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Chapter 7Lecture Outline

Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

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Bone Tissue

tissues and organs of the skeletalsystem

histology of osseous tissue

bone development

physiology of osseous tissue bone disorders

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What are the Functions of theSkeletal System?

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Functions of the Skeleton

support holds the body up, supports teeth movement limb movements, breathing, action of muscle

on bone

protection brain, spinal cord, heart, lungs

blood formationred bone marrowis the chief producerof blood cells

stores calcium and phosphate, influences blood levelsof Ca & P

acid-base balance buffers blood against excessive pHchanges

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What is the Anatomy of aBone?

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Bone Anatomy Most superficial

layer is theperiosteum.

Figure 7.5b

Periosteum

Endosteum

Perforating fibers

Perforating canal

Osteon

Lacuna

Nerve

Blood vessel

(b)

Spongy bone

Spicules

Centralcanal

Collagen

fibers

Concentric

lamellae

Circumferential

lamellae

Trabeculae

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

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layer is thePeriosteum.

Next (deeper) isCompact Bone.

osteon

Figure 7.5b

Periosteum

Endosteum

Perforating fibers

Perforating canal

Osteon

Lacuna

Nerve

Blood vessel

(b)

Spongy bone

Spicules

Centralcanal

Collagen

fibers

Concentric

lamellae

Circumferential

lamellae

Trabeculae


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osteon Next (deeper) is

Spongy Bone.

spicules

trabeculae

Figure 7.5b

Periosteum

Endosteum

Perforating fibers

Perforating canal

Osteon

Lacuna

Nerve

Blood vessel

(b)

Spongy bone

Spicules

Centralcanal

Collagen

fibers

Concentric

lamellae

Circumferential

lamellae

Trabeculae


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osteon Next (deeper) is

Spongy Bone.

spicules

trabeculae

Deepest is the

Medullary Cavity.

not present insome bones

Figure 7.5b

Periosteum

Endosteum

Perforating fibers

Perforating canal

Osteon

Lacuna

Nerve

Blood vessel

(b)

Spongy bone

Spicules

Centralcanal

Collagen

fibers

Concentric

lamellae

Circumferential

lamellae

Trabeculae


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Endosteum

The spongy bone is coated withreticular tissue (loose CTP) calledendosteum.

Recall that reticular tissue isassociated with Blood Cells.

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Bone Marrow bone marrowoccupies the

medullary cavity of a long bone andsmall spaces amid the trabeculae ofspongy bone

red marrow(hemopoietictissue)- produces blood cells inreticular tissue

yellow marrowfound in adults

fat tissue

no longer produces blood

Figure 7.7

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What Kinds of Cells areResponsible for Bones?

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Histology of Osseous Tissue

four principal typesof bone cells osteogenic (osteoprogenator) cells

Osteogenic cell Osteoblast Osteocyte

(a) Osteocyte development

Nucleus Mitochondrion

Roughendoplasmicreticulum

Secretoryvesicles


Figure 7.4a

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osteoblasts





Secretoryvesicles


Figure 7.4a

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osteoblasts

osteocytes





Secretoryvesicles


Figure 7.4a

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osteoblasts

osteocytes

osteoclasts





Secretoryvesicles


Figure 7.4a

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Histology of Osseous Tissue osteogenic (osteoprogenator) cells

only mitotic cells of bone (other than blood stem cells)

found in periosteum, endosteum

produce osteoblasts

osteoblasts bone forming cells

synthesize soft organic matter of matrix which hardens by mineraldeposition

are nonmitotic

osteocytes former osteoblasts that have become trapped

in the matrix lacunae tiny cavities where osteocytes reside canaliculi little channels that connect lacunae contribute to homeostatic mechanisms of bone density and Ca and P regulate bone remodeling

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The Bone Matrix

Bone matrix is a compositecombines 2 structural materials

Collagen Fibersgive bone tensile strength with some degree offlexibility

Ground Substance (Calcium Phosphate crystals)givescompression strength

combines optimal mechanical properties of each component

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The Bone Matrix What happens if one of the components is missing?

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The Bone Matrix What happens if one of the components is missing?

Rickets (in children)/Osteomalacia (in adults)Disease causing soft bones due to deficiency ofcalcium salts

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What Different Shapes ofBones are in our Bodies?

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Shapes of Bones long bones

longer than wide

short bones equal in length and width

flat bones protect soft organs

irregular bones unusual shape

Figure 7.1


Femur

Scapula

Sternum

Radius

Ulna

Irregular bonesFlat bones

Short bonesLong bones

Capitate(carpal) bone

Talus

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What is the Structure ofLong Bones?

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Structure of a Long Bone

epiphyses anddiaphysis

compact andspongy bone

Medullary cavity(marrow cavity)

articular cartilage

periosteum

Figure 7.2


(a) Living (b) Dried

Marrow cavity

Periosteum

Nutrient foramen

Site of endosteum

Compact bone

Spongy bone

Epiphysis

Epiphysis

Diaphysis

Articularcartilage

Epiphysealline

Red bonemarrow

Yellow bone marrow

Epiphysealline

Articularcartilage

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General Features of Long Bones

diaphysis(shaft)

epiphyses- ends of a long bone

medullary cavity(marrow cavity) - space in the diaphysisthatcontains bone marrow

compact (dense) boneused in outer shell

spongy bone(cancellous bone) composed of spicules andtrabeculae

articular cartilagehyaline cartilage locatedwhere onebone meets another

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Compact Bone Osteonbasic structural unit

of compact bone

concentric lamellaelike a tree trunk

central canalcarries

blood vessels andnerves

collagen fiberscorkscrew down the

matrix of the lamellagiving it a helicalarrangement

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Compact Bone

not all of the matrix isorganized into osteons

circumferentiallamellae -inner and

outer boundaries ofdense bone runparallel to bone surface

interstitial lamellae

remains of old osteons

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Spongy Bone

slivers of bone calledspicules

thin plates of bone calledtrabeculae

spaces between filled withbone marrow

provides strength withminimalweight

trabeculae develop along bones lines of stress

Spongy bone is also made of layers of lamellae,but NOT osteons NO central canals

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Structure of a Flat Bone

sandwich-likeconstruction

two layers of compactbone enclosing amiddle layer of spongybone (no medullary cavity)

spongy bone absorbsshock

marrow spaces linedwith endosteum


Suture

Outer compactbone

Spongy bone(diploe)

Inner compactbone

Trabeculae

Figure 7.3

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How are Bones Made?

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Bone Development

the formation of bone is calledossification (also known as osteogenesis)

two methods:

intramembranous ossification

endochondral ossification

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Intramembranous Ossification Used to produce theflat bonesof the skull

bonesdevelop within a fibrous sheetsimilar to dermis

1. Some of the fibroblast-like cells in the sheet change theirbehavior: they differentiate into osteogenic cells.

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2. The osteogenic cells produce osteoblasts. A periosteumdevelops to cover the outer surfaces.

3. The osteoblasts make spongy bone. Some of theosteoblasts become trapped in the bony matrix andbecome osteocytes. and endosteum develops to cover the

inner surfaces.

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2. The osteogenic cells produce osteoblasts. A periosteumdevelops to cover the outer surfaces.

3. The osteoblasts make spongy bone. Some of theosteoblasts become trapped in the bony matrix andbecome osteocytes. and endosteum develops to cover the

inner surfaces.4. The spongy bone towards the surfaces of the bone gets

converted into compact bone by more osteoblasts.

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Endochondral Ossification

bone developsfrom pre-existing hyaline cartilage model

most bones develop by this process

This is a 2 Step Process:

Step 1. Ossification of the Diaphysis to produce thePrimary Ossification Center:

a. Recall that hyaline cartilage is covered by perichondrium (denseirregular CTP). This is where cartilage stem cells live.

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Endochondral OssificationThis is a 2 Step Process:

Step 1.Ossification of the diaphysis to produce theprimary ossification center:

a. Recall that hyaline cartilage is covered by perichondrium(dense irregular CTP). This is where cartilage stem cells live.These cartilage stem cells change their behavior: they

become osteogenic cells. We now say that the perichondriumis a periosteum.

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Step 1.Ossification of the diaphysis to produce the primary ossificationcenter:

a. Recall that hyaline cartilage is covered by perichondrium (denseirregular CTP). This is where cartilage stem cells live. These cartilagestem cells change their behavior: they become osteogenic cells. Wenow say that the perichondrium is a periosteum.

b. The osteogenic cells produce osteoblasts. The osteoblastsstart producing bony matrix at the models outer surface,

creating a bony collar. The bony collar starts in the middleof the diaphysis then extends to either end.

E d h d l O ifi i

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Step 1.Ossification of the diaphysis to produce the primary ossificationcenter:

a. Recall that hyaline cartilage is covered by perichondrium (dense irregularCTP). This is where cartilage stem cells live. These cartilage stem cellschange their behavior: they become osteogenic cells. We now say thatthe perichondrium is a periosteum.

b. The osteogenic cells produce osteoblasts. The osteoblasts startproducing bony matrix at the models outer surface, creating a bony

collar. The bony collar starts in the middle of the diaphysis then extendsto either end.

c. Chondrocytes deep inside the middle of the diaphysis of the

model now change their behavior: they undergo hypertrophy.

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2 Ways Tissue can Grow

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Hypertrophy

Proliferation

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Hypertrophy of Chondrocytes

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Chondrocytes EXPAND, but tissue size stays the same.

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If Chondroblasts EXPAND, then Lacunae must EXPAND.

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If Chondroblasts EXPAND, then Lacunae must EXPAND.If Lacunae EXPAND and tissue size stays the same,

then matrix must SHRINK

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E d h d l O ifi ti

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Endochondral OssificationStep 1.Ossification of the diaphysis to produce the primary ossification center:

a. Recall that hyaline cartilage is covered by perichondrium (dense irregular

CTP). This is where cartilage stem cells live. These cartilage stem cellschange their behavior: they become osteogenic cells. We now say thatthe perichondrium is a periosteum.

b. The osteogenic cells produce osteoblasts. The osteoblasts startproducing bony matrix at the models outer surface, creating a bony collar.

The bony collar starts in the middle of the diaphysis then extends to either

end.c. Chondrocytes deep inside the middle of the diaphysis of the model now

change their behavior: they undergo hypertrophy. As the cells enlarge, thecartilage matrix around them is reduced to thin walls. These walls becomecalcified NOT true bone. The calcified matrix causes the chondrocytesto die.

d. The calcified cartilage gets chewed up by osteoclasts thatinvade and the resulting cavity is invaded by blood vesselsand osteoblasts invade to produce true bone.

P i O ifi ti C t d

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Primary Ossification Center andPrimary Marrow Cavity

Figure 7.10 (2-3)

Bony collar

Periosteum

2

Enlarging

chondrocytes

Primaryossificationcenter

Formation ofprimaryossification center,bony collar, andperiosteum


Vascular invasion,formation of primarymarrow cavity, andappearance ofsecondaryossification center

3

Secondaryossificationcenter

Primarymarrowcavity

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Step 1. Ossification of the diaphysis to form the primary ossificationcenter

Step 2. Ossification of the Epiphyses to form theSecondary Ossification Centers

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Step 2. Ossification of the Epiphyses to form the SecondaryOssification Centers

a. The bony collar extends over the epiphysis.

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a. The bony collar extends over the epiphysis.

b. Chondrocytes deep inside the epiphysis undergohypertrophy, the matrix becomes thin andcalcified, the cells die.

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a. The bony collar extends over the epiphysis.b. Chondrocytes deep inside the epiphysis undergo hypertrophy,

the matrix becomes thin and calcified, the cells die.

c. Osteoclasts invade and chew up the calcified

matrix, blood vessels invade then osteoblastsinvade to produce bone.

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The Epiphyseal Plate is Essential

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The Epiphyseal Plate is Essentialfor Bone Elongation

Figure 7.10 (4-6)


Metaphysis

Diaphysis

Epiphysis

Cartilage

Metaphysis

Spongy bone

Marrow cavity

Compact bone

Periosteum

4 5 6

Secondarymarrow cavity

Bloodvessel

Secondaryossificationcenter

Bone at birth, withenlarged primarymarrow cavity andappearance ofsecondary marrowcavity in one epiphysis

Bone of child, withepiphyseal plate

Adult bone with asingle marrowcavity and closedepiphyseal plate

Epiphysealplate

Articularcartilage

Epiphysealline

Nutrientforamen

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Interstitial Bone Growth

In bone elongation cartilage is replaced by bone

metaphysisis the name for the zone of

transition from cartilage to bone

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Histology of Metaphysis

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Interstitial Growth is very similar to EndochondrialOssification.

Just one extra pre-step:

proliferation of chondrocytes prior to hypertrophy


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Pneumonic: Remember: Pretty Hard CartilageOssifies

R stands for Reserve cartilage (the epiphyseal plate)

P stands for Proliferation Zone H stands for Hypertrophy Zone

C stands for Calcification Zone

O stands for Ossification Zone


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Histology of Metaphysis zone of reserve cartilage

typical hyaline cartilage farthest from marrow cavity

shows no sign of transforming into bone

zone of proliferation

chondrocytes multiply forming columns of flat lacunae

zone of hypertrophy

chondrocyteenlargement

matrix between lacunae becomes very thin

zone of calcification

mineral deposited in the matrix between columns of lacunae

zone of bone deposition (ossification)

chondrocytes die, osteoclasts dissolve the calcified cartilage,blood vessels enter, osteoblasts make bone

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Fetal Skeleton at 12 Weeks

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Fetal Skeleton at 12 Weeks

Figure 7.11


Humerus

Ulna

Femur

Radius

Mandible

Scapula

Ribs

Pelvis Biophoto Associates/Photo Researchers, Inc.

Cranialbones

Vertebrae

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What Causes Less Than

Typical Interstitial Growth?(Short Stature)

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Dwarfism

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Dwarfism

achondroplastic dwarfism long bones stop growing in

childhood Normal torso, short limbs

failure of cartilage growth in

metaphyses mutantdominant allele

pituitary dwarfism lack of growth hormone

normal proportions with shortstature

Figure 7.14


The McGraw-Hill Companies, Inc./Joe DeGrandis, photographer

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Bone Remodeling

*Wolffs law of bone - architecture ofbone determined by mechanical stresses

Bone grows thickest where the most stress isfelt

Trabeculae and spicules align with the stressforce

Bone that does not feel as much stress growsthinner to minimize weight

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Design of Spongy Bone

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Design of Spongy Bone

Figure 7.6


Greater trochanter

Compact bone

Head

Lines of stress

Shaft (diaphysis)

Trabeculae ofspongy bone

Robert Calentine/Visuals Unlimited

Calcium Homeostasis

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Calcium Homeostasis

about 99% of bodys calcium stored in skeleton

hypocalcemia- blood calcium deficiency

causes excess excitability of muscle, tremors,spasms or tetany (inability to relax)

hypercalcemia- blood calcium excess

RARE

Symptoms: sluggish reflexes, depression

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Calcium Homeostasis

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Calcium Homeostasis hypercalcemiais rare

hypocalcemiahas a wide variety of causes

vitamin D deficiency

diarrhea

thyroid tumors

underactive parathyroids pregnancy and lactation

accidental removal of parathyroid glands during thyroid surgery

Homeostasis depends on a balance between dietaryintake, urinary and fecal loses, and exchanges betweenosseous tissue

Calcium Homeostasis

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Calcium Homeostasis

regulated by three hormones:

Calcitriol := Vitamin D3 required to absorb Ca

Calcitonin:Decreases Blood Ca

Parathyroid hormone:Increases Blood Ca

Calcium Homeostasis

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Calcium Homeostasis

regulated by three hormones:

Calcitriol := Vitamin D3 required to absorb Ca

Calcitonin:Decreases Blood Ca

Parathyroid hormone(PTH): Increases Blood Ca

Calcitriol(Activated Vitamin D3)

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Ca c t o ( ct ated ta 3)

produced by sequential action of 3 organs:

skin liver kidneys

increases calcium absorption by small intestine

less calcium lost in urine

can also cause activation of osteoclasts: Ca released from bone

necessary for making bone

Deficiency causes abnormal softness of bones (rickets) inchildren and (osteomalacia)in adults

Calcitonin

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Calcitonin

secreted bythyroid glandwhen blood calcium

concentration risestoo high

lowers blood calcium concentrationin two ways: osteoclast inhibition

osteoblast stimulation

important in children, MINOReffect in adults

reduces bone loss in women during pregnancy & lactation

Correction for Hypercalcemia

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Co ect o o ype ca ce aCopyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

(a) Correction for hypercalcemia

Calcitoninsecretion

Blood Ca2+

excess

Blood Ca2+

returns tonormal

Reducedosteoclast

activity

Less boneresorption

Increasedosteoblast

activity

More bonedeposition

Figure 7.18a

Parathyroid Hormone (PTH)

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Parathyroid Hormone (PTH) secreted by the parathyroid glandswhen sense low blood

calcium(glands found on the posterior surface of thyroid gland)

PTH raises calcium blood levelby four mechanisms raises the osteoclast population size

less calcium lost in urine

promotes synthesis of calcitriol in the kidneys inhibits bone deposition

PTH also helps build bone - sporadic injection or secretionof low levels of PTH causes bone deposition and can

increase bone mass

Correction for Hypocalcemia

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Correction for HypocalcemiaCopyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

(b) Correction for hypocalcemia

Blood Ca2+

deficiency

Parathyroidhormonesecretion

Increasedosteoclast

activity

Blood Ca2+

returns tonormal

More boneresorption

Less bonedeposition

Prevention ofhydroxyapatite

formation

More urinaryphosphateexcretion

Reducedosteoblast

activity

Conservationof calcium

Less urinarycalcium

excretion

Figure 7.18b

H l C t l f C l i

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Hormonal Control of Calcium

calcitriol, calcitonin, and PTH maintain normalblood calcium concentration

Figure 7.17


Calcium Intake and Excretion

Digestive tract

Kidneys

Fecal loss350 mg/day

Urinary loss650 mg/day

Calcitriol

CalcitriolPTH

Blood

Calcitonin(weak effect)

CalcitriolPTH

Bone

Absorption bydigestive tract

Filtrationby kidneys

Reabsorptionby kidneys

Deposition byosteoblasts

Resorption byosteoclasts

Dietary requirement1,000 mg/day

Ca2+

(9.210.4 mg/dL) HydroxyapatiteCa10(PO4)6(OH)2

Calcium carbonateCaCO3

Other Factors Affecting Bone

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Other Factors Affecting Bone

Many hormones, vitamins, and growth factors affect

osseous tissue (examples:growth hormone, estrogen,and testosterone)

Use of anabolic steroidscauses growth to stop

epiphyseal plate closes prematurely Can result in abnormally short adult stature

Fractures and Their Repair

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Fractures and Their Repair

fracturesclassified by structural characteristics

break in the skin =open fracture, akacompound fracture

displaced= ends of bones NOT aligned properly

direction of fracture line (linear=parallel to bone, vs. oblique, transverse)

number of pieces (1=incomplete, 2=complete, 3 or more=comminuted)

pathological fracture break in a bone weakened bysome other disease

bone cancer or osteoporosis

usually caused by stress that would NOT break a healthy bone

Types of Bone Fractures

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yp

Figure 7.19


(a) Nondisplaced

(c) Comminuted (d) Greenstick

a: Custom Medical Stock Photo, Inc.; c: Lester V. Bergman/Corbis; d: Custom Medical Stock Photo, Inc.

Healing of Fractures

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gstages of healing bone fractures:

1. form blood clot (fracture hematoma) andform

granulation tissue blood capillaries, fibroblasts, macrophages, osteoclasts, and osteogenic

cells invade clot

2. soft callus formation formed by fibroblasts and chondroblasts depositing collagen and

fibrocartilage into granulation tissue

3. conversion to hard callus osteoblasts produce a bony collar in 6 weeks called a hard callus

acts as a temporary splint to join broken ends together

4. remodeling hard callus persists for 3 4 months

osteoclasts dissolve fragments of broken bone

osteoblasts deposit spongy bone to bridge to between the broken ends,later convert spongy compact bone, bone will be thicker in fracture area

uncomplicated fractures normally heal in 8 - 12 weeks, longer in elderly

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Healing of Fractures

Figure 7.20


Fibrocartilage

Soft callusHematoma

Compact bone

1 2 3 4

Marrowcavity

Hematoma formationThe hematoma is convertedto granulation tissue by invasionof cells and blood capillaries.

Hard callus formationOsteoblasts deposit a temporarybony collar around the fracture tounite the broken pieces whileossification occurs.

Bone remodelingSmall bone fragments areremoved by osteoclasts, whileosteoblasts deposit spongybone and then convert it tocompact bone.

Soft callus formationDeposition of collagen andfibrocartilage converts granulationtissue to a soft callus.

Hardcallus

Spongy

bone

New bloodvessels

Treatment of Fractures

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Treatment of Fractures Reduction = getting bones aligned properly

closed reductionbone fragments are manipulated intotheir normal positions without surgery

open reduction involves surgical exposure of the boneand the use of plates, screws, or pins to realign the

fragments

cast normally used to stabilize and immobilize healing bone

traction RARELY used ambulation (walking) encouraged to promote blood circulation/healing

to maintain alignment, may use traction in children to override muscles

electrical stimulation accelerates repair suppresses the effects of parathyroid hormone

orthopedics the branch of medicine that deals injuries and disorders of thebones, joints, and muscles

Fractures and Their Repairs

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Fractures and Their Repairs

Figure 7.21


SIU/Visuals Unlimited; 7.22a: Michael Klein/Peter Arnold, Inc.

Osteoporosis

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Osteoporosis osteoporosis the most common bone disease

severe loss of bone density

bones lose mass and become brittle affects spongy bone the most

subject to pathological fracturesof hip, wrist & vertebral column

kyphosis(widows hump) deformity of spine due to vertebral

bone loss, usually cervical vertebrae affected complications of loss of mobility are pneumonia and thrombosis

postmenopausal women at greatest risk begin to lose bone mass as early as 35 yoa

by age 70, average loss is 30% of bone mass in white women

risk factors - race, age, gender, smoking, diabetes mellitus, dietspoor in calcium, protein, vitamins C and D

best treatment isprevention- exercise and calcium intake

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Osteoporosis

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Osteopo os s estrogen maintains density in both sexes inhibits resorption

by osteoclasts testes and adrenals produce estrogen in men in women, rapid bone loss after menopause since estrogen blood

level drops below 30 ng/mL

osteoporosis is common in young female athletes with low

body fat causing them to stop ovulating and ovarianestrogen secretion is low

treatments estrogen replacement therapy (ERT) slows bone resorption, but

increases risk of breast cancer, stroke and heart disease

drugs Fosamax/Actonel destroys osteoclasts May cause loss of bone mass in mandible (lower jaw) and perhaps hip

PTH slows bone loss if given as daily injection Forteo (PTH derivative) increases density by 10% in 1 year

may promote bone cancer so use is limited to 2 years

Chapt 07 New

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Transcript of Chapt 07 New