UNIT 5 – BONE PHYSIOLOGY

5 FUNCTIONS OF THE SKELETAL SYSTEM

1. SUPPORT

• RIGID, STRONG BONE SUITED FOR WEIGHT BEARING & MAJOR SUPPORTING ELEMENT OF THE BODY

2. PROTECTION

• BONE IS HARD, PROTECTS ORGANS IT SURROUNDS

• EXAMPLES: BRAIN, LUNGS, HEART

3. MOVEMENT

• MUSCLES ATTACH TO BONES BY TENDONS & CONTRACTION OF MUSCLES CAUSES BONE TO MOVE

• LIGAMENTS CONNECT BONES& CARTILAGE COVERS ENDS & JOINTS

5 FUNCTIONS OF THE SKELETAL SYSTEM

4. STORAGE

• EXCESS MINERALS IN BLOOD ARE TAKING INTO BONE & STORED

• BLOOD LEVELS FALL & BONES RELEASE MINERALS (SUCH AS PHOSPHORUS & CALCIUM)

• STORES FAT

5. BLOOD CELL PRODUCTION

• BONE MARROW GIVES RISE TO BLOOD CELLS & PLATELETS

CLASSIFICATION OF BONES

• LONG BONES

• LONGER THAN THEY ARE WIDE

• EXAMPLES: UPPER & LOWER LIMBS

• SHORT BONES

• BROAD AS THEY ARE LONG

• CUBE-SHAPED AND/OR ROUND

• EXAMPLES: TARSALS & CARPALS

• FLAT BONES

• THIN, FLAT, & CURVED

• EXAMPLES: SKULL (PARIETAL), STERNUM, SCAPULAE

CLASSIFICATION OF BONES

• IRREGULAR BONES

• DON’T FIT IN THE OTHER CATEGORIES

• EXAMPLES: FACE & VERTEBRAE

• SESAMOID

• SESAME SEED

• EXAMPLES: PATELLA, SMALL & FLAT

• SUTURAL BONES

• WORMIAN BONES

• BORDERS LIKE A JIGSAW PUZZLE

GROSS STRUCTURE OF LONG BONES• DIAPHYSIS

• SHAFT

• MADE OF COMPACT BONE

• EPIPHYSES (PROXIMAL & DISTAL)

• THE ENDS OF THE LONG BONE

• THIN LAYER OF COMPACT BONE ENCLOSING AN AREA FILLED WITH SPONGY BONE

• EPIPHYSEAL LINE

• REMNANT OF THE EPIPHYSEAL PLATE

• EPIPHYSEAL PLATE

• CAUSE THE GROWTH OF A LONG BONE

• HYALINE CARTILAGE PLATE EVENTUALLY BECOMES COMPLETELY REPLACED BY BONE, LEAVING ONLY THE EPIPHYSEAL LINES TO MARK THEIR PREVIOUS LOCATION

• MEDULLARY CAVITY

• YELLOW MARROW & RED MARROW IS FOUND THERE

GROSS ANATOMY OF BONE• PERIOSTEUM

• FIBROUS CONNECTIVE TISSUE MEMBRANE THAT COVERS THE DIAPHYSIS

• SHARPEY’S FIBERS SECURE THE PERIOSTEUM TO THE UNDERLYING BONE

• ARTICULAR CARTILAGE

• GLASSY HYALINE CARTILAGE

• PROVIDES A SMOOTH, SLIPPERY SURFACE THAT DECREASES FRICTION AT JOINT SURFACES

• LOCATED ON THE EPIPHYSES OVER A THIN LAYER OF COMPACT BONE ENCLOSING AN AREA FILLED WITH SPONGY BONE

• MEDULLARY CAVITY

• STORAGE AREA FOR ADIPOSE TISSUE (YELLOW MARROW)

• IN INFANTS, THIS AREA FORMS BLOOD CELLS (RED MARROW)

• IN ADULT BONES, RED MARROW IS CONFINED TO THE CAVITIES OF SPONGY BONE OF FLAT BONES AND THE EPIPHYSES OF SOME LONG BONES

Endosteum

Medulary Cavity (Yellow Marrow)

Arteries

Sharpey’s Fibers

Periosteum

Compact Bone

Spongy Bone

Compact Bone

Articular Cartilage

COMPACT BONE

• COMPACT BONE IS MORE DENSE THAN CANCELLOUS BONE

• FUNCTIONAL UNIT = OSTEON (HAVERSIAN SYSTEM)

• CONSISTS OF A SINGLE HAVERSIAN CANAL, CONTENTS & CONCENTRIC LAMELLAE (CONCENTRIC LAYERS) & OSTEOCYTES

• OSTEOCYTES RECEIVE NUTRIENTS & ELIMINATE WASTE THROUGH CANALS IN COMPACT BONE

• BLOOD VESSELS FROM THE PERIOSTEUM ENTER BONE THROUGH THE VOLKMANN’S CANALS

• COMPACT BONE IS THICKEST WHERE STRESS IS GREATEST & OSTEONS RUN PARALLEL IN LONG BONES TO THE AXIS OF THE SHAFT

SPONGY BONE

• AKA CANCELLOUS BONE

• DOES NOT HAVE OSTEONS IN CONCENTRIC LAYERS

• MATRIX HAS CONNECTING RODS & PLATES OF BONE CALLED TRABECULAE

• TRABECULAE CONSISTS OF SEVERAL LAMELLAE WITH OSTEOCYTES THAT ARE LOCATED BETWEEN THE LAYERS

• TRABECULAE ARE ORIENTED ALONG LINES OF STRESS WITHIN BONES

Osteon

Lacuna

Canaliculus

Central Haversian Canal

Central Haversian Canal

Blood Vessel

Perforating Volkmann’s Canal

MICROSCOPIC ANATOMY OF BONE

• OSTEOCYTES

• MATURE BONE CELLS

• LACUNAE

• TINY CAVITIES WITHIN THE MATRIX ARRANGED IN CONCENTRIC CIRCLES AROUND CENTRAL (HAVERSIAN) CANALS

• OSTEON OR HAVESIAN SYSTEM

• COMPLEX CONSISTING OF CENTRAL CANAL & MATRIX RINGS

• CENTRAL CANALS RUN LENGTHWISE THROUGH THE BONY MATRIX, CARRYING BLOOD VESSELS AND NERVES TO ALL AREAS OF BONE

MICROSCOPIC ANATOMY OF BONE

• CANALICULI

• TINY CANALS RADIATE OUTWARD FROM THE CENTRAL CANALS TO ALL LACUNAE

• FORM A TRANSPORTATION SYSTEM THAT CONNECTS ALL THE BONE CELLS

• PERFORATING (VOLKMANN’S) CANALS

• COMMUNICATION PATWAY FROM THE OUTSIDE OF THE BONE TO ITS INTERIOR (AND THE CENTRAL CANALS)

• RUN INTO THE COMPACT BONE AT RIGHT ANGELS TO THE SHAFT

• THE CALCIUM SALTS DEPOSITED IN THE MATRIX GIVE BONE ITS HARNESS WHEREAS THE ORGANIC PARTS (ESPECIALLY THE COLLAGEN FIBERS) PROVIDE FOR BONE’S FLEXIBILITY AND GREAT TENSILE STRENGTH

COMPACT BONE

CALCIUM• BONES ARE ESSENTIAL IN MAINTAINING CALCIUM LEVELS IN THE BLOOD

• BONE IS THE PRIMARY STORAGE SITE OF CALCIUM

• MOST ABUNDANT MINERAL IN THE BODY

• 99% IS IN BONE

• CALCIUM IS USED FOR MUSCLE CONTRACTION & NERVE CELL POTENTIALS

• HIGH LEVELS CAN CAUSE CELLS TO BE NON-REACTIVE & LOW LEVELS CAN CAUSE CONVULSION

• CALCIUM MOVES INTO BONE WITH OSTEOBLASTS AND OUT OF BONE WITH OSTEOCLASTS

• WHEN BLOOD LEVELS FLUCTUATE, BLASTS & CLASTS CHANGE TO MEET THE NEED

• PARATHRYOID HORMONE

• PRIMARY REGULATOR OF BLOOD CALCIUM

• PH CAN STIMULATE OSTEOCLAST ACTIVITY & STIMULATE UPTAKE IN THE SMALL BOWEL BY CREATING MORE VITAMIN D

NUTRITION• BONE GROWTH REQUIRES OSTEOBLASTS & CHONDROBLASTS TO

PROLIFERATE

• CALCIUM IS CRITICAL!

• FOR GROWTH & VITAMIN D IS NECESSARY FOR CALCIUM ABSORPTION IN THE SMALL INTESTINE

• LACK OF CALCIUM RESULTS IN RICKETS IN KIDS AND OSTEOMALCIA IN ADULTS

• VITAMIN D IS ONLY SOLUBLE IN FAT, SO DISEASES THAT INTERFERE WITH FAT ABSORPTION AFFECT VITAMIN D

• VITAMIN C IS CRITICAL FOR COLLAGEN SYNTHESIS

• SCURVY IS THE MALADY WHERE A PERSON IS DEFICIENT IN VITAMIN C WHICH CAUSES BONES DEFICIENT IN COLLAGEN

• COLLAGEN IS ALSO IMPORTANT IN CONNECTIVE TISSUE PRODUCTION

• SCURVY CAUSES POOR WOUND HEALING & EASY HEMORRHAGE

HORMONES

• GROWTH HORMONE SECRETED FROM THE ANTERIOR PITUITARY INCREASES GENERAL TISSUE GROWTH, SPECIFICALLY APPOSITIONAL BONE GROWTH AND INTERSTITIAL CARTILAGE GROWTH

• THYROID HORMONES:

• CALCITONIN & THYROXINE

• CALCITONIN

• PROMOTES CALCIUM LOSS IN THE KIDNEYS & REDUCES BLOOD LEVELS

• INHIBITS OSTEOCLAST ACTIVITY

• THYROXINE

• STIMULATES OSTEOBLAST ACTIVITY & BONE MATRIX SYNTHESIS

• SEX HORHOMES

• ESTROGEN & TESTOSTERONE STIMULATES OSTEOBLAST ACTIVITY

BONE FORMATION, GROWTH, & REMODELING

• MOST BONES DEVELOP USING HYALINE CARTILAGE STRUCTURES AS THEIR “MODELS”

• IN EMBRYOS, THE SKELETON IS PRIMARILY MADE OF HYALINE CARTILAGE

• IN CHILDHOOD, MOST OF THE CARTILAGE HAS BEEN REPLACED BY BONE

• CARTILAGE REMAINS ONLY IN THE BRIDGE OF THE NOSE, PARTS OF THE RIBS, AND SURFACES OF THE JOINTS

• FLAT BONES FORM ON FIBROUS MEMEBRANES

BONE CELL TYPES• OSTEOCYTES

• MOST COMMON

• EACH OCCUPIES A LACUNA

• 2 PRIMARY FUNCTIONS:

1. MAINTAIN AND MONITOR PROTEIN & MINERAL CONTENT OF BONE MATRIX

2. PARTICIPATE IN BONE REPAIR

• OSTEOBLASTS

• BONE PRODUCING CELLS

• OSTEOCLASTS

• CELLS THAT BREAK DOWN BONE

• OSTEOPROGENITOR CELLS

• STEM CELLS THAT DIFFERENTIATE INTO OSTEOBLASTS

BONE OSSIFICATION

• OSSIFICATION

• THE FORMATION OF BONE BY OSTEOBLASTS & SYNTHESIS OF EXTRACELLULAR MATRIX AND ADDITION OF MINERALS TO MATRIX

• PROCESS OF REPLACING OTHER TISSUES WITH BONE

• CALCIFICATION

• DEPOSITION OF CALCIUM SALTS DURING OSSIFICATION

2 PROCESSES OF BONE OSSIFICATION

• INTRAMEMBRANOUS OSSIFICATION (DERMAL OSSIFICATION)• BONE THAT DEVELOPS FROM FIBROUS CONNECTIVE TISSUE

• OCCURS IN DEEP LAYERS OF DERMINS (DERMAL BONES) – SKULL (FONTANELS), MANDIBLE, CLAVICLE

• 3 STEPS

1. MESENCHYMAL CELLS (STEM CELLS THAT ARE PRESENT IN MANY CT) AGGREGATE & BEING THE OSSIFICATION PROCESS; BONE EXPANDS OUT FROM THE OSSIFICATION CENTERS AS A SERIES OF SPICULES (SMALL STRUTS); MESENCHYMAL CELLS DIFFERENTIATE & PRODUCE OSTEOBLASTS

2. BONE GROWTH IS ACTIVE & REQUIRES OXYGEN & FOOD; BLOOD VESSELS FORM & BECOME TRAPPED IN THE GROWING BONE

3. OVER TIME, INTRAMEMBRANOUS IS ONLY SPONGY BONE; AS THE BONE MATURES SPONGY BONE IS REMOVED FOR MARROW CAVITIES; SPONGY BONE FORMED IN THIS PROCESS CAN BECOME COMPACT

2 PROCESSES OF BONE OSSIFICATION

• ENDOCHONDRAL OSSIFICATION

• RESPONSIBLE FOR THE INCREASE IN LENGTH OF BONES

• IN LONG BONES, ENDOCHRONDRAL GROWTH AT THE EPIPHYSEAL PLATE RESULTS IN THE INCREASE OF THE DIAPHYSIS

• MOST BONE STARTS AS HYALINE CARTILAGE

• CARTILAGE IS A MINIATURE MODEL OF WHAT THE BONE WILL LOOK LIKE IN ADULTHOOD

• MODELS BECOME BONE IN ENDOCHONDRAL OSSIFICATION

2 PROCESSES OF BONE OSSIFICATION• ENDOCHONDRAL OSSIFICATION

• 6 STEPS

1. CARTILAGE ENLARGES, BY APPOSITIONAL GROWTH; CHONDROCYTES AT CENTER OF CARTILAGE GROW IN SIZE; MATRIX REDUCES IN SIZE & SPICULES CALCIFY; CHONDROCYTES DIE & LEAVE CAVITIES IN CARTILAGE

2. BLOOD VESSELS GROW AROUND EDGES OF CARTILAGE; OSTEOBLASTS FORM IN THE PERICHONDRIUM; CARTILAGE BECOMES ENCASED IN BONE

3. PERICHONDRIUM NEEDS OXYGEN & FOOD SO CAPILLARIES BEGIN TO GROW WHERE THE CARTILAGE HAS DIED OFF; FIBROBLASTS BECOME OSTEOBLASTS & REPLACE CARTILAGE WITH SPONGY BONE; HAPPENS IN AN AREA CALLED PRIMARY CENTER OF OSSIFICATION WHERE BONE GROWS TOWARDS THE ENDS OF THE BONE; ENTIRE DIAPHYSIS IS SPONGY BONE

4. AS THE BONE CONTINUES TO GROW, OSTEOCLASTS APPEAR BREAKING DOWN THE TRABECULAE OF SPONGY BONE STARTING A MARROW CAVITY; NOW BONE GROWS IN 2 WAYS: LENGTH & DIAMETER BY APPOSITIONAL GROWTH

5. CAPILLARIES & OSTEOBLASTS MIGRATE TO THE EPIPHYSIS CREATING SECONDARY OSSIFICATION CENTERS

6. EPIPHYSIS FILLS WITH SPONGY BONE; A SMALL LAYER OF CARTILAGE REMAINS & BECOMES ARTICULAR CARTILAGE

FETAL OSSIFICATION

• 4 STEPS

1. HYALINE CARTILAGE MODEL IS COMPLETELY COVERED WITH BONE MATRIX BY BONE-FORMING CELLS CALLED OSTEOBLASTS

2. FETUS HAS CARTILAGE “BONES” ENCLOSED BY “BONY” BONES

3. ENCLOSED HYALINE CARTILAGE MODEL IS DIGESTED AWAY, OPENING UP MEDULLARY CAVITY WITHIN NEWLY FORMED BONE

4. BY BIRTH OR SHORTLY AFTER, MOST HYALINE CARTILAGE MODELS HAVE BEEN COVERTED TO BONE

Bone Starting to Replace Cartilage

Hyaline Cartilage Model

Bone

Blood Vessel

Hyaline Cartilage

Yellow Marrow Cavity Forming

New Center of Bone Growth

Articular Cartilage

Bone

Bone Forming

Bone forming Epiphyseal plate

Growth in Wide Bone

Epiphyseal Plate

Cartilage forming Plate

BONE GROWTH

• BONES CANNOT GROW BY INTERSTITIAL GROWTH LIKE CARTILAGE, LIGAMENTS, & TENDONS

• BONES GROW BY 2 METHODS:

1. APPOSITIONAL GROWTH

2. ENDOCHONDRAL GROWTH

BONE GROWTH

• APPOSITIONAL GROWTH

• RESPONSIBLE FOR THE INCREASE IN DIAMETER OF LONG BONES AND MOST GROWTH OF OTHER BONES

• CELLS ON THE INNER LAYER OF PERIOSTEUM DIFFERENTIATE INTO OSTEOBLASTS & CASUE GROWTH OF THE BONE MATRIX; BECOME SURROUNDED WITH MATRIX & BECOME OSTEOCYTES

• ON THE SURFACE OF THE BONE, APPOSITIONAL GROWTH ADDS LAYERS OF BONE THAT BECOME LAMELLAE

• REMEMBER, BONE IS DEPOSITED BY OSTEOBLASTS ON THE SURFACE OF THE BONE & REABSORBED BY OSTEOCLASTS ON THE INNDER SURFACE OF THE BONE SO MARROW CAVITY ENLARGES AS BONE GROWS

BONE GROWTH• ENDOCHONDRAL GROWTH (LONGITUDINAL

GROWTH)

• “NEW” CARTILAGE IS FORMED CONTINUOUSLY ON THE EXTERNAL FACE OF THE ARTICULAR CARTILAGE AND ON THE EPIPHYSEAL PLATE SURFACE THAT IS FARTHER AWAY FROM THE MEDULLARY CAVITY

• AT THE SAME TIME, THE “OLD” CARTILAGE ABUTTING THE INTERNAL FACE OF THE ARTICULAR CARTILAGE AND THE MEDULLARY IS BROWN DOWN AND REPLACED BY BONY MATRIX

• PROCESS OF LONG BONE GROWTH IS CONTROLLED BY HORMONES – GROWTH HORMONES DURING PUBERTY & SEX HORMONES

• ENDS DURING ADOLESCENCE WHEN THE EPIPHYSEAL PLATES ARE COMPLETELY CONVERTED TO BONE

BLOOD & NERVE SUPPLY• BONE TISSUE IS WELL SUPPLIED WITH BLOOD – HIGHLY VASCULAR!!!

• BLOOD VESSELS SUPPLY THE DIAPHYSIS BY ENTERING THE CARTILAGE MODEL BEFORE OSSIFICATION OCCURS

• MAJORITY OF BONES HAVE ONLY ONE VESSEL TO SUPPLY BLOOD

• LONG BONES (FEMUR) HAVE 3 BLOOD VESSELS

• NUTRIENT FORAMINA TUNNELS IN THE BONE THAT BLOOD VESSELS ENTER THROUGH

• METAPHYSEAL VESSELS

• SUPPLY BLOOD TO THE INNER SURFACE OF THE EPIPHYSEAL CARTILAGE

• LOCATION WHERE CARTILAGE IS REPLACED BY BONE

• PERIOSTEAL VESSELS

• PROVIDE BLOOD TO THE SUPERFICIAL OSTEONS OF THE BONE SHAFT

• NERVES

• FOUND THROUGHOUT THE BONE, ESPECIALLY IN THE ENDOSTEUM

• WHY BONE BREAKS ARE SO PAINFUL

BONE REMODELING

• ESSENTIAL IF BONES ARE TO RETAIN NORMAL PROPORTIONS AND STRENGTH

• ACCOUNTS FOR BONES BECOMING THICKER

• FORMS LARGE PROJECTIONS FOR MUSCLES TO ATTACH

• OSTEOBLASTS LAY DOWN MATRIX & BECOME OSTEOCYTES

• PHYSICALLY INACTIVE PEOPLE LOSE BONE MASS & ATROPHY (CELL DEATH)

BONE IS DYNAMIC• BONES ARE REMODELED CONTINUALLY IN RESPONSE TO 2 FACTORS:

1. CALCIUM LEVELS IN BLOOD

2. PULL OF GRAVITY AND MUSCLES ON THE SKELETON

• BLOOD CALCIUM LEVELS DROP

• PARATHYROID GLANDS ARE STIMULATED TO RELEASE PARATHYROID HORMONE (PTH) INTO BLOOD

• PTH ACTIVATES OSTEOCLASTS (BONE-DESTROYING CELLS)

• OSTEOCLASTS BREAK DOWN BONE MATRIX & RELEASE CALCIUM IONS INTO BLOOD

• WHEN BLOOD CALCIUM LEVELS ARE TOO HIGH (HYPERCLACEMIA)

• OSTEOBLASTS DEPOSIT CALCIUM IN BONE MATRIX

• CALCITONIN IS RELEASED

BONE FRACTURES

• HEMATOMA IS FORMED

• BLOOD VESSELS ARE RUPTURED WHEN THE BONE BREAKS

• AS A RESULT, A BLOOD-FILLED SWELLING CALLED A HEMATOMA FORMS

• BREAK IS SPLINTED BY FIBROCARTILAGE CALLUS

• GROWTH OF NEW CAPILLARIES AT THE SITE OF DAMAGE

• PHAGOCYTES DISPOSE OF DEAD TISSUE

• CONNECTIVE TISSUE FORM A MASS OF REPAIR TISSUE

• BONY CALLUS IS FORMED

• OVER THE NEXT FEW MONTHS, THE BONY CALLUS IS REMODELED IN RESPONSE TO THE MECHANICAL STRESSES PLACED ON IT SO THAT IT FORMS A STRONG PERMANENT “PATCH” AT THE FRACTURE SITE

BONE FRACTURES

Internalcallus (fibrous tissue and cartilage)

HematomaHematoma

Internalcallus (fibrous tissue and cartilage) Healed fracture

Spongybonetrabecula

Bony callus of spongy bone