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Chapter 6 Part B

Bones and Skeletal Tissue

6.5 Bone Development

Ossification (osteogenesis) is the process of bone tissue formation

Formation of bony skeleton begins in month 2 of development

Postnatal bone growth occurs until early adulthood

Bone remodeling and repair are lifelong

Formation of the Bony Skeleton

Up to about week 8, fibrous membranes and hyaline cartilage of fetal skeleton are replaced with bone tissue

Endochondral ossification

Bone forms by replacing hyaline cartilage

Bones are called cartilage (endochondral) bones

Form most of skeleton

Intramembranous ossification

Bone develops from fibrous membrane

Bones are called membrane bones

Formation of the Bony Skeleton (cont.)

Endochondral ossification

Forms essentially all bones inferior to base of skull, except clavicles

Begins late in month 2 of development

Uses previously formed hyaline cartilage models

Requires breakdown of hyaline cartilage prior to ossification

Begins at primary ossification center in center of shaft

Blood vessels infiltrate perichondrium, converting it to periosteum

Mesenchymal cells specialize into osteoblasts

Formation of the Bony Skeleton (cont.)

Five main steps in the process of ossification:

Bone collar forms around diaphysis of cartilage model

Central cartilage in diaphysis calcifies, then develops cavities

Periosteal bud invades cavities, leading to formation of spongy bone

Bud is made up of blood vessels, nerves, red marrow, osteogenic cells, and osteoclasts

Formation of the Bony Skeleton (cont.)

Five main steps in the process of ossification (cont.):

Diaphysis elongates, and medullary cavity forms

Secondary ossification centers appear in epiphyses

Epiphyses ossify

Hyaline cartilage remains only in epiphyseal plates and articular cartilages

Figure 6.8 Endochondral ossification in a long bone.

Week 9

Hyaline

cartilage

Primary

ossification

center

Bone

collar

Bone collar forms around the diaphysis of the hyaline cartilage model.

Slide 2

Figure 6.8 Endochondral ossification in a long bone.

Week 9

Area of

deteriorating

cartilage matrix

Hyaline

cartilage

Primary

ossification

center

Bone

collar

Bone collar forms around the diaphysis of the hyaline cartilage model.

Cartilage in the center of the diaphysis calcifies and then develops cavities.

Slide 3

Figure 6.8 Endochondral ossification in a long bone.

Month 3

Week 9

Area of

deteriorating

cartilage matrix

Hyaline

cartilage

Spongy

bone

formation

Blood

vessel of

periosteal

bud

Primary

ossification

center

Bone

collar

Bone collar forms around the diaphysis of the hyaline cartilage model.

Cartilage in the center of the diaphysis calcifies and then develops cavities.

The periosteal bud invades the internal cavities and spongy bone forms.

Slide 4

Figure 6.8 Endochondral ossification in a long bone.

Month 3

Week 9

Birth

Secondary

ossification

center

Epiphyseal

blood vessel

Area of

deteriorating

cartilage matrix

Hyaline

cartilage

Medullary

cavity

Spongy

bone

formation

Blood

vessel of

periosteal

bud

Primary

ossification

center

Bone

collar

Bone collar forms around the diaphysis of the hyaline cartilage model.

Cartilage in the center of the diaphysis calcifies and then develops cavities.

The periosteal bud invades the internal cavities and spongy bone forms.

The diaphysis elongates and a medullary cavity forms. Secondary ossification centers appear in the epiphyses.

Slide 5

Figure 6.8 Endochondral ossification in a long bone.

Month 3

Week 9

Birth

Childhood to adolescence

Articular

cartilage

Secondary

ossification

center

Spongy

bone

Epiphyseal

blood vessel

Area of

deteriorating

cartilage matrix

Epiphyseal

plate

cartilage

Hyaline

cartilage

Medullary

cavity

Spongy

bone

formation

Blood

vessel of

periosteal

bud

Primary

ossification

center

Bone

collar

Bone collar forms around the diaphysis of the hyaline cartilage model.

Cartilage in the center of the diaphysis calcifies and then develops cavities.

The periosteal bud invades the internal cavities and spongy bone forms.

The epiphyses ossify. When completed, hyaline cartilage remains only in the epiphyseal plates and articular cartilages.

The diaphysis elongates and a medullary cavity forms. Secondary ossification centers appear in the epiphyses.

Slide 6

Formation of the Bony Skeleton (cont.)

Intramembranous ossification: begins within fibrous connective tissue membranes formed by mesenchymal cells

Forms frontal, parietal, occipital, temporal, and clavicle bones

Formation of the Bony Skeleton (cont.)

Four major steps are involved:

Ossification centers are formed when mesenchymal cells cluster and become osteoblasts

Osteoid is secreted, then calcified

Woven bone is formed when osteoid is laid down around blood vessels, resulting in trabeculae

Outer layer of woven bone forms periosteum

Lamellar bone replaces woven bone, and red marrow appears

Mesenchymal

cell

Osteoid

Osteoblast

Ossification centers appear in the fibrous connective tissue membrane.

• Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center that produces the first trabeculae of spongy bone.

Ossification

center

Collagen

fiber

Figure 6.9 Intramembranous ossification.

Slide 2

Mesenchymal

cell

Osteoblast

Osteoid

Osteocyte

Newly calcified

bone matrix

Osteoid

Osteoblast

Ossification centers appear in the fibrous connective tissue membrane.

Osteoid is secreted within the fibrous membrane and calcifies.

• Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center that produces the first trabeculae of spongy bone.

• Osteoblasts continue to secrete osteoid, which calcifies in a few days.

• Trapped osteoblasts become osteocytes.

Ossification

center

Collagen

fiber

Figure 6.9 Intramembranous ossification.

Slide 3

Mesenchymal

cell

Osteoblast

Osteoid

Osteocyte

Newly calcified

bone matrix

Osteoid

Osteoblast

Ossification centers appear in the fibrous connective tissue membrane.

Osteoid is secreted within the fibrous membrane and calcifies.

• Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center that produces the first trabeculae of spongy bone.

• Osteoblasts continue to secrete osteoid, which calcifies in a few days.

• Trapped osteoblasts become osteocytes.

Mesenchyme

condensing

to form the

periosteum

Trabeculae of

woven bone

Blood vessel

Woven bone and periosteum form.

• Accumulating osteoid is laid down between embryonic blood vessels in a manner that results in a network (instead of concentric lamellae) of trabeculae called woven bone.

• Vascularized mesenchyme condenses on the external face of the woven bone and becomes the periosteum.

Ossification

center

Collagen

fiber

Figure 6.9 Intramembranous ossification.

Slide 4

Mesenchymal

cell

Osteoblast

Osteoid

Osteocyte

Newly calcified

bone matrix

Osteoid

Osteoblast

Ossification centers appear in the fibrous connective tissue membrane.

Osteoid is secreted within the fibrous membrane and calcifies.

• Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center that produces the first trabeculae of spongy bone.

• Osteoblasts continue to secrete osteoid, which calcifies in a few days.

• Trapped osteoblasts become osteocytes.

Mesenchyme

condensing

to form the

periosteum

Fibrous

periosteum

Plate of

compact bone

Trabeculae of

woven bone

Diploë (spongy

bone) cavities

contain red

marrow

Blood vessel

Woven bone and periosteum form.

• Accumulating osteoid is laid down between embryonic blood vessels in a manner that results in a network (instead of concentric lamellae) of trabeculae called woven bone.

• Vascularized mesenchyme condenses on the external face of the woven bone and becomes the periosteum.

• Trabeculae just deep to the periosteum thicken. Mature

lamellar bone replaces them, forming compact bone plates.

• Spongy bone (diploë), consisting of distinct trabeculae, persists internally and its vascular tissue becomes red marrow.

Ossification

center

Collagen

fiber

Osteoblast

Lamellar bone replaces woven bone, just deep to the periosteum. Red marrow appears.

Figure 6.9 Intramembranous ossification.

Slide 5

Postnatal Bone Growth

Long bones grow lengthwise by interstitial (longitudinal) growth of epiphyseal plate

Bones increase thickness through appositional growth

Bones stop growing during adolescence

Some facial bones continue to grow slowly through life

Growth in Length of Long Bones

Interstitial growth requires presence of epiphyseal cartilage in the epiphyseal plate

Epiphyseal plate maintains constant thickness

Rate of cartilage growth on one side balanced by bone replacement on other

Epiphyseal plate consists of five zones:

Resting (quiescent) zone

Proliferation (growth) zone

Hypertrophic zone

Calcification zone

Ossification (osteogenic) zone

Growth in Length of Long Bones (cont.)

Resting (quiescent) zone

Area of cartilage on epiphyseal side of epiphyseal plate that is relatively inactive

Proliferation (growth) zone

Area of cartilage on diaphysis side of epiphyseal plate that is rapidly dividing

New cells formed move upward, pushing epiphysis away from diaphysis, causing lengthening

Growth in Length of Long Bones (cont.)

Hypertrophic zone

Area with older chondrocytes closer to diaphysis

Cartilage lacunae enlarge and erode, forming interconnecting spaces

Calcification zone

Surrounding cartilage matrix calcifies; chondrocytes die and deteriorate

Growth in Length of Long Bones (cont.)

Ossification zone

Chondrocyte deterioration leaves long spicules of calcified cartilage at epiphysis-diaphysis junction

Spicules are then eroded by osteoclasts and are covered with new bone by osteoblasts

Ultimately replaced with spongy bone

Medullary cavity enlarges as spicules are eroded

Resting zone

Proliferation zone

Cartilage cells undergo

mitosis.

Hypertrophic zone

Older cartilage cells

enlarge.

Calcification zone

Matrix calcifies; cartilage

cells die; matrix begins

deteriorating; blood

vessels invade cavity.

Calcified

cartilage spicule

Ossification zone

New bone forms.

Osseous tissue

(bone) covering

cartilage spicules

Osteoblast

depositing

bone matrix

Figure 6.10 Growth in length of a long bone occurs at the epiphyseal plate.

Growth in Length of Long Bones (cont.)

Near end of adolescence, chondroblasts divide less often

Epiphyseal plate thins, then is replaced by bone

Epiphyseal plate closure occurs when epiphysis and diaphysis fuse

Bone lengthening ceases

Females: occurs around 18 years of age

Males: occurs around 21 years of age

Growth in Width (Thickness)

Growing bones widen as they lengthen through appositional growth

Can occur throughout life

Bones thicken in response to increased stress from muscle activity or added weight

Osteoblasts beneath periosteum secrete bone matrix on external bone

Osteoclasts remove bone on endosteal surface

Usually more building up than breaking down which leads to thicker, stronger bone that is not too heavy

Figure 6.11 Long bone growth and remodeling during youth.

Bone growth

Bone remodeling

Articular cartilage

Cartilage

grows here.

Epiphyseal plate

Bone that was

here has been

resorbed.

Bone replaces

cartilage here.

Bone that was

here has been

resorbed.

Appositional

growth adds

bone here.

Cartilage

grows here.

Bone

replaces

cartilage

here.

Hormonal Regulation of Bone Growth

Growth hormone: most important hormone in stimulating epiphyseal plate activity in infancy and childhood

Thyroid hormone: modulates activity of growth hormone, ensuring proper proportions

Testosterone (males) and estrogens (females) at puberty: promote adolescent growth spurts

End growth by inducing epiphyseal plate closure

Excesses or deficits of any hormones cause abnormal skeletal growth

6.6 Bone Remodeling

About 5–7% of bone mass is recycled each week

Spongy bone replaced ~ every 3-4 years

Compact bone replaced ~ every 10 years

Bone remodeling consists of both bone deposit and bone resorption

Occurs at surfaces of both periosteum and endosteum

Remodeling units: packets of adjacent osteoblasts and osteoclasts coordinate remodeling process

Bone Deposit

New bone matrix is deposited by osteoblasts

Osteoid seam: band of unmineralized bone matrix that marks area of new matrix

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

Bone Deposit (cont.)

Trigger for deposit not confirmed but may include:

Mechanical signals

Increased concentrations of calcium and phosphate ions for hydroxyapatite formation

Matrix proteins that bind and concentrate calcium

Appropriate amount of enzyme alkaline phosphatase for mineralization

Bone Resorption

Resorption is function of osteoclasts

Dig depressions or grooves as they break down matrix

Secrete lysosomal enzymes and protons (H+) that digest matrix

Acidity converts calcium salts to soluble forms

Bone Resorption (cont.)

Osteoclasts also phagocytize demineralized matrix and dead osteocytes

Digested products are transcytosed across cell and released into interstitial fluid and then into blood

Once resorption is complete, osteoclasts undergo apoptosis

Osteoclast activation involves PTH (parathyroid hormone) and immune T cell proteins

Control of Remodeling

Remodeling occurs continuously but is regulated by genetic factors and two control loops

Hormonal controls

Negative feedback loop that controls blood Ca2+ levels

Calcium functions in many processes, such as nerve transmission, muscle contraction, blood coagulation, gland and nerve secretions, as well as cell division

99% of 1200–1400 gms of calcium are found in bone

Intestinal absorption of Ca2+ requires vitamin D

Response to mechanical stress

Control of Remodeling

Hormonal controls

Parathyroid hormone (PTH): produced by parathyroid glands in response to low blood calcium levels

Stimulates osteoclasts to resorb bone

Calcium is released into blood, raising levels

PTH secretion stops when homeostatic calcium levels are reached

Calcitonin: produced by parafollicular cells of thyroid gland in response to high levels of blood calcium levels

Effects are negligible, but at high pharmacological doses it can lower blood calcium levels temporarily

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

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

BALANCE

Stimulus

Falling blood

Ca2 levels

Thyroid

gland

Osteoclasts

degrade bone matrix and release

Ca2 into blood.

Parathyroid

glands

Parathyroid

glands release parathyroid hormone (PTH).

PTH

IMBALANCE

Clinical – Homeostatic Imbalance 6.1

Even minute changes in blood calcium levels can cause severe neuromuscular problems

Hypocalcemia: low levels of calcium cause hyperexcitablility

Hypercalcemia: high levels of calcium cause nonresponsiveness

Sustained high blood calcium levels can lead to deposits of calcium salts in blood vessels or kidneys and formation of kidney stones

Control of Remodeling (cont.)

Hormonal controls (cont.)

Other hormones play a role in bone density and turnover

Leptin

Hormone released by adipose tissue

May play role in bone density regulation by inhibiting osteoblasts

Serotonin

Neurotransmitter regulates mood and sleep; also interferes with osteoblast activity

Most serotonin made in gut

Secreted into blood after a meal

May inhibit bone turnover after a meal, so bone calcium is locked in when new calcium is flooding into bloodstream

Control of Remodeling (cont.)

Response to mechanical stress

Bones reflect stresses they encounter

Bones are stressed when weight bears on them or muscles pull on them

Wolf’s law states that bones grow or remodel in response to demands placed on them

Stress is usually off center, so bones tend to bend

Bending compresses one side, stretches other side

Diaphysis is thickest where bending stresses are greatest

Bone can be hollow because compression and tension cancel each other out in center of bone

Load here

(body weight)

Head of

femur

Compression

here

Tension

here

Point

of no

stress

Figure 6.13 Bone anatomy and bending stress.

Control of Remodeling (cont.)

Wolf’s law also explains:

Handedness (right- or left-handed) results in thicker and stronger bone of the corresponding upper limb

Curved bones are thickest where most likely to buckle

Trabeculae form trusses along lines of stress

Large, bony projections occur where heavy, active muscles attach

Weight lifters have enormous thickenings at muscle attachment sites of most used muscles

Bones of fetus and bedridden people are featureless because of lack of stress on bones

Control of Remodeling (cont.)

Mechanical stress causes remodeling by producing electrical signals when bone is deformed

Compressed and stretched regions are oppositely charged

Compression/tension changes fluid flows within canaliculi, which may also stimulate remodeling

Hormonal controls determine whether and when remodeling occurs in response to changing blood calcium levels, but mechanical stress determines where it occurs

6.7 Bone Repair

Fractures are breaks

During youth, most fractures result from trauma

In old age, most result from weakness of bone due to bone thinning

Fracture Classification

Three “either/or” fracture classifications

Position of bone ends after fracture

Nondisplaced: ends retain normal position

Displaced: ends are out of normal alignment

Completeness of break

Complete: broken all the way through

Incomplete: not broken all the way through

Whether skin is penetrated

Open (compound): skin is penetrated

Closed (simple): skin is not penetrated

Can also be described by location of fracture, external appearance, and nature of break

Table 6.2-1 Common Types of Fractures

Table 6.2-2 Common Types of Fractures (continued)

Table 6.2-3 Common Types of Fractures (continued)

Fracture Treatment and Repair

Treatment involves reduction, the realignment of broken bone ends

Closed reduction: physician manipulates to correct position

Open reduction: surgical pins or wires secure ends

Immobilization of bone by cast or traction is needed for healing

Time needed for repair depends on break severity, bone broken, and age of patient

Fracture Treatment and Repair (cont.)

Repair involves four major stages:

Hematoma formation

Fibrocartilaginous callus formation

Bony callus formation

Bone remodeling

Fracture Treatment and Repair (cont.)

Hematoma formation

Torn blood vessels hemorrhage, forming mass of clotted blood called a hematoma

Site is swollen, painful, and inflamed

Figure 6.14-1 Stages in the healing of a bone fracture.

Hematoma

A hematoma forms.

Fracture Treatment and Repair (cont.)

Fibrocartilaginous callus formation

Capillaries grow into hematoma

Phagocytic cells clear debris

Fibroblasts secrete collagen fibers to span break and connect broken ends

Fibroblasts, cartilage, and osteogenic cells begin reconstruction of bone

Create cartilage matrix of repair tissue

Osteoblasts form spongy bone within matrix

This mass of repair tissue is called fibrocartilaginous callus

Figure 6.14-2 Stages in the healing of a bone fracture.

External

callus

Internal

callus

(fibrous

tissue and

cartilage)

New

blood

vessels

Spongy

bone

trabecula

Fibrocartilaginous callus forms.

Fracture Treatment and Repair (cont.)

Bony callus formation

Within one week, new trabeculae appear in fibrocartilaginous callus

Callus is converted to bony (hard) callus of spongy bone

Bony callus formation continues for about 2 months until firm union forms

Figure 6.14-3 Stages in the healing of a bone fracture.

Bony

callus of

spongy

bone

Bony callus forms.

Fracture Treatment and Repair (cont.)

Bone remodeling

Begins during bony callus formation and continues for several months

Excess material on diaphysis exterior and within medullary cavity is removed

Compact bone is laid down to reconstruct shaft walls

Final structure resembles original structure

Responds to same mechanical stressors

Figure 6.14-4 Stages in the healing of a bone fracture.

Healed

fracture

Bone remodeling occurs.

Figure 6.14 Stages in the healing of a bone fracture.

Hematoma

External

callus

Bony

callus of

spongy

bone

Internal

callus

(fibrous

tissue and

cartilage)

Healed

fracture

New

blood

vessels

Spongy

bone

trabecula

A hematoma forms.

Fibrocartilaginous callus forms.

Bony callus forms.

Bone remodeling occurs.

6.8 Bone Disorders

Imbalances between bone deposit and bone resorption underlie nearly every disease that affects the human skeleton.

Three major bone diseases:

Osteomalacia and rickets

Osteoporosis

Paget’s disease

Osteomalacia and Rickets

Osteomalacia

Bones are poorly mineralized

Osteoid is produced, but calcium salts not adequately deposited

Results in soft, weak bones

Pain upon bearing weight

Rickets (osteomalacia of children)

Results in bowed legs and other bone deformities because bones ends are enlarged and abnormally long

Cause: vitamin D deficiency or insufficient dietary calcium

Osteoporosis

Osteoporosis is a group of diseases in which bone resorption exceeds deposit

Matrix remains normal, but bone mass declines

Spongy bone of spine and neck of femur most susceptible

Vertebral and hip fractures common

Figure 6.15 The contrasting architecture of normal versus osteoporotic bone.

Normal bone

Osteoporotic bone

Osteoporosis (cont.)

Risk factors for osteoporosis

Most often aged, postmenopausal women

Affects 30% of women aged 60–70 years and 70% by age 80

30% of Caucasian women will fracture bone because of osteoporosis

Estrogen plays a role in bone density, so when levels drop at menopause, women run higher risk

Men are less prone due to protection by the effects of testosterone

Osteoporosis (cont.)

Additional risk factors for osteoporosis:

Petite body form

Insufficient exercise to stress bones

Diet poor in calcium and protein

Smoking

Hormone-related conditions

Hyperthyroidism

Low blood levels of thyroid-stimulating hormone

Diabetes mellitus

Immobility

Males with prostate cancer taking androgen-suppressing drugs

Osteoporosis (cont.)

Treating osteoporosis

Traditional treatments

Calcium

Vitamin D supplements

Weight-bearing exercise

Hormone replacement therapy

Slows bone loss but does not reverse it

Controversial because of increased risk of heart attack, stroke, and breast cancer

Osteoporosis (cont.)

Other drugs for osteoporosis:

Bisphosphonates: decrease osteoclast activity and number

Partially reverse osteoporosis in spine

Selective estrogen receptor modulators: mimic estrogen without targeting breast and uterus

Denosumab

Monoclonal antibody shown to reduce fractures in men with prostate cancer

Improves bone density in elderly

Osteoporosis (cont.)

Preventing osteoporosis

Plenty of calcium in diet in early adulthood

Reduce consumption of carbonated beverages and alcohol

Leach minerals from bone, so decrease bone density

Plenty of weight-bearing exercise

Increases bone mass above normal for buffer against age-related bone loss

Paget’s Disease

Excessive and haphazard bone deposit and resorption cause bone to be made fast and poorly

Called Pagetic bone

Very high ratio of spongy to compact bone and reduced mineralization

Usually occurs in spine, pelvis, femur, and skull

Rarely occurs before age 40

Cause unknown: possibly viral

Treatment includes calcitonin and bisphosphonates

Developmental Aspects of Bone

Embryonic skeleton ossifies predictably, so fetal age is easily determined from X rays or sonograms

Most long bones begin ossifying by 8 weeks, with primary ossification centers developed by week 12

Developmental Aspects of Bone

Birth to Young Adulthood

At birth, most long bones ossified, except at epiphyses

Epiphyseal plates persist through childhood and adolescence

At ~ age 25, all bones are completely ossified, and skeletal growth ceases

Figure 6.17 Fetal primary ossification centers at 12 weeks.

Parietal

bone

Frontal

bone

of skull

Occipital

bone

Mandible

Clavicle

Radius

Femur

Tibia

Ribs

Vertebra

Scapula

Ulna

Humerus

Ilium

Age-Related Changes in Bone

In children and adolescents, bone formation exceeds resorption

Males tend to have greater mass than females

In young adults, both are balanced

In adults, bone resorption exceeds formation

Age-Related Changes in Bone (cont.)

Bone density changes over lifetime are largely determined by genetics

Gene for vitamin D’s cellular docking determines mass early in life and osteoporosis risk at old age

Bone mass, mineralization, and healing ability decrease with age beginning in fourth decade

Except bones of skull

Bone loss is greater in whites and in females