bonetissue ppt

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Skeletal System Composed of the body ¶s bones and associated ligaments, tendons, and cartilages. Functions: 1. Support The bone s of the leg s, pel vic gir dle , and ver tebr al column support the weight of the erect bo dy. The man dibl e (jawbone ) support s the tee th. Oth er bone s support var ious org ans and tiss ues. 2. Protection The bone s of the skull prot ect the bra in. Ribs and ste rnum (br eas tbone ) prot ect the lung s and heart. Vertebrae pro tect the spi nal cord.

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8/7/2019 BoneTissue ppt

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Skeletal System

� Functions:3. Movement

� Skeletal muscles use the bones as levers tomove the body.

4. Reservoir for minerals and adipose tissue

� 99% of the body¶s calcium is stored in bone.

� 85% of the body¶s phosphorous is stored inbone.

� Adipose tissue is found in the marrow of certain bones.

± What is really being stored in this case? (hint ± 

it starts with an E )

5. Hematopoiesis

� A.k.a. blood cell formation.

� All blood cells are made in the marrow of certain bones.

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Bone Classification� There are 206 named bones inthe human body.

� Each belongs to one of 2 largegroups:

± Axial skeleton

� Forms long axis of the body.

� Includes the bones of the skull,

vertebral column, and rib cage.� These bones are involved in

protection, support, andcarrying other body parts.

± Appendicular skeleton

� Bones of upper & lower limbsand the girdles (shoulder bonesand hip bones) that attach themto the axial skeleton.

� Involved in locomotion andmanipulation of the

environment.

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Bone Classification

� 4 types of bones:1. Long Bones

� Much longer than they are wide.

� All bones of the limbs except for the patella (kneecap),

and the bones of the wrist andankle.

� Consists of a shaft plus 2expanded ends.

� Your finger bones are long boneseven though they¶re

very short ± how can this be?

2. Short Bones

� Roughly cube shaped.

� Bones of the wrist and the ankle.

Femur 

Carpal Bones

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Bone Structure

� Bones are organs. Thus, they¶re composed of multiple tissue types. Bones are composed of:

± Bone tissue (a.k.a. osseous tissue).

± Fibrous connective tissue.± Cartilage.

± Vascular tissue.

± Lymphatic tissue.

± Adipose tissue.± Nervous tissue.

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Note the gross differences between the spongy bone and the

compact bone in the above photo.

Do you see the trabeculae?

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Compare compact and spongy bone as viewed with the light microscope

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Bone Structure

� Bone tissue is a type of connective tissue, so it mustconsist of cells plus asignificant amount of extracellular matrix.

� Bone cells:1. Osteoblasts

� Bone-building cells.

� Synthesize and secretecollagen fibers and other 

organic components of bone matrix.

� Initiate the process of calcification.

� Found in both theperiosteum and theendosteum

The blue arrows indicate the

osteoblasts. The yellow arrows indicate

the bone matrix they¶ve just secreted.

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Bone Structure

2. Osteocytes� Mature bone cells.

� Osteoblasts that havebecome trapped by the

secretion of matrix.� No longer secrete

matrix.

� Responsible for maintaining the bone

tissue.

Yellow arrows indicate

osteocytes ± noticehow they are

surrounded by the

pinkish bone matrix.

Blue arrow shows an

osteoblast in the

process of becoming an

osteocyte.

On the right, notice how the osteocyte

is ³trapped´ within the pink matrix

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3. Osteoclasts± Huge cells derived from the fusion of as many as 50 monocytes (a type of white blood cell).

± Cells that digest bone matrix ± this process is called bone resorption and ispart of normal bone growth, development, maintenance, and repair.

± Concentrated in the endosteum.

± On the side of the cell that faces the bone surface, the PM is deeply foldedinto a ruffled border. Here, the osteoclast secretes digestive enzymes (howmight this occur ?) to digest the bone matrix. It also pumps out hydrogen ions(how might this occur ?) to create an acid environment that eats away at thematrix. What advantage might a ruffled border confer?

± Why do we want a cell that eats away at bone? (Hint: bone is a verydynamic tissue.)

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�Here, we see a cartoon showing all 3 cell types. Osteoblasts and osteoclasts are indicated.

�Note the size of the osteoclast (compare it to the osteoblast), and note the ruffled border.

�Why is there a depression underneath the osteoclast?

�What is the name of the third cell type shown here?

�What do you think the tan material represents?

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Bone Structure

� Bone Matrix:

± Consists of organic and inorganic

components.

± 1/3 organic and 2/3 inorganic by

weight.

� Organic component consists of several

materials that are secreted by the

osteoblasts:± Collagen fibers and other organic materials

» These (particularly the collagen) provide

the bone with resilience and the ability

to resist stretching and twisting.

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� Inorganic componentof bone matrix± Consists mainly of 2

salts: calciumphosphate and calciumhydroxide. These 2salts interact to form acompound calledhydroxyapatite.

± Bone also containssmaller amounts of 

magnesium, fluoride,and sodium.

± These minerals givebone its characteristichardness and theability to resistcompression.

Three-dimensional array of 

collagen molecules. The rod-

shaped molecules lie in a

staggered arrangement which

acts as a template for bone

mineralization. Bone mineral is

laid down in the gaps.

Note collagen fibers in longitudinal & cross section

and how they occupy space btwn the black bone cells.

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This bone:

a. Has been demineralized

b. Has had its organic component removed

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Long Bone Structure

� Shaft plus 2 expanded ends.

� Shaft is known as the diaphysis.

± Consists of a thick collar of compactbone surrounding a central marrowcavity

� In adults, the marrow cavity containsfat - yellow bone marrow.

� Expanded ends are epiphyses

± Thin layer of compact bone coveringan interior of spongy bone.

± Joint surface of each epiphysis iscovered w/ a type of hyaline cartilageknown as articular cartilage. Itcushions the bone ends and reducesfriction during movement.

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Long Bone

Structure

� The external surface of the entirebone except for the joint surfaces of the epiphyses is covered by adouble-layered membrane known asthe periosteum.

± Outer fibrous layer is dense irregular connective tissue.

± Inner cellular layer containsosteoprogenitor cells and osteoblasts.

± Periosteum is richly supplied with

nerve fibers, lymphatic vessels andblood vessels.

� These enter the bone of the shaft via anutrient foramen.

± Periosteum is connected to the bonematrix via strong strands of collagen.

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Long Bone

Structure

� Internal bone surfaces are covered with a delicate

connective tissue membrane known as the

endosteum.

± Covers the trabeculae of spongy bone in the marrowcavities and lines the canals that pass through compact

bone.

± Contains both osteoblasts and osteoclasts.

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Structure of Short, Irregular, and

Flat Bones� Thin plates of periosteum-covered

compact bone on the outside andendosteum-covered spongy bonewithin.

� Have no diaphysis or epiphysisbecause they are not cylindrical.

� Contain bone marrow betweentheir trabeculae, but no marrowcavity.

� In flat bones, the internal spongybone layer is known as the diploë,and the whole arrangementresembles a stiffened sandwich.

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Bone Marrow

� Bone marrow is a general term for thesoft tissue occupying the medullarycavity of a long bone, the spaces amidthe trabeculae of spongy bone, and thelarger haversian canals.

� There are 2 main types: red & yellow.

� Red bone marrow = blood cellforming tissue = hematopoietic tissue

� Red bone marrow looks like blood but

with a thicker consistency.� It consists of a delicate mesh of reticular 

tissue saturated with immature red bloodcells and scattered adipocytes.

Notice the red marrow

and the compact bone

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Distribution of 

Marrow

� In a child, the medullarycavity of nearly every bone isfilled with red bone marrow.

� In young to middle-agedadults, the shafts of the long

bones are filled with fattyyellow bone marrow.

± Yellow marrow no longer produces blood, although inthe event of severe or chronicanemia, it can transform back 

into red marrow� In adults, red marrow is

limited to the axial skeleton,pectoral girdle, pelvic girdle,and proximal heads of the

humerus and the femur.

Note the compact bone on the

bottom and marrow on the bottom.

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Microscopic

Structure of 

Compact Bone

� Consists of multiple

cylindrical structuralunits known asosteons or haversiansystems.

� Imagine these osteons

as weight-bearingpillars that arearranged parallel toone another along thelong axis of a

compact bone.

The diagram below represents a long

bone shaft in cross-section. Each

yellow circle represents an osteon. The

blue represents additional matrix filling

in the space btwn osteons. The white in

the middle is the marrow cavity.

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Osteons

� Each osteon consists of a singlecentral canal, known as ahaversian canal, surrounded byconcentric layers of calcifiedbone matrix.

± Haversian canals allow the passageof blood vessels, lymphatic vessels,and nerve fibers.

± Each of the concentric matrix³tubes´ that surrounds a haversian

canal is known as a lamella.± All the collagen fibers in a particular lamella run in a single direction,while collagen fibers in adjacentlamellae will run in the oppositedirection. This allows bone to better 

withstand twisting forces.

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Running perpendicular to the haversian canals are Volkmann¶s canals.They connect the blood and nerve supply in the periosteum to those inthe haversian canals and the medullary cavity.

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Osteons

� Lying in between intact

osteons are incomplete

lamellae called

interstitial lamellae.

These fill the gapsbetween osteons or are

remnants of bone

remodeling.

� There are also circumferential lamellae that extend around the

circumference of the shaft. There are inner circumferential

lamellae surrounding the endosteum and outer circumferential

lamellae just inside the periosteum.

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� Spider-shapedosteocytes occupy smallcavities known aslacunae at the junctionsof the lamellae. Hairlikecanals called canaliculiconnect the lacunae to

each other and to thecentral canal.

� Canaliculi allow theosteocytes to exchange

nutrients, wastes, andchemical signals to eachother via intercellular connections known asgap junctions.

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Here, we have a close up and a far away view of compact bone. You

should be able to identify haversian

canals, concentric lamellae,

interstitial lamellae, lacunae, and

canaliculi.

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Microscopic

Structure of Spongy

Bone� Appears poorly organized

compared to compact bone.

� Lacks osteons.

� Trabeculae align along

positions of stress andexhibit extensive cross-bracing.

� Trabeculae are a few celllayers thick and contain

irregularly arrangedlamellae and osteocytesinterconnected by canaliculi.

� N o haversian or Volkmann¶s canals are

necessary. Why?

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Bone Development

� Osteogenesis (a.k.a.ossification) is theprocess of bone tissueformation.

� In embryos this leads to

the formation of thebony skeleton.

� In children and youngadults, ossificationoccurs as part of bone

growth.� In adults, it occurs as

part of bone remodelingand bone repair.

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Formation of the Bony Skeleton

� Before week 8, the humanembryonic skeleton is made of fibrous membranes and hyalinecartilage.

� After week 8, bone tissue

begins to replace the fibrousmembranes and hyalinecartilage.± The development of bone from a

fibrous membrane is called

intramembranous ossification.Why?

± The replacement of hyalinecartilage with bone is known asendochondral ossification. Why?

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Intramembranous Ossification� Some bones of the skull (frontal, parietal, temporal, and occipital

bones), the facial bones, the clavicles, the pelvis, the scapulae, andpart of the mandible are formed by intramembranous ossification

� Prior to ossification, these structures exist as fibrous membranesmade of embryonic connective tissue known as mesenchyme.

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� Mesenchymal cells firstcluster together and startto secrete the organic

components of bonematrix which thenbecomes mineralizedthrough the crystallizationof calcium salts. Ascalcification occurs, the

mesenchymal cellsdifferentiate intoosteoblasts.

� The location in the tissuewhere ossification begins

is known as anossification center .

� Some osteoblasts aretrapped w/i bony pockets.These cells differentiateinto osteocytes.

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� The developing bone grows outward from the ossification center in small struts called spicules.

� Mesenchymal cell divisions provide additional osteoblasts.

� The osteoblasts require a reliable source of oxygen and nutrients.

Blood vessels trapped among the spicules meet these demandsand additional vessels branch into the area. These vessels willeventually become entrapped within the growing bone.

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� Initially, the intramembranous bone consists only of 

spongy bone. Subsequent remodeling around trapped

blood vessels can produce osteons typical of compact

bone.

� As the rate of growth slows, the connective tissue aroundthe bone becomes organized into the fibrous layer of the

periosteum. Osteoblasts close to the bone surface become

the inner cellular layer of the periosteum.

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Endochondral Ossification

� Begins with the formation of a hyaline cartilage model whichwill later be replaced by bone.

� Most bones in the body develop via this model.

� More complicated than intramembranous because the hyaline

cartilage must be broken down as ossification proceeds.� We¶ll follow limb bone development as an example.

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Endochondral Ossification ± Step 1

� Chondrocytes near the center 

of the shaft of the hyaline

cartilage model increase

greatly in size. As these cells

enlarge, their lacunae expand,and the matrix is reduced to a

series of thin struts. These

struts soon begin to calcify.

� The enlarged chondrocytes

are now deprived of nutrients

(diffusion cannot occur 

through calcified cartilage)

and they soon die and

disintegrate.

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Endochondral Ossification ± Step 2

� Blood vessels grow into the perichondrium surrounding the shaftof the cartilage. The cells of the inner layer of the

perichondrium in this region then differentiate into osteoblasts.

� The perichondrium is now a periosteum and the inner osteogenic

layer soon produces a thin layer of bone around the shaft of thecartilage. This bony collar provides support.

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Endochondral Ossification ± Step 3

� Blood supply to the periosteum, andcapillaries and fibroblasts migrate intothe heart of the cartilage, invading thespaces left by the disintegratingchondrocytes.

� The calcified cartilaginous matrixbreaks down; the fibroblastsdifferentiate into osteoblasts that replaceit with spongy bone.

� Bone development begins at this

primary center of ossification andspreads toward both ends of thecartilaginous model.

� While the diameter is small, the entirediaphysis is filled with spongy bone.

Notice the primary

ossification centers in the

thigh and forearm bones

of the above fetus.

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Endochondral Ossification ± Step 4

� The primary ossification center enlarges

proximally and distally, while osteoclasts break 

down the newly formed spongy bone and open upa medullary cavity in the center of the shaft.

� As the osteoblasts move towards the epiphyses,

the epiphyseal cartilage is growing as well. T hus,

even though the shaft is getting longer, theepiphyses have yet to be transformed into bone.

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Endochondral Ossification ± Step 5

� Around birth, most long boneshave a bony diaphysis surroundingremnants of spongy bone, awidening medullary cavity, and 2cartilaginous epiphyses.

� At this time, capillaries andosteoblasts will migrate into theepiphyses and create secondaryossification centers. The epiphysiswill be transformed into spongybone. However, a smallcartilaginous plate, known as theepiphyseal plate, will remain atthe juncture between the epiphysisand the diaphysis.

Articular

cartilageEpiphyseal plate

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Growth in Bone

Length

� Epiphyseal cartilage(close to the epiphysis)of the epiphyseal platedivides to create more

cartilage, while thediaphyseal cartilage(close to the diaphysis)of the epiphyseal plate istransformed into bone.

This increases the lengthof the shaft.

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�As a result osteoblasts begin

producing bone faster than the rateof epiphyseal cartilage expansion.

Thus the bone grows while the

epiphyseal plate gets narrower and

narrower and ultimately

disappears. A remnant(epiphyseal line) is visible on X-

rays ( do you see them in the

adjacent femur, tibia, and fibula?)

At puberty, growth in bone length

is increased dramatically by the

combined activities of growth

hormone, thyroid hormone, andthe sex hormones.

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Growth in Bone Thickness

� Osteoblasts beneath the periosteum secrete bone

matrix on the external surface of the bone. This

obviously makes the bone thicker.

� At the same time, osteoclasts on the endosteumbreak down bone and thus widen the medullary

cavity.

� This results in an increase in shaft diameter even

though the actual amount of bone in the shaft isrelatively unchanged.

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Fractures

� Despite its mineral strength,bone may crack or even break 

if subjected to extreme loads,

sudden impacts, or stresses

from unusual directions.

± The damage produced constitutes

a fracture.

� The proper healing of a

fracture depends on whether or 

not, the blood supply andcellular components of the

periosteum and endosteum

survive.

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Fracture

Repair

� Step 1:

A. Immediately after the fracture,extensivebleeding occurs.Over a period of 

several hours, alarge blood clot,or fracturehematoma,develops.

B. Bone cells at the

site becomedeprived of nutrients and die.The site becomesswollen, painful,and inflamed.

� Step 2:A. Granulation tissue is formed as the hematoma is

infiltrated by capillaries and macrophages, which begin

to clean up the debris.B. Some fibroblasts produce collagen fibers that span the

break , while others differentiate into chondroblasts andbegin secreting cartilage matrix.

C. Osteoblasts begin forming spongy bone.

D. This entire structure is known as a fibrocartilaginous

callus and it splints the broken bone.

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� Step 3:A. Bone trabeculae

increase in number and convert thefibrocartilaginous

callus into a bonycallus of spongybone. Typicallytakes about 6-8weeks for this tooccur.

Fracture

Repair

� Step 4:A. During the next several months, the bony callus is continually

remodeled.

B. Osteoclasts work to remove the temporary supportive structureswhile osteoblasts rebuild the compact bone and reconstruct thebone so it returns to its original shape/structure.

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Fracture Types

� Fractures are often classified according to the position of thebone ends after the break:

Open (compound) bone ends penetrate the skin.

Closed (simple) bone ends don¶t penetrate the skin.

Comminuted bone fragments into 3 or more pieces.Common in the elderly (brittle

bones).

Greenstick  bone breaks incompletely. One side bent,one side broken. Common in

children whose bone contains morecollagen and are less mineralized.

Spiral ragged break caused by excessive twistingforces. Sports injury/Injury of abuse.

Impacted one bone fragment is driven into the

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What kind of fracture is this?It¶s kind of tough to tell, but 

this is a _ _ _ _ _ _ fracture.

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Bone Remodeling

� Bone is adynamic tissue.

±  What does that mean?

� Wolff¶s lawholds that bonewill grow or remodel inresponse to theforces or 

demands placedon it. Examinethis with thebone on the left.

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Check out the

mechanism of 

remodeling on the right!

Why might you suspect

someone whose been a

powerlifter for 15 years to

have heavy, massive

bones, especially at the

point of muscle insertion?

Astronauts tend to

experience bone atrophyafter they¶re in space for 

an extended period of 

time. Why?

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Nutritional Effects on Bone

� Normal bone growth/maintenancecannot occur w/o sufficient dietaryintake of calcium and phosphatesalts.

� Calcium and phosphate are not

absorbed in the intestine unless thehormone calcitriol is present.Calcitriol synthesis is dependent onthe availability of the steroidcholecalciferol (a.k.a. Vitamin D)

which may be synthesized in the skinor obtained from the diet.

� Vitamins C, A, K, and B12 are allnecessary for bone growth as well.

Hormonal Effects

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Hormonal Effects

on Bone

� Growth hormone, producedby the pituitary gland, andthyroxine, produced by thethyroid gland, stimulate bonegrowth.

± GH stimulates protein synthesisand cell growth throughout thebody.

± Thyroxine stimulates cellmetabolism and increases therate of osteoblast activity.

± In proper balance, thesehormones maintain normalactivity of the epiphyseal plate(what would you consider normal activity?) until roughlythe time of puberty.

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Hormonal Effects on Bone

� At puberty, the rising levels of sex hormones (estrogens infemales and androgens in males) cause osteoblasts toproduce bone faster than the epiphyseal cartilage candivide. This causes the characteristic growth spurt as wellas the ultimate closure of the epiphyseal plate.

� Estrogens cause faster closure of the epiphyseal growthplate than do androgens.

� Estrogen also acts to stimulate osteoblast activity.

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Hormonal Effects on Bone

� Other hormones that affect bone growth includeinsulin and the glucocorticoids.

± Insulin stimulates bone formation

± Glucocorticoids inhibit osteoclast activity.� Parathyroid hormone and calcitonin are 2

hormones that antagonistically maintain blood[Ca2+] at homeostatic levels.

± Since the skeleton is the body¶s major calciumreservoir, the activity of these 2 hormones affects boneresorption and deposition.

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Calcitonin

� Released by the C cells of the thyroid gland in response to high

blood [Ca2+].

� Calcitonin acts to ³tone down´ blood calcium levels.

� Calcitonin causes decreased osteoclast activity which results indecreased break down of bone matrix and decreased calcium

being released into the blood.� Calcitonin also stimulates osteoblast activity which means

calcium will be taken from the blood and deposited as bonematrix.

Notice the thyroidfollicles on the

right. The arrow

indicates a C cell

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Calcitonin Negative Feedback Loop

Increased Blood [Ca2+] Increased calcitonin release

from thyroid C cells.

Increased osteoblast activity

Decreased osteoclast activity

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ParathyroidHormone

� PTH increases calcitriol synthesis which increases Ca2+

absorption in the small intestine.

� PTH decreases urinary Ca2+ excretion and increases urinaryphosphate excretion.

� Released by the cells of theparathyroid gland in response to lowblood [Ca2+].Causes blood [Ca2+] toincrease.

� PTH will bind to osteoblasts and this

will cause 2 things to occur:� The osteoblasts will decrease their activity

and they will release a chemical known asosteoclast-stimulating factor .

� Osteoclast-stimulating factor will increaseosteoclast activity.

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Increased PTH release

by parathyroid gland

Binds to osteoblast

causing decreased

osteoblast activity and

release of osteoclast-

stimulating factor 

OSF causes increased

osteoclast activity

Decreased bone

deposition and increased

bone resorption

Increased calcitriol

synthesis

Increased intestinal

Ca2+ absorption

Decreased Ca2+

excretion

Increased Blood [Ca2+]

Decreased Blood [Ca2+]

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Clinical Conditions

� Osteomalacia± Literally ³soft bones.´

± Includes many disorders in whichosteoid is produced butinadequately mineralized.

� Causes can include insufficientdietary calcium

� Insufficient vitamin D fortificationor insufficient exposure to sunlight.

� Rickets

± Children's form of osteomalacia± More detrimental due to the fact

that their bones are still growing.

± Signs include bowed legs, anddeformities of the pelvis, ribs, andskull.

What about the above x-ray is

indicative of rickets?

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Clinical Conditions

� Osteomyelitis± Osteo=bone +

myelo=marrow +

itis=inflammation.

± Inflammation of bone andbone marrow caused by

pus-forming bacteria that

enter the body via a

wound (e.g., compound

fracture) or migrate from a

nearby infection.

± Fatal before the advent of 

antibiotics.

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Clinical Conditions

� Osteoporosis± Group of diseases in which

bone resorption occurs at afaster rate than bone deposition.

± Bone mass drops and bonesbecome increasingly porous.

± Compression fractures of thevertebrae and fractures of thefemur are common.

± Often seen in postmenopausalwomen because theyexperience a rapid decline inestrogen secretion; estrogenstimulates osteoblast andinhibits osteoclast activity.

� Based on the above, whatpreventative measures mightyou suggest?

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Clinical Conditions

� Gigantism± Childhood hypersecretion

of growth hormone by thepituitary gland causesexcessive growth.

� Acromegaly± Adulthood hypersecretion

of GH causes overgrowth of bony areas still responsiveto GH such as the bones of the face, feet, and hands.

� Pituitary dwarfism± GH deficiency in children

resulting in extremely shortlong bones and maximumstature of 4 feet.