Lecture 10 - Bone.pdf

7/27/2019 Lecture 10 - Bone.pdf

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Lecture 10: BONE

Everything is connected to everything else

The Skeletal System: Bone Tissue

Functions of Bone and Skeletal System

Structure of Bone

Histology of Bone Tissue

Blood and Nerve Supply of Bone

Bone Formation

Bones Role in Calcium Homeostasis

Exercise and Bone TissueAging and Bone Tissue

Overview

Bone tissue forms most of the SKELETON,

which allows us to move, provides support,

and protection.

The study of bone structure and bone

disorders is known as OSTEOLOGY.


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Overview

Functions of Bone:

1. SUPPORT - provides a point of attachment for

SKELETAL MUSCLE.

2. PROTECTION - Protects internal organs frominjury. Cranial bones protect the brain, the ribcage protects the thoracic cavity, etc

3. MOVEMENT - Assists in movement (muscleattaches to bone).

Overview

Functions of Bone (continued)

4. MINERAL HOMEOSTASIS

Bone tissue stores several minerals, especially

CALCIUM and PHOSPHORUS.

5. BLOOD CELL PRODUCTION

Red bone marrow is the site of production of red

and white blood cells and platelets. The

process of blood cell formation -

HEMOPOIESIS.

6. ENERGY STORAGE

Lipids are stored in YELLOW bone marrow.

Overview

The Skeletal System consists of bone tissue,

cartilage, red and yellow bone marrow,

periosteum and endosteum.


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Bone Anatomy

Basic Structure of typical LONG bone:

1. DIAPHYSIS - shaft or main LONG portion.

2. EPIPHYSIS - distal and proximal ENDS or

extremities.

Bone Anatomy

Basic Structure of typical LONG bone:

3. METAPHYSIS - region where the Diaphysis

joins the Epiphysis.

In a growing bone, each metaphysis includes an

EPIPHYSEAL PLATE which is a layer of hyaline

cartilage that allows the diaphysis of the bone to

grow in length.

4. ARTICULAR CARTILAGE - a thin layer ofhyaline cartilage covering the epiphysis wherebone forms an articulation or joint.


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Bone Anatomy

5. PERIOSTEUM - a membrane around the

surface of bone not covered by articular

cartilage.

6. MEDULLARY (MARROW) CAVITY

space within the Diaphysis that contains

YELLOW or fatty bone marrow.

7. ENDOSTEUM - lines the medullary cavity.


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Extracellular matrix surrounding widely

separated cells

Matrix

25% water

25% collagen fibers

50% crystallized mineral salts

The most abundant mineral salt is

calcium phosphate


A process called calcification is initiated

by bone-building cells called osteoblasts

Mineral salts are deposited and crystalize

in the framework formed by the collagen

fibers of the extracellular matrix

Bones flexibilitydepends on collagenfibers

Bone Histology

OSSEOUS TISSUE contains an abundant

matrix with widely separated cells.

4 types of cells in bone tissue:

1. OSTEOPROGENITOR CELLS - these candivide, are unspecialized cells, derived fromMESENCHYME (remember, we said allconnective tissue is derived from this).

Found in the periosteum and endosteum.

Can divide and become OSTEOBLASTS.


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Bone Histology

2. OSTEOBLASTS

CANT DIVIDE.

Osteoblasts secrete MATRIX.

Form bone, but have lost their ability to divide bymitosis.

Secrete components that build bone tissue.


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Bone Histology

3. OSTEOCYTES

CANT DIVIDE.

DO NOT secrete matrix.

Osteocytes are mature bone cells that are derivedfrom OSTEOBLASTS.

NO mitotic potential.

Osteoblasts initially form bone tissue, osteocytes

no longer secrete bone tissue materials, butmaintain the daily activities of bone tissue.

Bone Histology

4. OSTEOCLASTS

clast - break

Function in bone RESORPTION (destruction ofthe matrix), which is important in repairing andmaintaining bone.


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Bone

Bone is not completely solid, but has many

small spaces within it.

Depending on the size and distribution of these

spaces, regions of bone may be classified as:

1. COMPACT (DENSE) BONE

2. CANCELLOUS (SPONGY) BONE


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Compact Bone

The main difference between compact and

cancellous bone is that in compact bone,

there are concentric ring structures of

OSTEONS (HAVERSIAN SYSTEMS) in

compact bone and an irregular arrangement

of osteons in SPONGY BONE.


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Compact Bone

Central canals run longitudinally through

bone.

Around these canals are CONCENTRIC

LAMELLAE - rings of hard, calcified matrix.

Between the lamellae are spaces called

LACUNAE that contain OSTEOCYTES.

Remember, osteocytes are mature bone cells that

no longer secrete matrix.


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Compact Bone

Radiating in all directions form lacunae are

CANALICULI, which connect lacunae with

one another and with central canals.


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Spongy Bone

Compared to compact bone, spongy bone

has no formal osteons.

Instead, lamellae are arranged in irregular

configurations of thin plates called TRABECULAE.

Spongy bone makes up most of the bone

tissue in short, flat, and irregular shaped

bones and the epiphyses of long bones.


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Spongy Bone

Spongy bone in the hips, ribs, sternum,

vertebrae, skull, and ends of long bones is

the only site of HEMOPOIESIS in adults. Where blood cells are PRODUCED.

Compact Bone

How do nutrients actually get into bone?

From the PERIOSTEUM - blood vessels, nerves,etc, penetrate the compact bone tissue

through PERFORATING (VOLKMANNS)CANALS.

These connect with the MEDULLARY CAVITY,

PERIOSTEUM, and CENTRAL (HAVERSIAN)CANALS.


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Bone Formation: Ossification

Bones in infants are not hard or rigid.

There is a constant process of bone being

broken down and rebuilt.

This process by which bone forms is calledOSSIFICATION.

Ossification begins around the 6th or 7th

week of embryonic life and continues

throughout adulthood.


Bone formation follows one of two patterns:

1. INTRAMEMBRANOUS OSSIFICATION

2. ENDOCHONDRAL OSSIFICATION


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Intramembranous ossification:

Refers to bone formation DIRECTLY within loose

fibrous connective tissue membranes.

Forms DIRECTLY from MESENCHYME withoutgoing through a CARTILAGE stage first.

Fontanels in an infant skull (soft spots) are

composed of loose fibrous connective tissue and

are eventually replaced by bone through

Intramembranous Ossification.


Endochondral Ossification:

Refers to formation of bone IN hyaline cartilage.

Mesenchyme is transformed into

CHONDROBLASTS - cartilage precursors, thatproduce a hyaline cartilage matrix that is graduallyREPLACED BY BONE.


These two kinds of ossification DO NOT lead

to differences in STRUCTURE of mature

bones.

They simply indicate different methods in

bone FORMATION.


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The first stage in development of bone is

migration of MESENCHYMAL cells into an

area where bone formation is about to begin. These cells increase in number and size.

In some skeletal structures, they becomechondroblasts and produce cartilage; in othersthey become osteoblasts and will form bonetissue.


Intramembranous Ossification Steps:

1. At the site where bone will develop,MESENCHYME cells cluster together and

differentiate into OSTEOPROGENITOR CELLSand then into OSTEOBLASTS.

The place where this cluster occurs is called the

CENTER OF OSSIFICATION

Osteoblasts secrete matrix and become surrounded

by it.


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2. Matrix secretion stops and those cells become

OSTEOCYTES and lie within lacunae. Calcium and other minerals start to be deposited

and the MATRIX starts to calcify.



3. As bone matrix starts to form, it develops into

TRABECULAE that fuse with one another to form

precursor bone with the appearance of SPONGYbone.

Mesenchyme cells start to condense on the outer

surface of the developing bone.


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4. The condensed mesenchyme develops intoPERIOSTEUM.

Most surface layers of the spongy bone are

replaced by compact bone, but spongy bone

remains in the center of the bone.

Eventually, newly formed bone is remodeled and

reshaped until reaching its final adult shape and

size.


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Endochondral Ossification steps:

Replacement of CARTILAGE by bone.

Most bones in the body are formed this way.

1. Development of a cartilage precursor. At the site where bone will form, mesenchyme cells gather

in the rough shape of the future bone.

These cells differentiate into CHONDROBLASTS that

produce hyaline cartilage.

A PERICHONDRIUM develops around the cartilage

structure.


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Endochondral Ossification Steps:

2. GROWTH of CARTILAGE

Grows by continual cell division.

A nutrient artery penetrates the Perichondrium.

This stimulates OSTEOPROGENITOR CELLS in

the perichondrium to form OSTEOBLASTS.

Once the perichondrium starts to form bone, it is

now called PERIOSTEUM.



3. Development of the PRIMARY ossification

center:

Capillaries grow into disintegrating cartilage and

form the Primary ossification center.

This is where bone tissue will replace most of the

cartilage.

OSTEOBLASTS begin to deposit bone matrix over

the remnants of calcified cartilage.


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3. Development of the PRIMARY ossification

center: The ossification center enlarges towards the ends

of the bone.

Osteoclasts break down former spongy bone areas

leaving a new medullary cavity.

The cavity fills with red bone marrow.



4. Development of Diaphysis and Epiphysis:

The shaft (diaphysis), which was spongy bone, is

now replaced by compact bone with a core of red

bone marrow-filled MEDULLARY CAVITY.

When blood vessels enter the epiphyses (ends),

SECONDARY OSSIFICATION CENTERS develop,

usually around the time of birth.


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5. SECONDARY ossification centers:

Bone formation is similar to that in Primary areas.

However, SPONGY bone remains in the interior of

the epiphyses (no medullary cavity).

Hyaline cartilage remains covering the epiphyses


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Bone Growth During Infancy, Childhood

and Adolescence Growth in Length

The growth in length oflong bones involves two

major events: 1) Growth of cartilage

on the epiphysealplate

2) Replacement ofcartilage by bonetissue in theepiphyseal plate


and Adolescence

Osteoclasts dissolve the

calcified cartilage, andosteoblasts invade the arealaying down bone matrix

The activity of the epiphysealplate is the way bone canincrease in length

At adulthood, the epiphysealplates close and bone replacesall the cartilage leaving a bonystructure called the epiphysealline


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and Adolescence Growth in Thickness

Bones grow in thickness at the outer surface

Remodeling of Bone Bone forms before birth and continually renews

itself The ongoing replacement of old bone tissue by

new bone tissue

Old bone is continually destroyed and new bone isformed in its place throughout an individuals life

Bone Homeostasis

Just like skin, bone forms before birth, but

there is a constant RENEWAL of bone tissue

after birth.

REMODELING is the ongoing replacement of oldbone tissue by new bone tissue.

Ex. The distal end of the femur is replaced aboutevery 4 months.

But some areas in the femur may never be replaced

during an individuals lifetime.


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Remodeling

OSTEOCLASTS are responsible for BONE

RESPORTION (destruction of the matrix).

The body maintains a delicate balance betweenbuilding too much new bone too fast by

osteoblasts and osteoclasts removing mineralsand collagen.

Remodeling

OSTEOPOROSIS

Condition where the basic problem is that boneresorption outpaces bone formation and the

bones weaken.


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Remodeling

PAGETS DISEASE

When there is abnormal ACCELERATION of theremodeling process.

Osteoblastic bone formation is extensive andthere is irregular THICKENING of bone.


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Remodeling

OSTEOMYELITIS:

Inflammation of bone, especially bone marrow,

caused by a pathogenic organism, oftenStaphylococcusaureus.

Remodeling

In the basic process of resorption,

osteoclasts secrete protein-digesting

LYSOSOMAL enzymes that digest matrix

materials.

Factors Affecting Bone Growth and Bone

Remodeling Normal bone metabolism depends on several factors

Minerals Large amounts of calcium and phosphorus and

smaller amounts of magnesium, fluoride, andmanganese are required for bone growth andremodeling

Vitamins Vitamin A stimulates activity of osteoblasts

Vitamin C is needed for synthesis of collagen

Vitamin D helps build bone by increasing theabsorption of calcium from foods in the gastrointestinaltract into the blood

Vitamins K and B12 are also needed for synthesis ofbone proteins


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Remodeling Hormones

During childhood, the hormones most important to

bone growth are growth factors (IGFs), produced bythe liver IGFs stimulate osteoblasts, promote cell division at the

epiphyseal plate, and enhance protein synthesis

Thyroid hormones also promote bone growth bystimulating osteoblasts

Insulin promotes bone growth by increasing thesynthesis of bone proteins


Remodeling Hormones

Estrogen and testosterone cause a dramaticeffect on bone growth Cause of the sudden growth spurt that occurs

during the teenage year

Promote changes in females, such as widening ofthe pelvis

Shut down growth at epiphyseal plates

Parathyroid hormone, calcitriol, and calcitoninare other hormones that can affect bone

remodeling Weight Bearing Exercise

Fracture and Repair of Bone

Fracture Types Open (compound) fracture

The broken ends of the bone protrude through the skin

Closed (simple) fracture Does not break the skin

Comminuted fracture The bone is splintered, crushed, or broken into pieces

Greenstick fracture A partial fracture in which one side of the bone is broken and the other side

bends

Impacted fracture One end of the fractured bone is forcefully driven into another

Potts fracture Fracture of the fibula, with injury of the tibial articulation

Colles fracture A fracture of the radius in which the distal fragment is displaced

Stress fracture A series of microscopic fissures in bone


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Calcium and phosphorus needed to strengthen andharden new bone after a fracture are deposited onlygradually and may take several months

The repair of a bone fracture involves the followingsteps 1) Formation of fracture hematoma

Blood leaks from the torn ends of blood vessels, a clottedmass of blood forms around the site of the fracture

2) Fibrocartilaginous callus formation

Fibroblasts invade the fracture site and produce collagenfibers bridging the broken ends of the bone

3) Bony callus formation

Osteoblasts begin to produce spongy bone trabeculae joining

portions of the original bone fragments 4) Bone remodeling

Compact bone replaces spongy bone

Compact boneSpongy bone

Periosteum

Fracture hematoma

Fracturehematoma

Bonefragment

Osteocyte

Red bloodcell

Blood vessel

Formation of fracture hematoma

Phagocyte

Osteon

1

Phagocyte

Osteoblast

Fibroblast

Fibrocartilaginouscallus

Collagen fiber

Chondroblast

Cartilage

Fibrocartilaginous callus formation2


Periosteum

Fracture hematoma

Fracturehematoma

Bonefragment

Osteocyte

Red bloodcell

Blood vessel


Phagocyte

Osteon

1

Bony callus

Spongy bone

Osteoblast

Bony callus formation

Osteocyte

3


Periosteum

Fracture hematoma

Fracturehematoma

Bonefragment

Osteocyte

Red bloodcell

Blood vessel


Phagocyte

Osteon

1

Phagocyte

Osteoblast

Fibroblast


Collagen fiber

Chondroblast

Cartilage


Spongy bone

Osteoblast

Osteoclast

New compactbone

Bony callus formation Bone remodeling

Osteocyte

3 4


Periosteum

Fracture hematoma

Fracturehematoma

Bonefragment

Osteocyte

Red bloodcell

Blood vessel


Phagocyte

Osteon

1

Phagocyte

Osteoblast

Fibroblast


Collagen fiber

Chondroblast

Cartilage


Bony callus


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Bone Fractures

1. Formation of Fracture Hematoma Blood vessels crossing the bone are broken as

a result of the fracture.

Blood leaks into the area and forms a clotcalled a FRACTURE HEMATOMA.

Bone cells at the fracture site die due to lack ofblood flow.

The hematoma serves as a focus of cellularinvasion to help heal the fracture.

White blood cells start to flow into the area andbegin to clean up debris.

6-8 hours after fracture.


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Bone Fractures

2. Fibrocartilaginous Callus FOrmation Capillaries begin to grow into the hematoma

and organized tissue called a PROCALLUSforms.

A CALLUS is a mass of repair tissue thatbridges the ends of broken bones.

Fibroblasts begin to secrete collagen whichhelps join the ends of the fracture.

Precursor cells develop into chondroblasts(cartilage cells) and the procallus is now calleda FIBROCARTILAGINOUS (SOFT) CALLUS.

Lasts about 3 weeks.

Bone Fractures

3. Bony Callus Formation

Osteoprogenitor cells begin to develop into

osteoblasts which begin to produce new spongy

bone that bridges the ends of the broken bone.

The Callus is then referred to as a BONY (HARD)CALLUS.

3-4 months.


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Bone Fractures

4. Bone Remodeling

The final phase is remodeling of the callus.

Dead portions of the original fracture are gradually

resorbed by osteoclasts.

Compact bone replaces spongy bone.


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Calcium Homeostasis

Bone is a major storage area for calcium.

It stores more than 99% of the total calcium in the

body.

The role of bone in calcium homeostasis is tobuffer the level of calcium in the blood.

If there is too much calcium in the blood - bonewill take back calcium. If there is too little - bonewill release calcium into blood.

Hormones regulate these exchanges.

Bones Role in Calcium HomeostasisActions that help elevate blood Ca2+ level Parathyroid hormone (PTH) regulates

Ca2+ exchange between blood and bonetissue PTH increases the number and activity of

osteoclasts

PTH acts on the kidneys to decrease loss ofCa2+ in the urine

PTH stimulates formation ofcalcitriol ahormone that promotes absorption of

calcium from foods in the gastrointestinaltract


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Bones Role in Calcium HomeostasisActions that work to decrease blood Ca2+

level

The thyroid gland secretes calcitonin (CT)whichinhibits activity of osteoclasts

The result is that CT promotes boneformation and decreases blood Ca2+ level

Exercise and Bone Tissue Bone tissue alters its strength in response to

changes in mechanical stress Under stress, bone tissue becomes stronger through

deposition of mineral salts and production of collagenfibers by osteoblasts

Unstressed bones diminishes because of the loss ofbone minerals and decreased numbers of collagenfibers

The main mechanical stresses on bone arethose that result from the pull of skeletal musclesand the pull of gravity

Weight-bearing activities help build and retainbone mass

Aging and Bone Tissue

Principal Effects of Aging:

1. LOSS of calcium and other minerals.

Usually begins after 30 in females and accelerates

around age 40-45.

Does not begin until about age 60 in males.

Loss of calcium is one of the problems in

OSTEOPOROSIS.


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Aging and Bone Tissue

Principal Effects of Aging:

2. Second effect is a decrease in the rate of

protein synthesis. This causes the bones to lose tensile strength or

become more brittle and more susceptible to

fracture.

Documents

Lecture 10 - Bone.pdf