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Skeleton A 12 year-old boy is brought in with a bone fracture injury. The…

- - - - -A glistening white, double-layered membrane called the periosteum (per˝e-os´te-um; peri = around, osteo = bone) covers the external surface of the entire bone except the joint surfaces. The outer fibrous layer of the periosteum is dense irregular connective tissue. The inner osteogenic layer next to the bone surface contains osteoprogenitor cells (primitive stem cells that give rise to most bone cells). It also has bone-destroying cells (osteoclasts) and bone-forming cells (osteoblasts).
      - -The periosteum is richly supplied with nerve fibers and blood vessels, which is why broken bones are painful and bleed profusely. Perforating fibers—bundles of collagen fibers that extend into the bone matrix—secure the periosteum to the underlying bone. The periosteum also provides anchoring points for tendons and ligaments. At these points the perforating fibers are exceptionally dense.
      - -A delicate connective tissue membrane called the endosteum (en-dos´te-um; “within the bone”) covers internal bone surfaces. The endosteum covers the trabeculae of spongy bone and lines the canals that pass through the compact bone. The endosteum contains the same cell types as the inner layer of the periosteum.
    - - Unlike cartilage, bones are well vascularized. The main vessels serving the diaphysis are a nutrient artery and a nutrient vein. Together these run through a hole in the wall of the diaphysis, the nutrient foramen (fo-ra´men; “opening”). The nutrient artery runs inward to supply the bone marrow and the spongy bone. Branches then extend outward to supply the compact bone. Several epiphyseal arteries and veins serve each epiphysis in the same way. Nerves accompany blood vessels through the nutrient foramen into the bone.
    - - The epiphyses (e-pif′ĭ-sēz; singular: epiphysis) are the bone ends (epi = upon). An outer shell of compact bone forms the epiphysis exterior and the interior contains spongy bone. A thin layer of articular (hyaline) cartilage covers the joint surface of each epiphysis, cushioning the opposing bone ends during movement and absorbing stress.
        Between the diaphysis and each epiphysis of an adult long bone is an epiphyseal line, a remnant of the epiphyseal plate. The epiphyseal plate, commonly called the growth plate, is a disc of hyaline cartilage that grows during childhood to lengthen the bone. The flared portion of the bone where the diaphysis and epiphysis meet, whether it is the epiphyseal plate or line, is called the metaphysis (meta = between).
    - - A tubular diaphysis (di-af′ĭ-sis; dia = through, physis = growth), or shaft, forms the long axis of the bone. It is constructed of a relatively thick collar of compact bone that surrounds a central medullary cavity (med´u-lar-e; “middle”), or marrow cavity, that contains no bone tissue. Instead, the medullary cavity contains yellow marrow (fat) in adults and so is called the yellow marrow cavity. Between the marrow and the compact bone, there is often a thin layer of spongy bone.
    - - Every bone has a dense outer layer that looks smooth and solid to the naked eye. This external layer is compact bone. Internal to this is spongy bone (also called trabecular bone), a honeycomb of small needle-like or flat pieces called trabeculae (trah-bek´u-le; “little beams”). In living bones the open spaces between trabeculae are filled with red or yellow bone marrow.
    - - Hematopoietic (blood-forming) tissue is also called red marrow. It is found in different locations in infants and adults. In infants, the medullary cavity of the diaphysis and all areas of spongy bone contain red bone marrow. In adults, much of the red marrow, particularly in long bones, has been replaced by yellow marrow. In most adult long bones, the fat-containing yellow marrow extends well into the epiphysis, and little red marrow is present in the spongy bone cavities. As a result, red marrow in adults is only found in the cavities between trabeculae of spongy bones in:
      - • The flat bones of the skull, as well as the sternum, ribs, clavicles, scapulae, hip bones, and vertebrae
      - • The heads of the femur (thigh bone) and humerus (long bone of the arm)
      - Compared to long bones (femur and humerus), the red marrow found in the spongy bone of flat bones (such as the sternum) and in some irregular bones (such as the hip bone) is much more active in hematopoiesis. When clinicians suspect problems with the blood-forming tissue, they obtain red marrow samples from these sites. However, yellow marrow in the medullary cavity can revert to red marrow if a person becomes very anemic (has low oxygen-carrying capacity) and needs more red blood cells.
    - - The external surface of a bone is rarely smooth and featureless. Instead, it has distinct bone markings that provide a wealth of information about how that bone and its attached muscles and ligaments work together. Bone markings fit into three categories: (1) projections that are sites of muscle and ligament attachment, (2) surfaces that form joints, and (3) depressions and openings for blood vessels and nerves.
    - - Bone is composed of living cells and matrix. The extracellular matrix includes osteoid, organic substances that are secreted by osteoblasts and give the bone tensile strength. Its inorganic (mineral) components, the hydroxyapatites (calcium salts), make bone hard.
  - - - Look like frosted glass when freshly exposed, provide support with flexibility and resilience. They are the most abundant skeletal cartilages. Their chondrocytes are spherical, and the only fiber type in their matrix is fine collagen fibers (which are undetectable microscopically). Colored blue in, skeletal hyaline cartilages include:
        
        • Articular cartilages (artic = joint, point of connection), which cover the ends of most bones at movable joints
        
        • Costal cartilages, which connect the ribs to the sternum (breastbone)
        
        • Respiratory cartilages, which form the skeleton of the larynx (voice box) and reinforce other respiratory passageways
        
        • Nasal cartilages, which support the external nose
    - - Highly compressible with great tensile strength, fibrocartilages consist of roughly parallel rows of chondrocytes alternating with thick collagen fibers. Fibrocartilages occur in sites that are subjected to both pressure and stretch, such as the padlike cartilages (menisci) of the knee and the discs between vertebrae
    - - Resemble hyaline cartilages, but they contain more stretchy elastic fibers and so are better able to stand up to repeated bending. They are found in only two skeletal locations (shown in green in the external ear and the epiglottis (the flap that bends to cover the opening of the larynx each time we swallow).
    - - Unlike bone, which has a hard matrix, cartilage has a flexible matrix that can accommodate mitosis. It is the ideal tissue to use to rapidly lay down the embryonic skeleton and to provide for new skeletal growth.
        
        • Appositional growth
        In appositional growth, cartilage-forming cells in the surrounding perichondrium secrete new matrix against the external face of the existing cartilage tissue.
        
        • Interstitial growth.
        In interstitial growth, the lacunae-bound chondrocytes divide and secrete new matrix, expanding the cartilage from within. Typically, cartilage growth ends during adolescence when the skeleton stops growing.
    - - Bone is a dynamic and active tissue, and small-scale changes in bone architecture occur continually. Every year, remodeling replaces about 5–10% of our skeleton, and our entire skeleton is replaced about every 10 years. Spongy bone is replaced every three to four years; compact bone, every 10 years or so. This is essential because when bone remains in place for long periods, more of the calcium salts crystallize and the bone becomes more brittle—ripe conditions for fracture.
        In the adult skeleton, bone is deposited and removed primarily at the endosteal surface. Together, bone resorption and deposit constitute bone remodeling. Bone remodeling is coordinated by cohorts of adjacent osteoblasts and osteoclasts, which respond to signals from hormones and stress-sensing osteocytes (discussed shortly).
        Remodeling does not occur uniformly. For example, the distal part of the femur (thigh bone) is fully replaced every five to six months, whereas its shaft is altered much more slowly.
        
        Bone Deposition
        Following behind the osteoclasts, osteoblasts deposit new bone matrix. This begins as an osteoid seam—an unmineralized band of gauzy-looking bone matrix 10–12 micrometers (mm) wide. Between the osteoid seam and the older mineralized bone, there is an abrupt transition called the calcification front.
        How does the osteoid become calcified? The proteins of the newly deposited osteoid bind calcium ions (Ca2+), raising the local concentration of Ca2+. This in turn triggers osteoblasts to release matrix vesicles studded with the enzyme alkaline phosphatase. This enzyme cuts phosphate (Pi) ions off of the osteoid proteins, raising the local concentration of Pi. When the concentrations of Ca2+ and Pi are high enough, tiny calcium phosphate crystals form. These crystals then act as the seed around which hydroxyapatites (the mineral salts in bones) form. The result is that calcium salts are deposited throughout the osteoid, creating calcified bone matrix.
        
        Bone Resorption
        As noted earlier, the giant osteoclasts accomplish bone resorption. Osteoclasts move along a bone surface, digging depressions or grooves as they break down the bone matrix. The ruffled border of the osteoclast clings tightly to the bone, sealing off the area of bone destruction and secreting acid (H+) that dissolve the bone minerals and lysosomal enzymes that digest the organic matrix. The digested matrix end products and dissolved minerals are then endocytosed, transported across the osteoclast (by transcytosis), and released at the opposite side. There they enter the interstitial fluid and then the blood. Osteoclasts may also phagocytize dead osteocytes and any undigested demineralized matrix. When resorption of a given area of bone is completed, the osteoclasts undergo apoptosis (cell death).
        
        Control of Remodeling
        Remodeling goes on continuously in the skeleton, primarily regulated by two control loops that serve different purposes:
        -Maintaining Ca2+ homeostasis. A hormonal negative feedback loop involving parathyroid hormone maintains Ca2+ homeostasis in the blood.
        -Keeping bone strong. Mechanical and gravitational forces acting on a bone drive remodeling where it is required to strengthen that bone.
        -Hormonal controls determine whether and when remodeling occurs.
        -Mechanical stress determines where remodeling occurs.
        
        Mechanical stress
        The second set of controls regulating bone remodeling, bone’s response to mechanical stress (muscle pull and gravity), keeps the bones strong where stressors are acting.
        
        Wolff’s law holds that a bone grows or remodels in response to the demands placed on it. The first thing to understand is that a bone’s anatomy reflects the common stresses it encounters. For example, a bone is loaded (stressed) whenever weight bears down on it or muscles pull on it. This loading is usually off center and tends to bend the bone. Bending compresses the bone on one side and subjects it to tension (stretching) on the other
        
        In response to these mechanical stressors, the compact bone of long bones is thickest midway along the diaphysis, exactly where bending stresses are greatest (bend a stick and it will split near the middle). Both compression and tension are minimal toward the center of the bone (they cancel each other out), so a bone can “hollow out” for lightness (using spongy bone instead of compact bone) without jeopardy.
        
        Wolff’s law also explains the featureless bones of the fetus and the atrophied bones of bedridden people—situations in which bones are not stressed.
        
        How do mechanical forces communicate with the cells responsible for remodeling? Deforming bone pushes fluid containing ions through the canaliculi. This creates an electrical current. This electrical current is detected by osteocytes, which release chemical messengers that promote the formation of additional bone. This process underlies some of the electrical devices used to speed healing of fractures
        
        Wolff’s law also explains several other observations:
        -Handedness (being right- or left-handed) results in the bones of one upper limb being thicker than those of the less-used limb
        -Curved bones are thickest where they are most likely to buckle
        -The trabeculae of spongy bone form trusses, or struts, along lines of compression
        -Large, bony projections occur where heavy, active muscles attach. The bones of weight lifters have enormous thickenings at the attachment sites of the most-used muscles
        
        Hormonal controls
        To understand the hormonal control of bone remodeling, you need to understand calcium’s importance in the body. Maintaining extracellular fluid calcium levels within homeostatic levels is absolutely critical for maintaining the resting membrane potential of all cells. Without normal levels of blood calcium, nerves cannot fire as needed and muscles are unable to contract.
        
        The human body contains 1200–1400 g of calcium. More than 99% of this calcium is contained in bone minerals, 0.9% is inside cells, and less than 0.1% is in the extracellular fluid. Hormones use the vast amount of calcium in bone as a “storage bank” from which they can make withdrawals (resorption) or deposits as needed to maintain extracellular fluid calcium levels. Hormonal control normally maintains blood Ca2+ within the narrow range of 9–11 mg per dl (100 ml) of blood. Calcium is absorbed from the intestine under the control of the active form of vitamin D, called calcitriol.
        
        The hormonal controls primarily involve parathyroid hormone (PTH), produced by the parathyroid glands. When blood levels of Ca2+ decline, PTH is released (Figure 6.14). The increased PTH level stimulates osteoclasts to resorb bone, releasing Ca2+ into the blood. The PTH stimulation of osteoclasts is indirect—various cells (e.g., osteoblasts) respond to PTH secretion by producing another protein (RANK-L) that stimulates the formation and activity of osteoclasts.
        
        As blood concentrations of calcium rise, the stimulus for PTH release ends. The decline of PTH reverses its effects and causes blood Ca2+ levels to fall.
        
        Control by PTH acts to preserve blood calcium homeostasis, not the skeleton’s strength or well-being. Osteoclasts are no respecters of matrix age: When activated, they break down both old and new matrix. In fact, if blood calcium levels are low for an extended time, the bones become so demineralized that they develop large holes. We will discuss blood calcium regulation further in Chapter 16.
        
        Another hormone, calcitonin (kal˝sĭ-to´nin) produced by parafollicular cells of the thyroid gland, has been thought to regulate blood Ca2+ levels as well. However, in humans, calcitonin appears to be a hormone in search of a function. At normal levels, its effects on calcium homeostasis are negligible. When administered at pharmacological (abnormally high) doses, it does lower blood calcium levels temporarily.
        
        Various other hormones also affect bone resorption and deposition by either stimulating or inhibiting osteoclast activity. Like PTH, glucocorticoids (hormones from the adrenal cortex) and vitamin D indirectly stimulate osteoclast activity by increasing the synthesis of RANK-L and decreasing the synthesis of its antagonist (osteoprotegerin). Sex hormones, on the other hand, have the opposite effect—they increase the synthesis of RANK-L’s antagonist.
    - - Longitudinal bone growth mimics many of the events of endochondral ossification and depends on the presence of epiphyseal cartilage. The cartilage is relatively inactive on the side of the epiphyseal plate facing the epiphysis, a region called the resting zone (Figure 6.12). Below the resting zone, the cartilage cells form tall columns, like coins in a stack, that allow fast, efficient growth.
        
        1 Proliferation zone: The cells at the “top” (epiphysis-facing) side of the stack next to the resting zone comprise the proliferation or growth zone. These cells divide quickly, pushing the epiphysis away from the diaphysis and lengthening the entire long bone.
        
        2 Hypertrophic zone: The older chondrocytes in the stack, which are closer to the diaphysis, hypertrophy (enlarge). Their lacunae erode and enlarge, leaving large interconnecting spaces.
        
        3 Calcification zone: The surrounding cartilage matrix calcifies, the chondrocytes die, and the matrix begins to deteriorate, allowing blood vessels to invade. This leaves long, slender spicules of calcified cartilage at the epiphysis-diaphysis junctions, which look like stalactites hanging from the roof of a cave.
        
        4 Ossification zone: The calcified spicules are invaded by marrow elements from the medullary cavity. Osteoclasts partly erode the cartilage spicules, then osteoblasts cover them with new bone. Ultimately spongy bone replaces them. Eventually, as osteoclasts digest the spicule tips, the medullary cavity also lengthens.
    - - Growing bones widen as they lengthen. As with cartilages, bones increase in thickness or, in the case of long bones, diameter, by appositional growth. Osteoblasts in the periosteum secrete bone matrix on the external bone surface as osteoclasts on the endosteal surface of the diaphysis remove bone. Normally there is slightly more building up than breaking down. This unequal process produces a thicker, stronger bone but prevents it from becoming too heavy.
    - - The bone growth that occurs until young adulthood is exquisitely controlled by a symphony of hormones. During infancy and childhood, the single most important stimulus of epiphyseal plate activity is growth hormone released by the anterior pituitary gland. Thyroid hormones modulate the activity of growth hormone, ensuring that the skeleton has proper proportions as it grows.
        At puberty, sex hormones are released in increasing amounts. In both sexes, estrogens have a critical role in bone development. (In males, some circulating testosterone is converted to estrogens.) At low levels, estrogens stimulate the growth spurt typical of adolescence, but as estrogen levels increase over time, they induce epiphyseal closure, ending longitudinal bone growth. Masculinization or feminization of specific parts of the skeleton depends on the relative levels of estrogens and testosterone.
        Excesses or deficits of any of these hormones can result in abnormal skeletal growth. For example, hypersecretion of growth hormone in children results in excessive height (gigantism), and deficits of growth hormone or thyroid hormone produce characteristic types of dwarfism.
    - - A skeletal cartilage exhibits chondrocytes housed in lacunae (cavities) within the extracellular matrix (ground substance and fibers). It contains large amounts of water (which accounts for its resilience), lacks nerve fibers, is avascular, and is surrounded by a fibrous perichondrium that resists expansion
  - - - 1. A hematoma forms. When a bone breaks, blood vessels in the bone and periosteum (and perhaps in surrounding tissues) are torn. The hemorrhaged blood clots, forming a hematoma (he˝mah-to´mah) at the fracture site. Soon, bone cells deprived of nutrition die, and the tissue at the site becomes swollen, painful, and inflamed.
        
        2. Fibrocartilaginous callus forms. Within a few days, new blood vessels grow into the clot. Fibroblasts and chondroblasts invade the fracture site from the nearby periosteum and endosteum. The fibroblasts produce collagen fibers that span the break and connect the broken bone ends. The chondroblasts secrete a cartilaginous matrix that bulges externally and later calcifies, forming a fibrocartilaginous callus that spans the break and connects the broken bone ends. This entire mass of repair tissue, also called the soft callus (kal´us; “hard skin”), splints the broken bone.
        
        3. Bony callus forms. Within this mass of repair tissue, osteoblasts begin forming spongy bone. Within a week, osteoblasts begin to lay down trabeculae of new bone around and within the fibrocartilaginous callus. These trabeculae span the width of the callus and unite the two fragments of broken bone. Gradually the fibrocartilaginous callus is replaced by immature bone, converting it to a bony (hard) callus. Bony callus formation continues until a firm union forms about two months later. This process generally repeats the events of endochondral ossification.
        
        4. Bone remodeling occurs. Beginning during bony callus formation and continuing for several months after, the bony callus is remodeled. The excess material on the diaphysis exterior and within the medullary cavity is removed. Compact bone is laid down to reconstruct the shaft walls. The repaired area resembles the original unbroken bony region because it responds to the same set of mechanical stressors.
  - - - • Position of the bone ends after fracture: In nondisplaced fractures, the bone ends retain their normal position. In displaced fractures, the bone ends are out of normal alignment.
      - • Completeness of the break: If the bone is broken through, the fracture is a complete fracture. If not, it is an incomplete fracture.
      - • Whether the bone ends penetrate the skin: If so, the fracture is an open (compound) fracture. If not, it is a closed (simple) fracture.
      - In addition to these three classifications, all fractures can be described in terms of the location of the fracture, its external appearance, and/or the nature of the break
    - - Comminuted fracture
        -Bone Fragment into three or more pieces
        -Particularly common in the aged, whose bones are more brittle
      - Epiphyseal fracture
        -Epiphysis seperates from the diaphysis along the epiphyseal plate
        -Tends to occur where cartilage cells are dying and calcification of the matrix is occurring
      - Compression fracture
        -Bone is crushed
        -common in porous bones(osteoportic)
      - Depressed fracture
        -Broken bone portion is pressed inward
        -Typical of skull fracture
      - Spiral fracture
        -Ragged break occurs when excessive twisting forces are applied to a bone
        -Common sports fracture
      - Greenstick fracture
        -Bone breaks incompletely, much in the way a green twig breaks. Only one side of the shaft breaks; the other side bends
        -Common in children, whose bones have relativel;y more organic matrix and are more flexible than those adults