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6
Skeletal Cartilages (p. 173)
Basic Structure, Types, and Locations (p. 173)

Growth of Cartilage (p. 173)
Classification of Bones (pp. 173–175)
Functions of Bones (pp. 175–176)
Bone Structure (pp. 176–182)
Bones and
Gross Anatomy (pp. 177–179)
Microscopic Anatomy of Bone (pp. 179–180)
Chemical Composition of Bone (pp. 180–182)
Skeletal Tissues
Bone Development (pp. 182–185)
Formation of the Bony Skeleton (pp. 182–184)
Postnatal Bone Growth (pp. 184–185)
Bone Homeostasis: Remodeling

and Repair (pp. 185–189)
Bone Remodeling (pp. 185–188)
A
Bone Repair (pp. 188–189) ll of us have heard the expressions “bone tired” and “bag of
bones”—rather unflattering and inaccurate images of one of
Homeostatic Imbalances of Bone our most phenomenal tissues and our main skeletal elements.
(pp. 189–191, 194) Our brains, not our bones, convey feelings of fatigue. As for “bag of
Osteomalacia and Rickets (p. 189)
bones,” they are indeed more prominent in some of us, but without
bones to form our internal skeleton we would all creep along the
Osteoporosis (pp. 189–191) ground like slugs, lacking any definite shape or form. Along with its
Paget’s Disease (pp. 191, 194) bones, the skeleton contains resilient cartilages, which we briefly dis-
cuss in this chapter. However, our major focus is the structure and func-
Developmental Aspects of Bones: tion of bone tissue and the dynamics of its formation and remodeling
Timing of Events (p. 194) throughout life.
172
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Chapter 6 Bones and Skeletal Tissues 173
Skeletal Cartilages both heavy pressure and stretch, such as the padlike cartilages
(menisci) of the knee and the discs between vertebrae, colored
䉴 Describe the functional properties of the three types of car- red in Figure 6.1.
tilage tissue.
䉴 Locate the major cartilages of the adult skeleton. Growth of Cartilage
䉴 Explain how cartilage grows. Unlike bone, which has a hard matrix, cartilage has a flexible
matrix which can accommodate mitosis. It is the ideal tissue to
The human skeleton is initially made up of cartilages and fi- use to lay down the embryonic skeleton and to provide for new
brous membranes, but most of these early supports are soon re- skeletal growth. Cartilage grows in two ways. In appositional
placed by bone. The few cartilages that remain in adults are growth (ap⬙o-zish⬘un-al; “growth from outside”), cartilage-
found mainly in regions where flexible skeletal tissue is needed. forming cells in the surrounding perichondrium secrete new
matrix against the external face of the existing cartilage tissue. In
Basic Structure, Types, and Locations interstitial growth (in⬙ter-stish⬘al; “growth from inside”), the
lacunae-bound chondrocytes divide and secrete new matrix, ex-
A skeletal cartilage is made of some variety of cartilage tissue,
panding the cartilage from within. Typically, cartilage growth
which consists primarily of water. The high water content of
ends during adolescence when the skeleton stops growing.
cartilage accounts for its resilience, that is, its ability to spring
Under certain conditions—during normal bone growth in
back to its original shape after being compressed.
youth and during old age—calcium salts may be deposited in
The cartilage, which contains no nerves or blood vessels, is 6
the matrix and cause it to harden, a process called calcification.
surrounded by a layer of dense irregular connective tissue, the
Note, however, that calcified cartilage is not bone; cartilage and
perichondrium (per⬙ı̆-kon⬘dre-um; “around the cartilage”). The
bone are always distinct tissues.
perichondrium acts like a girdle to resist outward expansion
when the cartilage is compressed. Additionally, the perichon-
C H E C K Y O U R U N D E R S TA N D I N G
drium contains the blood vessels from which nutrients diffuse
through the matrix to reach the cartilage cells. This mode of nu- 1. Which type of cartilage is most plentiful in the adult body?
trient delivery limits cartilage thickness. 2. What two body structures contain flexible elastic cartilage?
As we described in Chapter 4, there are three types of carti- 3. Cartilage grows by interstitial growth. What does this mean?
lage tissue in the body: hyaline, elastic, and fibrocartilage. All
For answers, see Appendix G.
three types have the same basic components—cells called
chondrocytes, encased in small cavities (lacunae) within an
extracellular matrix containing a jellylike ground substance and
fibers. The skeletal cartilages contain representatives from all Classification of Bones
three types.
Hyaline cartilages, which look like frosted glass when freshly 䉴 Name the major regions of the skeleton and describe their
exposed, provide support with flexibility and resilience. They relative functions.
are the most abundant skeletal cartilages. When viewed under 䉴 Compare and contrast the structure of the four bone
the microscope, their chondrocytes appear spherical (see Fig- classes and provide examples of each class.
ure 4.8g). The only fiber type in their matrix is fine collagen
fibers (which, however, are not detectable microscopically). The 206 named bones of the human skeleton are divided into
Colored blue in Figure 6.1, skeletal hyaline cartilages include two groups: axial and appendicular. The axial skeleton forms
(1) articular cartilages, which cover the ends of most bones at the long axis of the body and includes the bones of the skull,
movable joints; (2) costal cartilages, which connect the ribs to vertebral column, and rib cage, shown in orange in Figure 6.1.
the sternum (breastbone); (3) respiratory cartilages, which form Generally speaking these bones are most involved in protecting,
the skeleton of the larynx (voicebox) and reinforce other respi- supporting, or carrying other body parts.
ratory passageways; and (4) nasal cartilages, which support the The appendicular skeleton (ap⬙en-dik⬘u-lar) consists of the
external nose. bones of the upper and lower limbs and the girdles (shoulder
Elastic cartilages look very much like hyaline cartilages (see bones and hip bones) that attach the limbs to the axial skeleton.
Figure 4.8h), but they contain more stretchy elastic fibers and so These bones are colored gold in Figure 6.1. Bones of the limbs
are better able to stand up to repeated bending. They are found help us to get from place to place (locomotion) and to manipu-
in only two skeletal locations, shown in green in Figure 6.1—the late our environment.
external ear and the epiglottis (the flap that bends to cover the Bones come in many sizes and shapes. For example, the pisi-
opening of the larynx each time we swallow). form bone of the wrist is the size and shape of a pea, whereas the
Fibrocartilages are highly compressible and have great ten- femur (thigh bone) is nearly 2 feet long in some people and has
sile strength. The perfect intermediate between hyaline and elas- a large, ball-shaped head. The unique shape of each bone fulfills
tic cartilages, fibrocartilages consist of roughly parallel rows of a particular need. The femur, for example, withstands great
chondrocytes alternating with thick collagen fibers (see Fig- weight and pressure, and its hollow-cylinder design provides
ure 4.8i). Fibrocartilages occur in sites that are subjected to maximum strength with minimum weight.
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174 UN I T 2 Covering, Support, and Movement of the Body
Epiglottis
Thyroid Larynx
cartilage
Cartilage in Cartilages in Cricoid
external ear nose cartilage
Trachea
Lung
Articular
cartilage
of a joint
Costal
cartilage
Cartilage
in intervertebral
disc
Respiratory
tube cartilages
in neck and thorax
Bones of skeleton
Axial skeleton
Pubic Appendicular skeleton
symphysis
Cartilages
Meniscus (padlike
cartilage in Hyaline cartilages
knee joint)
Elastic cartilages
Articular cartilage Fibrocartilages
of a joint
Figure 6.1 The bones and cartilages of the human skeleton. The cartilages that support
the respiratory tubes and larynx are drawn separately at the right.
For the most part, bones are classified by their shape as long, shape, not their overall size. The three bones in each of your
short, flat, and irregular (Figure 6.2). fingers are long bones, even though they are very small.
2. Short bones are roughly cube shaped. The bones of the
1. Long bones, as their name suggests, are considerably
wrist and ankle are examples (Figure 6.2d).
longer than they are wide (Figure 6.2a). A long bone has a
Sesamoid bones (ses⬘ah-moid; “shaped like a sesame
shaft plus two ends. All limb bones except the patella
seed”) are a special type of short bone that form in a tendon
(kneecap) and the wrist and ankle bones are long bones.
(for example, the patella). They vary in size and number in
Notice that these bones are named for their elongated
different individuals. Some sesamoid bones clearly act to
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(c) Flat bone (sternum)
(a) Long bone (humerus) 6
(b) Irregular bone (vertebra),

right lateral view (d) Short bone (talus)
Figure 6.2 Classification of bones on the basis of shape.
alter the direction of pull of a tendon. The function of oth- Functions of Bones
ers is not known.
3. Flat bones are thin, flattened, and usually a bit curved. The 䉴 List and describe five important functions of bones.
sternum (breastbone), scapulae (shoulder blades), ribs,
and most skull bones are flat bones (Figure 6.2c). Besides contributing to body shape and form, our bones per-
4. Irregular bones have complicated shapes that fit none of form several other important functions:
the preceding classes. Examples include the vertebrae and 1. Support. Bones provide a framework that supports the
the hip bones (Figure 6.2b). body and cradles its soft organs. For example, bones of
lower limbs act as pillars to support the body trunk when
we stand, and the rib cage supports the thoracic wall.
4. What are the components of the axial skeleton? 2. Protection. The fused bones of the skull protect the brain.
5. Contrast the general function of the axial skeleton to that of The vertebrae surround the spinal cord, and the rib cage
the appendicular skeleton. helps protect the vital organs of the thorax.
6. What bone class do the ribs and skull bones fall into? 3. Movement. Skeletal muscles, which attach to bones by ten-
dons, use bones as levers to move the body and its parts. As
a result, we can walk, grasp objects, and breathe. The design
of joints determines the types of movement possible.
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Articular
cartilage
Compact bone
Proximal
epiphysis
Spongy bone
Epiphyseal
line
Periosteum Endosteum
Compact bone
Medullary
cavity (lined
by endosteum) (b)
Yellow
Diaphysis bone marrow
6
Compact bone
Periosteum
Perforating
(Sharpey’s)
fibers
Nutrient
arteries
Distal
epiphysis
(a) (c)
Figure 6.3 The structure of a long bone of spongy bone and compact bone of the of (a). Note that the external surface of the
(humerus of arm). (a) Anterior view with epiphysis of (a). (See A Brief Atlas of the diaphysis is covered by periosteum, but the
bone sectioned frontally to show the inte- Human Body, Plates 20 and 21.) (c) Enlarged articular surface of the epiphysis is covered
rior at the proximal end. (b) Enlarged view cross-sectional view of the shaft (diaphysis) with hyaline cartilage.
4. Mineral and growth factor storage. Bone is a reservoir for 8. What two types of substances are stored in bone matrix?
minerals, most importantly calcium and phosphate. The 9. What are two functions of a bone’s marrow cavities?
stored minerals are released into the bloodstream as
needed for distribution to all parts of the body. Indeed,
“deposits” and “withdrawals” of minerals to and from the
bones go on almost continuously. Additionally, mineral-
ized bone matrix stores important growth factors such as Bone Structure
insulin-like growth factors, transforming growth factor,
䉴 Indicate the functional importance of bone markings.
bone morphogenic proteins, and others.
5. Blood cell formation. Most blood cell formation, or 䉴 Describe the gross anatomy of a typical long bone and a flat
hematopoiesis (hem⬙ah-to-poi-e⬘sis), occurs in the mar- bone. Indicate the locations and functions of red and yellow
row cavities of certain bones. marrow, articular cartilage, periosteum, and endosteum.
6. Triglyceride (fat) storage. Fat is stored in bone cavities and 䉴 Describe the histology of compact and spongy bone.
represents a source of stored energy for the body.
䉴 Discuss the chemical composition of bone and the advan-
tages conferred by the organic and inorganic components.
7. What is the functional relationship between skeletal muscles

and bones?
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(a) Osteogenic cell (b) Osteoblast (c) Osteocyte (d) Osteoclast
Stem cell Matrix-synthesizing cell Mature bone cell that Bone-resorbing cell
responsible for bone growth maintains the bone matrix
Figure 6.4 Comparison of different types of bone cells.

6
Because they contain various types of tissue, bones are organs. Structure of a Typical Long Bone
(Recall that an organ contains several different tissues.) Al- With few exceptions, all long bones have the same general
though bone (osseous) tissue dominates bones, they also contain structure, which includes a shaft, bone ends, and membranes
nervous tissue in their nerves, cartilage in their articular carti- (Figure 6.3).
lages, fibrous connective tissue lining their cavities, and muscle
and epithelial tissues in their blood vessels. We will consider Diaphysis A tubular diaphysis (di-af⬘ı̆-sis; dia = through,
bone structure at three levels: gross, microscopic, and chemical. physis = growth), or shaft, forms the long axis of the bone. It is
constructed of a relatively thick collar of compact bone that sur-
Gross Anatomy rounds a central medullary cavity (med⬘u-lar-e; “middle”), or
marrow cavity. In adults, the medullary cavity contains fat (yel-
Bone Markings low marrow) and is called the yellow marrow cavity.
The external surfaces of bones are rarely smooth and feature- Epiphyses The epiphyses (e-pif⬘ı̆-sēz; singular: epiphysis) are
less. Instead, they display projections, depressions, and openings the bone ends (epi = upon). In many cases, they are more ex-
that serve as sites of muscle, ligament, and tendon attachment, panded than the diaphysis. Compact bone forms the exterior of
as joint surfaces, or as conduits for blood vessels and nerves. epiphyses, and their interior contains spongy bone. The joint
These bone markings are named in different ways. surface of each epiphysis is covered with a thin layer of articular
Projections (bulges) that grow outward from the bone surface (hyaline) cartilage, which cushions the opposing bone ends
include heads, trochanters, spines, and others. Each has distin- during joint movement and absorbs stress. Between the diaph-
guishing features and functions. In most cases, bone projections ysis and each epiphysis of an adult long bone is an epiphyseal
are indications of the stresses created by muscles attached to and line, a remnant of the epiphyseal plate, a disc of hyaline carti-
pulling on them or are modified surfaces where bones meet and lage that grows during childhood to lengthen the bone. The re-
form joints. gion where the diaphysis and epiphysis meet, whether it is the
Depressions and openings include fossae, sinuses, foramina, epiphyseal plate or line, is sometimes called the metaphysis.
and grooves. They usually serve to allow passage of nerves and
blood vessels. The most important types of bone markings are Membranes A third structural feature of long bones is mem-
described in Table 6.1. You should familiarize yourself with branes. The external surface of the entire bone except the joint
these terms because you will meet them again as identifying surfaces is covered by a glistening white, double-layered mem-
marks of the individual bones studied in the lab. brane called the periosteum (per⬙e-os⬘te-um; peri = around,
osteo = bone). The outer fibrous layer is dense irregular connec-
Bone Textures: Compact and Spongy Bone tive tissue. The inner osteogenic layer, abutting the bone surface,
Every bone has a dense outer layer that looks smooth and solid consists primarily of bone-forming cells, called osteoblasts
to the naked eye. This external layer is compact bone (Figures (os⬘te-o-blasts; “bone germinators”), which secrete bone matrix
6.3 and 6.5). Internal to this is spongy bone (also called elements, and bone-destroying cells, called osteoclasts (“bone
cancellous bone), a honeycomb of small needle-like or flat breakers”). In addition, there are primitive stem cells, osteogenic
pieces called trabeculae (trah-bek⬘u-le; “little beams”). In liv- cells, that give rise to the osteoblasts (Figure 6.4).
ing bones the open spaces between trabeculae are filled with
red or yellow bone marrow.
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TABLE 6.1 Bone Markings

NAME OF
BONE MARKING DESCRIPTION ILLUSTRATIONS
Projections That Are Sites of Muscle and Ligament Attachment
Tuberosity Large rounded projection; may be Iliac

(too⬙bĕ-ros⬘ı̆-te) roughened crest
Crest Narrow ridge of bone; usually prominent Trochanter Intertrochanteric
line
Trochanter Very large, blunt, irregularly shaped process
(tro-kan⬘ter) (the only examples are on the femur)
Ischial
Line Narrow ridge of bone; less prominent than
spine
a crest
Tubercle Small rounded projection or process
Coxal Ischial
(too⬘ber-kl) bone tuberosity Adductor
Epicondyle Raised area on or above a condyle tubercle
(ep⬙ı̆-kon⬘dı-l)
Femur
Spine Sharp, slender, often pointed projection Vertebra of Medial
thigh epicondyle
Process Any bony prominence
Facet Condyle
6 Spinous
process
Projections That Help to Form Joints
Head Bony expansion carried on a narrow neck Head

Facet Smooth, nearly flat articular surface Condyle
Condyle Rounded articular projection

Facets Ramus
(kon⬘dı̄l)
Ramus Armlike bar of bone
Rib Mandible
(ra⬘mus)
Depressions and Openings
For Passage of Blood Vessels and Nerves

Groove Furrow
Fissure Narrow, slitlike opening
Inferior
Meatus
Foramen Round or oval opening through a bone orbital
(fo-ra⬘men) Sinus fissure
Notch Indentation at the edge of a structure Fossa Foramen
Others Notch
Meatus Canal-like passageway Groove
(me-a⬘tus) Skull
Sinus Cavity within a bone, filled with air and lined
with mucous membrane
Fossa Shallow, basinlike depression in a bone, often
(fos⬘ah) serving as an articular surface
The periosteum is richly supplied with nerve fibers, lym- Internal bone surfaces are covered with a delicate connective
phatic vessels, and blood vessels, which enter the diaphysis via tissue membrane called the endosteum (en-dos⬘te-um; “within
nutrient foramina (fo-ra⬙me-nah; “openings”). the bone”) (Figure 6.3). The endosteum covers the trabeculae of
The periosteum is secured to the underlying bone by perfo- spongy bone and lines the canals that pass through the compact
rating (Sharpey’s) fibers (Figure 6.3), tufts of collagen fibers that bone. Like the periosteum, the endosteum contains both bone-
extend from its fibrous layer into the bone matrix. The perios- forming and bone-destroying cells.
teum also provides anchoring points for tendons and ligaments.
At these points the perforating fibers are exceptionally dense.
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referred to as red marrow cavities. In newborn infants, the
medullary cavity of the diaphysis and all areas of spongy bone
contain red bone marrow. In most adult long bones, the fat-
containing medullary cavity extends well into the epiphysis, and
little red marrow is present in the spongy bone cavities. For this
reason, blood cell production in adult long bones routinely oc-
curs only in the heads of the femur and humerus (the long bone
of the arm).
The red marrow found in the diploë of flat bones (such as the
sternum) and in some irregular bones (such as the hip bone) is
much more active in hematopoiesis, and these sites are rou-
tinely used for obtaining red marrow samples when problems
with the blood-forming tissue are suspected. However, yellow
marrow in the medullary cavity can revert to red marrow if a
person becomes very anemic and needs enhanced red blood cell
production.
Spongy
bone
(diploë)
Microscopic Anatomy of Bone
Compact 6
Essentially, four major cell types populate bone tissue: os-
bone
teogenic cells, osteoblasts, osteocytes, and osteoclasts. These,
like other connective tissue cells, are surrounded by an extracel-
lular matrix of their making. The osteogenic cells, also called
osteoprogenitor cells, are mitotically active stem cells found in the
membranous periosteum and endosteum. Some of their prog-
eny differentiate into osteoblasts (bone-forming cells) while
Trabeculae others persist as bone stem cells to provide osteoblasts in the fu-
ture. We describe the structure and function of the remaining
two types of bone cells below.
Compact Bone
Although compact bone looks dense and solid, a microscope re-
veals that it is riddled with passageways that serve as conduits
for nerves, blood vessels, and lymphatic vessels (see Figure 6.7).
The structural unit of compact bone is called either the osteon
(os⬘te-on) or the Haversian system (ha-ver⬘zhen). Each osteon
Figure 6.5 Flat bones consist of a layer of spongy bone sand- is an elongated cylinder oriented parallel to the long axis of the
wiched between two thin layers of compact bone. bone. Functionally, osteons are tiny weight-bearing pillars.
(Photomicrograph at bottom, 25⫻.) As shown in the “exploded” view in Figure 6.6, an osteon is a
group of hollow tubes of bone matrix, one placed outside the
Structure of Short, Irregular, and Flat Bones
next like the growth rings of a tree trunk. Each matrix tube is a
lamella (lah-mel⬘ah; “little plate”), and for this reason compact
Short, irregular, and flat bones share a simple design: They all bone is often called lamellar bone. Although all of the collagen
consist of thin plates of periosteum-covered compact bone on fibers in a particular lamella run in a single direction, the colla-
the outside and endosteum-covered spongy bone within. How- gen fibers in adjacent lamellae always run in different directions.
ever, these bones are not cylindrical and so they have no shaft or This alternating pattern is beautifully designed to withstand
epiphyses. They contain bone marrow (between their trabecu- torsion stresses—the adjacent lamellae reinforce one another to
lae), but no significant marrow cavity is present. resist twisting. You can think of the osteon’s design as a “twister
Figure 6.5 shows a typical flat bone of the skull. In flat bones, resister.” Collagen fibers are not the only part of bone lamellae
the spongy bone is called the diploë (dip⬘lo-e; “folded”) and the that are beautifully ordered. The tiny crystals of bone salts align
whole arrangement resembles a stiffened sandwich. with the collagen fibers and thus also alternate their direction in
adjacent lamellae.
Location of Hematopoietic Tissue in Bones Running through the core of each osteon is the central canal,
Hematopoietic tissue, red marrow, is typically found within the or Haversian canal, containing small blood vessels and nerve
trabecular cavities of spongy bone of long bones and in the fibers that serve the needs of the osteon’s cells. Canals of a sec-
diploë of flat bones. For this reason, both these cavities are often
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Artery with
capillaries
interstitial lamellae (in⬙ter-stish⬘al) (Figure 6.7c, right pho-
Structures tomicrograph). They either fill the gaps between forming osteons
in the Vein or are remnants of osteons that have been cut through by bone
central Nerve fiber
canal
remodeling (discussed later). Circumferential lamellae, located
just deep to the periosteum and just superficial to the endos-
Lamellae teum, extend around the entire circumference of the diaphysis
(Figure 6.7a) and effectively resist twisting of the long bone.
Collagen
fibers
run in Spongy Bone
different
directions In contrast to compact bone, spongy bone looks like a poorly
organized, even haphazard, tissue (see Figure 6.5 and Fig-
ure 6.3b). However, the trabeculae in spongy bone align pre-
cisely along lines of stress and help the bone resist stress as much
as possible. These tiny bone struts are as carefully positioned as
the flying buttresses that help to support a Gothic cathedral.
Only a few cells thick, trabeculae contain irregularly arranged
lamellae and osteocytes interconnected by canaliculi. No osteons
Twisting are present. Nutrients reach the osteocytes of spongy bone by
6 force
diffusing through the canaliculi from capillaries in the endos-
teum surrounding the trabeculae.
Figure 6.6 A single osteon. The osteon is drawn as if pulled out
like a telescope to illustrate the individual lamellae.
Chemical Composition of Bone
Bone has both organic and inorganic components. Its organic
ond type called perforating canals, or Volkmann’s canals
components include the cells (osteogenic cells, osteoblasts, os-
(folk⬘mahnz), lie at right angles to the long axis of the bone and
teocytes, and osteoclasts) and osteoid (os⬘te-oid), the organic
connect the blood and nerve supply of the periosteum to those
part of the matrix. Osteoid, which makes up approximately
in the central canals and the medullary cavity (Figure 6.7a). Like
one-third of the matrix, includes ground substance (composed
all other internal bone cavities, these canals are lined with
of proteoglycans and glycoproteins) and collagen fibers, both of
endosteum.
which are made and secreted by osteoblasts. These organic sub-
Spider-shaped osteocytes (Figures 6.4c and 6.7b) occupy
stances, particularly collagen, contribute not only to a bone’s
lacunae (lac = hollow; una = little) at the junctions of the
structure but also to the flexibility and great tensile strength that
lamellae. Hairlike canals called canaliculi (kan⬙ah-lik⬘u-li)
allow the bone to resist stretch and twisting.
connect the lacunae to each other and to the central canal. The
Bone’s exceptional toughness and tensile strength has been
manner in which canaliculi are formed is interesting. When
the subject of intense research. It now appears that this re-
bone is being formed, the osteoblasts secreting bone matrix
silience comes from the presence of sacrificial bonds in or be-
surround blood vessels and maintain contact with one another
tween collagen molecules. These bonds break easily on impact,
by tentacle-like projections containing gap junctions. Then, as
dissipating energy to prevent the force from rising to a fracture
the newly secreted matrix hardens and the maturing cells
value. In the absence of continued or additional trauma, most
become trapped within it, a system of tiny canals—the cana-
of the sacrificial bonds re-form.
liculi, filled with tissue fluid and containing the osteocyte
The balance of bone tissue (65% by mass) consists of inor-
extensions—is formed. The canaliculi tie all the osteocytes in
ganic hydroxyapatites (hi-drok⬙se-ap⬘ah-tı̄tz), or mineral salts,
an osteon together, permitting nutrients and wastes to be re-
largely calcium phosphates present in the form of tiny, tightly
layed from one osteocyte to the next throughout the osteon.
packed, needle-like crystals in and around the collagen fibers in
Although bone matrix is hard and impermeable to nutrients,
the extracellular matrix. The crystals account for the most no-
its canaliculi and cell-to-cell relays (via gap junctions) allow
table characteristic of bone—its exceptional hardness, which al-
bone cells to be well nourished.
lows it to resist compression.
One function of osteocytes is to maintain the bone matrix. If
The proper combination of organic and inorganic matrix
they die, the surrounding matrix is resorbed. The osteocytes
elements allows bones to be exceedingly durable and strong
also act as stress or strain “sensors” in cases of bone deformation
without being brittle. Healthy bone is half as strong as steel in
or other damaging stimuli. They communicate this information
resisting compression and fully as strong as steel in resisting
to the cells responsible for bone remodeling (osteoblasts and os-
tension.
teoclasts) so that countermeasures can be taken or repairs
Because of the salts they contain, bones last long after death
made. We discuss the bone-destroying osteoclast on p. 186 in
and provide an enduring “monument.” In fact, skeletal remains
conjunction with the topic of bone remodeling.
many centuries old have revealed the shapes and sizes of ancient
Not all the lamellae in compact bone are part of osteons. Ly-
peoples, the kinds of work they did, and many of the ailments
ing between intact osteons are incomplete lamellae called
they suffered, such as arthritis.
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Compact bone Spongy bone
Central Perforating
(Haversian) canal (Volkmann’s) canal
Endosteum lining bony canals

and covering trabeculae
Osteon
(Haversian system)
6
Circumferential
lamellae
(a)
Perforating (Sharpey’s) fibers
Lamellae Periosteal blood vessel

Periosteum
Nerve
Vein
Lamellae
Artery
Central
Canaliculus canal
Osteocyte Lacunae
in a lacuna
(b) (c) Interstitial Lacuna (with osteocyte)
lamellae
Figure 6.7 Microscopic anatomy of compact bone. (a) Diagrammatic view of a pie-shaped
segment of compact bone. (b) Close-up of a portion of one osteon. Note the position of osteo-
cytes in the lacunae. (c) SEM (left) of cross-sectional view of an osteon (180⫻). Light photomi-
crographs (right) of a cross-sectional view of an osteon (160⫻).
SOURCE: (c, left) Kessel and Kardon/Visuals Unlimited.
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Mesenchymal
cell 10. Are crests, tubercles, and spines bony projections or concavities?
Collagen 11. How does the structure of compact bone differ from that of
fiber
spongy bone when viewed with the naked eye?
Ossification 12. What membrane lines the internal canals and covers the tra-
center
beculae of a bone?
Osteoid 13. Which component of bone—organic or inorganic—makes
Osteoblast it hard?
14. What name is given to a cell that has a ruffled border and
1 Ossification centers appear in the fibrous connective tissue acts to break down bone matrix?
membrane.
• Selected centrally located mesenchymal cells cluster and For answers, see Appendix G.
differentiate into osteoblasts, forming an ossification center.
Osteoblast
Osteoid
Bone Development
䉴 Compare and contrast intramembranous ossification and
Osteocyte endochondral ossification.
6 Newly calcified 䉴 Describe the process of long bone growth that occurs at
bone matrix the epiphyseal plates.
Ossification and osteogenesis (os⬙te-o-jen⬘ĕ-sis) are synonyms

2 Bone matrix (osteoid) is secreted within the fibrous membrane
and calcifies.
meaning the process of bone formation (os = bone, genesis = be-
• Osteoblasts begin to secrete osteoid, which is calcified within a ginning). In embryos this process leads to the formation of the
few days. bony skeleton. Later another form of ossification known as bone
• Trapped osteoblasts become osteocytes. growth goes on until early adulthood as the body continues to
Mesenchyme
increase in size. Bones are capable of growing in thickness
condensing throughout life. However, ossification in adults serves mainly
to form the for bone remodeling and repair.
periosteum
Trabeculae of
woven bone
Formation of the Bony Skeleton
Before week 8, the skeleton of a human embryo is constructed en-
Blood vessel tirely from fibrous membranes and hyaline cartilage. Bone tissue
begins to develop at about this time and eventually replaces most
of the existing fibrous or cartilage structures. When a bone devel-
3 Woven bone and periosteum form.
• Accumulating osteoid is laid down between embryonic blood
ops from a fibrous membrane, the process is intramembranous os-
vessels in a random manner. The result is a network (instead of sification, and the bone is called a membrane bone. Bone
lamellae) of trabeculae called woven bone. development by replacing hyaline cartilage is called endochondral
• Vascularized mesenchyme condenses on the external face of the
woven bone and becomes the periosteum.
ossification (endo = within, chondro = cartilage), and the resulting
bone is called a cartilage, or endochondral, bone. The beauty of
Fibrous using structures (membranes and cartilages) that are flexible and
periosteum resilient to fashion the embryonic skeleton is that they can ac-
Osteoblast commodate mitosis. Were the early skeleton composed of bone
tissue from the outset, growth would be much more difficult.
Plate of
compact bone
Intramembranous Ossification
Diploë (spongy
bone) cavities Intramembranous ossification results in the formation of cra-
contain red nial bones of the skull (frontal, parietal, occipital, and temporal
marrow
bones) and the clavicles. Most bones formed by this process are
4 Lamellar bone replaces woven bone, just deep to the flat bones. At about week 8 of development, ossification begins
periosteum. Red marrow appears.
• Trabeculae just deep to the periosteum thicken, and are later on fibrous connective tissue membranes formed by mesenchymal
replaced with mature lamellar bone, forming compact bone
plates.
• Spongy bone (diploë), consisting of distinct trabeculae, persists Figure 6.8 Intramembranous ossification. Diagrams 3 and 4
internally and its vascular tissue becomes red marrow. represent much lower magnification than diagrams 1 and 2 .
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Week 9 Month 3 Birth Childhood to adolescence
Articular
cartilage
Secondary
ossification Spongy
center bone
Epiphyseal
Area of blood vessel
deteriorating Epiphyseal
cartilage matrix plate
cartilage
Hyaline
cartilage Medullary
Spongy
bone cavity
formation
Bone Blood
collar vessel of
Primary periosteal
ossification bud
6
center
1 Bone collar forms 2 Cartilage in the 3 The periosteal 4 The diaphysis 5 The epiphyses ossify.
around hyaline center of the diaphysis bud invades the elongates and a When completed, hyaline
cartilage model. calcifies and then internal cavities and medullary cavity forms cartilage remains only in
develops cavities. spongy bone begins as ossification continues. the epiphyseal plates and
to form. Secondary ossification articular cartilages.
centers appear in the
epiphyses in preparation
for stage 5.
Figure 6.9 Endochondral ossification in a long bone.
cells. Essentially, the process involves the four major steps de- periosteum secrete osteoid against the hyaline cartilage di-
picted in Figure 6.8. aphysis, encasing it in bone. This freshly formed layer of
bone is called the periosteal bone collar.
Endochondral Ossification 2 Cartilage in the center of the diaphysis calcifies and then
Except for the clavicles, essentially all bones of the skeleton be- develops cavities. As the bone collar forms, chondrocytes
low the base of the skull form by endochondral ossification within the shaft hypertrophy (enlarge) and signal the sur-
(en⬙do-kon⬘dral). Beginning in the second month of develop- rounding cartilage matrix to calcify. Then, because calcified
ment, this process uses hyaline cartilage “bones” formed earlier cartilage matrix is impermeable to diffusing nutrients, the
as models, or patterns, for bone construction. It is more com- chondrocytes die and the matrix begins to deteriorate. This
plex than intramembranous ossification because the hyaline deterioration opens up cavities, but the hyaline cartilage
cartilage must be broken down as ossification proceeds. We will model is stabilized by the bone collar. Elsewhere, the carti-
use a forming long bone as our example. lage remains healthy and continues to grow briskly, causing
The formation of a long bone typically begins in the center of the cartilage model to elongate.
the hyaline cartilage shaft at a region called the primary ossifi- 3 The periosteal bud invades the internal cavities and spongy
cation center. First, the perichondrium covering the hyaline bone forms. In month 3, the forming cavities are invaded
cartilage “bone” is infiltrated with blood vessels, converting it to by a collection of elements called the periosteal bud, which
a vascularized periosteum. As a result of this change in nutri- contains a nutrient artery and vein, lymphatic vessels, nerve
tion, the underlying mesenchymal cells specialize into os- fibers, red marrow elements, osteoblasts, and osteoclasts.
teoblasts. The stage is now set for ossification to begin, as The entering osteoclasts partially erode the calcified carti-
illustrated in Figure 6.9: lage matrix, and the osteoblasts secrete osteoid around the
remaining fragments of hyaline cartilage, forming bone-
1 A bone collar is laid down around the diaphysis of the hya-
covered cartilage trabeculae. In this way, the earliest version
line cartilage model. Osteoblasts of the newly converted
of spongy bone in a developing long bone forms.
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ondary centers in both epiphyses, whereas the small long

bones form only one secondary ossification center.) The
cartilage in the center of the epiphysis calcifies and deterio-
Resting zone
rates, opening up cavities that allow a periosteal bud to
enter. Then bone trabeculae appear, just as they did earlier
in the primary ossification center. (In short bones, only the
primary ossification center is formed. Most irregular bones
1 Proliferation develop from several distinct ossification centers.)
zone Secondary ossification reproduces almost exactly the events
Cartilage cells
undergo mitosis.
of primary ossification, except that the spongy bone in the
interior is retained and no medullary cavity forms in the
epiphyses. When secondary ossification is complete, hyaline
cartilage remains only at two places: (1) on the epiphyseal
surfaces, as the articular cartilages, and (2) at the junction
2 Hypertrophic of the diaphysis and epiphysis, where it forms the epiphyseal
zone plates.
Older cartilage cells
enlarge.
Postnatal Bone Growth
6 3 Calcification
Calcified
zone During infancy and youth, long bones lengthen entirely by in-
Matrix becomes terstitial growth of the epiphyseal plate cartilage and its replace-
cartilage
calcified; cartilage
spicule ment by bone, and all bones grow in thickness by appositional
cells die; matrix
Osteoblast begins deteriorating. growth. Most bones stop growing during adolescence. However,
depositing some facial bones, such as those of the nose and lower jaw, con-
bone matrix
tinue to grow almost imperceptibly throughout life.
Osseous 4 Ossification
tissue zone Growth in Length of Long Bones
(bone) New bone formation
covering is occurring. Longitudinal bone growth mimics many of the events of endo-
cartilage chondral ossification. The cartilage is relatively inactive on the
spicules
side of the epiphyseal plate facing the epiphysis, a region called the
resting or quiescent zone. But the epiphyseal plate cartilage abut-
Figure 6.10 Growth in length of a long bone occurs at the ting the diaphysis organizes into a pattern that allows fast, efficient
epiphyseal plate. The side of the epiphyseal plate facing the epiph-
growth. The cartilage cells here form tall columns, like coins in a
ysis (distal face) contains resting cartilage cells. The cells of the epiph-
yseal plate proximal to the resting cartilage area are arranged in four
stack. The cells at the “top” (epiphysis-facing side) of the stack
zones—proliferation, hypertrophic, calcification, and ossification— abutting the resting zone comprise the proliferation or growth zone
from the region of the earliest stage of growth 1 to the region (Figure 6.10). These cells divide quickly, pushing the epiphysis
where bone is replacing the cartilage 4 (150⫻). away from the diaphysis, causing the entire long bone to lengthen.
Meanwhile, the older chondrocytes in the stack, which are
closer to the diaphysis (hypertrophic zone in Figure 6.10), hyper-
4 The diaphysis elongates and a medullary cavity forms. As trophy, and their lacunae erode and enlarge, leaving large inter-
the primary ossification center enlarges, osteoclasts break connecting spaces. Subsequently, the surrounding cartilage
down the newly formed spongy bone and open up a matrix calcifies and these chondrocytes die and deteriorate,
medullary cavity in the center of the diaphysis. Throughout producing the calcification zone. This leaves long slender
the fetal period (week 9 until birth), the rapidly growing spicules of calcified cartilage at the epiphysis-diaphysis junc-
epiphyses consist only of cartilage, and the hyaline cartilage tion, which look like stalactites hanging from the roof of a cave.
models continue to elongate by division of viable cartilage These calcified spicules ultimately become part of the ossification
cells at the epiphyses. Ossification “chases” cartilage forma- or osteogenic zone, and are invaded by marrow elements from
tion along the length of the shaft as cartilage calcifies, is the medullary cavity. The cartilage spicules are partly eroded by
eroded, and then is replaced by bony spicules on the epiph- osteoclasts, then quickly covered with new bone—called woven
yseal surfaces facing the medullary cavity. bone—by osteoblasts, and ultimately replaced by spongy bone.
5 The epiphyses ossify. At birth, most of our long bones have The spicule tips are eventually digested by osteoclasts, and in
a bony diaphysis surrounding remnants of spongy bone, a this way, the medullary cavity also grows longer as the long bone
widening medullary cavity, and two cartilaginous epiphy- lengthens. During growth, the epiphyseal plate maintains a
ses. Shortly before or after birth, secondary ossification constant thickness because the rate of cartilage growth on its
centers appear in one or both epiphyses, and the epiphyses epiphysis-facing side is balanced by its replacement with bony
gain bony tissue. (Typically, the large long bones form sec- tissue on its diaphysis-facing side.
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Longitudinal growth is accompanied by almost continuous Bone growth Bone remodeling
remodeling of the epiphyseal ends to maintain the proper pro-
portions between the diaphysis and epiphyses (Figure 6.11).
Bone remodeling involves both new bone formation and bone Articular cartilage
Cartilage
resorption (destruction). It is described in more detail later in grows here.
conjunction with the changes that occur in adult bones. Epiphyseal plate
As adolescence ends, the chondroblasts of the epiphyseal Cartilage
plates divide less often and the plates become thinner and thin- is replaced Bone is
by bone here. resorbed here.
ner until they are entirely replaced by bone tissue. Longitudinal
bone growth ends when the bone of the epiphysis and diaphysis Cartilage
grows here. Bone is added
fuses. This process, called epiphyseal plate closure, happens at by appositional
about 18 years of age in females and 21 years of age in males. Cartilage growth here.
However, as noted earlier, an adult bone can still increase in is replaced
by bone here. Bone is
diameter or thickness by appositional growth if stressed by ex-
resorbed here.
cessive muscle activity or body weight.
Growth in Width (Thickness) Figure 6.11 Long bone growth and remodeling during youth.
The events at the left depict endochondral ossification that occurs
Growing bones widen as they lengthen. As with cartilages, at the articular cartilages and epiphyseal plates as the bone grows in
bones increase in thickness or, in the case of long bones, diame- length. Events at the right show bone remodeling during long bone 6
ter, by appositional growth. Osteoblasts beneath the periosteum growth to maintain proper bone proportions.
secrete bone matrix on the external bone surface as osteoclasts
on the endosteal surface of the diaphysis remove bone
(Figure 6.11). However, there is normally slightly less breaking Bone Homeostasis:
down than building up. This unequal process produces a
thicker, stronger bone but prevents it from becoming too heavy.
Remodeling and Repair
䉴 Compare the locations and remodeling functions of the
C H E C K Y O U R U N D E R S TA N D I N G osteoblasts, osteocytes, and osteoclasts.
15. Bones don’t begin as bones. What do they begin as? 䉴 Explain how hormones and physical stress regulate bone
16. When describing endochondral ossification, some say “bone remodeling.
chases cartilage.” What does that mean? 䉴 Describe the steps of fracture repair.
17. Where is the primary ossification center located in a long
bone? Where is (are) the secondary ossification center(s) Bones appear to be the most lifeless of body organs, and may
located? even summon images of a graveyard. But as you have just
18. As a long bone grows in length, what is happening in the learned, this appearance is deceiving. Bone is a dynamic and ac-
hypertrophic zone of the epiphyseal plate? tive tissue, and small-scale changes in bone architecture occur
For answers, see Appendix G. continually. Every week we recycle 5–7% of our bone mass, and
as much as half a gram of calcium may enter or leave the adult
skeleton each day! Spongy bone is replaced every three to four
Hormonal Regulation of Bone Growth years; compact bone, every ten years or so. This is fortunate be-
cause when bone remains in place for long periods more of
The growth of bones that occurs until young adulthood is ex- the calcium salts crystallize (see description below) and the
quisitely controlled by a symphony of hormones. During infancy bone becomes more brittle—ripe conditions for fracture. And
and childhood, the single most important stimulus of epiphyseal when we break bones—the most common disorder of bone
plate activity is growth hormone released by the anterior pituitary homeostasis—they undergo a remarkable process of self-repair.
gland. Thyroid hormones modulate the activity of growth hor-
mone, ensuring that the skeleton has proper proportions as it
grows. At puberty, male and female sex hormones (testosterone Bone Remodeling
and estrogens, respectively) are released in increasing amounts. In the adult skeleton, bone deposit and bone resorption (re-
Initially these sex hormones promote the growth spurt typical moval) occur both at the surface of the periosteum and the sur-
of adolescence, as well as the masculinization or feminization of face of the endosteum. Together, the two processes constitute
specific parts of the skeleton. Later the hormones induce epiph- bone remodeling, and they are coupled and coordinated by
yseal plate closure, ending longitudinal bone growth. “packets”of adjacent osteoblasts and osteoclasts called remodeling
Excesses or deficits of any of these hormones can result in units (with help from the stress-sensing osteocytes). In healthy
obviously abnormal skeletal growth. For example, hypersecre- young adults, total bone mass remains constant, an indication
tion of growth hormone in children results in excessive height that the rates of bone deposit and resorption are essentially
(gigantism), and deficits of growth hormone or thyroid hor- equal. Remodeling does not occur uniformly, however. For
mone produce characteristic types of dwarfism.
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example, the distal part of the femur, or thigh bone, is fully The hormonal feedback becomes much more meaningful
replaced every five to six months, whereas its shaft is altered when you understand calcium’s importance in the body. Ionic
much more slowly. calcium is necessary for an amazing number of physiological
Bone deposit occurs wherever bone is injured or added bone processes, including transmission of nerve impulses, muscle
strength is required. For optimal bone deposit, a healthy diet contraction, blood coagulation, secretion by glands and nerve
rich in proteins, vitamin C, vitamin D, vitamin A, and several cells, and cell division. The human body contains 1200–1400 g
minerals (calcium, phosphorus, magnesium, and manganese, to of calcium, more than 99% present as bone minerals. Most of
name a few) is essential. the remainder is in body cells. Less than 1.5 g is present in blood,
New matrix deposits by osteocytes are marked by the pres- and the hormonal control loop normally maintains blood Ca2+
ence of an osteoid seam, an unmineralized band of gauzy-looking within the very narrow range of 9–11 mg per dl (100 ml) of
bone matrix 10–12 micrometers (␮m) wide. Between the os- blood. Calcium is absorbed from the intestine under the control
teoid seam and the older mineralized bone, there is an abrupt of vitamin D metabolites. The daily calcium requirement is
transition called the calcification front. Because the osteoid seam 400–800 mg from birth until the age of 10, and 1200–1500 mg
is always of constant width and the change from unmineralized from ages 11 to 24.
to mineralized matrix is sudden, it seems that the osteoid must
mature for about a week before it can calcify. Hormonal Controls The hormonal controls primarily involve
The precise trigger for calcification is still controversial. How- parathyroid hormone (PTH), produced by the parathyroid
ever, one critical factor is the product of the local concentrations glands. To a much lesser extent calcitonin (kal⬙sı̆-to⬘nin), pro-
of calcium and phosphate (Pi) ions (the Ca2+· Pi product). Ini- duced by parafollicular cells (C cells) of the thyroid gland, may be
6
tially the bone salts are laid down in a noncrystalline form, but involved. As Figure 6.12 illustrates, PTH is released when blood
when the Ca2+· Pi product reaches a certain level, tiny crystals of levels of ionic calcium decline. The increased PTH level stimu-
hydroxyapatite form spontaneously and then catalyze further lates osteoclasts to resorb bone, releasing calcium to the blood.
crystallization of calcium salts in the area. Other factors involved Osteoclasts are no respecters of matrix age. When activated, they
are matrix proteins that bind and concentrate calcium, and the break down both old and new matrix. Only osteoid, which lacks
enzyme alkaline phosphatase (shed by the osteoblasts), which is calcium salts, escapes digestion. As blood concentrations of cal-
essential for mineralization. Once proper conditions are present, cium rise, the stimulus for PTH release ends. The decline of PTH
calcium salts are deposited all at once and with great precision reverses its effects and causes blood Ca2+ levels to fall.
throughout the “matured” matrix. Normally, a small percentage In humans, calcitonin appears to be a hormone in search of
of the calcified salts remain in the noncrystallized form to pro- a function because its effects on calcium homeostasis are negli-
vide a readily available source of calcium ions when blood cal- gible. When administered at pharmacological (abnormally
cium levels decline toward nonhomeostatic values. high) doses, it does lower blood calcium levels temporarily.
Bone resorption is accomplished by osteoclasts, giant mul- These hormonal controls act not to preserve the skeleton’s
tinucleate cells that arise from the same hematopoietic stem cells strength or well-being but rather to maintain blood calcium
that differentiate into macrophages. Osteoclasts move along a homeostasis. In fact, if blood calcium levels are low for an ex-
bone surface, digging grooves as they break down the bone ma- tended time, the bones become so demineralized that they de-
trix. The part of the osteoclast that touches the bone is highly velop large, punched-out-looking holes. Thus, the bones serve
folded to form a ruffled membrane (see Figure 6.4d) that clings as a storehouse from which ionic calcium is drawn as needed.
tightly to the bone, sealing off the area of bone destruction. The
ruffled border secretes (1) lysosomal enzymes that digest the or-
H O M E O S TAT I C I M B A L A N C E
ganic matrix and (2) hydrochloric acid that converts the calcium
salts into soluble forms that pass easily into solution. Osteoclasts Minute changes from the homeostatic range for blood calcium
may also phagocytize the demineralized matrix and dead osteo- can lead to severe neuromuscular problems ranging from hy-
cytes. The digested matrix end products, growth factors, and dis- perexcitability (when blood Ca2+ levels are too low) to nonre-
solved minerals are then endocytosed, transported across the sponsiveness and inability to function (with high blood Ca2+
osteoclast (by transcytosis), and released at the opposite side levels). In addition, sustained high blood levels of Ca2+, a condi-
where they enter first the interstitial fluid and then the blood. tion known as hypercalcemia (hi⬙per-kal-se⬘me-ah), can lead to
There is much to learn about osteoclast activation, but proteins undesirable deposits of calcium salts in the blood vessels, kid-
secreted by T cells of the immune system appear to be important. neys, and other soft organs, which may hamper the functioning
of these organs. ■
Control of Remodeling In addition to the hormones that regulate bone remodeling
The remodeling that goes on continuously in the skeleton is reg- in response to blood calcium levels, it is now established that
ulated by two control loops that serve different “masters.” One is leptin, a hormone released by adipose tissue, plays a role in reg-
a negative feedback hormonal loop that maintains Ca2+ homeo- ulating bone density. Best known for its effects on weight and
stasis in the blood. The other involves responses to mechanical energy balance (see pp. 946–947), in animal studies leptin appears
and gravitational forces acting on the skeleton. to inhibit osteoblasts through an additional pathway mediated
by the hypothalamus which activates sympathetic nerves serving
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IMB
AL
AN
CE
Calcium homeostasis of blood: 9–11 mg/100 ml

BALANCE BALANCE
Stimulus
Falling blood
IMB
AL Ca2+ levels
AN
CE
Thyroid
gland
Osteoclasts
degrade bone Parathyroid
matrix and release glands
Parathyroid
Ca2+ into blood.
glands release
parathyroid
hormone (PTH).
PTH 6
Figure 6.12 Parathyroid hormone (PTH) control of blood calcium levels.
bones. However, the full scope of leptin’s bone-modifying activ- Load here
ity in humans is still being worked out. (body weight)
Response to Mechanical Stress The second set of controls

regulating bone remodeling, bone’s response to mechanical
stress (muscle pull) and gravity, serves the needs of the skeleton
by keeping the bones strong where stressors are acting. Wolff’s
law holds that a bone grows or remodels in response to the de- Head of
mands placed on it. The first thing to understand is that a bone’s femur
anatomy reflects the common stresses it encounters. For exam-
ple, a bone is loaded (stressed) whenever weight bears down on
it or muscles pull on it. This loading is usually off center, how-
ever, and tends to bend the bone. Bending compresses the bone
on one side and subjects it to tension (stretching) on the other
(Figure 6.13). As a result of these mechanical stressors, long
bones are thickest midway along the diaphysis, exactly where
Tension Compression
bending stresses are greatest (bend a stick and it will split near here
the middle). Both compression and tension are minimal toward here
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. Point of
no stress
Other observations explained by Wolff’s law include these:
(1) Handedness (being right or left handed) results in the bones
of one upper limb being thicker than those of the less-used
limb, and vigorous exercise of the most-used limb leads to large
increases in bone strength (Figure 6.14). (2) Curved bones are
thickest where they are most likely to buckle. (3) The trabeculae
of spongy bone form trusses, or struts, along lines of compres-
sion. (4) Large, bony projections occur where heavy, active mus- Figure 6.13 Bone anatomy and bending stress. Body weight
transmitted to the head of the femur (thigh bone) threatens to bend
cles attach. (The bones of weight lifters have enormous
the bone along the indicated arc, compressing it on one side (con-
thickenings at the attachment sites of the most-used muscles.) verging arrows on right) and stretching it on the other side (diverging
Wolff’s law also explains the featureless bones of the fetus and arrows on left). Because these two forces cancel each other internally,
the atrophied bones of bedridden people—situations in which much less bone material is needed internally than superficially.
bones are not stressed.
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stimulation, so that bone in the least stressed areas (which is

temporarily dispensable) is broken down.
Bone Repair
Despite their remarkable strength, bones are susceptible to
fractures, or breaks. During youth, most fractures result from
exceptional trauma that twists or smashes the bones (sports in-
juries, automobile accidents, and falls, for example). Excessive
intake of vitamin A appears to increase fracture risk in some
people. Elevated blood levels of the amino acid derivative ho-
mocysteine were also believed to increase fracture risk, but re-
cent studies indicate that it is actually a marker of low bone
density and bone frailty. In old age, most fractures occur as
bones thin and weaken.
(a) Fractures may be classified by
1. Position of the bone ends after fracture. In nondisplaced
Cross-
fractures the bone ends retain their normal position; in
6 sectional displaced fractures the bone ends are out of normal
dimension alignment.
of the
humerus
2. Completeness of the break. If the bone is broken through,
the fracture is a complete fracture; if not, it is an incomplete
Added fracture.
bone matrix 3. Orientation of the break relative to the long axis of the bone.
counteracts
added stress If the break parallels the long axis, the fracture is linear; if the
break is perpendicular to the bone’s long axis, it is transverse.
Serving arm Nonserving arm 4. Whether the bone ends penetrate the skin. If so, the frac-
(b) ture is an open (compound) fracture; if not, it is a closed
(simple) fracture.
Figure 6.14 Vigorous exercise can lead to large increases in
bone strength. The diagrams show the average difference in the
In addition to these four either-or classifications, all fractures
cross-sectional dimensions of the humerus of the arm in the serving can be described in terms of the location of the fracture, the ex-
and nonserving arms of professional tennis players. The data re- ternal appearance of the fracture, and/or the nature of the
vealed average increases in bone rigidity and strength of 62% and break. Table 6.2 summarizes the various descriptions.
45%, respectively, in the serving arms. The structural changes were A fracture is treated by reduction, the realignment of the bro-
more pronounced in players who began training at an early age. ken bone ends. In closed (external) reduction, the bone ends are
SOURCE: C. B. Ruff, “Gracilization of the Modern Human Skeleton,” coaxed into position by the physician’s hands. In open (internal)
American Scientist 94(6): p. 513, Nov–Dec 2006. reduction, the bone ends are secured together surgically with
pins or wires. After the broken bone is reduced, it is immobi-
How do mechanical forces communicate with the cells re- lized either by a cast or traction to allow the healing process to
sponsible for remodeling? Although the mechanisms by which begin. For a simple fracture the healing time is six to eight weeks
bone responds to mechanical stimuli are still uncertain, we do for small or medium-sized bones in young adults, but it is much
know that deforming a bone produces an electrical current. Be- longer for large, weight-bearing bones and for bones of elderly
cause compressed and stretched regions are oppositely charged, people (because of their poorer circulation).
it has been suggested that electrical signals direct remodeling. Repair in a simple fracture involves four major stages (Fig-
This principle underlies some of the devices currently used to ure 6.15):
speed bone repair and the healing of fractures. 1 A hematoma forms. When a bone breaks, blood vessels in
The skeleton is continuously subjected to both hormonal in- the bone and periosteum, and perhaps in surrounding tis-
fluences and mechanical forces. At the risk of constructing too sues, are torn and hemorrhage. As a result, a hematoma
large a building on too small a foundation, we can speculate that (he⬙mah-to⬘mah), a mass of clotted blood, forms at the
the hormonal loop determines whether and when remodeling fracture site. Soon, bone cells deprived of nutrition die, and
occurs in response to changing blood calcium levels, and me- the tissue at the site becomes swollen, painful, and inflamed.
chanical stress determines where it occurs. For example, when 2 Fibrocartilaginous callus forms. Within a few days, several
bone must be broken down to increase blood calcium levels, events lead to the formation of soft granulation tissue, also
PTH is released and targets the osteoclasts. However, mechani- called the soft callus (kal⬘us; “hard skin”). Capillaries grow
cal forces determine which osteoclasts are most sensitive to PTH into the hematoma and phagocytic cells invade the area and
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External
callus
Hematoma Bony
callus of
spongy
bone
Internal New Healed
callus blood fracture
(fibrous vessels
tissue and
cartilage) Spongy
bone
trabecula
1 A hematoma forms. 2 Fibrocartilaginous 3 Bony callus forms. 4 Bone remodeling

callus forms. occurs.
Figure 6.15 Stages in the healing of a bone fracture.

6
begin cleaning up the debris. Meanwhile, fibroblasts and Homeostatic Imbalances of Bone
osteoblasts invade the fracture site from the nearby perios-
teum and endosteum and begin reconstructing the bone. 䉴 Contrast the disorders of bone remodeling seen in osteo-
The fibroblasts produce collagen fibers that span the break porosis, osteomalacia, and Paget’s disease.
and connect the broken bone ends, and some differentiate
into chondroblasts that secrete cartilage matrix. Within this Imbalances between bone deposit and bone resorption underlie
mass of repair tissue, osteoblasts begin forming spongy nearly every disease that affects the adult skeleton.
bone, but those farthest from the capillary supply secrete
an externally bulging cartilaginous matrix that later calci-
Osteomalacia and Rickets
fies. This entire mass of repair tissue, now called the
fibrocartilaginous callus, splints the broken bone. Osteomalacia (os⬙te-o-mah-la⬘she-ah; “soft bones”) includes a
3 Bony callus forms. Within a week, new bone trabeculae
number of disorders in which the bones are inadequately min-
eralized. Osteoid is produced, but calcium salts are not de-
begin to appear in the fibrocartilaginous callus and gradually
posited, so bones soften and weaken. The main symptom is pain
convert it to a bony (hard) callus of spongy bone. Bony
when weight is put on the affected bones.
callus formation continues until a firm union is formed
Rickets is the analogous disease in children. Because young
about two months later.
bones are still growing rapidly, rickets is much more severe than
4 Bone remodeling occurs. Beginning during bony callus for- adult osteomalacia. Bowed legs and deformities of the pelvis,
mation and continuing for several months after, the bony skull, and rib cage are common. Because the epiphyseal plates
callus is remodeled. The excess material on the diaphysis cannot be calcified, they continue to widen, and the ends of long
exterior and within the medullary cavity is removed, and bones become visibly enlarged and abnormally long.
compact bone is laid down to reconstruct the shaft walls. Osteomalacia and rickets are caused by insufficient calcium
The final structure of the remodeled area resembles that of in the diet or by a vitamin D deficiency. For this reason, drink-
the original unbroken bony region because it responds to ing vitamin D–fortified milk and exposing the skin to sunlight
the same set of mechanical stressors. (which spurs the body to form vitamin D) usually cure these
disorders. Although the seeming elimination of rickets in the
C H E C K Y O U R U N D E R S TA N D I N G United States has been heralded as a public health success, rick-
19. If osteoclasts in a long bone are more active than ets still rears its head in isolated situations. For example, if a
osteoblasts, what change in bone mass is likely? mother who breast-feeds her infant becomes vitamin D defi-
20. Which stimulus—PTH (a hormone) or mechanical forces act- cient because of dreary winter weather, the infant too will be
ing on the skeleton—is more important in maintaining ho- vitamin D deficient and will develop rickets.
meostatic blood calcium levels?
21. How does an open fracture differ from a closed fracture?
Osteoporosis
22. How do bone growth and bone remodeling differ?
For most of us, the phrase “bone problems of the elderly”
For answers, see Appendix G. brings to mind the stereotype of a victim of osteoporosis—a
hunched-over old woman shuffling behind her walker.
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TABLE 6.2 Common Types of Fractures

FRACTURE FRACTURE
TYPE DESCRIPTION AND COMMENTS TYPE DESCRIPTION AND COMMENTS
Comminuted Bone fragments into three or more pieces. Compression Bone is crushed.
Particularly common in the aged, whose bones are Common in porous bones (i.e., osteoporotic bones)
more brittle subjected to extreme trauma, as in a fall
Crushed
vertebra
6
Spiral Ragged break occurs when excessive twisting forces Epiphyseal Epiphysis separates from the diaphysis along the
are applied to a bone. epiphyseal plate.
Common sports fracture Tends to occur where cartilage cells are dying and
calcification of the matrix is occurring
Depressed Broken bone portion is pressed inward. Greenstick Bone breaks incompletely, much in the way a green
twig breaks. Only one side of the shaft breaks; the
other side bends.
Typical of skull fracture Common in children, whose bones have relatively
more organic matrix and are more flexible than
those of adults
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osteoporosis include a petite body form, insufficient exercise to
stress the bones, immobility, a diet poor in calcium and protein,
abnormal vitamin D receptors, smoking (which reduces estro-
gen levels), and hormone-related conditions such as hyperthy-
roidism, low blood levels of thyroid-stimulating hormone
(better known for its role in stimulating the secretion of thyroid
hormones), and diabetes mellitus. In addition, recent research
indicates that a particular gene, dubbed LRP5, may play a role in
osteoporosis. It inhibits release of serotonin by cells of the gut.
Because serotonin inhibits osteoblast growth, reducing its syn-
thesis increases bone density.
Osteoporosis has traditionally been treated with calcium and
vitamin D supplements, weight-bearing exercise, and hormone
(estrogen) replacement therapy (HRT). Frustratingly, HRT only
(a) Normal bone slows the loss of bone but does not reverse it. Additionally, be-
cause of the increased risk of heart attack, stroke, and breast
cancer associated with estrogen replacement therapy, it is a con-
troversial treatment these days.
Newer drugs are available. These include alendronate (Fos-
6
amax), a drug that decreases osteoclast activity and number, and
shows promise in reversing osteoporosis in the spine; and selec-
tive estrogen receptor modulators (SERMs), such as raloxifene,
dubbed “estrogen light” because it mimics estrogen’s beneficial
bone-sparing properties without targeting the uterus or breast.
Additionally, statins, drugs used by tens of thousands of people to
lower cholesterol levels, have been shown to have an unexpected
side effect of increasing bone mineral density up to 8% over four
years. Although not a substitute for HRT, estrogenic compounds
in soy protein (principally the isoflavones daidzein and genis-
tein) offer a good addition or adjunct for some patients.
(b) Osteoporotic bone How can osteoporosis be prevented (or at least delayed)? The
first requirement is to get enough calcium while your bones are
Figure 6.16 The contrasting architecture of normal versus still increasing in density (bones reach their peak density during
osteoporotic bone. Scanning electron micrographs, 300⫻. early adulthood). Second, drinking fluoridated water hardens
bones (as well as teeth). Conversely, excessive intake of carbon-
Osteoporosis (os⬙te-o-po-ro⬘sis) refers to a group of diseases ated beverages leaches minerals from bone and decreases bone
in which bone resorption outpaces bone deposit. The bones density. Finally, getting plenty of weight-bearing exercise (walk-
become so fragile that something as simple as a hearty sneeze ing, jogging, tennis, etc.) throughout life will increase bone mass
or stepping off a curb can cause them to break. The composi- above normal values and provide a greater buffer against age-
tion of the matrix remains normal but bone mass is reduced, related bone loss.
and the bones become porous and light (Figure 6.16). Even
though osteoporosis affects the entire skeleton, the spongy
bone of the spine is most vulnerable, and compression frac- Paget’s Disease
tures of the vertebrae are common. The femur, particularly its Often discovered by accident when X rays are taken for some
neck, is also very susceptible to fracture (called a broken hip) in other reason, Paget’s disease (paj⬘ets) is characterized by exces-
people with osteoporosis. sive and haphazard bone deposit and resorption. The newly
Osteoporosis occurs most often in the aged, particularly in formed bone, called Pagetic bone, is hastily made and has an ab-
postmenopausal women. Although men develop it to a lesser normally high ratio of spongy bone to compact bone. This,
degree, 30% of American women between the ages of 60 and 70 along with reduced mineralization, causes a spotty weakening
have osteoporosis, and 70% have it by age 80. Moreover, 30% of of the bones. Late in the disease, osteoclast activity wanes, but
all Caucasian women (the most susceptible group) will experi- osteoblasts continue to work, often forming irregular bone
ence a bone fracture due to osteoporosis. Sex hormones, partic- thickenings or filling the marrow cavity with Pagetic bone.
ularly estrogen, help to maintain the health and normal density Paget’s disease may affect any part of the skeleton, but it is
of the skeleton by restraining osteoclast activity and by promot- usually a localized condition. The spine, pelvis, femur, and skull
ing deposit of new bone. After menopause, however, estrogen are most often involved and become increasingly deformed and
secretion wanes, and estrogen deficiency is strongly implicated painful. It rarely occurs before the age of 40, and it affects about
in osteoporosis in older women. Other factors that contribute to 3% of North American elderly people. Its cause is unknown, but
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M A K I N G C O N N E C T I O N S
Homeostatic Interrelationships Between the Skeletal

System and Other Body Systems
Endocrine System
■ Skeletal system provides some bony protection; stores calcium
needed for second-messenger signaling mechanisms
■ Hormones regulate uptake and release of calcium from bone;
promote long bone growth and maturation
Cardiovascular System
■ Bone marrow cavities provide site for blood cell formation; ma-
trix stores calcium needed for cardiac muscle activity
■ Cardiovascular system delivers nutrients and oxygen to bones;
carries away wastes
Lymphatic System/Immunity
■ Skeletal system provides some protection to lymphatic organs;
6 bone marrow is site of origin for lymphocytes involved in im-
mune response
■ Lymphatic system drains leaked tissue fluids; immune cells pro-
tect against pathogens
Respiratory System
■ Skeletal system protects lungs by enclosure (rib cage)
■ Respiratory system provides oxygen; disposes of carbon dioxide
Digestive System
■ Skeletal system provides some bony protection to intestines,
pelvic organs, and liver
■ Digestive system provides nutrients needed for bone health and
growth
Urinary System
Integumentary System
■ Skeletal system protects pelvic organs (urinary bladder, etc.)
■ Urinary system activates vitamin D; disposes of nitrogenous
■ Skeletal system provides support for body organs including wastes
the skin
■ Skin provides vitamin D needed for proper calcium absorption Reproductive System
and use
■ Skeletal system protects some reproductive organs by enclosure
Muscular System
■ Gonads produce hormones that influence the form of the skele-
ton and epiphyseal closure
■ Skeletal system provides levers plus ionic calcium for muscle
activity
■ Muscle pull on bones increases bone strength and viability;
helps determine bone shape
Nervous System
■ Skeletal system protects brain and spinal cord; provides depot
for calcium ions needed for neural function
■ Nerves innervate bone and joint capsules, providing for pain
and joint sense
192
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The Skeletal System and Interrelationships with the

Muscular, Endocrine, and Integumentary Systems
Our skeleton supports us, protects our “innards” (the protection Endocrine System
our brain gets from the skull is indispensable), gives us stature (for Although mechanical factors are undeniably important in shaping
some reason, tall people get more respect), contributes to our the skeleton and helping to keep it strong, hormones acting indi-
shape (women are shaped differently than men), and allows us to vidually and in concert direct skeletal growth during youth, and en-
move. Obviously, the skeletal system has important interactions hance (or impair) skeletal strength in adults. Growth hormone is
with many other body systems, not the least of which are the en- essential for normal skeletal growth and maintenance throughout
docrine and integumentary systems. However, its most intimate life, whereas thyroid and sex hormones ensure that normal skeletal
and mutually beneficial relationship is with the muscular system, proportions are established during childhood and adolescence.
so we will consider that first. Conversely, PTH serves not the skeleton but a different master—
homeostasis of blood calcium levels. Any interference with normal
Muscular System hormonal functioning is soon apparent as a skeletal abnormality or
The codependence of the skeletal and muscular systems is malproportion.
striking—as one system goes, so goes the other. If we participate
in weight-bearing exercise (run, play tennis, do aerobics) regularly, Integumentary System
our muscles become more efficient and exert more force on our The skeletal system is absolutely dependent on the integumentary
bones. As a result, our bones stay healthy and strong and in- system (the skin) for the calcium that keeps the bones hard and 6
crease their mass to assume the added stress. strong. The relationship is indirect: In the presence of sunlight, a
Since both spongy and compact bone reach peak density dur- vitamin D precursor is produced in the dermal capillary blood. It is
ing midlife, weight-bearing exercise during youth is important, es- activated elsewhere, and (among its other roles) it regulates the
pecially in females who have less bone mass than males and lose carrier system that absorbs calcium from ingested foods into the
it faster. blood. Because calcium is required for so many body functions,
Regular exercise also stretches the connective tissues binding and bones provide the “calcium bank,” the bones become in-
bones to muscles and to other bones, and reinforcing joints. Since creasingly soft and weak in the absence of vitamin D because no
this increases overall flexibility, we have fewer injuries, allowing us daily rations of calcium are allowed to enter the blood from the di-
to stay active well into old age. (Pain makes couch potatoes.) gestive tract.
Skeletal System
Case study: Remember Mrs. DeStephano? When we last heard 3. What is internal reduction? Why was a cast applied?
about her she was being admitted for further studies. Relative to 4. Given an uncomplicated recovery, approximately how long
her skeletal system, the following notes have been added to her should it take before Mrs. DeStephano has a good solid bony
chart. callus?
■ Fracture of superior right tibia (shinbone of leg); skin lacerated; 5. What complications might be predicted by the fact that the nu-
area cleaned and protruding bone fragments subjected to inter- trient artery is damaged?
nal (open) reduction and casted
■ Nutrient artery of tibia damaged 6. What new techniques might be used to enhance fracture repair
■ Medial meniscus (fibrocartilage disc) of right knee joint crushed; if healing is delayed or impaired?
knee joint inflamed and painful 7. How likely is it that Mrs. DeStephano’s knee cartilage will regen-
Relative to these notes: erate? Why?
1. What type of fracture does Mrs. DeStephano have? (Answers in Appendix G)
2. What problems can be predicted with such fractures and how
are they treated?
193
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mesenchymal cells, which in turn produce the membranes and

cartilages that form the embryonic skeleton. These structures
Parietal
then ossify according to an amazingly predictable timetable that
bone allows fetal age to be determined easily from either X rays or
Occipital sonograms. Although each bone has its own developmental
bone Frontal schedule, most long bones begin ossifying by 8 weeks after con-
bone of
Mandible skull ception and have well-developed primary ossification centers
by 12 weeks (Figure 6.17).
Clavicle
At birth, most long bones of the skeleton are well ossified ex-
cept for their epiphyses. After birth, secondary ossification cen-
Scapula ters develop in a predictable sequence. The epiphyseal plates
Radius persist and provide for long bone growth all through childhood
Ulna
and the sex hormone–mediated growth spurt at adolescence. By
the age of 25 years, nearly all bones are completely ossified and
skeletal growth ceases.
Ribs Humerus In children and adolescents, bone formation exceeds bone
resorption. In young adults, these processes are in balance, and
Vertebra in old age, resorption predominates. Despite the environmental
factors (discussed earlier) that influence bone density, genetics
6 Ilium
still plays the major role in determining how much a person’s
bone density will change over a lifetime. A single gene that codes
Tibia
for vitamin D’s cellular docking site helps determine both the
tendency to accumulate bone mass during early life and a per-
Femur son’s risk of osteoporosis later in life.
Beginning in the fourth decade of life, bone mass decreases
with age. The only exception appears to be in bones of the skull.
Among young adults, skeletal mass is generally greater in males
than in females, and greater in blacks than in whites. Age-related
Figure 6.17 Fetal primary ossification centers at 12 weeks. The bone loss is faster in whites than in blacks (who have greater
darker areas indicate primary ossification centers in the skeleton of a
bone density to begin with) and faster in females than in males.
12-week-old fetus.
Qualitative changes also occur: More osteons remain incom-
pletely formed, mineralization is less complete, and the amount
it may be initiated by a virus. Drug therapies include calcitonin of nonviable bone increases, reflecting a diminished blood sup-
(now administered by a nasal inhaler), and the newer bisphos- ply to the bones in old age. These age-related changes are also
phonates (etidronate, alendronate, and others) which have bad news because fractures heal more slowly in old people.
shown success in preventing bone breakdown. Daily ultrasound treatments are helpful in hastening repair of
fractures, and electrical stimulation of fracture sites dramati-
C H E C K Y O U R U N D E R S TA N D I N G cally increases the speed of healing. (Presumably electrical fields
inhibit PTH stimulation of osteoclasts and induce formation of
23. Which bone disorder is characterized by excessive deposit of
growth factors that stimulate osteoblasts at the fracture site.)
weak, poorly mineralized bone?
24. What are three measures that may help to maintain healthy
bone density?
25. What name is given to “adult rickets”? 26. What is the status of bone structure at birth?
27. The decrease in bone mass that begins in the fourth decade
of life affects nearly all bones. What are the exceptions?
Developmental Aspects of Bones: Skeletal cartilages and bones—their architecture, composi-

Timing of Events tion, and dynamic nature—have been examined in this chapter.
We have also discussed the role of bones in maintaining overall
䉴 Describe the timing and cause of changes in bone archi- body homeostasis, as summarized in Making Connections. Now
tecture and bone mass throughout life. we are ready to look at the individual bones of the skeleton and
how they contribute to its functions, both collectively and
Bones are on a precise schedule from the time they form until individually.
death. The mesoderm germ layer gives rise to embryonic

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qxd 12/2/2011 1:20 PM Page 172

Growth of Cartilage (p. 173)

Classification of Bones (pp. 173–175)

Functions of Bones (pp. 175–176)

Bone Structure (pp. 176–182)

Microscopic Anatomy of Bone (pp. 179–180)

Chemical Composition of Bone (pp. 180–182)

Postnatal Bone Growth (pp. 184–185)

Bone Homeostasis: Remodeling

Chapter 6 Bones and Skeletal Tissues 173

174 UN I T 2 Covering, Support, and Movement of the Body

Chapter 6 Bones and Skeletal Tissues 175

(c) Flat bone (sternum)

(a) Long bone (humerus) 6

(b) Irregular bone (vertebra),

Figure 6.2 Classification of bones on the basis of shape.

176 UN I T 2 Covering, Support, and Movement of the Body

7. What is the functional relationship between skeletal muscles

Chapter 6 Bones and Skeletal Tissues 177

(a) Osteogenic cell (b) Osteoblast (c) Osteocyte (d) Osteoclast

Figure 6.4 Comparison of different types of bone cells.

TABLE 6.1 Bone Markings

Projections That Are Sites of Muscle and Ligament Attachment

Tuberosity Large rounded projection; may be Iliac

Projections That Help to Form Joints

Head Bony expansion carried on a narrow neck Head

Condyle Rounded articular projection

Depressions and Openings

For Passage of Blood Vessels and Nerves

Chapter 6 Bones and Skeletal Tissues 179

180 UN I T 2 Covering, Support, and Movement of the Body

Chapter 6 Bones and Skeletal Tissues 181

Endosteum lining bony canals

Perforating (Sharpey’s) fibers

Lamellae Periosteal blood vessel

182 UN I T 2 Covering, Support, and Movement of the Body

Ossification and osteogenesis (os⬙te-o-jen⬘ĕ-sis) are synonyms

Chapter 6 Bones and Skeletal Tissues 183

Figure 6.9 Endochondral ossification in a long bone.

184 UN I T 2 Covering, Support, and Movement of the Body

ondary centers in both epiphyses, whereas the small long

Chapter 6 Bones and Skeletal Tissues 185

186 UN I T 2 Covering, Support, and Movement of the Body

Chapter 6 Bones and Skeletal Tissues 187

Calcium homeostasis of blood: 9–11 mg/100 ml

Figure 6.12 Parathyroid hormone (PTH) control of blood calcium levels.

Response to Mechanical Stress The second set of controls

188 UN I T 2 Covering, Support, and Movement of the Body

stimulation, so that bone in the least stressed areas (which is

Chapter 6 Bones and Skeletal Tissues 189

1 A hematoma forms. 2 Fibrocartilaginous 3 Bony callus forms. 4 Bone remodeling

Figure 6.15 Stages in the healing of a bone fracture.

190 UN I T 2 Covering, Support, and Movement of the Body

TABLE 6.2 Common Types of Fractures

Chapter 6 Bones and Skeletal Tissues 191

Homeostatic Interrelationships Between the Skeletal

The Skeletal System and Interrelationships with the

194 UN I T 2 Covering, Support, and Movement of the Body