Skeletal Organization
• Typically there are about 206 bones in the human
skeleton
• For convenience the skeleton is divided into the:
• Axial skeleton
• Appendicular skeleton
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Divisions of the Skeleton
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• Axial Skeleton
• Skull
• Spinal column
• Ribs
• Sternum
• Hyoid bone
Cranium
Skull
Face
Hyoid
Clavicle
Scapula
Sternum
Humerus
Ribs
Vertebral
column
Vertebral
column
Hip
bone
Carpals
Sacrum
Radius
Coccyx
Ulna
Femur
Metacarpals
• 80 bones
Phalanges
Patella
Tibia
Fibula
Tarsals
Metatarsals
Phalanges
(a)
(b)
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Divisions of the Skeleton
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Cranium
Skull
Face
Hyoid
Clavicle
Scapula
Sternum
Humerus
Ribs
Vertebral
column
• Appendicular Skeleton
• Upper limbs
• Lower limbs
• Shoulder girdle
• Pelvic girdle
Vertebral
column
Hip
bone
Carpals
Sacrum
Radius
Coccyx
Ulna
Femur
Metacarpals
Phalanges
Patella
Tibia
Fibula
• 126 bones
Tarsals
Metatarsals
Phalanges
(a)
(b)
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7.3: Bone Development
and Growth
• Before week 8, the human
embryonic skeleton is made of
fibrous membranes and hyaline
cartilage.
• After week 8, bone tissue begins
to replace the fibrous membranes
and hyaline cartilage.
– The development of bone from a
fibrous membrane is called
intramembranous ossification.
Why?
– The replacement of hyaline
cartilage with bone is known as
endochondral ossification. Why?
Intramembranous Bones
• Intramembranous Ossification
• These bones originate within sheet-like layers of
connective tissues (mesenchyme)
• They are the broad, flat bones
• Ex: Skull bones (except mandible), the facial bones,
the clavicles, the pelvis and the scapulae
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Endochondral Bones
• Endochondral Ossification
•Begins in the second month of development
•Requires breakdown of hyaline cartilage prior to
ossification
•Bones begin as hyaline cartilage
• Form models for future bones
•These are most bones of the skeleton
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Endochondral Ossification
• Hyaline cartilage model
• Primary ossification center
• Secondary ossification centers
• Epiphyseal plate
• Osteoblasts vs. osteoclasts
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Cartilaginous
model
Developing
periosteum
Remnants of
epiphyseal
plates
Secondary
ossification
center
Compact bone
developing
Spongy
bone
Epiphyseal
plates
Blood
vessel
Calcified
cartilage
(a)
(b)
Medullary
cavity
(c)
Medullary
cavity
Compact
bone
Medullary
cavity
Remnant of
epiphyseal
plate
Epiphyseal
plate
Primary
ossification
center
Secondary
ossification
center
(d)
Articular
cartilage
Spongy
bone
Articular
cartilage
(e)
(f)
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Endochondral Ossification
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Osteogenesis - 10 week fetus
Osteogenesis - 16 week fetus
Video
http://www.youtube.com/watch?v=78RBpWSOl08
Video
http://www.youtube.com/watch?v=0dV1Bwe2v6c
Lab
Skull Lab Exercise 13
Catalyst
Catalyst
Catalyst
Catalyst
Criteria for SUCCESS!!!
I will be able to:
1. Identify and describe the functions of the four layers of cells involved in
growth at the epiphyseal plate.
2. List the steps in the process of bone reabsorption.
3. List the steps in the process of bone deposition.
4. List the steps in the process of appositional growth.
5. Identify 3 nutritional needs to maintain bone growth/maintenance.
6. List the effects of 4 hormones on bone growth.
7. Describe the causes and effects of two types of homeostatic imbalance
disorders in bone.
Growth at the Epiphyseal Plate
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• First layer of cells
Bone tissue
of epiphysis
• Closest to the end of
epiphysis
• Resting cells
• Anchors epiphyseal plate
to epiphysis
1 Zone of
resting
cartilage
2 Zone of
proliferating
cartilage
3 Zone of
hypertrophic
cartilage
• Second layer of cells
4 Zone of
calcified
cartilage
• Many rows of young
cells
• Undergoing mitosis
Ossified
bone of
diaphysis
(a)
(b)
b: © The McGraw-Hill Companies, Inc./Al Telser, photographer
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Growth at the Epiphyseal Plate
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
• Third layer of cells
Bone tissue
of epiphysis
• Older cells
• Left behind when new
cells appear
• Cells enlarging and
becoming calcified
1 Zone of
resting
cartilage
2 Zone of
proliferating
cartilage
3 Zone of
hypertrophic
cartilage
• Fourth layer of cells
4 Zone of
calcified
cartilage
• Thin
• Dead cells
• Calcified
extracellular matrix
Ossified
bone of
diaphysis
(a)
(b)
b: © The McGraw-Hill Companies, Inc./Al Telser, photographer
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Homeostasis of Bone Tissue
• Bone Resorption – action of osteoclasts via stimulation from
parathyroid hormone (PTH)
• Bone Deposition – action of osteoblasts and via stimulation
from calcitonin
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Developing
medullary
cavity
Osteoclast
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© Biophoto Associates/Photo Researchers, Inc.
Animation: Bone Growth in Width
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Check out the mechanism of
remodeling on the right!
Why might you suspect someone
whose been a powerlifter for 15
years to have heavy, massive
bones, especially at the point of
muscle insertion?
Astronauts tend to experience
bone atrophy after they’re in
space for an extended period of
time. Why?
Long Bone Growth and Remodeling
Figure 6.10
Nutritional Effects on Bone
• Normal bone growth/maintenance
cannot occur without sufficient
dietary intake of calcium and
phosphate salts.
• Calcium and phosphate are not
absorbed in the intestine unless the
hormone calcitriol is present.
Calcitriol synthesis is dependent on
the availability of the steroid
cholecalciferol (a.k.a. Vitamin D)
which may be synthesized in the skin
or obtained from the diet.
• Vitamins C, A, K, and B12 are all
necessary for bone growth as well.
Hormonal Effects on Bone
• Growth hormone, produced by the
pituitary gland, and thyroxine,
produced by the thyroid gland,
stimulate bone growth.
.
Hormonal Effects on Bone
• At puberty, the rising levels of sex hormones (estrogens in
females and androgens in males) cause osteoblasts to
produce bone faster than the epiphyseal cartilage can
divide. This causes the characteristic growth spurt as well
as the ultimate closure of the epiphyseal plate.
• Estrogens cause faster closure of the epiphyseal growth
plate than do androgens.
• Estrogen also acts to stimulate osteoblast activity.
At puberty, growth in bone length is
increased dramatically by the combined
activities of growth hormone, thyroid
hormone, and the sex hormones.
•As a result osteoblasts begin producing
bone faster than the rate of epiphyseal
cartilage expansion. Thus the bone grows
while the epiphyseal plate gets narrower and
narrower and ultimately disappears. A
remnant (epiphyseal line) is visible on X-rays
(do you see them in the adjacent femur, tibia,
and fibula?)
Calcitonin
• Released by the C cells of the thyroid gland in response to high
blood [Ca2+].
• Calcitonin acts to “tone down” blood calcium levels.
• Calcitonin causes decreased osteoclast activity which results in
decreased break down of bone matrix and decreased calcium
being released into the blood.
• Calcitonin also stimulates osteoblast activity which means
calcium will be taken from the blood and deposited as bone
matrix.
Notice the thyroid
follicles on the
right. The arrow
indicates a C cell
Factors Affecting Bone
Development, Growth and Repair
• Deficiency of Vitamin A – retards bone development
• Deficiency of Vitamin C – results in fragile bones
• Deficiency of Vitamin D – rickets, osteomalacia
• Insufficient Growth Hormone – dwarfism
• Excessive Growth Hormone – gigantism, acromegaly
• Insufficient Thyroid Hormone – delays bone growth
•Physical Stress – stimulates bone growth
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Animation: Bone Growth in Width
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Homeostatic
Imbalances
Homeostatic Imbalances
• Rickets
– Bones of children are inadequately mineralized
causing softened, weakened bones
– Bowed legs and deformities of the pelvis, skull,
and rib cage are common
– Caused by insufficient calcium in the diet, or by
vitamin D deficiency
Homeostatic
Imbalances
Homeostatic Imbalances
• Osteoporosis
– Group of diseases in which bone reabsorption
outpaces bone deposit
– Spongy bone of the spine is most vulnerable
– Occurs most often in postmenopausal women
– Bones become so fragile that sneezing or stepping
off a curb can cause fractures
Animation: Osteoporosis
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