Transcript Chapter 7 Lecture Outline See PowerPoint Image Slides for all figures and tables pre-inserted into PowerPoint without notes. 7-1 Copyright (c) The McGraw-Hill Companies, Inc.

Chapter 7
Lecture
Outline
See PowerPoint Image Slides
for all figures and tables pre-inserted into
PowerPoint without notes.
7-1
Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Bone as a Tissue
• Connective tissue with a matrix hardened
by minerals (calcium phosphate)
• Individual bones consist of bone tissue,
marrow, blood, cartilage and periosteum
• Continually remodels itself
• Functions of the skeletal system
– support, protection, movement, electrolyte
balances, acid-base balance and blood
formation
7-2
I. Components and Functions of
the Skeletal System
Functions of the skeletal system
A. Support
B. Protection
C. Movement Facilitation
D. Mineral Storage
E. Blood Cell Production
F. Energy Storage
7-3
II. Macroscopic Structure of Bones
• A. Two types of bone
• 1. compact- dense white osseous tissue
• 2. spongy- more loosely organized form of
osseous tissue
• We will discuss differences between compact
and spongy bone
– Where located
– Microscopic anatomy
7-4
B. Parts of a Long Bone
•
•
•
•
•
1.
2.
3.
4.
5.
diaphysis
epiphysis
articular surfaces
periosteum
endosteum
7-5
General Features of Bones
• 1. Shaft (diaphysis) = cylinder of compact bone
– marrow cavity (medullary cavity) lined with
endosteum (osteogenic cells and reticular
connective tissue)
• 2. Enlarged ends (epiphyses)
– spongy bone covered by compact bone
– enlarged to strengthen joint and attach ligaments
• 3. Joint surface covered with articular cartilage
• 4. Shaft covered with periosteum (sheath)
– outer fibrous layer of collagen
– inner osteogenic layer of bone forming cells
• 5. Endosteum– lines the internal surface of the bone
7-6
Structure of a Long Bone
• Compact and
spongy bone
• Marrow cavity
• Articular cartilage
• Periosteum
• Epiphyseal plate
=growth plate
7-7
Structure of a Flat Bone
• External and
internal surfaces
composed of
compact bone
• Middle layer is
spongy bone and
bone marrow
• Skull fracture may
leave inner layer
of compact bone
unharmed
7-8
D. Bone Cells
•
•
•
•
1.
2.
3.
4.
Osteogenic cells
Osteoblasts
Osteocytes
Osteoclasts
7-9
Cells of Osseous Tissue (1)
• Osteogenic cells in endosteum, periosteum or central
canals give rise to new osteoblasts
– arise from embryonic fibroblasts
– multiply continuously
• Osteoblasts mineralize organic matter of matrix
• Osteocytes are osteoblasts trapped in the matrix they
formed
– cells in lacunae connected by gap junctions inside canaliculi7-10
Cells of Osseous Tissue (2)
• Osteoclasts develop in bone marrow by fusion
of 3-50 stem cells
• Reside in pits that they ate into the bone
7-11
A. Bone Matrix
• Matrix is 25% water, 25% proteins (mostly
collagen), 50% calcium salts
– Calcium salts: mostly hydroxyapatite
(Ca10(PO4)6(OH)2
• Combination provides for strength and
resilience
– minerals resist compression; collagen resists
tension
– bone adapts by varying proportions
7-12
Histology of Bone
7-13
B. Compact Bone
• Osteon = basic structural unit= haversian system
central canal =osteonic canal=haversian canal
and its lamellae (cylinders formed from
layers)
osteocytes connected to each other and their
blood supply by tiny cell processes in
canaliculi
• Perforating canals or Volkmann canals
– vascular canals perpendicularly joining
central canals
7-14
B. Compact Bone
• Osteon = basic structural unit= haversian system
• Two types of vascular channels
1. Haversian canals
2. Volkmann canals (perforating canals)
– vascular canals perpendicularly joining
central canals
– Not all of the matrix organized into osteons
– Inner and outer boundaries of dense bone are
organized in circumferential lamellae, run
parallel to bone surface
7-15
Blood Vessels of Bone
7-16
C. Spongy Bone
• Spongelike appearance formed by
plates of bone called trabeculae
– spaces filled with red bone marrow
– no osteocyte is far from blood of bone
marrow
• Provides strength with little weight
– trabeculae develop along bone’s lines of
stress
7-17
Spongy Bone Structure and
Stress
7-18
Bone Marrow
• In medullary cavity (long bone) and
among trabeculae (spongy bone)
• Red marrow like thick blood
– reticular fibers and immature cells
– Hemopoietic (produces blood cells)
– in vertebrae, ribs, sternum, pelvic
girdle and proximal heads of femur
and humerus in adults
• Yellow marrow
– fatty marrow of long bones in adults
• Gelatinous marrow of old age
– yellow marrow replaced with reddish
jelly
7-19
IV. Ossification
• Replacement of other tissues with bones
• A.
Intramembranous Ossification
-process that forms flat bones (skull, mandible)
• B. Endochondral Ossification
-bones are formed from a hyaline cartilage model
-bone tissue forms within the model
-process that forms long and short bones
7-20
A. Intramembranous Ossification
• 1. mesenchyme (embryonic connective tissue)
– forms a richly vascularized layer with cell-to-cell contact
• 2. collagen fibers are laid down randomly
– forms a gel-like material
• 3. mesenchymal cells differentiate into osteoblasts
• 4. new osteoblasts continue to secrete and
mineralize matrix
• 5. trabeculae are formed (ossification centers)
– becomes middle of bone
• 6. vascular mesenchyme condenses to form periand endosteum
7-21
A. Intramembranous Ossification
7. red bone marrow invades spaces between
trabeculae
8. new periosteum develops osteoblasts
-these form trabeculae which grow together to form
compact bone on outer surface
7-22
Intramembranous Ossification 1
• Produces flat bones of skull and clavicle.7-23
Intramembranous Ossification 2
• Note the periosteum and osteoblasts.
7-24
B. Endochondral Ossification
• 1. Mesenchyme condenses in shape of future bone
• Differentiate into chondroblasts
• Develops perichondrium
• 2. Model grows as chondroblasts divide
• Chondroblasts hypertrophy and die
• Matrix becomes calcified
• 3. Perichondrium converts to periosteum
• Forms a thin periosteal collar in mid-diaphysis
• 4. Blood vessels invade model
• Carries osteoblasts, osteoclasts, and red marrow to interior of model
7-25
B. Endochondral Ossification
5. Interior osteoclasts break down calcified
cartilage matrix
• Interior osteoblasts produce bone matrix of
trabeculae, this is primary ossification center
6. Similar events begin to occur in each
epiphysis
• These are secondary ossification centers
7. As primary ossification center enlarges,
early trabeculae are removed to form
medullary cavitiy
• This becomes populated with red marrow
7-26
Stages of Endochondral
Ossification
7-27
Primary Ossification Center and
Primary Marrow Cavity
7-28
Secondary Ossification Centers
and Secondary Marrow Cavities
7-29
Fetal Skeleton at 12 Weeks
7-30
V. Bone Growth and Remodeling
A. Interstitial growth
–
–
–
–
–
Growth in length of bones
1. zone of cell proliferation
2. zone of cell hypertrophy
3. zone of calcification
4. zone of bone deposition
B. Appositional growth
– Growth in diameter
– Occurs by subperiosteal intramembraneous
ossification
7-31
C. Remodeling
Occurs for four reasons
1. bone growth in length and width
2. changes in use of bone
3. bone tissue turnover-internal
remodeling
4. plasma Ca2+ levels
7-32
V. Bone Growth and Remodeling
• Bones increase in length
– interstitial growth of epiphyseal plate
– epiphyseal line is left behind when cartilage gone
• Bones increase in width = appositional growth
– osteoblasts lay down matrix in layers on outer
surface and osteoclasts dissolve bone on inner
surface
• Bones remodeled throughout life
– Wolff’s law of bone = architecture of bone
determined by mechanical stresses
• action of osteoblasts and osteoclasts
– greater density and mass of bone in athletes or
manual worker is an adaptation to stress
7-33
Hormonal Regulation of
Bone Growth and Replacement
• A. Growth Hormone
• B. Sex steroids
•
Bone growth especially rapid in puberty and adolescence when surges of GH,
estrogen, and testosterone promote ossification
•
•
•
•
C.
D.
E.
F.
Thyroid hormones increased GH
Parathyroid hormones
Calcitriol
Calcitonin
7-34
Ion Imbalances
• Changes in phosphate levels = little effect
• Changes in calcium can be serious
– hypocalcemia is deficiency of blood calcium
• causes excitability of nervous system if too low
– muscle spasms, tremors or tetany ~6 mg/dL
– laryngospasm and suffocation ~4 mg/dL
• with less calcium, sodium channels open more easily,
sodium enters cell and excites neuron
– hypercalcemia is excess of blood calcium
• binding to cell surface makes sodium channels less likely to
open, depressing nervous system
– muscle weakness and sluggish reflexes, cardiac arrest ~12
mg/dL
• Calcium phosphate homeostasis depends on
calcitriol, calcitonin and PTH hormone
regulation
7-35
Carpopedal Spasm
• Hypocalcemia demonstrated by muscle spasm
of hands and feet.
7-36
Hormonal Control of Calcium
Balance
• Calcitriol, PTH and calcitonin maintain
normal blood calcium concentration.
7-37
Calcitriol (Activated Vitamin D)
• Produced by the following process
– UV radiation and epidermal keratinocytes convert
steroid derivative to cholecalciferol - D3
– liver converts it to calcidiol
– kidney converts that to calcitriol (vitamin D)
• Calcitriol behaves as a hormone that raises
blood calcium concentration
– increases intestinal absorption and absorption from
the skeleton
– increases stem cell differentiation into osteoclasts
– promotes urinary reabsorption of calcium ions
• Abnormal softness (rickets) in children and
(osteomalacia) in adults without vitamin D
7-38
Calcitriol Synthesis and
Action
7-39
Calcitonin
(tones down blood Ca2+ levels)
• Secreted (C cells of thyroid gland) when
calcium concentration rises too high
• Functions
– reduces osteoclast activity as much as 70%
– increases the number and activity of
osteoblasts
• Important in children, little effect in adults
– osteoclasts more active in children
– deficiency does not cause disease in adults
• Reduces bone loss in osteoporosis
7-40
Correction for Hypercalcemia
7-41
Parathyroid Hormone (PTH)
• Glands on posterior surface of thyroid
• Released with low calcium blood levels
• Function = raise calcium blood level
– causes osteoblasts to release osteoclast-stimulating
factor (RANKL) increasing osteoclast population
– promotes calcium resorption by the kidneys
– promotes calcitriol synthesis in the kidneys
– inhibits collagen synthesis and bone deposition by
osteoblasts
• Sporatic injection of low levels of PTH causes
7-42
bone deposition
Correction for Hypocalcemia
7-43
Other Factors Affecting Bone
• Hormones, vitamins and growth factors
• Growth rapid at puberty
– hormones stimulate osteogenic cells, chondrocytes
and matrix deposition in growth plate
– girls grow faster than boys and reach full height
earlier (estrogen stronger effect)
– males grow for a longer time and taller
• Growth stops (epiphyseal plate “closes”)
– teenage use of anabolic steroids = premature closure
of growth plate and short adult stature
7-44
Osteoporosis 1
• Bones lose mass and become brittle (loss
of organic matrix and minerals)
– risk of fracture of hip, wrist and vertebral
column
– complications (pneumonia and blood
clotting)
• Postmenopausal white women at greatest
risk
– by age 70, average loss is 30% of bone mass
– black women rarely suffer symptoms
7-45
Osteoporosis 2
• Estrogen maintains density in both sexes
(inhibits resorption)
– testes and adrenals produce estrogen in men
– rapid loss after menopause, if body fat too low or
with disuse during immobilizaton
• Treatment
– ERT slows bone resorption, but increases risk
breast cancer, stroke and heart disease
– PTH slows bone loss if given daily injection
• Forteo increases density by 10% in 1 year
• may promote bone cancer
– best treatment is prevention -- exercise and
calcium intake (1000 mg/day) between ages 25
and 40
7-46
Spinal Osteoporosis
7-47
VII. Effect of Exercise on Bone
• Increased exercise causes increased
mechanical stress on bone
• Stimulates remodeling and increased
bone mass
• Stimulates release of calcitonin
• Lack of exercise causes atrophy of
bone
7-48