Anatomy & Physiologyjacusers.johnabbott.qc.ca/~paul.anderson/8052012/805... · 2012. 1. 10. ·...

Anatomy & Physiology101-805

Unit 6

The Skeletal

System

Paul Anderson 2011

2

Claviclescapula

humerus

pelvis

femur

Skeletal System: Components

Martini &

Bartholomew fig

1-2b

cranium

costal (rib)cartilages

•Bones major organs of system, have allfunctions of system.

•Cartilages connect & protect bones atjoints, form smooth articular surfaces of

moveable bones.

•Ligaments connect bones at joints &stabilise joints.

•Joints (Articulations): regions where

bones meet: form fulcrum of levers.

Elbow jointKnee joint

Patellar

ligament

Meniscus cartilage patella

Moveable

fulcrum of

lever

ligament

3

Skeletal System: Major Functions:

1. Support of soft tissues.2. Body shape.3. Protection of vital organs

(brain by cranium, heart & lungs by rib cage, spinal cord by spine.4. Allows for adaptive (i.e. homeostatic) movements

- forms attachment sites for muscles- has moveable joints- forms levers with muscles: movement occurs when muscles pull on bones

5. Production of blood cells (Hemopoiesis)- in adult red bone marrow forms all red blood cells, platelets & mostwhite blood cells

6. Storage of minerals (Ca/P) in bone matrix & fat (in yellow marrow)- minerals harden bones for their normal functions- Bone deposition & resorption are controlled by hormones (e.g. PTH)- vit D required for absorption of Ca/P

Blood

Ca+2

PO4 -3

Ca/P stored asHydroxyapatite,Ca5(PO4)3OHin bone matrix

Diet

Vit D

Bone deposition

Bone resorption

4

Muscles, Bones & Joints form Levers

Tendon of musclepulls on bone

Joint (allows movement)

Movementof bone

Bone

Skeletal System: Tissues

Bones are organs consisting of several tissues.

• Bone (osseous tissue)• Cartilage• Fibrous connective tissue (in the surface layeror periosteum)

• Hemopoietic (blood forming) tissue in redmarrow)- hemopoietic (myeloid) tissue occurs in vertebrae,sternum, ribs, skull, scapula, pelvis & proximal epiphysesof femur, and humerus

• Adipose tissue (in yellow marrow)- source of energy: can form red marrow in emergencies.

Cartilage vs Bone Tissue in the Skeletal System

Cartilage and bone are distributed according to their properties.

•Resiliency is due to the organic matrix ground substance.•Strength is due to the organic matrix collagen fibers.•Hardness & rigidity are due to calcified inorganic matrix.

Bone•Properties of rigidity, hardness &strength.

•Calcified matrix- hard and rigid.

•Mature bone cells osteocytes.

•Vascular (vessels run in canals).

•Grows by appositional growth only,due to its calcified matrix.

•In development bone graduallyreplaces cartilage to form themajor tissue of all adult bones.

Cartilage•Properties of resiliency & strength.

•Non – calcified matrix -firm but notrigid.

•Mature cartilage cells chondrocytes.

•Non vascular so thin & slow to heal.

•Grows by appositional (surface) &interstitial (internal) growth.

•Forms most of embryonic skeleton.

•In adults found mainly at joints andin the upper respiratory tract.

Two Types of Growth Occur in Skeletal Tissues:

•Appositional Growth means growth at a skeletal surface.•Appositional Growth occurs by cell division of osteogenic (orchondrogenic) cells in the periosteum or endosteum of bone or in theperichondrium of cartilage.

•Interstitial Growth means internal growth by cell division &production of new matrix internally, expanding the tissue fromwithin.

•Interstitial growth occurs in cartilage but not in bone since itsmatrix is calcified (i.e. hardened).

Growth inSkeletalTissues

Appositional(surface)Growth

Interstitial(internal)Growth

In CartilageTissue only

At surface ofBone & Cartilage

Tissues

Appositional Growth occurs in Bone & Cartilage

Appositional Growth in Cartilage

Perichondrium(surface membraneof cartilage)

Fibrous layer:outer protectivecollagenous layer

Cellular layer: innerchondrogenic layerwith fibroblasts

Newchondrocytes

Collagenfibers

fibroblastsform

old

matrix

new matrix

Newmatrix

Martini, Figure 4-13

new matrix

• Interstitial growth means internal growth by celldivision and production of new matrix internally, thusexpanding the tissue from within.

• Interstitial growth occurs in cartilage but not inbone since its matrix is calcified (i.e. hardened).

Interstitial Growth in Cartilage

old

matrixNon - calcified

matrix

• Cartilage has a non -calcified matrix so can grow by Interstitial Growth.• Bone has a calcified matrix so can only grow by Appositional Growth.

Martini, Figure 4-13

Cartilage Tissues

in the Skeletal

System

Marieb, 5th ed., Figure 7-1

Two types ofcartilage occur inthe skeletal system.

•Hyaline Cartilage

•Fibrous Cartilage

11

Types of Cartilage : Hyaline Cartilage

Hyaline Cartilage•Matrix appears smooth buthas many thin collagen fibers.

•Provides firmness, resiliency,strength and a smoothsurface for joints.

•Found in articular surfaces ofbones, embryonic skeleton,costal cartilages, upperrespiratory tract.

•There arethree types ofcartilage.

•Only fibrousand hyalinecartilage occurin the skeletalsystem.

Martini & Bartholomew, Figure 4-10(a)

(surface

membrane)

articular

cartilage

12

Fibrous Cartilage

- Matrix has many thick parallel collagen fibers- Provides extreme strength- Fibrous cartilage is found in skeletal system•pubic symphyses•intervertebral disks•menisci cartilages in knee joint

Martini & Bartholomew, Figure 4-10(c)

13

Bone Tissue

In Bone tissue the extracellular matrix secretedby bone cells consists of an organic component(osteoid) and a hardened inorganic component.

•The organic component (osteoid) consists ofcollagen fibers in a firm glycoprotein groundsubstance.

•Collagen provides strength to withstandtensile forces (due to stretching, bending andtwisting) without breaking.

•The inorganic component consists mainly ofhydroxyapatite, Ca5(PO4)3OH, a hard mineral

•The inorganic component provides hardnessand rigidity to withstand compression forceswithout bending.

14

Bone Tissue: Components & Properties

Bone Tissue

ExtracellularMatrix

Bone Cells(Osteocytes)

Inorganic Matrix(hydroxyapatite)

Organic Matrix(Osteoid)

GroundSubstance(glycoprotein)

CollagenFibers

Strength Hardness & rigidity

Properties of bone tissue

15

Bone Cells

•Mature bone cells (osteocytes) are connected to each other and to thenearest blood supply via many cytoplasmic processes which run throughtiny canals (canaliculi) in the extracellular matrix.

•Unlike cartilage, bone matrix is impermeable so does not allow diffusion,except via canaliculi which are therefore “lifelines” for bone cells.

Osteocytesnon - dividing mature bone cells

O2

nutrients

CO2

wastes

Lacuna: space

surrounding

osteocyte

Extracellularcalcified matrix

Cytoplasmic

processes of

osteocytes in

canaliculi

Canaliculi: allow diffusion

between osteocytes

& blood vessels

Nucleus of

osteocyte

16

Compact Bone Tissue

Fig. 6-3, Martini & Bartholomew;

Two types of bone tissue occur, Compact Bone and Spongy Bone.Compact Bone has

• No marrow spaces• Parallel osteons resist forces primarily in one direction• Has no trabeculae• Occurs externally on bones

External

membrane

(periosteum)

of bone organ

HaversianSystem(osteon)

Blood vessels

in Central

Canal

Concentric

layers of

bone tissue

(lamellae)

Osteocyte

in lacuna

17

Compact Bone Tissue: Haversian Systems

•Haversian Systems (osteons) consist of concentriclayers (lamellae) of bone tissue surrounding acentral (Haversian) canal containing blood vessels.

•Radiating canaliculi connect the osteocytes with thecentral canal.

calcified


18

Spongy Bone Tissue

•Contains many spaces with marrow•Spongy bone reduces the weight of bones and (where it contains redmarrow) is a source of blood cells.

•Has lamellae but no osteons•Consists of irregular bony bars or struts (trabeculae) aligned towithstand forces from many directions.

•Occurs internally in bones

Fig. 6-4, Martini

Lamellae but

no osteons

Trabeculae

Spaces

containing

marrow

Osteocyte in

lacuna

Internal

surface

(endosteum)

Opening of

canaliculi

19

Bone Tissues - 1


Fig. 6-4, Martini

Surrounds

bone organs

Between

osteonsSurrounds osteons

Perforating or

“Volkmann’s canal

20

Bone Tissues - 2


Fig. 6-4, Martini

strengthens

osteon

Concentric

lamellae

lines

internal

surfaces of

bones

alternate

21

Structure

of a Long

Bone


Fig. 6-2, 6-11, Martini

22

Structure of a Long Bone - 2

Long bones consist of a diaphysis (or shaft) the walls of which are mostly ofcompact bone. The shaft of a long bone withstands forces mainly parallel tothe bone. The diaphysis contains interstitial and circumferential lamellae aswell as concentric lamellae.

• Perforating or Volkmann’s canals connect the Haversian canals to themain blood supply.

• The diaphysis is hollow with a marrow cavity containing fatty yellowmarrow.

• An expanded end at each end of the diaphysis called the epiphysis. Thisforms joints with other bones and contains spongy bone so is able towithstand forces from many directions. Yellow or red marrow occurs inthe spaces between trabeculae.

• In adults red marrow occurs in the proximal epiphyses of the femur andhumerus.

• The epiphysis is covered by a thin cortex of compact bone and, at thejoint surfaces by an articular cartilage (hyaline cartilage).

23

Structure of a Long

Bone -3

•The metaphysis is the junction between diaphysis and epiphysis.

•During growth years a layer of hyaline cartilage occurs on theepiphyseal side of the metaphysis called the epiphyseal plate.

•This is responsible for longitudinal growth (lengthening of long bones)until maturity by interstitial growth of cartilage and appositionalgrowth of bone.

•At maturity the epiphyseal plate is completely ossified and is nowcalled the epiphyseal line

epiphysis

diaphysis

metaphysis

Epiphyseal plate

(immature bone) or

epiphyseal line

(mature ossified bone)


Fig. 6-11, Martini

24

Bone Tissues: Periosteum

•The external surfaces of bones (except at joint surfaces) arecovered by the periosteum.

•This has two layers, an outer collagenous fibrous layer and an innercellular layer.- The outer fibrous layer of the periosteum protects bones and binds tendons and ligaments to bones (via perforating or Sharpey’sfibers).

- The inner cellular layer of the periosteum is osteogenic, i.e. functions in appositional growth, remodeling and repair of bones

Periosteum

Fibrouslayer

Cellularlayer

Forms new boneby Appositional

Growth

Anchors bones toligaments & tendons

Protectsbones

•Growth

•Remodeling

•Fracture repair

25

The Periosteum


Fig. 6-6, Martini

contains•stem cells•osteoblasts•osteoclasts

anchor

periosteum to

bone tissue

26

The Endosteum

•Internally the cavitiesof bones are lined witha thin cellularEndosteum whichfunctions like thecellular layer of theperiosteum.

•It therefore contains - stem cells(osteoprogenitor cells) - osteoblasts, the

source of new bonetissue

- osteoclasts whichdestroy bone tissue.

Fig. 6-8, Martini

27

Fig. 6-3, Martini

Types of

Bone Cells

Osteocytescannot

normally divideOsteoblastsraise pH to form

inorganic matrix

Osteoclastslower pH to

dissolve

inorganic matrix

Endosteum

PeriosteumCompact bone

BoneDeposition

BoneResorption

formsforms

28

Functions of Bone Cells

mobile cells

29

Appositional Growth of Bone Tissue

•Osteogenic (bone – forming) cells in the periosteum or endosteumare called osteoblasts.•Osteoblasts exchange chemicals via cytoplasmic processesconnecting the cells,,•Osteoblasts secrete the organic matrix first and then create thealkaline environment causing precipitation of the inorganic matrixof hydroxyapatite around themselves.•The osteoblasts are now mature non- dividing cells calledosteocytes and are imprisoned within their lacunae in the calcifiedmatrix and connected to their blood supply via canaliculi.

organic matrixsecretes

Raises pH

to form

calcified

30

Appositional Growth of Long Bone Diaphysis


Increased diameter of marrow cavity dueto resorption by osteoclasts in endosteum.

Increased bone circumference due toappositional growth by osteoblasts in periosteum.

31

Ossification

Bone Formation occurs by Ossification and byAppositional Growth, processes that occur

•during the growth of the skeleton to maturity

•during remodelling of bone throughout life

•in the repair of bones.

•Ossification is the replacement of cartilage orfibrous connective tissues with bone tissue.•Ossification occurs in development of theskeleton to maturity & in fracture repair.

32

Development of Skeleton

In the embryo mostbones are first formed ashyaline cartilage bone“models” which aregradually replaced bybone (osseous) tissue atmaturity in a process

called EndochondralOssification.

A few bones however, areformed instead as fibrousmembrane models (mostskull bones and theclavicle) in a differentprocess called

IntramembranousOssification.

Fig. 6-4, Martini &

Bartholomew;

Skeleton

of 16 week

old fetus

33

Intramembranous Ossification

• In both types of ossification, centers of bone forming tissue (called

ossification centers) are formed within the model in a vascularised

environment.

•Osteoblasts first secrete the organic matrix followed by

calcification.

•Ossification then proceeds by appositional growth away from the

ossification center.

•In Intramembranous Ossificationembryonic mesenchyme cellsdifferentiate to become osteoblasts(bone forming cells) within a fibrousmembrane under the skin.

•Osteoblasts then form spongy boneto which is added compact bone,externally, beneath the newlyformed periosteum.

Fig. 6-2, Martini

Periosteum

34

Endochondral Ossification: Summary

•For most bones embryonic mesenchyme cells firstdifferentiate to become chondroblasts surrounded bya perichondrium.

•Hyaline cartilage is formed which grows byinterstitial and appositional growth forming a cartilagebone “model”.

•In Endochondral Ossification calcification of thehyaline cartilage bone model occurs which causes deathof most chondrocytes.

•The bone model is then invaded by vascularised tissuewhich form Ossification Centers within the model.

•Cartilage is replaced by spongy bone tissue asossification spreads by appositional growth away fromthe ossification centers.

35

Endochondral Ossification: Initial Steps

•In the center of the diaphysis the cartilage model calcifies andchondrocytes die.

•Increased vascularisation of the perichondrium forms a periosteumwhich forms an external collar of compact bone around the diaphysisof the cartilage model.

•This collar spreads along the diaphysis.

Blood

vessels(Bone collar)

1.Death of

chondrocytesin cartilage

model

2.Bone CollarFormation

Fig. 6-5, Martini &

Bartholomew;

36

Endochondral Ossification: Steps

•Vascularised bone - forming tissue from the periosteum (a periostealbud) invades the center of the diaphysis forming a PrimaryOssification Center.

•Osteoclasts digest away the calcified cartilage while osteoblastsform new spongy bone around the remnants of the cartilage withinthe diaphysis.

•Calcification of cartilage continues within the diaphysis andossification follows this, spreading along the diaphysis.

3.Formation of

PrimaryOssificationCenter incenter ofdiaphysis

4.Ossificationof diaphysis

Spongy

bone

Periosteal

bud

Fig. 6-5, Martini &

Bartholomew;

Spongy

bone

37

Endochondral Ossification: Steps

•Osteoclasts erode the newly formedspongy bone to create a marrow cavityin the center of the diaphysis whichspreads along the diaphysis.

•Calcification of cartilage then occursin each epiphysis at or after birth,followed by invasion by a periostealbud, forming a Secondary OssificationCenter in each epiphysis.

5.Formation of SecondaryOssification Centers in

EpiphysesMarrow

cavity

Secondary

ossification

center

Fig. 6-5, Martini &

Bartholomew;

38

Endochondral Ossification:

Final Steps

•Ossification forms spongybone in each epiphysisbetween a layer of epiphysealcartilage (the epiphysealplate) and articular cartilage.

•Epiphyseal plate cartilagecontinue to grow byinterstitial growth as fast asit replaced by bone tissue onthe diaphyseal side of theplate.

•Therefore the long bonecontinues to grow in lengthuntil maturity when theepiphyseal plate iscompletely ossified (“closureof epiphyses”) forming anepiphyseal line.

•After this stage no furtherlengthening of bones can occurbut bones continue to increasein thickness.

6.Ossification(closure) of

Epiphyseal Platesby end of puberty

Fig. 6-8, Martini

39

Development of the Skeleton - 1

Intramembranousossification

forming dermalbone

Hyalinecartilage

bone modelsare sites forendochondralossification

Secondary ossificationCenters in epiphyses

40


Epiphyseal plates shrinking

Articularcartilage

41


•Epiphysealplate almostcompletelyossified.

•Eventuallycloses tobecomeepiphysealline.

•No morelengtheningof bones canthen occur.

Articularcartilageremainsthroughoutlife

42

Bone Remodeling

Bone remodeling refers to the changes in shape andthickness of bones throughout life due to twoantagonistic processes, bone deposition and boneresorption at the periosteum and endosteum.

Bone deposition and resorption occur• in response to the need for a constant blood calcium

level• in response to mechanical stresses• for repair of fractures and• during bone growth to maturity.

43

Bone Deposition & Bone Resorption

•Bone deposition means appositional growth of newbone tissue by the activity of osteoblasts.

•Osteoblasts first secrete the organic matrix then theinorganic matrix.

•Formation of inorganic matrix is catalysed by locallyincreased concentrations of Ca+2 and PO4

-3 and by thecreation of an alkaline environment for enzymessecreted by the osteoblasts.

•Bone resorption refers to the digestion of bonematrix by enzymes and acids secreted by osteoclastswhich also phagocytose the cellular products.

44

Bone Tissue Responds to Mechanical Stress

Wolff’s law states that bones respond to the levelof mechanical stress by structural changes (e.g.trabeculae of spongy bones form along lines which willresist the most stress).

• The fetal skeleton is relatively featureless.

• Athletes show increased bone mass.

• Astronauts & bedridden patients show decreased bonemass (Atrophy of Disuse).

•Bone remodeling occurs in response to the mechanicalstresses placed upon bones.

•Bone: Use it or lose it!

Bone is a living tissue and is constantly responding to theneeds of the body to resist mechanical stress (Wolf’s law).

45

Bone Tissue Responds to Body’s Needs for Ca/P

Bone is a living tissue and is constantly respondingto the needs of the body for adequate blood levelsof Ca+2 and PO4 -3.

•PTH raises blood calcium levels sois hypercalcemic

•Calcitonin lowers blood [calcium] sois hypocalcemic

Two antagonistic hormones (Parathyryroid Hormone,PTH and Calcitonin) respond to the needs for adequateblood calcium and therefore affect bone remodeling.

46

How PTH & Calcitonin Control Blood Ca levels

!Blood[Ca+2]

Parathyroidgland

ParathyroidHormone(PTH)

osteoclasts

! Bonedeposition

" Blood[Ca+2]

Thyroidgland

Calcitonin

! BoneResorption

!Blood Ca " Blood Ca

++ -

-ve

feedback

osteoclasts

-vefeedback

stimulus stimulus

47

PTH Causes Bone Resorption & Increases Blood Ca

BoneResorption

!Blood Ca

Stimulus for PTH" Blood [Ca]

•PTH is released when blood calcium levels fall.•PTH stimulates osteoclasts so increasing Bone Resorption.

Ca+2

Ca+2 returnedto blood

Ca+2

Ca+2Ca+2

PTH

PTH

Bone

IntestineKidney

Ca+2 removedfrom bone

Ca+2 absorbed

into to blood

PTH withcalcitriol

48

Calcitonin Causes Bone Deposition & Lowers Blood Ca

BoneDeposition

" Blood [Ca]

Stimulus forCalcitonin!Blood [Ca]

•Calcitonin is released when blood calcium levels rise.•Calcitonin inhibits osteoclasts allowing osteoblasts toincrease Bone Deposition.

Ca+2

Ca+2 lostin urine

Ca+2

Ca+2

Ca+2 added

to bone

Ca+2 excreted

Kidney

Bone

calcitonin

calcitonin

49

Thyroid glandsecretes

calcitonin

Increased excretionof calciumin kidneys

Calcium deposition inbone (inhibitionof osteoclasts)

Blood calciumlevels decline

HOMEOSTASISDISTURBED

Rising calciumlevels in blood

HOMEOSTASISRESTORED

HOMEOSTASISNormal calcium

levels(8.5-11 mg/dl) HOMEOSTASIS

RESTORED

HOMEOSTASISDISTURBED

Falling calciumlevels in blood Release of stored

calcium from bone(stimulation of

osteoclasts, inhibitionof osteoblasts)

Enhancedreabsorption

of calcium in kidneys

Stimulation ofcalcitriol production

at kidneys;enhanced Ca2+, PO4

3-

absorption bydigestive tract

Parathyroidglands secrete

parathyroidhormone (PTH)

Blood calciumlevels

increase

Martini & Bartholomew

Figure 10-10

Homeostatic Control of Blood Ca by Calcitonin & PTH

50

Factors Affecting Growth of the Skeleton

Extrinsic Growth Factors include•vitamin D (for Ca/P absorption & inorganic matrix formation)

•sunlight (for synthesis of vitamin D)•vitamin C (for collagen synthesis)•vitamin A (for osteoblast activity & normal bone growth in children)

•vitamins K & B12 (for protein synthesis)•dietary protein (for synthesis of organic matrix)•dietary calcium and phosphorus (for inorganic matrixformation)•carbohydrate (for energy.

Intrinsic Growth Factors include Genes, GrowthHormone (GH), Thyroid Hormones & Sex Hormones.

Growth of the skeleton requires Extrinsic Factorsand Intrinsic Factors.

51

Factors Affecting Growth of the Skeleton - 2

EXTRINSIC GROWTH

FACTORS

VITAMINS

MINERALS

DIETARY PROTEIN

DIETARY

CARBOHYDRATE

INTRINSIC

GROWTH FACTORS

HORMONES

GENES

SUNLIGHT

CDA K B12

Ca PMg, Mn, F, I, Fe

Amino

acids

energy

•Calcitriol •(from vit D)

•Growth Hormone

•Estrogens

•Calcitonin

•Thyroxine

•Androgens

•PTH

collagen

•Vit C promotes formation of collagen & organic matrix.•Vit D promotes Ca/P absorption & formation of inorganic matrix.

vit C

I

Formation & Functions of Vitamin D

Integumentary System

Martini & Bartholomew

fig 1-2a

sunlight

diet

Vit D precursor

(vit D3)

• Vitamin D is synthesed from cholesterol inthe skin in the presence of sunlight.

• Vitamin D promotes Ca and P absorptionfrom the diet.

• Vit D is converted by the kidneys into thehormone calcitriol which targets the smallintestine, increasing Ca/P absorption.

Cholesterol in

skin

Liver

stores vit D3Kidney

activates vit D3 to hormone

calcitriol (activated vit D)

Small

Intestine

Calcitriol

via blood

Increased

absorption

of Ca/P

via blood

via blood

Bones &

teeth

via blood

53

Rickets: a Childhood Bone Disorder due to

Calcium or Vitamin D Deficiency

2 years later,with calcium & vit Dsupplements

Softening of bonescauses bowing of legs &other bone deformities

Lack of vit Dcauses Rickets

• inadequateabsorption of Ca

• Hypocalcemia• Loss of inorganic

bone matrix• Softening of

bones.• Inadequate

ossification ofepiphyses whichbecomeenlarged.

54

Scurvy: a Connective Tissue Disorder From

Deficiency of Vitamin C

Deficiency of Vitamin C causes Scurvy• Inadequate synthesis of collagen.• With less collagen in organic matrix

of bone, bones lose mass & strength.• Bones become thin & fragile & break

more easily.

Inadequate collagencauses loose teeth &bleeding gums,

Inadequate collagencauses bruising &bleeding under the skin

55

Effect of Growth Hormone on the Skeleton

•Growth hormone (GH) causesprotein synthesis and celldivision of osteogenic cellsthroughout the growing years.

•Growth Hormone causes thejuvenile growth spurt andgeneral growth of the skeletonto maturity .

•Pituitary Dwarf has shortstature with normal skeletalproportions.

Hypopituitary Dwarf

•"Height

•Normal proportions

56

Effect of Thyroid Hormone on the Skeleton

•Thyroid hormone (Thyroxine)causes energy release forbone growth and controlschanges in skeletalproportions as bones grow.

•Thyroid hormone (thyroxine)works synergistically with GHto cause skeletal growth andcontrols changes in skeletalproportions.

•Hypothyroid Dwarf has shortstature and infantile skeletalproportions.

Hypothyroid Dwarf

•"Height

•Infantile proportions

57

Effect of Sex Hormones

on the Skeleton

•Sex Hormones(Androgens & Estrogens)cause

•Growth spurt of puberty.•Ossification ("closure")of the epiphyseal platesat the end of puberty

•Secondary Sexualskeletal changes

•Bone Depositionthroughout life

(preventing osteoporosis).

Bones

porous &

brittle

Normal spongybone

Martini fig 6-17

Bone withOsteoporosis

58

Summary of Effects of Hormones on Bones

GH has indirect action on bones by acting

as a trophic hormone for the liver

T4

gonadotropin

•GH - Juvenile growth spurt

•T4 - Normal Skeletal proportions

- energy for growth

•Sex hormones - adolescent growth spurt

- closure of epiphyses

liverhormone from liver

59

Changes in the Human Skeleton with Age

• Bone mass is not constant but increases and decreasesduring life due to two processes, bone deposition andbone resorption.

• Hormones help control these skeletal changes (alongwith diet and normal bone use).

•During growth years (0 - 20} the rate of deposition exceedsthe rate of resorption and there is a net increase in bone mass.

•During adulthood (ages 20 - 35 in females; 20 - 60 in males) therate of deposition equals the rate of resorption and bone massis fairly constant.

•During later years (35+ in females; 60 +in males) the rate ofdeposition is less than the rate of absorption and there is anet decrease in bone mass.

60

Changes in the Human Skeleton with Age - 2

growth years

(0 - 20yrs}

deposition >

resorption

Juvenile

growth spurt

Adolescent

growth spurt

•GH

•Thyroxine

Sex

Hormones

androgens

estrogens

Growth

hormone

Thyroxine

•Relative importance ofhormones at various ages•All continue to besecreted throughout life

Closure of

epiphyses

Middle years: deposition = resorption

Old age:

deposition < resorption

"Sex hormones

"Bone mass (osteopenia)

osteoporosis

Bone mass

-25%

-30%menopause

70 //

61

Specific Skeletal Changes with Age

Changes in Body Proportions•skull becomes proportionately smaller (rest of body grows faster)•face becomes proportionately larger (compared to cranium)•cranium becomes proportionately smaller (compared to face)•legs become proportionately longer•trunk becomes proportionately smaller•female pelvis widens (during puberty)

•thorax changes shape (from round to elliptical)

Face 1 1

Skull 4 2

Marieb fig 7-34

62

Specific Skeletal Changes with Age - 2

Ossification and Closure of Epiphyseal Plates (by 18 in females; 21 in males) due to sex hormones.

Martini fig 6-10

Epiphyseal plates of

growing long bones

Epiphyseal lines of fully

ossified long bones

63


Appearance of Secondary Spinal Curvatures.•Cervical curvature by 3 months as infant lifts head up.•Lumbar curvature by 1 year as child stands upright.

Secondary

Spinal

Curvatures

cervical

lumbar

Adult

spinePrimary Spinal

Curvatures

Primary

Spinal

Curvatures

1 - 3 years

64


Cranium ofnewborn Infant

Martini fig 7-15

Cranium ofadult

Martini fig 7-3b

•Closure of Fontanels of Skull and formation of Sutures.- Fontanels are fibrous connections between cranial bones allowingcranial distortion during birth: fontanels disappear by age 4.

•Sutures start to form when brain stops growing at age 5.•Sutures fuse in old age.

65

Repair of Bone

Fractures - Early

Stages

1. Breakage ofblood vesselscause death ofBone Tissue &Formation ofFractureHematoma (< 48h)

2. Formation ofInternal &External Callusfrom Cells ofPeriosteum &Endosteum(48h to 3-4weeks)

Callus: a bridgeof spongy bone &fibrocartilagebetween severedbone segments

Fibro

Martini &

Bartholomew

fig 6-7

66

Repair of Bone

Fractures -

Later Stages

3. Fusion of Calluses& Ossification ofCartilage(3/4 weeks - 2/3months): cast can beremoved

4. Remodeling of Callusesby osteoclasts respondingto stresses on bones (by3 months upperextremity- 6 monthslower extremity).

New spongy bone in center of diaphysis resorbed by osteoclastsleaving marrow cavity - similar to ossification process during growth.

Anatomy & Physiologyjacusers.johnabbott.qc.ca/~paul.anderson/8052012/805... · 2012. 1. 10. ·...

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Transcript of Anatomy & Physiologyjacusers.johnabbott.qc.ca/~paul.anderson/8052012/805... · 2012. 1. 10. ·...