins to calcify. With the calcification of the matrix, most of the chondrocytes die. The dead cells and parts of the matrix are removed, leaving behind some vertical columns of calcified matrix. Blood vessels and other red marrow constituents fill in the spaces between the columns of remaining calcified cartilage matrix, and osteogenic cells accompanying them line up on the columns and begin to deposit a layer of osteoid upon the cartilage remnants. At the same time, chondrocytic proliferation on the epiphyseal side of the plate continues, adding to the total mass of viable cartilage.

Figure 4.14. Structure and dynamics of an epiphyseal plate in a growing long bone.

 From Saladin (2007), with permission.

Under the influence of growth hormone, the process of forming new cartilage on one side of the epiphyseal plate and its removal and replacement by new spongy bone on the other continues as long as the bone is growing. As an individual reaches the end of the overall growth period, caused by increased concentrations of sex steroid hormones during puberty, the cartilage of the epiphyseal plate diminishes and is finally replaced by bone to form the epiphyseal line. Called closure of the epiphyseal plate, this marks the end of growth of that particular bone. Estrogen in both sexes is critical for proper closure of the epiphyseal plate and the cessation of growth. In its absence, growth continues into adulthood. The two epiphyseal plates within a single bone may close at different times, as do those of different bones. Recognition of these sequences allows anthropologists to accurately age the skeleton of an individual who has died in the late teenage years or early 20s.

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Calcium and Phosphorus Homeostasis II

Joseph Feher , in Quantitative Human Physiology, 2012

•

Identify the parts of bone including endosteum, periosteum, diaphysis, epiphysis, and epiphyseal plate

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Identify the three major cell types in bone: osteoblast, osteocyte, and osteoclast

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Describe the organic matrix of bone and its mineralization

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Describe the location and function of osteoblasts

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Describe the recruitment of osteoclasts from hematopoeitic stem cells

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Describe the mechanism of osteoclastic resorption of bone

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Describe remodeling of bone

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List the sequential steps in Ca and Pi absorption from the intestine

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Describe how vitamin D increases Ca and Pi absorption from the intestine

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Describe how the intestine adapts to diets containing differing amounts of Ca and Pi

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Describe the actions of PTH and vitamin D on Ca and Pi reabsorption by the kidney tubule

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Compare the overall effect of PTH on Ca and Pi homeostasis to that of vitamin D

•

Trace the negative feedback loops involved in the homeostatic response to low plasma Ca

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Calcium and Phosphorus Homeostasis II

Joseph Feher , in Quantitative Human Physiology (Second Edition), 2017

•

Identify the parts of bone including endosteum, periosteum, diaphysis, epiphysis, and epiphyseal plate

•

Identify the three major cell types in bone: osteoblast, osteocyte, and osteoclast

•

Describe the organic matrix of bone and its mineralization

•

Describe the location and function of osteoblasts

•

Describe the recruitment of osteoclasts from hematopoietic stem cells

•

Describe the mechanism of osteoclastic resorption of bone

•

Describe remodeling of bone

•

List the sequential steps in Ca and Pi absorption from the intestine

•

Describe how vitamin D increases Ca and Pi absorption from the intestine

•

Describe how the intestine adapts to diets containing differing amounts of Ca and Pi

•

Describe the actions of PTH, vitamin D, and FGF23 on Ca and Pi reabsorption by the kidney tubule

•

Compare the overall effect of PTH on Ca and Pi homeostasis to that of vitamin D and FGF23

•

Trace the negative feedback loops involved in the homeostatic response to low plasma Ca

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Gigantism

W.W. de Herder , ... A.J. van der Lely , in Reference Module in Biomedical Sciences, 2016

High Dose Sex Steroid Administration

Administration of high dose estradiol or testosterone has been used to limit final height prognosis by promoting closure of the epiphyseal plates. However, their use has declined over the last 30 years because of side-effects during treatment and social acceptance of taller stature ( Rayner et al., 2010). Of concern is the fact that girls treated with high dose estrogen appear to have a dose-dependent influence on fertility in adulthood with a depleted follicular pool and the development of primary ovarian insufficiency (Hendriks et al., 2012). To date, high dose testosterone treatment has not been shown to affect male fertility in adulthood (Hendriks et al., 2010).

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Disease conditions in small animals

Charles E. DeCamp DVM, MS , ... Susan L. Schaefer MS, DVM , in Brinker, Piermattei and Flo's Handbook of Small Animal Orthopedics and Fracture Repair (Fifth Edition), 2016

Radiographic signs

Radiographically, the initial finding in hypertrophic osteodystrophy is a thin, radiolucent line in the metaphysis parallel to the epiphyseal plate, especially in the radius ( Figure 24-7). Secondarily, there is an extraperiosteal cuff of calcification along the metaphysis (Figure 24-8). The lucent line disappears and is replaced by an increased radiodensity. If relapses occur, a new radiolucent line appears between the physis and the radiodense region. 21 As the dog matures, these extraperiosteal thickenings often regress (Figures 24-8 and 24-9) but may leave a permanently thickened metaphysis. 22 Stunting of axial growth and long-bone angular deformity may be observed in a small percentage of severely affected dogs. Pathologic fracture has been documented but is extremely rare. 23

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The Development and Evolution of Cartilage

J. Andrew Gillis , in Reference Module in Life Sciences, 2019

Articular Cartilage

Additional zones of cartilage usually persist at the ends of developing long bones. This tissue will form the articular cartilage of the joint region, and unlike the epiphyseal plate, will remain cartilaginous indefinitely. Articular cartilage performs a vital buffering function, with the ECM providing a smooth, low-friction surface at sites of skeletal articulation. Aggrecan, the principal proteoglycan of cartilage matrix, consists of a protein core with covalently bound sulphated glycosaminoglycan (GAG) chains, and these GAGs retain water in order to maintain themselves in an optimally spaced configuration. Upon compression, water is squeezed from the matrix, and sulphated GAGs are brought into close contact with one another. Upon release of compression, repulsive interactions and the re-absorption of water returns GAGs to their optimally spaced configuration, returning the cartilage ECM to its turgid state ( Roughley and Mort, 2014). The dynamic expulsion and re-absorption of water by cartilage matrix allows this tissue to act as an effective buffer against compressive forces.

Articular cartilage is organised into three zones, each with matrix and cellular properties reflecting specialised functional adaptations (Decker, 2017) (Fig. 3). The thin 'superficial zone' sits at the articular surface, and consists of specialised flattened chondrocytes that secrete glycoproteins, such as lubricin/proteoglycan 4 (encoded through alternative splicing of Prg4 – Marcelino et al., 1999; Jay et al., 2001), to maintain frictionless motion between articulating bones. Beneath the superficial zone lies the 'intermediate zone', in which round chondrocytes are organised into stacks, and produce/maintain typical cartilage ECM products, such as type II collagen and aggrecan. The intermediate zone transitions into an underlying 'deep zone', which consists of stacks of larger, chondrocytes in a partially calcified ECM that grades into subchondral bone. This zonal architecture develops largely postnatally, in conjunction with the expansion of the articular cartilage by proliferation of progenitor cells in the superficial zone (and possible also in the deeper zone), through local cellular rearrangements, and through increases in cell size in the middle and deep zones (Mankin, 1962; Archer et al., 1994; Hayes et al., 2001; Dowthwaite et al., 2003; Hunziker et al., 2007; Williams et al., 2010; Decker et al., 2017). Evidence for the presence of persistent cartilage progenitor cells in adult articular cartilage is scant, and this – combined with the avascular nature of the tissue and the low turnover of ECM proteins – may account for why articular cartilage has such a limited capacity to heal spontaneously following injury (e.g., in osteoarthritis – Hunziker, 1999; Heinemeier et al., 2016).

Fig. 3

Fig. 3. Mammalian articular cartilage. A Safranin-O/Fast Green-stained section through the proximal tibial articular cartilage of a 6 week-old mouse reveals the organization of chondrocytes into superficial, intermediate and deep zones.

 Image by Dr. Rebekah Decker, Genomics Institute of the Novartis Foundation.

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Metals and Minerals

Konnie H. Plumlee DVM, MS, Dipl ABVT, ACVIM , in Clinical Veterinary Toxicology, 2004

Lesions.

Animals do not present gross or histopathologic lesions characteristic of Mo-induced copper deficiency that are specifically diagnostic. The most common observation is an emaciated carcass. Lesions of periosteosis and abnormal epiphyseal plate growth may be observed, but must be differentiated from a primary copper deficiency.

Lesions observed at necropsy in cattle that were fed a diet containing approximately 7400 ppm sodium molybdate included swollen and friable livers and pale, swollen kidneys with perirenal edema. Histopathology revealed hydropic hepatocellular degermation progressing to periacinar necrosis and hemorrhage. In some animals hepatocytes were only observed in the periportal areas. Histopathology of the kidney ranged from hydropic degeneration of the kidney to marked necrosis of the proximal and distal tubular cells. Limited regeneration was observed 4 days after exposure ceased.

Two sheep were administered daily doses of 35 mg Na2MoO4/kg body weight (sheep 1) and 33.9 mg Na2MoO4/kg body weight (sheep 2). Sheep 1 received two 35-mg/kg doses and was euthanized at 48 hours; sheep 2 received three doses and was euthanized at 60 hours. Sheep 1 was anorectic at 48 hours, and sheep 2 was anorectic at 60 hours. Necropsy findings included diffuse subcutaneous petechiae and tan discoloration of the liver with multiple 3- to 5-mm subcapsular ecchymosis. The kidneys were mottled and had areas of pallor on the capsular surface. Histopathology revealed diffuse hemorrhagic hepatic necrosis with a thin rim of hepatocytes in the periportal areas. There was diffuse hydropic degeneration to necrosis of the renal convoluted tubular cells. Lesions were not observed in the gastrointestinal tract, heart, spleen, or lung. Plasma levels of Mo at 48 hours were 48 and 51 ppm for sheep 1 and 2, respectively. For sheep 1, the liver and kidney concentrations of Mo were 26 ppm (wet weight) and 50 ppm, respectively. For sheep 2, the liver concentration was 96 ppm and kidney concentration was 180 ppm.

Rats were exposed to inhaled molybdenum trioxide (MoO3) at exposure levels of 0, 10, 30, and 100 mg/m3 for 6 hours per day, 5 days a week for 2 years. 25 Lesions observed in the exposed rats were chronic inflammatory lesions located at the peribronchiolar and subpleural sites. The giant cells and macrophages contained cholesterol clefts. Metaplasia of the alveoli consisted of ciliated cuboidal and columnar cells. Hyaline degeneration was observed at level II of the nasal respiratory epithelium, and at levels II and III of the respiratory epithelium. Male rats had an increased occurrence of alveolar and bronchiolar adenomas compared with the control rats.

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Vitamin C Deficiency Scurvy

Megan Brickley , Rachel Ives , in The Bioarchaeology of Metabolic Bone Disease, 2008

Histological Features of Infantile Scurvy

Key features linked to infantile scurvy that can be identified histologically are listed in Table 4.6. Investigations by Follis et al. (1950) suggest that scurvy is characterised by fractures within the trabecular bone at the epiphyseal plate in individuals in whom endochondral bone formation should be taking place. This leads to an area with limited trabecular development, as illustrated in sections of a scorbutic and normal guinea pig rib shown in Figure 4.11. These investigators observed fragments of mineralised trabecular bone lying at various angles in individuals who had scurvy, or who had recently started to recover (but importantly not all individuals with scurvy showed such changes). Fractures caused by scurvy may be present for a couple of months after recovery, but, this type of fracture is not pathognomic (Follis et al., 1950). Histological changes can be used to help suggest a diagnosis in archaeological bone, but other features (macroscopic and radiological) would need to be present for a firm diagnosis to be considered.

TABLE 4.6. Histological Features of Juvenile Scurvy

Tissue type Features Code Differential diagnosis Sources
Cortical bone Metaphyseal fractures D Trauma Milgram (1990)
Trabecular bone Fractures in trabecular bone elements D Trauma Bourne (1942b), Follis et al. (1950), Milgram (1990)
Broken or irregular ossified cartilage columns D Leukaemia

Note: See Table 4.2 for definition of codes used in diagnosis.

FIGURE 4.11. 1. Un-decalcified section of costochondral junction of rib of guinea pig receiving ample diet of greenstuff. Numerous calcified trabeculae may be seen extending from the junction. 2. Un-decalcified section of costochondral junction of rib of guinea pig on a scorbutic diet for two weeks. Number of trabeculae greatly reduced (Ca., cartilage; T., trabeculae; C.R., cortex of rib; M., marrow; B., deposit of bone salt in cartilage).

 Courtesy of Geoffrey H. Bourne. 1943. Some experiments on the possible relationship between vitamin C and calcification. Journal of Physiology, Wiley-Blackwell Publishing Ltd. Copyright © 1943 Wiley-Blackwell Publishing Ltd.

An important point noted by Follis et al. (1950) was the difficulty of identifying features linked to scurvy using histology if severe rickets was present (see Figure 4.12). Schultz (2001) also states that some aspects of the histological appearance of scurvy and anaemia are very similar, although the cases discussed in this paper are all archaeological so an exact diagnosis is not known. However, Schultz does provide information in differentiating between changes caused by scurvy and anaemia (Schultz, 2001:134). There are difficulties with the histological analyses of bone sections especially where diseases co-exist, but microscopic analysis is worth considering where invasive investigative techniques are possible, as it may provide additional information that can assist with a diagnosis. As shown by Brickley and Ives (2006) microscopic analysis of bone surfaces, which is relatively easy to undertake, is particularly useful for characterising the extent and type of porosity abnormal surface present in early stages of the condition.

FIGURE 4.12. Camera lucida drawing of transverse sections of a typical scorbutic and rachitic rib. The upper borders correspond to the outer surfaces of the costochondral junctions. In rickets the sharp angle of junction between cartilage and shaft is not apt to be present because of the deep rachitic intermediate zone interposed between the proliferative cartilage and the shaft.

 Reproduced with permission from the BMJ Publishing Group ©. Archives of Disease in Childhood, Park et al. 1935. 10:265–294, Figure 37. Copyright © 1935

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