Chapter 6 Check point questions 1. How does the skeletal system function in support, protection, movement, and storage of minerals? 2. Describe the role of bones in blood cell production. 3. Which bones contain red bone marrow?We also discuss several other topics like What are the microorganisms found in the intestinal gut?
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4. How do red bone marrow and yellow bone marrow differ in composition and function? 6. Why is bone considered a connective tissue? 7. What factors contribute to the hardness and tensile strength of bone? 8. List the four types of cells in bone tissue and their functions. 9. What is the composition of the extracellular matrix of bone tissue? 10. How are compact and spongy bone tissues different in microscopic appearance, location, and function? 11. What is a bone scan and how is it used clinically? 12. Explain the location and roles of the nutrient arteries, nutrient foramina, epiphyseal arteries, and periosteal arteries. 13. Which part of a bone contains sensory nerves associated with pain? 14. Describe one situation in which these sensory neurons are important. 15. How is a bone marrow needle biopsy performed? What conditions are diagnosed through this procedure? 16. What are the major events of intramembranous ossification and endochondral ossification, and how are they different? 17. Describe the zones of the epiphyseal (growth) plate and their functions, and the significance of the epiphyseal line. 18. Explain how bone growth in length differs from bone growth in thickness. 19. How could the metaphyseal area of a bone help determine the age of a skeleton? 20. Define remodeling, and describe the roles of osteoblasts and osteoclasts in the process. 21. What factors affect bone growth and bone remodeling? 22. List the types of fractures and outline the four steps involved in fracture repair. 23. How do hormones act on bone to regulate calcium homeostasis? 24. How do mechanical stresses strengthen bone tissue? 25. Would children raised in space ever be able to return to Earth? 26. Why is it important to engage in weightbearing exercises before the epiphyseal plates close? 27. What is demineralization, and how does it affect the functioning of bone?28. What changes occur in the organic part of bone extracellular matrix with aging? Chapter 7 1. On what basis is the skeleton grouped into the axial and appendicular divisions? 2. Give examples of long, short, flat, and irregular bones. 3. What are surface markings? What are their general functions? 4. Describe the cavities within the skull and the nasal septum. 5. Which foramina and fissures are associated with the orbit? 6. What structures make up the nasal septum? 7. Define the following: foramen, suture, paranasal sinus, and fontanel. 8. What structures pass through the supraorbital foramen? 9. How do the parietal bones relate to the cranial cavity? 10. What structures form the zygomatic arch? 11. What structures pass through the hypoglossal canal? 12. Why is the sphenoid bone called the keystone of the cranial floor? 14. Which bones form the hard palate? Which bones form the nasal septum? 15. What are the functions of the hyoid bone? 16. What are the functions of the vertebral column? 17. Describe the four curves of the vertebral column. 18. What are the three main parts of a typical vertebra? 19. What are the principal distinguishing characteristics of the bones of the various regions of the vertebral column? 23. How do the atlas and axis differ from the other cervical vertebrae? 24. Describe several distinguishing features of thoracic vertebrae. 25. What are the distinguishing features of the lumbar vertebrae? 26. How many vertebrae fuse to form the sacrum and coccyx? 28. How are ribs classified?The skeletal system performs several basic functions: 1. Support. The skeleton serves as the structural framework for the body by supporting soft tissues and providing attachment points for the tendons of most skeletal muscles. 2. Protection. The skeleton protects the most important internal organs from injury. For example, cranial bones protect the brain, and the rib cage protects the heart and lungs. 3. Assistance in movement. Most skeletal muscles attach to bones; when they contract, they pull on bones to produce movement. This function is discussed in detail in Chapter 10. 4. Mineral homeostasis (storage and release). Bone tissue makes up about 18% of the weight of the human body. It stores several minerals, especially calcium and phosphorus, which contribute to the strength of bone. Bone tissue stores about 99% of the body's calcium. On demand, bone releases minerals into the blood to maintain critical mineral balances (homeostasis) and to distribute the minerals to other parts of the body. 5. Blood cell production. Within certain bones, a connective tissue called red bone marrow produces red blood cells, white blood cells, and platelets, a process called hemopoiesis (hēmōpoyēsis; hemo = blood; poiesis = making). Red bone marrow consists of developing blood cells, adipocytes, fibroblasts, and macrophages within a network of reticular fibers. It is present in developing bones of the fetus and in some adult bones, such as the hip (pelvic) bones, ribs, sternum (breastbone), vertebrae (backbones), skull, and ends of the bones of the humerus (arm bone) and femur (thigh bone). In a newborn, all bone marrow is red and is involved in hemopoiesis. With increasing age, much of the bone marrow changes from red to yellow. Blood cell production is considered in detail in Section 19.2. 6. Triglyceride storage. Yellow bone marrow consists mainly of adipose cells, which store triglycerides. The stored triglycerides are a potential chemical energy reserve. Macroscopic bone structure may be analyzed by considering the parts of a long bone, such as the humerus (the arm bone) A long bone is one that has greater length than width. A typical long bone consists of the following parts: 1. The diaphysis (dīAFisis = growing between) is the bone's shaft or body—the long, cylindrical, main portion of the bone. 2. The epiphyses (ePIFisēz = growing over; singular is epiphysis) are the proximal and distal ends of the bone. 3. The metaphyses (meTAFisēz; meta = between; singular is metaphysis) are the regions between the diaphysis and the epiphyses. In a growing bone, each metaphysis contains an epiphyseal (growth) plate (ep iFIZ ′ ēal), a layer of hyaline cartilage that allows the diaphysis of the bone to grow in length (described later in the chapter). When a bone ceases to grow in length at about ages 14–24, the cartilage in the epiphyseal plate is replaced by bone; the resulting bony structure is known as the epiphyseal line. 4. The articular cartilage is a thin layer of hyaline cartilage covering the part of the epiphysis where the bone forms an articulation (joint) with another bone. Articular cartilage reduces friction and absorbs shock at freely movable joints. Because articular cartilage lacks a perichondrium and lacks blood vessels, repair of damage is limited. 5. The periosteum (perēOStēum; peri = around) is a tough connective tissue sheath and its associated blood supply that surrounds the bone surface wherever it is not covered by articular cartilage. It is composed of an outer fibrous layer of dense irregular connective tissue and an inner osteogenic layer that consists of cells. Some of the cells enable bone to grow in thickness, but not in length. The periosteum also protects the bone, assists in fracture repair, helps nourish bone tissue, and serves as an attachment point for ligaments and tendons. The periosteum is attached to the underlying bone by perforating fibers or Sharpey's fibers, thick bundles of collagen that extend from the periosteum into the bone extracellular matrix. 6. The medullary cavity (MEDulerē; medulla = marrow, pith), or marrow cavity, is a hollow, cylindrical space within the diaphysis that contains fatty yellow bone marrow and numerous blood vessels in adults. This cavity minimizes the weight of the bone by reducing the dense bony material where it is least needed. The long bones' tubular design provides maximum strength with minimum weight. 7. The endosteum (endOStēum; endo = within) is a thin membrane that lines the medullary cavity. It contains a single layer of boneforming cells and a small amount of connective tissue.Parts of a long bone. The spongy bone tissue of the epiphyses and metaphyses contains red bone marrow, and the medullary cavity of the diaphysis contains yellow bone marrow (in adults). FUNCTIONS OF BONE TISSUE 1. Supports soft tissue and provides attachment for skeletal muscles. 2. Protects internal organs. 3. Assists in movement, along with skeletal muscles. 4. Stores and releases minerals. 5. Contains red bone marrow, which produces blood cells. 6. Contains yellow bone marrow, which stores triglycerides (fats). The structure of bone at the microscopic level. Like other connective tissues, bone, or osseous tissue (OSēus), contains an abundant extracellular matrix that surrounds widely separated cells. The extracellular matrix is about 15% water, 30% collagen fibers, and 55% crystallized mineral salts. The most abundant mineral salt is calcium phosphate [Ca3(PO4)2]. It combines with another mineral salt, calcium hydroxide [Ca(OH)2], to form crystals of hydroxyapatite [Ca10(PO4)6(OH)2] (hīdroksēAPatīt). As the crystals form, they combine with still other mineral salts, such as calcium carbonate (CaCO3), and ions such as magnesium, fluoride, potassium, and sulfate. As these mineral salts are deposited in the framework formed by the collagen fibers of the extracellular matrix, they crystallize and the tissue hardens. A bone's hardness depends on the crystallized inorganic mineral salts, a bone's flexibility depends on its collagen fibers. Like reinforcing metal rods in concrete, collagen fibers and other organic molecules provide tensile strength, resistance to being stretched or torn apart. Soaking a bone in an acidic solution, such as vinegar, dissolves its mineral salts, causing the bone to become rubbery and flexible. bone cells called osteoclasts secrete enzymes and acids that break down both the mineral salts and the collagen fibers of the extracellular matrix of bone. Four types of cells are present in bone tissue: osteogenic cells, osteoblasts, osteocytes, and osteoclasts 1. Osteoprogenitor cells (os t ′ ēōprōJENitor; genic = producing) are unspecialized bone stem cells derived from mesenchyme, the tissue from which almost all connective tissues are formed. They are the only bone cells to undergo cell division; the resulting cells develop into osteoblasts. Osteoprogenitor cells are found along the inner portion of the periosteum, in the endosteum, and in the canals within bone that contain blood vessels. 2. Osteoblasts (OStēōblasts ; blasts = buds or sprouts) are bonebuilding cells. They ′ synthesize and secrete collagen fibers and other organic components needed to build the extracellular matrix of bone tissue, and they initiate calcification (described shortly). As osteoblasts surround themselves with extracellular matrix, they become trapped in their secretions and become osteocytes. (Note: The ending blast in the name of a bone cell or any other connective tissue cell means that the cell secretes extracellular matrix.) 3. Osteocytes (OStēōsīts ; cytes = cells), mature bone cells, are the main cells in bone ′ tissue and maintain its daily metabolism, such as the exchange of nutrients and wastes with the blood. Like osteoblasts, osteocytes do not undergo cell division. (Note: The ending cyte in the name of a bone cell or any other tissue cell means that the cell maintains and monitors the tissue.) 4. Osteoclasts (OStēōklasts ; clast = break) are huge cells derived from the fusion of as ′ many as 50 monocytes (a type of white blood cell) and are concentrated in the endosteum. On the side of the cell that faces the bone surface, the osteoclast's plasma membrane is deeply folded into a ruffled border. Here the cell releases powerful lysosomal enzymes and acids that digest the protein and mineral components of the underlying extracellular bone matrix. This breakdown of bone extracellular matrix, termed resorption (rēSORPshun), is part of the normal development, maintenance, and repair of bone. (Note: The ending clast means that the cell breaks down extracellular matrix.) As you will see later, in response to certain hormones, osteoclasts help regulate blood calcium level (see Section 6.7). They are also target cells for drug therapy used to treat osteoporosis (see Disorders: Homeostatic Imbalances at the end of this chapter). A mnemonic that will help you remember the difference between the function of osteoblasts and osteoclasts is as follows: osteoBlasts Build bone, while osteoClasts Carve out bone. Bone is not completely solid but has many small spaces between its cells and extracellular matrix components. Some spaces serve as channels for blood vessels that supply bone cells with nutrients. Other spaces act as storage areas for red bone marrow. Depending on the size and distribution of the spaces, the regions of a bone may be categorized as compact or spongy Compact Bone Tissue Compact bone tissue contains few spaces (Figure 6.3a) and is the strongest form of bone tissue. It is found beneath the periosteum of all bones and makes up the bulk of the diaphyses of long bones. Compact bone tissue provides protection and support and resists the stresses produced by weight and movement. Compact bone tissue is composed of repeating structural units called osteons, or haversian systems (haVERshan). Each osteon consists of concentric lamellae arranged around a central canal or haversian canal. Resembling the growth rings of a tree, the concentric lamellae (la MELē) are circular plates of mineralized extracellular matrix of increasing diameter, surrounding a small network of blood vessels and nerves located in the central canal (Figure 6.3a). These tubelike units of bone generally form a series of parallel cylinders that, in long bones, tend to run parallel to the long axis of the bone. Between the concentric lamellae are small spaces called lacunae (laKOOnē = little lakes; singular is lacuna), which contain osteocytes. Radiating in all directions from the lacunae are tiny canaliculi (kanaLIKūlī = small channels), which are filled with extracellular fluid. Inside the canaliculi are slender fingerlike processes of osteocytes. Neighboring osteocytes communicate via gap junctions. The canaliculi connect lacunae with one another and with the central canals, forming an intricate, miniature system of interconnected canals throughout the bone. This system provides many routes for nutrients and oxygen to reach the osteocytes and for the removal of wastes. Osteons in compact bone tissue are aligned in the same direction and are parallel to the length of the diaphysis. As a result, the shaft of a long bone resists bending or fracturing even when considerable force is applied from either end. Compact bone tissue tends to be thickest in those parts of a bone where stresses are applied in relatively few directions. The lines of stress in a bone are not static. They change as a person learns to walk and in response to repeated strenuous physical activity, such as weight training. The lines of stress in a bone also can change because of fractures or physical deformity. Thus, the organization of osteons is not static but changes over time in response to the physical demands placed on the skeleton. The areas between neighboring osteons contain lamellae called interstitial lamellae (in ter ′ STISHal), which also have lacunae with osteocytes and canaliculi. Interstitial lamellae are fragments of older osteons that have been partially destroyed during bone rebuilding or growth. Blood vessels and nerves from the periosteum penetrate the compact bone through transverse perforating canals or Volkmann's canals (FOLKmans). The vessels and nerves of the perforating canals connect with those of the medullary cavity, periosteum, and central canals. Arranged around the entire outer and inner circumference of the shaft of a long bone are lamellae called circumferential lamellae (ser kumferENsh ′ ēal). They develop during initial bone formation. The circumferential lamellae directly deep to the periosteum are called outer circumferential lamellae. They are connected to the periosteum by perforating (Sharpey's) fibers. The circumferential lamellae that line the medullary cavity are called inner circumferential lamellae (Figure 6.3a). Spongy Bone Tissue In contrast to compact bone tissue, spongy bone tissue, also referred to as trabecular or cancellous bone tissue, does not contain osteons (Figure 6.3b, c). Spongy bone tissue is always located in the interior of a bone, protected by a covering of compact bone. It consists of lamellae that are arranged in an irregular pattern of thin columns called trabeculae (traBEKūlē = little beams; singular is trabecula). Between the trabeculae are spaces that are visible to the unaided eye. These macroscopic spaces are filled with red bone marrow in bones that produce blood cells, and yellow bone marrow (adipose tissue) in other bones. Both types of bone marrow contain numerous small blood vessels that provide nourishment to the osteocytes. Each trabecula consists of concentric lamellae, osteocytes that lie in lacunae, and canaliculi that radiate outward from the lacunae. Spongy bone tissue makes up most of the interior bone tissue of short, flat, sesamoid, and irregularly shaped bones. In long bones it forms the core of the epiphyses beneath the paperthin layer of compact bone, and forms a variable narrow rim bordering the medullary cavity of the diaphysis. Spongy bone is always covered by a layer of compact bone for protection. At first glance, the trabeculae of spongy bone tissue may appear to be less organized than the osteons of compact bone tissue. However, they are precisely oriented along lines of stress, a characteristic that helps bones resist stresses and transfer force without breaking. Spongy bone tissue tends to be located where bones are not heavily stressed or where stresses are applied from many directions. The trabeculae do not achieve their final arrangement until locomotion is completely learned. In fact, the arrangement can even be altered as lines of stress change due to a poorly healed fracture or a deformity. Spongy bone tissue is different from compact bone tissue in two respects. First, spongy bone tissue is light, which reduces the overall weight of a bone. This reduction in weight allows the bone to move more readily when pulled by a skeletal muscle. Second, the trabeculae of spongy bone tissue support and protect the red bone marrow. Spongy bone in the hip bones, ribs, sternum (breastbone), vertebrae, and the proximal ends of the humerus and femur is the only site where red bone marrow is stored and, thus, the site where hemopoiesis (blood cell production) occurs in adults. Bone is richly supplied with blood. Blood vessels, which are especially abundant in portions of bone containing red bone marrow, pass into bones from the periosteum. We will consider the blood supply of a long bone such as the mature tibia (shin bone) shown in Figure 6.4. Periosteal arteries (perēOStēal), small arteries accompanied by nerves, enter the diaphysis through many perforating (Volkmann's) canals and supply the periosteum and outer part of the compact bone (see Figure 6.3a). Near the center of the diaphysis, a large nutrient artery passes through a hole in compact bone called the nutrient foramen (foramina is plural). On entering the medullary cavity, the nutrient artery divides into proximal and distal branches that course toward each end of the bone. These branches supply both the inner part of compact bone tissue of the diaphysis and the spongy bone tissue and red bone marrow as far as the epiphyseal plates (or lines). Some bones, like the tibia, have only one nutrient artery; others, like the femur (thigh bone), have several. The ends of long bones are supplied by the metaphyseal and epiphyseal arteries, which arise from arteries that supply the associated joint. The metaphyseal arteries (metaFIZēal) enter the metaphyses of a long bone and, together with the nutrient artery, supply the red bone marrow and bone tissue of the metaphyses. The epiphyseal arteries (ep i ′ FIZēal) enter the epiphyses of a long bone and supply the red bone marrow and bone tissue of the epiphyses.Veins that carry blood away from long bones are evident in three places: (1) One or two nutrient veins accompany the nutrient artery and exit through the diaphysis; (2) numerous epiphyseal veins and metaphyseal veins accompany their respective arteries and exit through the epiphyses and metaphyses, respectively; and (3) many small periosteal veins accompany their respective arteries and exit through the periosteum. Nerves accompany the blood vessels that supply bones. The periosteum is rich in sensory nerves, some of which carry pain sensations. These nerves are especially sensitive to tearing or tension, which explains the severe pain resulting from a fracture or a bone tumor. For the same reason there is some pain associated with a bone marrow needle biopsy. In this procedure, a needle is inserted into the middle of the bone to withdraw a sample of red bone marrow to examine it for conditions such as leukemias, metastatic neoplasms, lymphoma, Hodgkin's disease, and aplastic anemia. As the needle penetrates the periosteum, pain is felt. Once it passes through, there is little pain. Ossification The process by which bone forms is called ossification (os ifiK ′ Āshun; ossi = bone; fication = making) or osteogenesis (os t ′ ēōJENesis). Bone formation occurs in four principal situations: (1) the initial formation of bones in an embryo and fetus, (2) the growth of bones during infancy, childhood, and adolescence until their adult sizes are reached, (3) the remodeling of bone (replacement of old bone by new bone tissue throughout life), and (4) the repair of fractures (breaks in bones) throughout life. ormation in an Embryo and Fetus In the first type of ossification, called intramembranous ossification (in traMEMbranus; ′ intra = within; membran = membrane), bone forms directly within mesenchyme, which is arranged in sheetlike layers that resemble membranes. In the second type, endochondral ossification (en d′ ōKONdral; endo = within; chondral = cartilage), bone forms within hyaline cartilage that develops from mesenchyme. Intramembranous Ossification Intramembranous ossification is the simpler of the two methods of bone formation. The flat bones of the skull, most of the facial bones, mandible (lower jawbone), and the medial part of the clavicle (collar bone) are formed in this way. Also, the “soft spots” that help the fetal skull pass through the birth canal later harden as they undergo intramembranous ossification, which occurs as follows (Figure 6.5): Development of the ossification center. At the site where the bone will develop, specific chemical messages cause the cells of the mesenchyme to cluster together and differentiate, first into osteoprogenitor cells and then into osteoblasts. The site of such a cluster is called an ossification center. Osteoblasts secrete the organic extracellular matrix of bone until they are surrounded by it. Calcification. Next, the secretion of extracellular matrix stops, and the cells, now called osteocytes, lie in lacunae and extend their narrow cytoplasmic processes into canaliculi that radiate in all directions. Within a few days, calcium and other mineral salts are deposited and the extracellular matrix hardens or calcifies (calcification). Formation of trabeculae. As the bone extracellular matrix forms, it develops into trabeculae that fuse with one another to form spongy bone around the network of blood vessels in the tissue. Connective tissue associated with the blood vessels in the trabeculae differentiates into red bone marrow. Development of the periosteum. In conjunction with the formation of trabeculae, the mesenchyme condenses at the periphery of the bone and develops into the periosteum. Eventually, a thin layer of compact bone replaces the surface layers of the spongy bone, but spongy bone remains in the center. Much of the newly formed bone is remodeled (destroyed and reformed) as the bone is transformed into its adult size and shape. Endochondral Ossification The replacement of cartilage by bone is called endochondral ossification. Although most bones of the body are formed in this way, the process is best observed in a long bone. It proceeds as follows (Figure 6.6): Development of the cartilage model. At the site where the bone is going to form, specific chemical messages cause the cells in mesenchyme to crowd together in the general shape of the future bone, and then develop into chondroblasts. The chondroblasts secrete cartilage extracellular matrix, producing a cartilage model consisting of hyaline cartilage. A covering called the perichondrium (per i ′ KONdrēum) develops around the cartilage model. Growth of the cartilage model. Once chondroblasts become deeply buried in the cartilage extracellular matrix, they are called chondrocytes. The cartilage model grows in length by continual cell division of chondrocytes, accompanied by further secretion of the cartilage extracellular matrix. This type of cartilaginous growth, called interstitial (endogenous) growth (growth from within), results in an increase in length. In contrast, growth of the cartilage in thickness is due mainlyto the deposition of extracellular matrix material on the cartilage surface of the model by new chondroblasts that develop from the perichondrium. This process is called appositional (exogenous) growth (apōZISHonal), meaning growth at the outer surface. Interstitial growth and appositional growth of cartilage are described in more detail in Section 4.5. As the cartilage model continues to grow, chondrocytes in its midregion hypertrophy (increase in size) and the surrounding cartilage extracellular matrix begins to calcify. Other chondrocytes within the calcifying cartilage die because nutrients can no longer diffuse quickly enough through the extracellular matrix. As these chondrocytes die, the spaces left behind by dead chondrocytes merge into small cavities called lacunae. Development of the primary ossification center. Primary ossification proceeds inward from the external surface of the bone. A nutrient artery penetrates the perichondrium and the calcifying cartilage model through a nutrient foramen in the midregion of the cartilage model, stimulating osteoprogenitor cells in the perichondrium to differentiate into osteoblasts. Once the perichondrium starts to form bone, it is known as the periosteum. Near the middle of the model, periosteal capillaries grow into the disintegrating calcified cartilage, inducing growth of a primary ossification center, a region where bone tissue will replace most of the cartilage. Osteoblasts then begin to deposit bone extracellular matrix over the remnants of calcified cartilage, forming spongy bone trabeculae. Primary ossification spreads from this central location toward both ends of the cartilage model. Development of the medullary (marrow) cavity. As the primary ossification center grows toward the ends of the bone, osteoclasts break down some of the newly formed spongy bone trabeculae. This activity leaves a cavity, the medullary (marrow) cavity, in the diaphysis (shaft). Eventually, most of the wall of the diaphysis is replaced by compact bone. Development of the secondary ossification centers. When branches of the epiphyseal artery enter the epiphyses, secondary ossification centers develop, usually around the time of birth. Bone formation is similar to what occurs in primary ossification centers. However, in the secondary ossification centers spongy bone remains in the interior of the epiphyses (no medullary cavities are formed here). In contrast to primary ossification, secondary ossification proceeds outward from the center of the epiphysis toward the outer surface of the bone. Formation of articular cartilage and the epiphyseal (growth) plate. The hyaline cartilage that covers the epiphyses becomes the articular cartilage. Prior to adulthood, hyaline cartilage remains between the diaphysis and epiphysis as the epiphyseal (growth) plate, the region responsible for the lengthwise growth of long bones that you will learn about next.Bone Growth during Infancy, Childhood, and Adolescence During infancy, childhood, and adolescence, bones throughout the body grow in thickness by appositional growth, and long bones lengthen by the addition of bone material on the diaphyseal side of the epiphyseal plate by interstitial growth. Growth in Length The growth in length of long bones involves the following two major events: (1) interstitial growth of cartilage on the epiphyseal side of the epiphyseal plate and (2) replacement of cartilage on the diaphyseal side of the epiphyseal plate with bone by endochondral ossification. To understand how a bone grows in length, you need to know some of the details of the structure of the epiphyseal plate. The epiphyseal (growth) plate (epiFIZēal) is a layer of hyaline cartilage in the metaphysis of a growing bone that consists of four zones (Figure 6.7b): 1. Zone of resting cartilage. This layer is nearest the epiphysis and consists of small, scattered chondrocytes. The term “resting” is used because the cells do not function in bone growth. Rather, they anchor the epiphyseal plate to the epiphysis of the bone. 2. Zone of proliferating cartilage. Slightly larger chondrocytes in this zone are arranged like stacks of coins. These chondrocytes undergo interstitial growth as they divide and secrete extracellular matrix. The chondrocytes in this zone divide to replace those that die at the diaphyseal side of the epiphyseal plate. 3. Zone of hypertrophic cartilage (hīperTRŌfik). This layer consists of large, maturing chondrocytes arranged in columns. 4. Zone of calcified cartilage. The final zone of the epiphyseal plate is only a few cells thick and consists mostly of chondrocytes that are dead because the extracellular matrix around them has calcified. Osteoclasts dissolve the calcified cartilage, and osteoblasts and capillaries from the diaphysis invade the area. The osteoblasts lay down bone extracellular matrix, replacing the calcified cartilage by the process of endochondral ossification. Recall that endochondral ossification is the replacement of cartilage with bone. As a result, the zone of calcified cartilage becomes the “new diaphysis” that is firmly cemented to the rest of the diaphysis of the bone. The activity of the epiphyseal plate is the only way that the diaphysis can increase in length. As a bone grows, chondrocytes proliferate on the epiphyseal side of the plate. New chondrocytes replace older ones, which are destroyed by calcification. Thus, the cartilage is replaced by bone on the diaphyseal side of the plate. In this way the thickness of the epiphyseal plate remains relatively constant, but the bone on the diaphyseal side increases in length (Figure 6.7c). If a bone fracture damages the epiphyseal plate, the fractured bone may be shorter than normal once adult stature is reached. This is because damage to cartilage, which is avascular, accelerates closure of the epiphyseal plate due to the cessation of cartilage cell division, thus inhibiting lengthwise growth of the bone.Growth in Thickness Like cartilage, bone can grow in thickness (diameter) only by appositional growth (Figure 6.8a): At the bone surface, periosteal cells differentiate into osteoblasts, which secrete the collagen fibers and other organic molecules that form bone extracellular matrix. The osteoblasts become surrounded by extracellular matrix and develop into osteocytes. This process forms bone ridges on either side of a periosteal blood vessel. The ridges slowly enlarge and create a groove for the periosteal blood vessel. Eventually, the ridges fold together and fuse, and the groove becomes a tunnel that encloses the blood vessel. The former periosteum now becomes the endosteum that lines the tunnel. Osteoblasts in the endosteum deposit bone extracellular matrix, forming new concentric lamellae. The formation of additional concentric lamellae proceeds inward toward the periosteal blood vessel. In this way, the tunnel fills in, and a new osteon is created. As an osteon is forming, osteoblasts under the periosteum deposit new circumferential lamellae, further increasing the thickness of the bone. As additional periosteal blood vessels become enclosed as in step , the growth process continues. Animation: Bone Elongation and Bone Widening Remodeling of Bone Like skin, bone forms before birth but continually renews itself thereafter. Bone remodeling is the ongoing replacement of old bone tissue by new bone tissue. It involves bone resorption, the removal of minerals and collagen fibers from bone by osteoclasts, and bone deposition, the addition of minerals and collagen fibers to bone by osteoblasts. Thus, bone resorption results in the destruction of bone extracellular matrix, while bone deposition results in the formation of bone extracellular matrix. At any given time, about 5% of the total bone mass in the body is being remodeled. The renewal rate for compact bone tissue is about 4% per year, and for spongy bone tissue it is about 20% per year. Remodeling also takes place at different rates in different regions of the body. The distal portion of the femur is replaced about every four months. By contrast, bone in certain areas of the shaft of the femur will not be replaced completely during an individual's life. Even after bones have reached their adult shapes and sizes, old bone is continually destroyed and new bone is formed in its place. Remodeling also removes injured bone, replacing it with new bone tissue. Remodeling may be triggered by factors such as exercise, sedentary lifestyle, and changes in diet.benefits. Since the strength of bone is related to the degree to which it is stressed, if newly formed bone is subjected to heavy loads, it will grow thicker and therefore be stronger than the old bone. Also, the shape of a bone can be altered for proper support based on the stress patterns experienced during the remodeling process. Finally, new bone is more resistant to fracture than old bone. . Factors Affecting Bone Growth and Bone Remodeling Normal bone metabolism—growth in the young and bone remodeling in the adult—depends on several factors.. 1. Minerals. Large amounts of calcium and phosphorus are needed while bones are growing, as are smaller amounts of magnesium, fluoride, and manganese. These minerals are also necessary during bone remodeling. 2. Vitamins. Vitamin A stimulates activity of osteoblasts. Vitamin C is needed for synthesis of collagen, the main bone protein. As you will soon learn, vitamin D helps build bone by increasing the absorption of calcium from foods in the gastrointestinal tract into the blood. Vitamins K and B12 are also needed for synthesis of bone proteins. 3. Hormones. During childhood, the hormones most important to bone growth are the insulinlike growth factors (IGFs), which are produced by the liver and bone tissue (see Section 18.6). IGFs stimulate osteoblasts, promote cell division at the epiphyseal plate and in the periosteum, and enhance synthesis of the proteins needed to build new bone. IGFs are produced in response to the secretion of human growth hormone (hGH) from the anterior lobe of the pituitary gland (see Section 18.6). Thyroid hormones (T3 and T4) from the thyroid gland also promote bone growth by stimulating osteoblasts. In addition, the hormone insulin from the pancreas promotes bone growth by increasing the synthesis of bone proteins. At puberty, the secretion of hormones known as sex hormones causes a dramatic effect on bone growth. The sex hormones include estrogens (produced by the ovaries) and androgens such as testosterone (produced by the testes A fracture (FRAKchoor) is any break in a bone. Fractures are named according to their severity, the shape or position of the fracture line, or even the physician who first described them. In some cases, a bone may fracture without visibly breaking. A stress fracture is a series of microscopic fissures in bone that forms without any evidence of injury to other tissues. In healthy adults, stress fractures result from repeated, strenuous activities such as running, jumping, or aerobic dancing. Stress fractures are quite painful and also result from disease processes that disrupt normal bone calcification, such as osteoporosis (discussed in Disorders: Homeostatic Imbalances at the end of this chapter The repair of a bone fracture involves the following phases Reactive phase. This phase is an early inflammatory phase. Blood vessels crossing the fracture line are broken. As blood leaks from the torn ends of the vessels, a mass of blood (usually clotted) forms around the site of the fracture. This mass of blood, called a fracture hematoma (hē′ maTŌma; hemat = blood; oma = tumor), usually forms 6 to 8 hours after the injury. Because the circulation of blood stops at the site where the fracture hematoma forms, nearby bone cells die. Swelling and inflammation occur in response to dead bone cells, producing additional cellular debris. Phagocytes (neutrophils and macrophages) and osteoclasts begin to remove the dead or damaged tissue in and around the fracture hematoma. This stage may last up to several weeks. Reparative phase: Fibrocartilaginous callus formation. The reparative phase is characterized by two events: the formation of a fibrocartilaginous callus and a bony callus to bridge the gap between the broken ends of the bones. Blood vessels grow into the fracture hematoma and phagocytes begin to clean up dead bone cells. Fibroblasts from the periosteum invade the fracture site and produce collagen fibers. In addition, cells from the periosteum develop into chondroblasts and begin to produce fibrocartilage in this region. These events lead to the development of a fibrocartilaginous (soft) callus (fibrōkartiLAJinus), a mass of repair tissue consisting of collagen fibers and cartilage that bridges the broken ends of the bone. Formation of the fibrocartilaginous callus takes about 3 weeks. Reparative phase: Bony callus formation. In areas closer to wellvascularized healthy bone tissue, osteoprogenitor cells develop into osteoblasts, which begin to produce spongy bone trabeculae. The trabeculae join living and dead portions of the original bone fragments. In time, the fibrocartilage is converted to spongy bone, and the callus is then referred to as a bony (hard) callus. The bony callus lasts about 3 to 4 months. Bone remodeling phase. The final phase of fracture repair is bone remodeling of the callus. Dead portions of the original fragments of broken bone are gradually resorbed by osteoclasts. Compact bone replaces spongy bone around the periphery of the fracture. Sometimes, the repair process is so thorough that the fracture line is undetectable, even in a radiograph (xray). However, a thickened area on the surface of the bone remains as evidence of a healed fracture. Bone heals more rapidly than cartilage because its blood supply is more plentiful. Treatments for Fractures Treatments for fractures vary according to age, type of fracture, and the bone involved. The ultimate goals of fracture treatment are realignment of the bone fragments, immobilization to maintain realignment, and restoration of function. For bones to unite properly, the fractured ends must be brought into alignment. This process, called reduction, is commonly referred to as setting a fracture. In closed reduction, the fractured ends of a bone are brought into alignment by manual manipulation, and the skin remains intact. In open reduction, the fractured ends of a bone are brought into alignment by a surgical procedure using internal fixation devices such as screws, plates, pins, rods, and wires. Following reduction, a fractured bone may be kept immobilized by a cast, sling, splint, elastic bandage, external fixation device, or a combination of these devices. Although bone has a generous blood supply, healing sometimes takes months. The calcium and phosphorus needed to strengthen and harden new bone are deposited only gradually, and bone cells generally grow and reproduce slowly. The temporary disruption in their blood supply also helps explain the slowness of healing of severely fractured bones. Bone is the body's major calcium reservoir, storing 99% of total body calcium. One way to maintain the level of calcium in the blood is to control the rates of calcium resorption from bone into blood and of calcium deposition from blood into bone. Both nerve and muscle cells depend on a stable level of calcium ions (Ca2+) in extracellular fluid to function properly. Blood clotting also requires Ca2+. Also, many enzymes require Ca2+ as a cofactor (an additional substance needed for an enzymatic reaction to occur). For this reason, the blood plasma level of Ca2+ is very closely regulated between 9 and 11 mg/100 mL. Even small changes in Ca2+ concentration outside this range may prove fatal—the heart may stop (cardiac arrest) if the concentration goes too high, or breathing may cease (respiratory arrest) if the level falls too low. The role of bone in calcium homeostasis is to help “buffer” the blood Ca2+ level, releasing Ca2+ into blood plasma (using osteoclasts) when the level decreases, and absorbing Ca2+ (using osteoblasts) when the level rises. Ca2+ exchange is regulated by hormones, the most important of which is parathyroid hormone (PTH) secreted by the parathyroid glands (see Figure 18.13). This hormone increases blood Ca2+ level. PTH secretion operates via a negative feedback system (Figure 6.10). If some stimulus causes the blood Ca2+ level to decrease, parathyroid gland cells (receptors) detect this change and increase their production of a molecule known as cyclic adenosine monophosphate (cyclic AMP). The gene for PTH within the nucleus of a parathyroid gland cell (the control center) detects the intracellular increase in cyclic AMP (the input). As a result, PTH synthesis speeds up, and more PTH (the output) is released into the blood. The presence of higher levels of PTH increases the number and activity of osteoclasts (effectors), which step up the pace of bone resorption. The resulting release of Ca2+ from bone into blood returns the blood Ca2+ level to normal. PTH also acts on the kidneys (effectors) to decrease loss of Ca2+ in the urine, so more is retained in the blood. And PTH stimulates formation of calcitriol (the active form of vitamin D), a hormone that promotes absorption of calcium from foods in the gastrointestinal tract into the blood. Both of these actions also help elevate blood Ca2+ level. Another hormone works to decrease blood Ca2+ level. When blood Ca2+ rises above normal, parafollicular cells in the thyroid gland secrete calcitonin (CT) (kalsiTŌnin). CT inhibits activity of osteoclasts, speeds blood Ca2+ uptake by bone, and accelerates Ca2+ deposition into bones. The net result is that CT promotes bone formation and decreases blood Ca2+ level. Despite these effects, the role of CT in normal calcium homeostasis is uncertain because it can be completely absent without causing symptoms. Nevertheless, calcitonin harvested from salmon (Miacalcin®) is an effective drug for treating osteoporosis because it slows bone resorption. Figure 18.14 summarizes the roles of parathyroid hormone, calcitriol, and calcitonin in regulation of blood Ca2+ level. Animation : Regulation of Blood Calcium , Regulation of Bone Growth and Blood Calcium Release of calcium from bone matrix and retention of calcium by the kidneys are the two main ways that blood calcium level can be increased. Within limits, bone tissue has the ability to alter its strength in response to changes in mechanical stress. When placed under stress, bone tissue becomes stronger through increased deposition of mineral salts and production of collagen fibers by osteoblasts. Without mechanical stress, bone does not remodel normally because bone resorption occurs more quickly than bone formation. Research has shown that highimpact intermittent strains more strongly influence bone deposition as compared with lowerimpact constant strains. Therefore, running and jumping stimulate bone remodeling more dramatically than walking. The main mechanical stresses on bone are those that result from the pull of skeletal muscles and the pull of gravity. If a person is bedridden or has a fractured bone in a cast, the strength of the unstressed bones diminishes because of the loss of bone minerals and decreased numbers of collagen fibers. Astronauts subjected to the microgravity of space also lose bone mass. In any of these cases, bone loss can be dramatic—as much as 1% per week. In contrast, the bones of athletes, which are repetitively and highly stressed, become notably thicker and stronger than those of astronauts or nonathletes. Weightbearing activities, such as walking or moderate weight lifting, help build and retain bone mass. Adolescents and young adults should engage in regular weightbearing exercise prior to the closure of the epiphyseal plates to help build total mass prior to its inevitable reduction with aging. However, people of all ages can and should strengthen their bones by engaging in weightbearing exercise. Animation: Bone Processes Response to Stress in Adult Bones From birth through adolescence, more bone tissue is produced than is lost during bone remodeling. In young adults the rates of bone deposition and resorption are about the same. As the level of sex hormones diminishes during middle age, especially in women after menopause, a decrease in bone mass occurs because bone resorption by osteoclasts outpaces bone deposition by osteoblasts. In old age, loss of bone through resorption occurs more rapidly than bone gain. Because women's bones generally are smaller and less massive than men's bones to begin with, loss of bone mass in old age typically has a greater adverse effect in females. These factors contribute to the higher incidence of osteoporosis in females. There are two principal effects of aging on bone tissue: loss of bone mass and brittleness. Loss of bone mass results from demineralization (dēmin eraliZ ′ Āshun), the loss of calcium and other minerals from bone extracellular matrix. This loss usually begins after age 30 in females, accelerates greatly around age 45 as levels of estrogens decrease, and continues until as much as 30% of the calcium in bones is lost by age 70. Once bone loss begins in females, about 8% of bone mass is lost every 10 years. In males, calcium loss typically does not begin until after age 60, and about 3% of bone mass is lost every 10 years. The loss of calcium from bones is one of the problems in osteoporosis (see Disorders section). The second principal effect of aging on the skeletal system, brittleness, results from a decreased rate of protein synthesis. Recall that the organic part of bone extracellular matrix, mainly collagen fibers, gives bone its tensile strength. The loss of tensile strength causes the bones to become very brittle and susceptible to fracture. In some elderly people, collagen fiber synthesis slows, in part due to diminished production of human growth hormone. In addition to increasing the susceptibility to fractures, loss of bone mass also leads to deformity, pain, loss of height, and loss of teeth.