101-805 unit 6 the skeletal system - john abbott...

Anatomy & Physiology 101-805

Unit 6 The Skeletal

System

Paul Anderson 2012

2

Clavicle scapula

humerus

pelvis

femur

Skeletal System: Components

Martini & Bartholomew fig 1-2b

cranium

costal (rib) cartilages

• Bones major organs of system, have all functions of system.

• Cartilages connect & protect bones at joints, 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 joint Knee 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 (affects bone shape, bone markings) - 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 & most

white 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 as Hydroxyapatite, Ca5(PO4)3OH in bone matrix

Diet Vit D

Bone deposition

Bone resorption

Calcitonin

PTH

4

Muscles, Bones & Joints form Levers

The skeleto - muscular system is a system of levers (devices for performing work). A Lever is a rigid bar (in the body, a bone) that turns about an axis of rotation or a fulcrum (in the body, a joint).

•  The Power point (P) of the lever is the insertion point of a muscle.

•  The Fulcrum (F) of the lever is the moveable joint at which movement occur.

•  The Resistance (R) is the weight of the part being moved.

P

R

F Power point (P), where tendon of muscle pulls on bone

Resistance (R), Weight of body part moved

Fulcrum (F), Joint that allows movement

bone

Tissues in the Skeletal System

Bones are organs consisting of several tissues. • Bone (osseous tissue) • Cartilage • Fibrous connective tissue: in the surface layer of bones (periosteum), cartilages (perichondrium) & in ligaments.

• Hemopoietic (blood forming) tissue in red marrow)

- hemopoietic (myeloid) tissue occurs in vertebrae, sternum, ribs, skull, scapula, pelvis & proximal epiphyses of 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 gradually replaces cartilage to form the major tissue of all adult bones.

Cartilage • Properties of resiliency & strength. • Non – calcified matrix -firm but not rigid.

• 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 and in 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 (or chondrogenic) cells in the periosteum or endosteum of bone or in the perichondrium of cartilage.

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

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

Growth in Skeletal Tissues

Appositional (surface) Growth

Interstitial (internal)

Growth In Cartilage Tissue only

At surface of Bone & Cartilage

Tissues

Appositional Growth occurs in Bone & Cartilage

Appositional Growth in Cartilage

Perichondrium (surface membrane of cartilage)

Fibrous layer: outer protective collagenous layer

Cellular layer: inner chondrogenic layer with fibroblasts

New chondrocytes

Collagen fibers

fibroblasts form

old matrix

new matrix

New matrix

new matrix

Martini, 8th ed. Figure 4-13

• Interstitial growth means internal growth by cell division and production of new matrix internally, thus expanding the tissue from within.

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

Interstitial Growth in Cartilage

old matrix

Non - 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.


Cartilage Tissues in the Skeletal

System

Marieb, 5th ed., Figure 7-1

Two types of cartilage occur in the skeletal system.

• Hyaline Cartilage

• Fibrous Cartilage

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Types of Cartilage : Hyaline Cartilage

Hyaline Cartilage • Matrix appears smooth but has many thin collagen fibers.

• Provides firmness, resiliency, strength and a smooth surface for joints.

• Found in articular surfaces of bones, embryonic skeleton, costal cartilages, upper respiratory tract.

• There are three types of cartilage.

• Only fibrous and hyaline cartilage occur in the skeletal system.

Martini & Bartholomew, Figure 4-10(a)

(surface membrane)

articular cartilage


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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)

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

• The organic component (osteoid) consists of collagen fibers in a firm glycoprotein ground substance.

• Collagen provides strength to withstand tensile forces (due to stretching, bending and twisting) without breaking.

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

• The inorganic component provides hardness and rigidity to withstand compression forces without bending.

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Bone Tissue: Components & Properties

Bone Tissue

Extracellular Matrix

Bone Cells (Osteocytes)

Inorganic Matrix (hydroxyapatite)

Organic Matrix (Osteoid)

Ground Substance (glycoprotein)

Collagen Fibers

Strength Hardness & rigidity Properties of bone tissue

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Bone Cells • Mature bone cells (osteocytes) are connected to each other and to the nearest blood supply via many cytoplasmic processes which run through tiny 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.

Osteocyte non - dividing mature bone cell

O2 nutrients

CO2 wastes

Lacuna: space surrounding osteocyte

Extracellular calcified matrix

Cytoplasmic processes of osteocytes in

canaliculi

Canaliculi: allow diffusion

between osteocytes & blood vessels

Nucleus of osteocyte

From Martini, 8th ed. Figure 6-3

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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 •  No trabeculae •  Occurs externally on bones

External membrane (periosteum) of bone organ

Haversian System (osteon)

Blood vessels in Central Canal

Concentric layers of bone tissue (lamellae)

Osteocyte in lacuna

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Compact Bone Tissue: Haversian Systems

• Haversian Systems (osteons) consist of concentric layers (lamellae) of bone tissue surrounding a central (Haversian) canal containing blood vessels.

• Radiating canaliculi connect the osteocytes with the central canal.

calcified


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

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

• Occurs internally in bones

Lamellae but no osteons

Trabeculae

Spaces containing marrow

Osteocyte in lacuna

Internal surface (endosteum)

Opening of canaliculi


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Bone Tissues - 1

Fig. 6-3, Martini & Bartholomew; Fig. 6-5, Martini, 8th ed.

Surrounds bone organs

Between osteons

Surrounds osteons

Perforating or “Volkmann’s canal

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Bone Tissues - 2


strengthens osteon

Concentric lamellae

lines internal surfaces of bones

alternate

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Structure of a Long

Bone


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Structure of a Long Bone - 2

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

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

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

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

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

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

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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 the epiphyseal 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 appositional growth of bone.

• At maturity the epiphyseal plate is completely ossified and is now called 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

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Bone Tissues: Periosteum

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

• This has two layers, an outer collagenous fibrous layer and an inner cellular layer.

- The outer fibrous layer of the periosteum protects bones and binds tendons and ligaments to bones (via perforating or Sharpey’s fibers).

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

Periosteum

Fibrous layer

Cellular layer

Forms new bone by Appositional

Growth

Anchors bones to ligaments & tendons

Protects bones

• Growth • Remodeling • Fracture repair

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The Periosteum

Fig. 6-3, Martini & Bartholomew; Fig. 6-6, Martini 8th ed.

contains • stem cells • osteoblasts • osteoclasts

anchor periosteum to

bone tissue

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The Endosteum

• Internally the cavities of bones are lined with a thin cellular Endosteum which functions like the cellular layer of the periosteum.

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

source of new bone tissue

- osteoclasts which destroy bone tissue.

Fig. 6-8, Martini

Martini, 8th ed. Figure 6-8 Osteoid

organic bone matrix is first to form.

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Fig. 6-3, Martini, 8th ed.

Types of Bone Cells

Osteocytes cannot

normally divide Osteoblasts raise pH to form inorganic matrix

Osteoclasts lower pH to

dissolve inorganic matrix

Endosteum

Periosteum Compact bone

Bone Deposition

Bone Resorption

forms forms

Osteocyte Osteoblast Osteoprogenitor cell Osteoclast

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Functions of Bone Cells

• Osteoclasts are multinucleated cells derived from hemopoietic stem cells in bone marrow.

• Osteoclasts are mobile cells that move to sites of injury or resorption.

• Osteoclast activity is increased by PTH which raises blood [Ca+2].

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Appositional Growth of Bone Tissue • Osteogenic (bone – forming) cells in the periosteum or endosteum are called osteoblasts. • Osteoblasts exchange chemicals via cytoplasmic processes connecting the cells. • Osteoblasts secrete the organic matrix first and then create the alkaline environment causing precipitation of the inorganic matrix of hydroxyapatite around themselves. • The osteoblasts are now mature non- dividing cells called osteocytes and are imprisoned within their lacunae in the calcified matrix and connected to their blood supply via canaliculi.

organic matrix secretes

Raises pH to form

calcified


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Appositional Growth of Long Bone Diaphysis


Increased diameter of marrow cavity due to resorption by osteoclasts in endosteum.

Increased bone circumference due to appositional growth by osteoblasts in periosteum.

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Ossification

Bone Formation occurs by Ossification and by Appositional 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 or fibrous connective tissues with bone tissue. • Ossification occurs in development of the skeleton to maturity & in fracture repair.

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Development of Skeleton

In the embryo most bones are first formed as hyaline cartilage bone “models” which are gradually replaced by bone (osseous) tissue at maturity in a process called Endochondral Ossification.

A few bones however, are formed instead as fibrous membrane models (most skull bones and the clavicle) in a different process called Intramembranous Ossification.


Skeleton of 16 week old fetus

Intramembranous bones

Endochondral bones

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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 Ossification embryonic connective tissue (mesenchyme) cells differentiate to become osteoblasts (bone forming cells) within a fibrous membrane under the skin.

• Osteoblasts then form spongy bone to which is added compact bone, externally, beneath the newly formed periosteum.

• Bones formed in this way are called “Dermal bones” & include the flat bones of the skull, the mandible & clavicle.

Fig. 6-2, Martini, 8th ed.

Periosteum

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Endochondral Ossification: Summary

• For most bones embryonic mesenchyme cells first differentiate to become chondroblasts surrounded by a perichondrium.

• Hyaline cartilage is formed which grows by interstitial and appositional growth forming a cartilage bone “model”.

• In Endochondral Ossification calcification of the hyaline cartilage bone model occurs which causes death of most chondrocytes.

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

• Cartilage is replaced by spongy bone tissue as ossification spreads by appositional growth away from the ossification centers.

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Endochondral Ossification: Initial Steps

• In the center of the diaphysis the cartilage model calcifies and chondrocytes die.

• Increased vascularisation of the perichondrium forms a periosteum which forms an external collar of compact bone around the diaphysis of the cartilage model.

• This collar spreads along the diaphysis.

Blood vessels (Bone collar)

1. Death of

chondrocytes in cartilage

model

2. Bone Collar Formation


36

Endochondral Ossification: Steps

• Vascularised bone - forming tissue from the periosteum (a periosteal bud) invades the center of the diaphysis forming a Primary Ossification Center.

• Osteoclasts digest away the calcified cartilage while osteoblasts form new spongy bone around the remnants of the cartilage within the diaphysis.

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

3. Formation of

Primary Ossification Center in center of diaphysis

4. Ossification of diaphysis

Spongy bone

Periosteal bud


Spongy bone

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Endochondral Ossification: Steps

• Osteoclasts erode the newly formed spongy bone to create a marrow cavity in the center of the diaphysis which spreads along the diaphysis.

• Calcification of cartilage then occurs in each epiphysis at or after birth, followed by invasion by a periosteal bud, forming a Secondary Ossification Center in each epiphysis.

5. Formation of Secondary Ossification Centers in

Epiphyses Marrow cavity

Secondary ossification center


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Endochondral Ossification: Final Steps

• Ossification forms spongy bone in each epiphysis between a layer of epiphyseal cartilage (the Epiphyseal Plate) and articular cartilage.

• Epiphyseal plate cartilage continue to grow by interstitial growth as fast as it replaced by bone tissue on the diaphyseal side of the plate.

• Therefore the long bone continues to grow in length until maturity when the epiphyseal plate is completely ossified (“closure of epiphyses”) forming an epiphyseal line.

• After this stage no further lengthening of bones can occur but bones continue to increase in thickness.

6. Ossification (closure) of

Epiphyseal Plates by end of puberty

Fig. 6-8, Martini

39

Development of the Skeleton - 1

Intramembranous ossification

forming dermal bone

Hyaline cartilage

bone models are sites for endochondral ossification Secondary ossification

Centers in epiphyses

Human Embryo at 7 weeks. The skeleton consists entirely

of cartilage and membrane

40


Epiphyseal plates shrinking

Articular cartilage

41


• Epiphyseal Plate almost completely ossified.

• Eventually closes to become Epiphyseal Line.

• No more lengthening of bones can then occur.

Articular cartilage

remains throughout

life

42

Bone Remodeling Bone remodeling refers to the changes in shape and thickness of bones throughout life due to two antagonistic processes, bone deposition and bone resorption 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.

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Bone Deposition & Bone Resorption

• Bone Deposition means appositional growth of new bone tissue by the activity of osteoblasts.

• Osteoblasts first secrete the organic matrix then help form the inorganic matrix.

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

-3 and by the creation of an alkaline environment for enzymes secreted by the osteoblasts.

• Bone Resorption refers to the digestion of bone matrix by enzymes and acids secreted by osteoclasts which also phagocytose the cellular products.

44

Bone Tissue Responds to Mechanical Stress

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

• The fetal skeleton is relatively featureless.

• Athletes show increased bone mass.

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

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

• Bone: “Use it or Lose it”!

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

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

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

• PTH raises blood calcium levels so is hypercalcemic

• Calcitonin lowers blood [calcium] so is hypocalcemic

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

46

How PTH & Calcitonin Control Blood Ca levels

↑Blood [Ca+2]

Parathyroid Gland

Parathyroid Hormone

(PTH)

osteoclasts

↑ Bone deposition

↓ Blood [Ca+2]

Thyroid Gland

Calcitonin

↑ Bone Resorption ↑Blood Ca ↓ Blood Ca

++ -

-ve feedback

osteoclasts

-ve feedback

stimulus stimulus

47

PTH Causes Bone Resorption & Increases Blood Ca

Bone Resorption

↑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 returned to blood

Ca+2

Ca+2 Ca+2 PTH

PTH

Bone

Intestine Kidney

Ca+2 removed from bone

Ca+2 absorbed into to blood

PTH with calcitriol

After Martini, 8th ed. Figure 6-16

48

Calcitonin Causes Bone Deposition & Lowers Blood Ca

Bone Deposition

↓ Blood [Ca]

Stimulus for Calcitonin ↑Blood [Ca]

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

Ca+2

Ca+2 lost in urine

Ca+2

Ca+2

Ca+2 added to bone

Ca+2 excreted

Kidney

Bone

calcitonin

calcitonin

After Martini, 8th ed. Figure 6-16

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Thyroid Gland Secretes

Calcitonin

Increased excretion of calcium in kidneys

Calcium deposition in bone (inhibition of osteoclasts)

Blood calcium levels decline

HOMEOSTASIS DISTURBED

Rising calcium levels in blood

HOMEOSTASIS RESTORED

HOMEOSTASIS Normal calcium levels

(8.5-11 mg/dl) HOMEOSTASIS RESTORED

HOMEOSTASIS DISTURBED

Falling calcium levels in blood Release of stored

calcium from bone (stimulation of

osteoclasts, inhibition of osteoblasts)

Enhanced reabsorption

of calcium in kidneys Stimulation of

calcitriol production at kidneys;

enhanced Ca2+, PO43-

absorption by digestive tract

Parathyroid glands secrete Parathyroid

Hormone (PTH)

Blood calcium levels

increase

Martini & Bartholomew Figure 10-10

Homeostatic Control of Blood Ca by Calcitonin & PTH

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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 matrix formation) • carbohydrate (supplies energy for growth).

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

Growth of the skeleton requires Extrinsic Factors and Intrinsic Factors.

51

Factors Affecting Growth of the Skeleton - 2

Amino acids

energy

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 in the skin in the presence of sunlight.

•  Vitamin D promotes Ca and P absorption from the diet.

•  Vit D is converted by the kidneys into the hormone calcitriol which targets the small intestine, increasing Ca/P absorption.

Cholesterol in skin

Liver stores vit D3

Kidney activates vit D3 to hormone Calcitriol (activated vit D) Calcitriol released by into blood by PTH

Small Intestine

Calcitriol Increased absorption of Ca/P

via blood

via blood

Bones & teeth

via blood

Kidney

53

Rickets: a Childhood Bone Disorder due to Calcium or Vitamin D Deficiency

2 years later, with calcium & vit D

supplements

Softening of bones causes bowing of legs & other bone deformities

Lack of vit D causes Rickets

•  inadequate absorption of Ca

•  Hypocalcemia

•  Loss of inorganic bone matrix

•  Softening of bones.

•  Inadequate ossification of epiphyses which become enlarged.

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 collagen causes loose teeth & bleeding gums,

Inadequate collagen causes bruising & bleeding under the skin

55

Effect of Growth Hormone on the Skeleton • Growth hormone (GH) causes protein synthesis and cell division of osteogenic cells throughout the growing years.

• Growth Hormone causes the Juvenile Growth Spurt and general growth of the skeleton to maturity .

• Pituitary Dwarf has short stature with normal skeletal proportions.

Hypopituitary Dwarf • ↓Height • Normal proportions

From Ganong, Review of Medical Physiology

56

Effect of Thyroid Hormone on the Skeleton

• Thyroid hormone (Thyroxine) causes energy release for bone growth and controls changes in skeletal proportions as bones grow.

• Thyroid hormone (thyroxine) works synergistically with GH to cause skeletal growth and controls changes in skeletal proportions.

• Hypothyroid Dwarf has short stature and infantile skeletal proportions.

Hypothyroid Dwarf • ↓Height • Infantile proportions

From Ganong, Review of Medical Physiology

57

Effect of Sex Hormones on the Skeleton

• Sex Hormones (Androgens & Estrogens) cause

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

• Secondary Sexual skeletal changes

• Bone Deposition throughout life

(preventing osteoporosis).

Bones porous & brittle

Normal spongy bone

Martini , 8th ed. fig 6-19

Bone with Osteoporosis

58

Summary of Effects of Hormones on Bones GH has indirect action on bones by acting as a trophic hormone for the liver

gonadotropin

• GH - Juvenile Growth Spurt

• T4 - Normal Skeletal Proportions - Energy for Growth

• Sex Hormones - Adolescent Growth Spurt - Closure of Epiphyses

Insulin –like growth factor (hormone) stimulates osteoblasts

Anterior Pituitary

Thyroid Gland

Gonads

Bones

Liver

Androgens Estrogens

Thyroxine (T4)

Growth Hormone (GH)

Gn

TSH

59

Changes in the Human Skeleton with Age

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

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

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

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

• During later years (35+ in females; 60 +in males) the rate of deposition is less than the rate of absorption and there is a net 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 of hormones at various ages • All continue to be secreted 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 //

Osteopenia: normal decline in bone mass

with age

Osteoporosis: pathological loss of bone

mass: weakens

bones

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 6-11

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 spine Primary Spinal

Curvature

Primary Spinal

Curvatures

1 - 3 years

64


Cranium of newborn Infant Martini fig 7-15

Martini & Bartholomew fig 6-15

Cranium of adult

Martini fig 7-3b

• Closure of Fontanels of Skull and formation of Sutures. - Fontanels are fibrous connections between cranial bones allowing cranial 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 of blood vessels cause death of Bone Tissue & Formation of Fracture Hematoma (< 48h)

2. Formation of Internal & External Callus from Cells of Periosteum & Endosteum (48h to 3-4 weeks)

Callus: a bridge of spongy bone & fibrocartilage between severed bone segments

Fibro

Martini & Bartholomew

fig 6-7

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Repair of Bone Fractures - Later Stages

3. Fusion of Calluses & Ossification of Cartilage (3/4 weeks - 2/3 months): cast can be removed

4. Remodeling of Calluses by osteoclasts responding to stresses on bones (by 3 months upper extremity- 6 months lower extremity).

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

101-805 unit 6 the skeletal system - john abbott...

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