Chapter 6 Bones and Skeletal Tissues Part C Bone Development and Growth.

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Transcript of Chapter 6 Bones and Skeletal Tissues Part C Bone Development and Growth.

Page 1: Chapter 6 Bones and Skeletal Tissues Part C Bone Development and Growth.
Page 2: Chapter 6 Bones and Skeletal Tissues Part C Bone Development and Growth.
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Chapter 6Bones and Skeletal

Tissues

Part CBone

Development and Growth

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Bone Development• Ossification (Osteogenesis)–the process of bone tissue formation

• Starts with the formation of the bony skeleton in 8 week old embryos as bone replaces cartilage and membranes

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Bone Development

• Bone grows in length until early adulthood (Bone growth)

• Bone is capable of growing in thickness throughout life (by appostional growth)

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Changes in the Human Skeleton

• In embryos, the skeleton is made of fibrous membranes and hyaline cartilage

• During development, much of the fibrous or cartilage structures are replaced by bone

• Cartilage remains in isolated areas–Bridge of the nose–Parts of ribs–Joints

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Formation of the Bony Skeleton

• Intramembranous ossification – bone develops from a fibrous membrane–The bone called a membrane bone

• Endochondral ossification – bone forms by replacing hyaline cartilage–The bone is called a cartilage bone

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Intramembranous Ossification

• Begins at the 8th week of development – All are flat bones

• Formation of most of the flat bones of the skull and the clavicles

• Fibrous connective tissue membranes are the structures on which ossification begins

• Four Stages

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Stages of Intramembranous Ossification

1. An ossification center appears in the fibrous connective tissue membrane

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Stages of Intramembranous Ossification

2. Bone matrix (osteoid) is secreted within the fibrous membrane

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Stages of Intramembranous Ossification

• 3. Woven bone (with trabeculae) and periosteum form

• 4. Bone collar of compact bone forms, and red marrow appears

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Endochondral Ossification

• Begins in the second month of development

• Uses hyaline cartilage “bones” as models for bone construction

• Requires breakdown of hyaline cartilage prior to ossification

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Stages of Endochondral Ossification

• Formation of bone collar

• Cavitation of the hyaline cartilage

• Invasion of internal cavities by the periosteal bud, and spongy bone forms – happens during the 3rd month

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Stages of Endochondral Ossification

• Formation of the medullary cavity; appearance of secondary ossification centers in the epiphyses–Secondary ossification centers appear right before or right after birth

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Stages of Endochondral Ossification

• Ossification of the epiphyses, with hyaline cartilage remaining only in the epiphyseal plates

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Stages of Endochondral Ossification

• Short bones will usually have just the primary ossification center

• Irregular bones have several distinct secondary ossification centers

• When complete, hyaline cartilage will remain in the epiphyseal plates and as articular cartilage

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Formation of bone collar around hyaline cartilage model.

1

2

3

4

Cavitation of the hyaline cartilage within the cartilage model.

Invasion of internal cavities by the periosteal bud and spongy bone formation.

5 Ossification of the epiphyses; when completed, hyaline cartilage remains only in the epiphyseal plates and articular cartilages

Formation of the medullary cavity as ossification continues; appearance of secondary ossification centers in the epiphyses in preparation for stage 5.

Hyaline cartilage

Primary ossification center

Bone collar

Deteriorating cartilage matrix

Spongy bone formation

Blood vessel of periosteal bud

Secondary ossification center

Epiphyseal blood vessel

Medullary cavity

Epiphyseal plate cartilage

Spongy bone

Articular cartilage

Stages of Endochondral Ossification

Figure 6.8

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Bone Growth

During infancy and youth

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Bone GrowthDuring infancy and youth

• During infancy and youth, long bones lengthen entirely by interstitial growth of the epiphyseal plates

• All bones grow in thickness by appositional growth

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Bone Growth of long bonesDuring infancy and youth

–Cells of the epiphyseal plate form three functionally different zones: •Growth zone•Transformation•osteogenic

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Functional Zones in Long Bone Growth

• Growth zone –cartilage cells undergo mitosis, pushing the epiphysis away from the diaphysis

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Functional Zones in Long Bone Growth

• Transformation zone –older cells enlarge, the matrix becomes calcified, cartilage cells die, and the matrix begins to deteriorate

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Functional Zones in Long Bone Growth

• Osteogenic zone –new bone formation occurs

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Bone Growth• Epiphyseal plates allow for

growth of long bone during childhood–New cartilage is continuously formed

–Older cartilage becomes ossified•Cartilage is broken down•Bone replaces cartilage

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Bone Growth• Bones are remodeled and

lengthened until growth stops

• Epiphyseal plate become thinner and thinner until entirely replaced by bone tissue–Called epiphyseal plate closure

–Happens about 18 in females and 21 in males

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Long Bone Formation and Growth

Slide 5.14b

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Figure 5.4b

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Bone Growth

• In Adults–Bones change shape somewhat

–Bones can continue to grow in width by appositional growth•When stressed by excessive muscle activity or body weight

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• During infancy and childhood, epiphyseal plate activity is stimulated by growth hormone

Hormonal Regulation of Bone Growth During Youth

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• During puberty, testosterone and estrogens: –Initially promote adolescent growth spurts

–Cause masculinization and feminization of specific parts of the skeleton

Hormonal Regulation of Bone Growth During Youth

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• During puberty, testosterone and estrogens: –Later induce epiphyseal plate closure, ending longitudinal bone growth

Hormonal Regulation of Bone Growth During Youth

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Hormonal Regulation of Bone Growth During Youth

• Excesses or deficits of any of these hormones can result in abnormal skeletal growth–Hypersecretion of growth hormone in children results in excessive height (gigantism)

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World's Tallest Man 8' 11"

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Hormonal Regulation of Bone Growth During Youth

• Excesses or deficits of any of these hormones can result in abnormal skeletal growth–Deficits of growth hormone or thyroid hormone produce types of dwarfism

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23" tall Pituitary Dwarf

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Chapter 6Bones and Skeletal

Tissues

Part DBone

Remodeling and Repair

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Bones• We may picture bones as lifeless structures – like we see them in movie graveyards or hanging in front of our classroom – But this isn’t at all the truth!

• Bones are very active, dynamic tissues!

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Bone remodeling

• Changes in bone architecture occur continually

• Every week we recycle 5 – 7% of our bone mass

• A half a gram of calcium enters or leaves the adult skeleton each day

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Bone remodeling

• Spongy bone is replaced every 3 to 4 years

• Compact bone is replaced every 10 years

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Types of Bone Cells• Osteocytes

–Mature bone cells• Osteoblasts

–Bone-forming cells• Osteoclasts

–Bone-destroying cells–Break down bone matrix for remodeling and release of calcium

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Bone Remodeling

• Bone remodeling is a process by both osteoblasts and osteoclasts

• Remodeling units – adjacent osteoblasts and osteoclasts deposit and resorb bone at periosteal and endosteal surfaces

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Bone Resorption

• Accomplished by osteoclasts

• Resorption bays – grooves formed by osteoclasts as they break down bone matrix

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Bone Resorption

• Resorption involves osteoclast secretion of:–Lysosomal enzymes that digest organic matrix

–Acids that convert calcium salts into soluble forms

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Bone Resorption

• Dissolved matrix is transcytosed across the osteoclast’s cell where it is secreted into the interstitial fluid and then into the blood

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Bone Deposition

• Occurs where bone is injured or added strength is needed

• Requires a diet rich in protein, vitamins C, D, and A, calcium, phosphorus, magnesium, and manganese

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Bone Deposition• Alkaline phosphatase is essential for

mineralization of bone

• Sites of new matrix deposition are revealed by the:–Osteoid seam – unmineralized band of bone matrix

–Calcification front – abrupt transition zone between the osteoid seam and the older mineralized bone

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Control of Remodeling

• Two control loops regulate bone remodeling–Hormonal mechanism maintains calcium homeostasis in the blood

–Mechanical and gravitational forces acting on the skeleton

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Importance of Ionic Calcium in the Body

• Calcium is necessary for:–Transmission of nerve impulses–Muscle contraction–Blood coagulation–Secretion by glands and nerve cells

–Cell division

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Homeostatic Imbalances of Ionic Calcium in the Body

• When blood Ca2 are too low, severe neuromuscular problems may occur -like hyperexcitability

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Homeostatic Imbalances of Ionic Calcium in the Body

• When blood Ca2 are too high (hypercalcemia), nonresponsiveness and inability to function may occur

• With hypercalcemia deposits of calcium may occur in blood vessels, kidneys, and other soft organs, which can lead them to stop functioning

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Hormonal Mechanism• Rising blood Ca2+ levels trigger the

thyroid to release calcitonin• Calcitonin stimulates calcium salt

deposit in bone• Falling blood Ca2+ levels signal the

parathyroid glands to release PTH• PTH signals osteoclasts to degrade

bone matrix and release Ca2+ into the blood

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Response to Mechanical Stress

• Wolff’s law –– a bone grows or remodels in response to the forces or demands placed upon it

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Response to Mechanical Stress

• Observations supporting Wolff’s law include–Long bones are thickest midway along the shaft (where bending stress is greatest)

–Curved bones are thickest where they are most likely to buckle

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Response to Mechanical Stress

• Trabeculae form along lines of stress

• Large, bony projections occur where heavy, active muscles attach

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Response to Mechanical Stress

Figure 6.13

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Bone Repair

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Bone Fractures (Breaks)

• Bone fractures are classified by:–The position of the bone ends after fracture

–The completeness of the break–The orientation of the break to the long axis of the bone

–Whether or not the bones ends penetrate the skin

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Common Types of Fractures

• Epiphyseal – epiphysis separates from diaphysis along epiphyseal line; occurs where cartilage cells are dying

• Greenstick – incomplete fracture where one side of the bone breaks and the other side bends; common in children

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Common Types of Fractures

Table 6.2.1

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Common Types of Fractures

Table 6.2.2

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Common Types of Fractures

Table 6.2.3

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Stages in the Healing of a Bone Fracture

• Hematoma formation–Torn blood vessels hemorrhage

–A mass of clotted blood (hematoma) forms at the fracture site

–Site becomes swollen, painful, and inflamed

Figure 6.14.1

1

Hematoma

Hematoma formation

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Stages in the Healing of a Bone Fracture• Fibrocartilaginou

s callus forms• Granulation

tissue (soft callus) forms a few days after the fracture

• Capillaries grow into the tissue and phagocytic cells begin cleaning debris Figure 6.14.2

2Fibrocartilaginous callus formation

External callus

New blood vessels

Spongy bone trabeculae

Internal callus (fibrous tissue and cartilage)

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Stages in the Healing of a Bone Fracture

• The fibrocartilaginous callus forms when:–Osteoblasts and fibroblasts migrate to the fracture and begin reconstructing the bone

–Fibroblasts secrete collagen fibers that connect broken bone ends

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Stages in the Healing of a Bone Fracture

• The fibrocartilaginous callus forms when:–Osteoblasts begin forming spongy bone

–Osteoblasts furthest from capillaries secrete an externally bulging cartilaginous matrix that later calcifies

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Stages in the Healing of a Bone Fracture

• Bony callus formation–New bone trabeculae appear in the fibrocartilaginous callus

–Fibrocartilaginous callus converts into a bony (hard) callus

Figure 6.14.3

3 Bony callus formation

Bony callus of spongy bone

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Stages in the Healing of a Bone Fracture

• Bony callus formation–Bone callus begins 3-4 weeks after injury, and continues until firm union is formed 2-3 months later

Figure 6.14.3

3 Bony callus formation

Bony callus of spongy bone

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Stages in the Healing of a Bone Fracture

• Bone remodeling–Excess material on the bone shaft exterior and in the medullary canal is removed

–Compact bone is laid down to reconstruct shaft walls

Figure 6.14.4

4 Bone remodeling

Healing fracture

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Clinical Advances in Bone Repair

• Electrical stimulation of fraction sites–Increases speed of healing

• Ultrasound treatments–Daily exposure to ultrasound reduces healing time of broken arms and legs by 35 to 45% by stimulating the production of the callus

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Clinical Advances in Bone Repair

• Bone grafts using the fibula–Grafts from hip bones often fail–Blood vessels are grafted with the fibula, having a better success rate

–Bone graphs more successful in adults than children

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Clinical Advances in Bone Repair

• VEGF (vascular endothelial growth factor)–Protein that stimulates growth of blood vessels- speeds

• Bone substitutes molded to the shape of desired bone or inserted into existing bone – replacing bone grafts

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Clinical Advances in Bone Repair

• Bone substitutes–May be crushed bone from cadavers •Small risk of hepatitis or HIV, or may be rejected

–synthetic bone material•Can be rejected

–Heat treated coral (to kill living coral cells) mixed with mineral salts of bone (calcium phosphate ) - new

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Homeostatic Imbalances of

Bone

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Homeostatic Imbalances

• Osteomalacia

–Bones are inadequately mineralized causing softened, weakened bones

–Main symptom is pain when weight is put on the affected bone

–Caused by insufficient calcium in the diet, or by vitamin D deficiency

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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

This is an xray of a child with bowed legs due to rickets (thanks to Dr. Mike Richardson)

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Homeostatic Imbalances

• Rickets–Caused by insufficient calcium in the diet, or by vitamin D deficiency

This is an xray of a child with bowed legs due to rickets (thanks to Dr. Mike Richardson)

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Homeostatic Imbalances• Osteoporosis

–Group of diseases in which bone reabsorption outpaces bone deposit

–Spongy bone of the spine is most vulnerable

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Homeostatic Imbalances• Osteoporosis

–Occurs most often in postmenopausal women

–Bones become so fragile that sneezing or stepping off a curb can cause fractures

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Osteoporosis: Treatment

• Calcium and vitamin D supplements

• Increased weight-bearing exercise

• Hormone (estrogen) replacement therapy (HRT) slows bone loss

• Natural progesterone cream prompts new bone growth

• Statins increase bone mineral density

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Developmental Aspects of Bones

Bones are on a precise schedule from the time

they form until a person’s death

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Developmental Aspects of Bones

• Mesoderm gives rise to embryonic mesenchymal cells, which produce membranes and cartilages that form the embryonic skeleton

• The embryonic skeleton ossifies in a predictable timetable that allows fetal age to be easily determined from sonograms

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Developmental Aspects of Bones

• At birth, most long bones are well ossified (except for their epiphyses)

• Epiphyseal plates persist and provide long-bone growth during childhood

• Epiphyseal plates provide the sex-hormone-mediated growth spurt at adolescence

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Developmental Aspects of Bones

• By age 25, nearly all bones are completely ossified and skeletal growth ceases

• In children and adolescents, bone formation exceeds bone resorption

• In young adults formation and resorption are balanced

• In old age, bone resorption predominates

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Developmental Aspects of Bones

• A single gene that codes for vitamin D docking determines both the tendency to accumulate bone mass early in life, and the risk for osteoporosis later in life

• In your 40’s bone mass will start decreasing with age, except bones in the skull

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Developmental Aspects of Bones

• In young adults skeletal mass is greater in males than females

• With age, the rate of bone loss is faster in females than in males

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