Chapter 6

Bone Tissue
 Functions of Skeletal System
• Support
• Protection
• Movement
• Mineral homeostasis
• Hemopoiesis (blood cell formation)
• Fat storage
 Structure of a Long Bone
• Diaphysis, metaphysis, epiphysis
• Medullary cavity
• Articular cartilage (hyaline cartilage)
• Periosteum (does not cover articular
cartilage)
• Endosteum
 Articular cartilage

Proximal epiphysis Spongy bone (contains red bone

marrow)
Metaphysis Red bone marrow
Epiphyseal line

Compact bone
Endosteum (lines medullary cavity)
Nutrient artery
Diaphysis
Medullary cavity (contains
yellow bone marrow in adults)
Periosteum
Humerus

Metaphysis

Distal epiphysis Articular cartilage

(a) Partially sectioned humerus

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 Proximal epiphysis

Epiphyseal line
Spongy bone
Metaphysis

Compact bone

Medullary cavity in diaphysis

(b) Partially sectioned humerus

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 Bone Cells
Osteogenic cells differentiate into osteoblasts
(“builders”) that secrete matrix and then
differentiate further into osteocytes, the
mature bone cells that maintain bone tissue.
Osteoclasts (“carvers”) secrete HCl and
enzymes, sculpt and shape bone by
reabsorption of matrix.
 From bone cell lineage From white blood cell lineage

Ruffled
border

OSTEOGENIC CELL OSTEOBLAST (forms OSTEOCYTE OSTEOCLAST (functions in

(develops into an bone extracellular (maintains bone resorption, the breakdown
osteoblast) matrix) tissue) of bone extracellular
matrix)

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 Bone Matrix
Hydroxyapatite (calcium and phosphorus salts)
provides rigidity
Collagen fibers provide flexibility, makes a
framework for calcification
 Compact Bone
Forms outer layer of all bones
Made of osteons (layers of matrix surrounding a
central canal, osteocytes found in lacunae,
linked by canaliculi)
Compact bone
Medullary
cavity
Spongy
Osteocyte
bone Interstitial Outer Concentric
Periosteum lamellae Canaliculi
circumferential lamellae
lamellae Lacuna
See Figure 6.3b for Blood
details vessels

Medullary
cavity

Osteon
Trabeculae

Inner Periosteal vein

circumferential Periosteal artery
lamellae Periosteum:
Outer fibrous layer
Inner osteogenic layer
Central canal
Spongy bone
Perforating canal
Compact bone Perforating (Sharpey’s)
fibers
(a) Osteons (haversian systems) in compact bone and trabeculae in spongy bone
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 Spongy Bone
Made of trabeculae – lattice of bone, spaces
may be filled with red marrow
All formed elements of the blood (rbcs, wbcs,
and platelets) produced in the red marrow
 Lacuna
Lamellae

Space for red Canaliculi

bone marrow Osteocyte

Trabeculae Osteoclast

Osteoblasts aligned
along trabeculae of
new bone

(b) Enlarged aspect of spongy bone trabeculae (c) Details of a section of a trabecula

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 Blood Supply of Bone
Rich blood supply of bone: Branches from
periosteal vessels pass through perforating
canals and into central canals of osteons.
Nutrient foramina allow vessels to pass into
medullary cavity.
 Articular cartilage
Epiphysis Epiphyseal artery
Epiphyseal vein

Epiphyseal line
Metaphysis
Metaphyseal artery

Metaphyseal vein
Medullary cavity
Compact bone
Nutrient artery
Diaphysis Periosteal artery
Periosteal vein
Periosteum
Nutrient foramen

Nutrient vein
Partially sectioned tibia (shin bone)
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 Osteocytes
Osteocytes connect within canaliculi by
cytoplasmic processes, linked by gap
junctions
Nutrients and wastes diffuse from cell to cell
 Ossification
Bone formation (ossification):
• Intramembranous – bone forms on/within a
fibrous connective tissue membrane, no
cartilage stage (skull, mandible)
• Endochondral – bone forms from a hyaline
cartilage model in the fetus (most other
bones). Cartilage proliferates and is replaced
by bone tissue.
(b) Twelve-week fetus. The red areas represent
bones that are forming (calcified). Clear areas
represent cartilage (uncalcified).

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 Perichondrium

Proximal Hyaline
epiphysis cartilage
Periosteum
Uncalcified
Primary
extracellular Nutrient
Diaphysis ossification
matrix artery center
Calcified Spongy bone
extracellular
Distal matrix
epiphysis

1 Development of 2 Growth of cartilage 3 Development of primary

cartilage model: model: growth ossification center: in this
mesenchymal cells occurs by cell region of the diaphysis,
develop into division of bone tissue replaces
chondroblasts, chondrocytes. most of the cartilage.
which form the
cartilage model.

(a) Sequence of events

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Uncalcified Secondary
extracellular ossification Articular
matrix center cartilage
Epiphyseal
artery and
Calcified vein Spongy bone
extracellular
matrix
Uncalcified Epiphyseal
Periosteum extracellular plate
matrix
Medullary
cavity
Nutrient artery
and vein

4 Development of the 5 Development of 6 Formation of articular

medullary (marrow) secondary ossification cartilage and epiphyseal
cavity: bone centers: these occur in plate: both structures
breakdown by the epiphyses of the consist of hyaline cartilage.
osteoclasts forms the bone.
medullary cavity.

(a) Sequence of events

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 Bone Growth
• Length – interstitial growth, happens within
the bone.
Epiphyseal plate (made of hyaline cartilage) is
the center of new bone formation. Once the
epiphyses “close” at age 18-25 years, the bone
cannot grow longer.
• Thickness – appositional growth (adding on
layers) from periosteum
 Bone formed by
osteoblasts
Bone destroyed
by osteoclasts
Medullary
cavity

Infant Child Young adult Adult

(b) Macroscopic changes

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 Factors Affecting Bone Growth
• Nutritional factors –
– Minerals: calcium and phosphorus (for
extracellular matrix)
– Vitamins: D (absorption of calcium from food),
C (synthesis of collagen), B12 and K (synthesis of
bone proteins), A (stimulates osteoblasts)
 Factors Affecting Bone Growth
• Hormones
– Insulin-like growth factors (IGFs produced by liver and bone)
stimulate osteoblasts and protein synthesis, cell division in
hyaline cartilage at growth plate
– human growth hormone (hGH stimulates production of IGFs)
– thyroid hormones (T3, T4 stimulate osteoblasts)
– Insulin (stimulates protein synthesis)
– sex steroids (estrogens and androgens increase osteoblast
activity, promote apoptosis of osteoclasts, responsible for
“growth spurt”, estrogens stop bone growth by closing
growth plate)
 Bone Remodeling
Bone remodeling is a process of homeostasis:
Balanced activity of osteoblasts and
osteoclasts.
Continues throughout adult life, helps
maintain strength of bone tissue.
Osteons and trabeculae are aligned in the
bone along lines of mechanical stress.
Osteocytes detect changing stresses, send
signals to osteoblasts and osteoclasts
 Bone Fracture
Stress fractures – microscopic fissures in bone due to
repeated stress/overuse
Fracture repair leads to formation of a bony callus that is
remodeled into compact bone
Four steps of fracture repair:
1. Formation of a fracture hematoma-6 to 8 hours

2. Fibrocartilaginous callus formation-3 weeks

3. Bony callus formation-3-4 months
4. Bone remodeling
 Periosteum

Fracture
hematoma
Bony
New blood (hard)
vessel callus

Spongy Healed
bone fracture
trabeculae
Fibrocartilaginous
callus (soft)

1 Reactive phase: 2a Reparative phase: 2b Reparative phase: 3 Bone

formation of fibrocartilaginous bony callus remodeling
fracture hematoma callus formation formation phase

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 Calcium
Calcium homeostasis: concentration of calcium
in blood is closely regulated; a crucial factor in
conduction of nerve impulses, action of
muscles, blood clotting, enzyme activity
Bone tissue is the body’s calcium reservoir
Parathyroid hormone: causes increase in blood
calcium concentration
Calcitonin: causes decrease in blood calcium
concentration
 STIMULUS

Disrupts homeostasis
by decreasing

CONTROLLED CONDITION
Blood calcium (Ca2+) level

RECEPTORS
Parathyroid
gland cells

Detect lowered Ca2+

Input concentration which increases
production of cyclic AMP

CONTROL CENTER
Parathyroid hormone gene
Return to
homeostasis when
response brings
Gene “turned on” which blood Ca2+ level
Output
increases release of PTH back to normal

EFFECTORS

Osteoclasts Kidneys
Kidneys retain Ca2+ in
Osteoclasts blood, excrete
increase bone phosphate in urine, and
resorption produce calcitriol

RESPONSE
Increase in blood
Ca2+ level
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 Bone Mineralization
Exercise (weight-bearing type) promotes
mineralization and collagen production,
leading to stronger, thicker bones which are
less susceptible to fracture
 Aging
• Aging results in demineralization and
decreased collagen synthesis: increased
fragility
• Osteoporosis: lack of sex steroids (estrogen or
testosterone) causes bone resorption to
outpace bone formation, leading to a
decrease in bone mass and increased
susceptibility to fracture
 SEM 30x SEM 30x

(a) Normal bone (b) Osteoporotic bone

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 Failure of Mineralization
Rickets/osteomalacia: failure of mineralization
(due to vitamin D or calcium deficiency)
 Figure Questions
• 6.1-6.11