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
Fig. 4-11, Martini & Bartholomew;
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. 6-3, Martini & Bartholomew;
Fig. 6-4, Martini
Surrounds
bone organs
Between
osteonsSurrounds osteons
Perforating or
“Volkmann’s canal
20
Bone Tissues - 2
Fig. 6-3, Martini & Bartholomew;
Fig. 6-4, Martini
strengthens
osteon
Concentric
lamellae
lines
internal
surfaces of
bones
alternate
21
Structure
of a Long
Bone
Fig. 6-2, Martini & Bartholomew;
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. 6-2, Martini & Bartholomew;
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. 6-3, Martini & Bartholomew;
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
Fig. 6-6, Martini & Bartholomew;
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
Development of the Skeleton - 2
Epiphyseal plates shrinking
Articularcartilage
41
Development of the Skeleton - 3
•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
Specific Skeletal Changes with Age - 3
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
Specific Skeletal Changes with Age - 4
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.
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