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Which is likely to heal faster, a bone injury or a cartilage injury? Why?

A bone injury because bone has more blood vessels and with cartilage you have to rely on diffusion.

Fossa

Flattened or shallow depression

How do bones respond to mechanical stress?

Typically, the bones of athletes become noticeably thicker as a result of repetitive and stressful exercise. Weight-bearing activities, such as weight lifting, walking, or running help build and retain bone mass. Research has shown that regular weight-bearing exercise can increase total bone mass in adolescents and young adults prior to its inevitable reduction later in life. In fact, research suggests that even 70- and 80-year- olds who perform moderate weight training can increase their bone mass.

Compare and contrast compact bone with spongy bone.

Unlike compact bone, spongy bone contains no osteons.

Describe the role of vitamins A and C in the formation of bones.

Vitamin D is necessary for the normal absorption of calcium from the intestines. Vitamin C is necessary for collagen synthesis by osteoblasts. Vitamin A is a family of fat-soluble compounds that play an important role in vision, bone growth, reproduction, cell division, and cell differentiation. Vitamin A is important for healthy bones. However, too much vitamin A has been linked to bone loss and an increase in the risk of hip fracture. Scientists believe that excessive amounts of vitamin A trigger an increase in osteoclasts, the cells that break down bone. They also believe that too much vitamin A may interfere with vitamin D, which plays an important role in preserving bone. Retinol is the form of vitamin A that causes concern. In addition to getting retinol from their diets, some people may be using synthetic retinoid preparations that are chemically similar to vitamin A to treat acne, psoriasis, and other skin conditions. These preparations have been shown to have the same negative impact on bone health as dietary retinol. Use of these medications in children and teens also has been linked to delays in growth. Beta-carotene, on the other hand, is largely considered to be safe and has not been linked to adverse effects in bone or elsewhere in the body.

Osteoporosis

meaning porous bones, is a disease that results in decreased bone mass and leads to weakened bones that are prone to fracture. The occurrence of osteoporosis is greatest among the elderly, especially Caucasian women, and the severity is closely linked to both age and onset of menopause. Smoking is also a risk factor for osteoporosis. Postmenopausal women are at risk because (1) women have less bone mass than men, (2) women begin losing bone mass earlier and faster in life (sometimes around 35 years of age), and (3) postmenopausal women no longer produce significant amounts of estrogen, which appears to help protect against osteoporosis by stimulating bone growth. As a result of osteoporosis, the incidence of fractures increases, most frequently in the wrist, hip, and vertebral column. The best treatment for osteoporosis seems to be prevention. Young adults should maintain good nutrition and physical activity to ensure adequate bone density, thus allowing for the normal, age-related loss later in life. Calcium supplements with vitamin D help maintain bone health, but by themselves will not stimulate new bone growth. Medical treatments involve two strategies: (1) slowing the rate of bone loss and (2) attempting to stimulate new bone growth. A class of medications called bisphosphonates (e.g., alendronate [Fosamax], risedronate [Actonel], ibandro- nate [Boniva]) currently are prescribed to slow the pro- gression of osteoporosis. These drugs work by interfering with osteoclast function and thus retarding the removal of bone during remodeling. Unfortunately, these drugs have also been implicated in increased risk of osteonecrosis (bone death) of the jaw and some other bone growth abnormalities, so patients are recommended not to take the drugs for longer than 5 years at a time.

What are the factors affecting bone remodeling?

Bone growth and bone remodeling both begin during embryologic development. We examine both processes here and the major hormones that regulate them. Even when adult bone size has been reached, the bone continues to renew and reshape itself throughout a person's lifetime. This constant, dynamic process of continual addition of new bone tissue (bone deposition) and removal of old bone tissue (bone resorption) is a process called bone remodeling. This ongoing process occurs at both the periosteal and endosteal surfaces of a bone. It is estimated that about 20% of the adult human skeleton is replaced yearly. However, bone remodeling does not occur at the same rate everywhere in the skeleton. For example, the compact bone in our skeleton is replaced at a slower rate than the spongy bone. The distal part of the femur (thigh bone) is replaced every 4 to 6 months, whereas the diaphysis of this bone may not be completely replaced during an individual's lifetime. Clearly, bone remodeling is dependent upon the coordinated activities of osteoblasts, osteocytes, and osteoclasts. The relative activities of these cells is influenced by two primary factors: hormones (described in the next section) and mechanical stress to the bone. Mechanical stress. Serotonin was previously discussed in section 1.6. Researchers have discovered that most bone cells have serotonin receptors, and specifically that when levels of circulating serotonin are too high, osteoprogenitor cells are prevented from differentiating into osteoblasts. Thus, serotonin appears to play a role in the rate and regulation of normal bone remodeling because it affects osteoblast differentiation. Further research is ongoing to see if abnormally high levels of serotonin are linked to low bone density disorders. Three additional hormones—parathyroid hormone, calcitriol, and calcitonin—participate in both regulating bone remodeling and regulating blood calcium levels. These hormones are discussed in detail in the next section.

Summarize the process of endochondral ossification (two paragraphs).

Boys Cant Pee During Erections Bone Collar Formation Cavitation Periosteal Bud Invasion Diaphysis Elongation Epiphiseal Ossification

Achondroplasia

(a type of dwarfism). Normal endochondral ossification of bones. Achondroplasia is a form of short-limbed dwarfism. The word achondroplasia literally means "without cartilage formation." Cartilage is a tough but flexible tissue that makes up much of the skeleton during early development. However, in achondroplasia the problem is not in forming cartilage but in converting it to bone 9 (a process called ossification), particularly in the long bones of the arms and legs. Achondroplasia is similar to another skeletal disorder called hypochondroplasia, but the features of achondroplasia tend to be more severe. All people with achondroplasia have short stature. The average height of an adult male with achondroplasia is 131 centimeters (4 feet, 4 inches), and the average height for adult females is 124 centimeters (4 feet, 1 inch). Characteristic features of achondroplasia include an average-size trunk, short arms and legs with particularly short upper arms and thighs, limited range of motion at the elbows, and an enlarged head (macrocephaly) with a prominent forehead. Fingers are typically short and the ring finger and middle finger may diverge, giving the hand a three-pronged (trident) appearance. People with achondroplasia are generally of normal intelligence. Health problems commonly associated with achondroplasia include episodes in which breathing slows or stops for short periods (apnea), obesity, and recurrent ear infections. In childhood, individuals with the condition usually develop a pronounced and permanent sway of the lower back (lordosis) and bowed legs. Some affected people also develop abnormal front-to-back curvature of the spine (kyphosis) and back pain. A potentially serious complication of achondroplasia is spinal stenosis, which is a narrowing of the spinal canal that can pinch (compress) the upper part of the spinal cord. Spinal stenosis is associated with pain, tingling, and weakness in the legs that can cause difficulty with walking. Another uncommon but serious complication of achondroplasia is hydrocephalus, which is a buildup of fluid in the brain in affected children that can lead to increased head size and related brain abnormalities.

Calcitonin

(calx = lime, tonos = stretching) is another hormone that aids in regulating blood calcium levels— however, it has a less significant role than either PTH or calcitriol. Calcitonin is released from the thyroid gland—specifically, from its parafollicular cells (see section 17.8b) in response to high blood calcium levels; it is also secreted in response to stress from exercise. • Although the entire function of calcitonin is unclear, it is known that calcitonin primarily inhibits osteoclast activity. In addition, calcitonin stimulates the kidneys to increase the loss of calcium in the urine. The result is a reduction in blood calcium levels. The following limitations are observed with calcitonin: • Calcitonin seems to have the greatest effect under conditions where there is the greatest turnover of bone, such as in growing children. • If high doses of calcitonin are administered, blood calcium levels decrease only temporarily. Thus, therapeutic injections of calcitonin cannot provide long-term decrease in blood calcium.

Osteocytes

(cyt = cell) are mature bone cells derived from osteoblasts that have lost their bone-forming ability when enveloped by calcified osteoid. Connections between the original neighboring osteoblasts are maintained as they become osteocytes. Osteocytes maintain the bone matrix and detect mechanical stress on a bone. If stress is detected, osteoblasts are signaled, and it may result in the deposition of new bone matrix at the surface.

Osteoclasts

(klastos = broken) are large, multi- nuclear, phagocytic cells. They are derived from fused bone mar- row cells similar to those that produce monocytes (described in section 18.3c). These cells exhibit a ruffled border where they contact the bone, which increases their surface area exposure to the bone. An osteoclast is often located within or adjacent to a depression or pit on the bone surface called a resorption lacuna (Howship's lacuna). Osteoclasts are involved in breaking down bone in an important process called bone resorption (described shortly). Osteoblasts perform the important function of synthesizing and secreting the initial semisolid organic form of bone matrix called osteoid

Describe the growth of a long bone; indicate what occurs in the 5 layers of the growth area.

A long bone grows in length my multiplication of cells in the epiphyseal plate of cartilage. The cartilage cells divide and increase in number. The zone of active division in the epiphyseal plate of cartilage lies towards the epiphysis (end of the bone). This means that newly formed cartilage cells will push the older, larger cells towards the diaphysis (shaft of the bone). Eventually these cartilage cells are replaced by osteocytes (bone 6 cells), thus increasing the length of the bone. It should be kept in mind that after puberty, when the epiphyseal plate of cartilage no more exists, the growth in length of a bone stops completely.

Ramus

Angular extension of a bone relative to the rest of the structure.

Endochondral ossification

Bone Collar Formation The primary ossification center develops in the center of the bone. Osteoblasts found in the bone will secrete osteoid against the walls of the diaphysis. This bone collar gives the developing bone structural support to begin hardening. Cavitation -The chondrocytes go through enlargement and signal the hyalin cartilage to harden into bone. The calcified hyalin cartilage is impermeable to the diffusion of nutrients. Since the chondrocytes cant receive any nutrients they begin to die and leave small cavities. These small cavities leave room in the hardened bone for blood vessels to travel through. Periosteal bud invasion is the introduction of a nutrient highway to the bone. Periosteal region is invaded by a bud containing blood vessels and nerves. This allows not only nutrients, but osteoblasts and osteoclasts cells to enter into the cavities. The osteoblasts secrete osteoid into the remaining hyalin cartilage and give rise to early spongy bone. Diaphysis Elongation - After the nutrient source is delivered to the center of the bone, the diaphysis region has the resources to elongate. The elogated region is powered by cells dividing in the primary center of ossification. This elongated region is known as the medullary cavity. The medullary cavity is where the bone marrow is contained. Epiphyseal Ossification - Just before birth the ends of the bone or Epiphysis will develop their own centers of ossification. These centers are known as the secondary centers of ossification. They go through the same process as the primary center of ossification: hypertrophication, calcification, cavitation, and periosteal bud invasion.

How do osteocytes communicate?

Canaliculi are tiny, interconnecting channels within the bone connective tissue that extend from each lacuna, travel through the lamellae, and connect to other lacunae and the central canal. Canaliculi house osteocyte cytoplasmic projections that permit intercellular contact and communication. Nutrients, minerals, gases, and wastes are transported through the cytoplasmic extensions within these passageways, allowing their exchange between the blood vessels of the central canal and the osteocytes.

What is an osteon, and what are its components?

Functional unit of compact bone tissue; also called a Haversian system. The process of the formation of osteons and their accompanying Haversian canals begins when immature woven bone and primary osteons are destroyed by large cells called osteoclasts, which hollow out a channel through the bone, usually following existing blood vessels. The central (Haversian) canal is a cylindrical channel that lies in the center of the osteon and runs parallel to it. Extending through the central canal are the blood vessels and nerves that supply the bone.

What are the functions of the skeletal system?

Functions include: Support, protection, movement, hemopoiesis, storage or mineral and energy reserves.

Disorders of Growth Hormone Secretion

Growth hormone deficiency, also known as pituitary dwarfism, is a condition that exists at birth as a result of inadequate growth hormone production due to a hypothalamic or pituitary problem. Growth retardation is typically not evident until a child reaches 1 year of age, because the influence of growth hormone (GH) is minimal during the first 6 to 12 months of life. In addition to short stature, children with pituitary dwarfism often have periodic low blood sugar (hypoglycemia). Injections of growth hormone over a period of many years can bring about improvement, but not a normal state. Oversecretion of growth hormone in childhood causes pituitary gigantism. Beyond extraordinary height (sometimes up to 8 feet), these people have enormous internal organs, a large and protruding tongue, and significant problems with blood glucose management. If untreated, a pituitary giant dies at a comparatively early age, often from complications of diabetes or heart failure. Excessive growth hormone production in an adult results in acromegaly instead of gigantism because the epiphyseal plate is closed in an adult. The individual does not grow in height, but the bones of the face, hands, and feet enlarge and widen (appositional growth), along with growth in cartilage. An increase in mandible size leads to a protruding jaw (prognathism). Internal organs, especially the liver, increase in size, and increased release of glucose lead to the development of diabetes in all individuals with acromegaly. Acromegaly may result from loss of feedback control of growth hormone at either the hypothalamic or pituitary level, or it may develop because of a GH-secreting tumor of the pituitary. Current treatment includes using a growth-inhibiting hormone analog, which acts to inhibit the release of growth hormone from the anterior pituitary.

How do the following hormones effect the bones: growth hormone, thyroid hormone, glucocorticoids, and serotonin?

Growth hormone is also called somatotropin, and is produced by the anterior pituitary gland. It affects bone growth by stimulating the liver to form another hormone called insulin-like growth factor (IGF) (also called somatomedin). Both growth hormone and IGF directly stimulate growth of cartilage in the epiphyseal plate. Thyroid hormone is secreted by the thyroid gland and stimulates bone growth by influencing the basal metabolic rate of bone cells (see section 17.8b). If maintained in proper balance, growth hormone and thyroid hormone regulate and maintain normal activity at the epiphyseal plates until puberty. Glucocorticoids are a group of steroid hormones that are released from the adrenal cortex and regulate blood glucose levels. High amounts increase bone loss and, in children, impairs growth at the epiphyseal plate. It is because of this relationship that a child's growth is monitored if receiving high doses of glucocorticoids as an anti-inflammatory, such as a treatment for children with severe asthma. Serotonin was previously discussed in section 1.6. Researchers have discovered that most bone cells have serotonin receptors, and specifically that when levels of circulating serotonin are too high, osteoprogenitor cells are prevented from differentiating into osteoblasts. Thus, serotonin appears to play a role in the rate and regulation of normal bone remodeling because it affects osteoblast differentiation. Further research is ongoing to see if abnormally high levels of serotonin are linked to low bone density disorders. Three additional hormones—parathyroid hormone, calcitriol, and calcitonin—participate in both regulating bone remodeling and regulat- ing blood calcium levels. These hormones are discussed in detail in the next section.

Fissure

Narrow slitlike opening through a bone.

What are the three different cartilages in the body and where are they found?

Hyaline = Location Tip of nose; trachea; most of larynx, costal cartilage; articular ends of long bones; most of fetal skeleton Elastic = External ear; epiglottis of larynx Fibrocartilage = Intervertebral discs; pubic symphysis; menisci of knee joints Cartilage is a semirigid connective tissue that is more flexible than bone. Recall from section that there are three subtypes of cartilage; the two most common subtypes are described below. •Hyaline cartilage attaches ribs to the sternum (costal cartilage), covers the ends of some bones (articular cartilage), and is the cartilage within growth plates (epiphyseal plates). Hyaline cartilage also provides a model for the formation of most of the bones in the body. •Fibrocartilage is a weight-bearing cartilage that withstands compression. It forms the intervertebral discs, the pubic symphysis (cartilage between bones of the pelvis), and cartilage pads of the knee joints (menisci).

Endochondral ossification can be summed into 5 major steps:

Hypertrophication: Chondrocyte cells grow. Calcification: Hardening of hyalin cartilage matrix. Cavitation: Chrondrocytes die and leave cavities in the bone. Periosteal bud invasion: Nutrients are delivered to the bone via blood vessels, and nerves also enter. Epiphyseal Ossification: the bone ends develop (secondary) ossification centers.

Unlike compact bone, spongy bone contains no osteons

Instead, its is an open lattice of narrow rods and plates of bone, called trabeculae. Bone marrow (when present) fills in between the trabeculae. When a segment of spongy bone is examined microscopically, you can see parallel lamellae composed of bone matrix. Between adjacent lamellae are osteocytes resting in lacunae, with numerous canaliculi radiating from the lacunae. Nutrients reach the osteocytes by diffusion through cytoplasmic processes within the canaliculi that open onto the surfaces of the trabeculae. Note that the trabeculae often form a meshwork of crisscross- ing bars and plates of small bone pieces. This structure provides great resistance to stresses applied in many directions by distributing the stress throughout the entire framework. As an analogy, visualize the jungle gym climbing apparatus on a children's playground. It is capa- ble of supporting the weight of numerous children whether they are distributed throughout its structure or all localized in one area. This is accomplished because stresses and forces are distributed throughout the structure.

Osteolysis

Osteolysis is an active resorption of bone matrix by osteoclasts and can be interpreted as the reverse of ossification. Although osteoclasts are active during the natural formation of healthy bone the term "osteolysis" specifically refers to a pathological process.

Which organs are involved in the production of vitamin D?

Kidney AND Liver (kidney responsible for distribution). Metabolic Regulation Vitamin D3, also called cholecalciferol, is synthesized from a steroid precursor by the keratinocytes when they are exposed to ultraviolet radiation. Vitamin D3 is then released into the blood and transported to the liver, where it is converted to another intermediate molecule (calcidiol), and then transported to the kidney, where it is converted to calcitriol. Calcitriol is the active form of vitamin D and is considered a hormone. It increases absorption of calcium and phosphate from the small intestine into the blood. Thus, the synthesis of vitamin D3 is important in regulating the levels of calcium and phosphate in the blood. As little as 10 to 15 minutes of direct sunlight a day provides your body with its daily vitamin D through this process. Ultraviolet light converts the precursor molecule in keratinocytes of the skin (7-dehydrocholesterol, a modified cholesterol molecule) to vitamin D3 (cholecalciferol), which is released into the blood. Vitamin D3 also is absorbed from the small intestine into the blood from the diet. 2 Vitamin D3 circulates throughout the blood. As it passes through the blood vessels of the liver, it is converted by liver enzymes to calcidiol by the addition of a hydroxyl group (—OH). Both steps 1 and 2 occur continuously with limited regulation. 3 Ultraviolet light Calcidiol circulates in the blood: As it passes through blood vessels of the kidney, it is con- verted to calcitriol by kidney enzymes (when another —OH group is added). Calcitriol is the active form Vitamin D3. The presence of parathyroid hormone increases the rate of this final enzymatic step in the kidney. Thus, greater amounts of calcitriol are formed when PTH is present.

Tuberosity

Large rough projection.

What are the structural components of a long bone and why are the right proportions of these components important?

Long bones are greater in length than width. These bones have an elongated, cylindrical shaft (diaphysis). This is the most common bone shape. Long bones are found in the upper limbs (namely, the arm, forearm, palm, and fingers) and lower limbs (thigh, leg, sole of the foot, and toes). Long bones vary in size. The small bones in the fingers and toes are long bones, as are the larger tibia and fibula of the lower limb.

Trochanter

Massive, rough projection found only on the femur.

What is the effect of mechanical stress on bone?

Mechanical stress occurs in the form of weight-bearing movement and exercise, and it is required for normal bone remodeling. Stress is detected by osteocytes and communicated to osteoblasts. Osteoblasts increase synthesis of osteoid, and this is followed by deposition of mineral salts. Bone strength increases over a period of time in response to mechanical stress. Mechanical stresses that significantly affect bone result from skeletal muscle contraction and gravitational forces.

Regions of a Long Bone

One of the principal gross features of a long bone is its shaft, which is called the diaphysis (diaphyses, growing between). The elongated, usually cylindrical, diaphysis provides for the leverage and major weight support of a long bone. Extending inward from the compact bone along the length of the diaphysis are spicules (think spike-like structures) of spongy bone. The hollow, cylindrical space within the diaphysis is called the medullary (marrow) cavity. In children, this cavity contains red bone mar- row, which later is replaced by yellow bone marrow in adults. An expanded knobby region called the epiphysis (epi = upon, physis = growth) is at each end of a long bone. A proximal epiphysis is the end of the bone closest to the body trunk, and a distal epiphysis is the end farthest from the trunk. An epiphysis is composed of an outer thin layer of compact bone and an inner, more extensive region of spongy bone. Spongy bone within the epiphysis resists stress that is applied from many directions. Covering the joint surface of an epiphysis is a thin layer of hyaline cartilage called the articular cartilage. This cartilage helps reduce friction and absorb shock in move- able joints. The metaphysis (mĕ-taf′i-sis) is the region in a mature bone sandwiched between the diaphysis and the epiphysis. This region contains the epiphyseal (ep-i- fiz′ē-ăl), or growth, plate in a growing bone. It is a thin layer of hyaline cartilage that provides for the 1 continued length- wise growth of the bone. The remnant of the epiphyseal plate in adults is a thin, defined area of compact bone called the epiphyseal line.

osteogenesis

Ossification (facio = to make), or osteogenesis ( genesis = beginning), refers to the formation and development of bone connective tissue. Ossification begins in the embryo and continues as the skeleton grows during childhood and adolescence. By the eighth through twelfth weeks of embryonic development, the skeleton begins forming from either thickened condensations of mesenchyme (intramembranous ossification) or a hyaline cartilage model of bone (endochondral ossification).

osteoblast

Osteoprogenitor cells are stem cells derived from mesenchyme. When they divide through the process of cellular division, another stem cell is produced along with a "committed cell" that matures to become an osteoblast. As previously described, these stem cells are located in both the periosteum and the endosteum. Osteoblasts (blast = germ) are formed from osteoprogenitor stem cells. Often, osteoblasts are positioned side by side on bone surfaces. Active osteoblasts exhibit a somewhat cuboidal shape and have abundant rough endoplasmic reticulum and Golgi apparatus, reflecting the activity of these cells. Osteoblasts perform the important function of synthesizing and secreting the initial semisolid organic form of bone matrix called osteoid (oeidos = resemblance). Osteoid later calcifies as a result of salt crystal deposition. As a consequence of this mineral deposition on osteoid, osteoblasts become entrapped within the matrix they produce and secrete, and thereafter they differentiate into osteocytes.

What is the function of red marrow in the bones and how does it differ in adults and infants?

Red bone marrow (myeloid tissue) is hemopoietic (blood cell forming) and contains reticular connective tissue, immature blood cells, and fat. (a) Red bone marrow distribution in the adult Yellow bone marrow Red bone marrow The locations of red bone marrow differ between children and adults. In children, red bone marrow is located in the spongy bone of most of the bones of the body as well as the medullary cavity of long bones. Much of the red bone marrow degenerates as children mature into adults, and the marrow primarily in the medullary cavities of long bones turns into a fatty substance called yellow bone marrow. As a result, adults have red bone marrow only in selected portions of the axial skeleton, such as the flat bones of the skull, the vertebrae, the ribs, the sternum, and the ossa coxae (hip bone). Adults also have red bone marrow in the proximal epiphyses of each humerus and femur. Note that severe anemia—a condition in which erythrocyte (red blood cell) numbers are lower than normal, resulting in insufficient oxygen reaching the cells of the body —may trigger conversion of yellow bone marrow back to red bone marrow, a change that facilitates the production of additional erythrocytes.

What are the effects of thyroid and parathyroid hormones on blood calcium levels?

Regulating calcium concentration in blood (between 8.9 and 10.1 milligrams per deciliter [mg/dL]) is essential because calcium is required for numerous physiologic processes such as initiation of muscle contraction; exocytosis of molecules from cells, including nerve cells (neurons); stimulation of the heart by pacemaker cells; and blood clotting. The two primary hormones that regulate blood calcium are calcitriol (an active form of vitamin D) and parathy- roid hormone. We describe blood calcium regulation here because of 10 the role of the skeleton in storage of calcium. (Also see Table R.2 for information about the hormones involved in regulating blood calcium levels.)

Foramen

Rounded passageway through a bone.

Tubercle

Small round projection.

Facet

Small, flat, shallow surface

What are the organic and inorganic components of the bone matrix, and what specific roles do they play?

The matrix of bone connective tissue has both organic and inorganic components. The organic component is osteoid, which is produced by osteoblasts. Osteoid is composed of both collagen protein plus a semisolid ground substance of proteoglycans (including chondroitin sulfate) and glycoproteins that suspends and supports the collagen fibers. These organic components give bone tensile strength by resisting stretching and twisting, and contribute to its overall flexibility. The inorganic portion of the bone matrix is made up of salt crystals that are primarily calcium phosphate, Ca3(PO4)2. Calcium phosphate and calcium hydroxide interact to form crystals of hydroxyapatite (h ̄ı-drok′se ̄-ap-a-t ̄ıt), which is Ca10(PO4)6(OH)2. The crystals also incorporate other salts (e.g., calcium carbonate) and ions (e.g., sodium, magnesium, sulfate, and fluoride) during the process of calcification. These crystals deposit around the long axis of collagen fibers in the extracellular matrix. The crystals harden the matrix and account for the rigidity or relative inflexibility of bone that provide its compressional strength. The correct proportion of organic and inorganic substances in the matrix of bone allows it to function optimally. A loss of protein, or the presence of abnormal protein, results in brittle bones; insufficient calcium results in soft bones.

What is the epiphyseal line?

The metaphysis is the region in a mature bone sandwiched between the diaphysis and the epiphysis. This region contains the epiphyseal or growth, plate in a growing bone. It is a thin layer of hyaline cartilage that provides for the continued length- wise growth of the bone. The remnant of the epiphyseal plate in adults is a thin, defined area of compact bone called the epiphyseal line.

What are the components of the bone matrix?

The primary component of bone is bone connective tissue, also called osseous (os′e ̄ -u ̆ s; os = bone) connective tissue. Bone is composed of both cells and extracellular matrix, like all connective tissue. We now describe the cells and matrix that compose bone connective tissue, how the matrix is formed and resorbed, and then the two microscopic arrangements (compact bone and spongy bone). Composition of the Bone Matrix The matrix of bone connective tissue has both organic and inorganic components. The organic component is osteoid, which is produced by osteoblasts. Osteoid is composed of both collagen protein plus a semisolid ground substance of proteoglycans (including chondroitin sulfate) and glycoproteins that suspends and supports the collagen fibers. These organic components give bone tensile strength by resist- ing stretching and twisting, and contribute to its overall flexibility. The inorganic portion of the bone matrix is made up of salt crystals that are primarily calcium phosphate, Ca3(PO4)2. Calcium phosphate and calcium hydroxide interact to form crystals of hydroxyapatite which is Ca10(PO4)6(OH)2. The crystals also incorporate other salts (e.g., calcium carbonate) and ions (e.g., sodium, magnesium, sulfate, and fluoride) during the process of calcification. These crystals deposit around the long axis of collagen fibers in the extracellular matrix. The crystals harden the matrix and account for the rigidity or relative inflexibility of bone that provide its compressional strength. The correct proportion of organic and inorganic substances in the matrix of bone allows it to function optimally. A loss of protein, or the presence of abnormal protein, results in brittle bones; insufficient calcium results in soft bones.

Spinal Curvature Abnormalities

There are three main spinal curvature deformities: kyphosis, lordosis, and scoliosis. Kyphosis (k ̄ı-fo ̄′sis) is an exaggerated thoracic curvature that is directed posteriorly, producing a hunchback look. Kyphosis often results from osteoporosis, but also may occur due to a vertebral compression fracture, osteomalacia (a disease in which adult bones become demineralized), abnormal vertebral growth, or chronic contractions in muscles that insert on the vertebrae.

During the Industrial Revolution, many children in cities spent little time outdoors and most of their time working in factories, leading to an increase in a disorder called rickets. Rickets is a bone disorder caused by inadequate vitamin D. Based on your knowledge of skin function, why do you think these children developed rickets?

These children already were not getting enough vitamin D in their diet, and they were spending all of their daylight hours indoors. Since the children were not exposed to much sunlight, their skin could not synthesize vitamin D from the UV rays of the sun. Without adequate amounts of vitamin D, the children developed rickets. Rickets is on the rise in the United States again among poor urban children who spend little time outdoors and who drink soda instead of milk.

How are bones classified based on their shape?

They are classified by Long bones, short bones, irregular bones, flat bones.

Effects of Parathyroid Hormone

and calcitriol on blood calcium Levels. Blood calcium levels are closely regulated by a negative feedback mechanism that involves the parathyroid gland, calcitriol, and various effectors (bone, kidneys, and small intestine). A low blood calcium level is the initial stimulus for the parathyroid glands to release parathyroid hormone. Together, PTH and calcitriol target various effectors to ultimately instigate a rise in blood calcium levels and return to homeostasis.

Rickets

is a disease caused by a vitamin D deficiency in childhood and characterized by overproduction and deficient calcification of osteoid tissue. Patients with rickets acquire a bowlegged appearance as their weight increases and the bones in their lower limbs bend. The disease also is characterized by disturbances in growth, hypocalcemia, and sometimes tetany (cramps and muscle twitches), usually caused by low blood calcium. During the Industrial Revolution, the incidence of rickets increased as children in cities were forced to work indoors in factories. Rickets continues to occur in some developing na- tions. The incidence recently has increased among urban U.S. chil- dren, who spend much of their time indoors and typically do not drink enough milk, opting instead for soft drinks.

Process

is a projection or outgrowth of tissue from a larger body. Also, any marked bony prominence.

Achondroplastic Dwarfism

is characterized by abnormal conversion of hyaline cartilage to bone. The most common form is achondroplastic dwarfism, in which the long bones of the limbs stop growing in childhood, whereas the other bones usually continue to grow normally. Thus, an indi- vidual with achondroplastic dwarfism is short in stature but generally has a large head. Those affected may have bowed lower limbs and lordosis (exaggerated curvature of the lumbar spine). Achondroplastic dwarfism results from a failure of chondrocytes in the second and third zones of the epiphyseal plate (figure 7.12a) to multiply and enlarge. As a result, there is inadequate endochondral ossification. Most cases result from a spontaneous mutation during DNA replication, whereas other cases are due to inheriting the disorder from an affected parent.

Compact bone

is composed of small cylindrical structures called osteons, or Haversian systems. An osteon is the basic functional and structural unit of mature compact bone. Osteons are oriented parallel to the diaphysis of the long bone. When an osteon is viewed in cross section, it has the appearance of a bull's-eye target. An osteon has several components as follows: • The central (Haversian) canal is a cylindrical channel that lies in the center of the osteon and runs parallel to it. Extending through the central canal are the blood vessels and nerves that supply the bone. • Concentric lamellae (lamina = plate, leaf) are rings of bone connective tissue that surround the central canal and form the bulk of the osteon. The numbers of concentric lamellae vary among osteons. Each lamella contains collagen fibers oriented at an angle in one direction; adjacent lamellae contain collagen fibers oriented at an angle that is 90 degrees different from both the previous and next lamellae. This alternating pattern of collagen fiber direction gives bone part of its strength and resilience. • Osteocytes are mature bone cells found in small spaces (see next) between adjacent concentric lamellae. These cells maintain the bone matrix. • Lacunae are the small spaces that each house an osteocyte. • Canaliculi are tiny, interconnecting channels within the bone connective tissue that extend from each lacuna, travel through the lamellae, and connect to other lacunae and the central canal. Canaliculi house osteocyte cytoplasmic projections that permit intercellular contact and communication. Nutrients, minerals, gases, and wastes are transported through the cytoplasmic extensions within these passageways, allowing their exchange between the blood vessels of the central canal and the osteocytes. • Perforating (Volkmann) canals resemble central canals in that they also contain blood vessels and nerves. However, perforating canals run perpendicular to the central canals and help connect multiple central canals within different osteons, thus forming a vascular and innervation connection among the multiple osteons. • Circumferential lamellae are rings of bone immediately internal to the periosteum of the bone (external circumferential lamellae) or internal to the endosteum (internal circumferential lamellae). Both external and internal circumferential lamellae run the entire circumference of the bone itself (hence, their name). • Interstitial lamellae (interstitial systems) are either the components of compact bone that are between osteons or are the leftover parts of osteons that have been partially resorbed—thus they often look like a 2 "bite" has been taken out of them. The interstitial lamellae are incomplete and typically have no central canal.

Parathyroid hormone (PTH)

is secreted and released by the parathy- roid glands (see section 17.10b) in response to reduced blood calcium levels (figure 7.15). The final enzymatic step converting calcidiol to calcitriol in the kidney occurs more readily in the presence of PTH. PTH and calcitriol interact with selected major organs as follows: • Bone connective tissue of the skeleton. PTH and calcitriol act synergistically (their combined effect is greater than the sum of their individual effects) to increase the release of calcium from the bone into the blood, by increasing osteoclast activity. • Kidneys. PTH and calcitriol act synergistically to stimulate the kidney to excrete less calcium in the urine (and thus retain more calcium in the blood). This occurs by increasing calcium reabsorption in the tubules in the kidney (see section 24.6). • Small intestine. A function unique to calcitriol is to increase absorption of calcium from the small intestine into the blood. The removal of calcium from bone, the decrease in loss of calcium from the kidney, and increase in calcium absorption from the gastrointestinal tract result in elevating blood calcium and returning it to within the normal homeostatic range. Subsequently, the release of additional PTH is inhibited by negative feedback.


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