OBJECTIVES
• DISTINGUISH BETWEEN
INTRAMEMBRANOUS AND ENDOCHONDRAL
BONES, AND EXPLAIN HOW SUCH BONES
DEVELOP AND GROW
• DESCRIBE THE EFFECTS
OF SUNLIGHT,
NUTRITION, HORMONAL SECRETION, AND
EXERCISE ON BONE DEVELOPMENT AND
GROWTH
BONE DEVELOPMENT
• PARTS OF THE SKELETAL SYSTEM BEGIN TO FORM
DURING THE FIRST FEW WEEKS OF PRENATAL
DEVELOPMENT
• BONY STRUCTURES CONTINUE TO GROW AND DEVELOP
INTO ADULTHOOD
• THE PROCESS OF BONE DEVELOPMENT IS CALLED
OSTEOGENESIS
• BONES FORM WHEN BONE TISSUE REPLACES EXISTING
CONNECTIVE TISSUE IN ONE OF TWO WAYS
• INTRAMEMBRANOUS
• ENDOCHONDRAL
INTRAMEMBRANOUS BONES
• ARE BONES THAT
ORIGINATED WITHIN
SHEET-LIKE LAYERS
OF CONNECTIVE
TISSUE
• INCLUDE THE BONES
OF THE SKULL,
CLAVICLES, STERNUM,
MANDIBLE, MAXILLAE
AND ZYGOMATIC
ENDOCHONDRAL BONES
• ARE BONES THAT BEGIN
AS MASSES OF CARTILAGE
LATER REPLACED BY BONE
TISSUE
• INCLUDES MAJORITY OF
THE BONES OF THE
SKELETON
• THE PROCESS OF FORMING
ENDOCHONDRAL BONES IS
CALLED ENDOCHONDRAL
OSSIFICATION
OSTEOGENESIS OF
INTRAMEMBRANOUS BONES
1.
SHEETS OF UNSPECIALIZED CONNECTIVE TISSUES APPEAR
AT THE SITE OF FUTURE BONES
2. PARTIALLY DIFFERENTIATED CONNECTIVE TISSUE CELLS
COLLECT AROUND BLOOD VESSELS IN THESE LAYERS
3. CONNECTIVE TISSUE CELLS FURTHER DIFFERENTIATE
INTO OSTEOBLASTS, WHICH DEPOSIT SPONGY BONE
4. OSTEOBLASTS BECOME OSTEOCYTES WHEN BONY MATRIC
COMPLETELY SURROUNDS THEM
5. CONNECTIVE TISSUE ON THE SURFACE OF EACH
DEVELOPING STRUCTURE FORMS A PERIOSTEUM
6. OSTEOBLASTS ON THE INSIDE OF THE PERIOSTEUM
DEPOSIT COMPACT BONE OVER THE SPONGY BONE
OSTEOGENESIS OF ENDOCHONDRAL
BONES
1.
MASSES OF HYALINE CARTILAGE FORM MODELS OF
FUTURE BONES
2. CARTILAGE TISSUE BREAKS DOWN AND PERIOSTEUM
DEVELOPS
3. BLOOD VESSELS AND DIFFERENTIATING OSTEOBLASTS
FROM THE PERIOSTEUM INVADE THE DISINTEGRATING
TISSUE
4. OSTEOBLASTS FORM SPONGY BONE IN THE SPACE
OCCUPIED BY CARTILAGE
5. OSTEOBLASTS BENEATH THE PERIOSTEUM DEPOSIT A
THIN LAYER OF COMPACT BONE
6. OSTEOBLASTS BECOME OSTEOCYTES WHEN BONY MATRIX
COMPLETELY SURROUNDS THEM
LONG BONE DEVELOPMENT
• BONE TISSUE BEGINS TO REPLACE HYALINE
CARTILAGE IN THE CENTER OF DIAPHYSIS
• THIS REGION IS CALLED THE PRIMARY
OSSIFICATION CENTER, IN WHICH BONE DEVELOPS
FROM IT TOWARD THE ENDS OF THE
CARTILAGINOUS STRUCTURE
• OSTEOBLASTS FROM THE PERIOSTEUM DEPOSIT A
THIN LAYER OF COMPACT BONE AROUND THE
PRIMARY OSSIFICATION CENTER
LONG BONE DEVELOPMENT CONT.
• THE EPIPHYSES OF THE DEVELOPING BONE REMAIN
CARTILAGINOUS AND CONTINUE TO GROW
• A SECONDARY OSSIFICATION CENTER APPEARS IN
THE EPIPHYSES AND SPONGY BONE FORMS IN ALL
DIRECTIONS
• AS SPONGY BONE IS DEPOSITED IN THE DIAPHYSIS
AND IN THE EPIPHYSIS, A BAND OF CARTILAGE
CALLED THE EPIPHYSEAL PLATE REMAINS BETWEEN
THE TWO OSSIFICATION CENTERS
ENDOCHONDRAL OSSIFICATION
GROWTH AT THE EPIPHYSEAL PLATE
• THE CARTILAGINOUS CELLS OF THE
EPIPHYSEAL PLATE FORM FOUR LAYERS:
• ZONE OF RESTING CARTILAGE
• ZONE OF PROLIFERATING CARTILAGE
• ZONE OF HYPERTROPHIC CARTILAGE
• ZONE OF CALCIFIED CARTILAGE
ZONE OF RESTING CARTILAGE
• IS CLOSEST TO THE END OF THE EPIPHYSIS
• IT IS COMPOSED OF RESTING CELLS THAT
DO NOT ACTIVELY PARTICIPATE IN
GROWTH
• THIS LAYER ANCHORS THE EPIPHYSEAL
PLATE TO THE BONY TISSUE OF THE
EPIPHYSIS
ZONE OF PROLIFERATING CARTILAGE
• THIS IS THE SECOND LAYER
• IT INCLUDES ROWS OF MANY YOUNG
CELLS UNDERGOING MITOSIS
• AS NEW CELLS APPEAR AND AS
EXTRACELLULAR MATRIX FORMS AROUND
THEM, THE CARTILAGINOUS PLATE
THICKENS
ZONE OF HYPERTROPHIC CARTILAGE
• COMPOSED OF ROWS OF OLDER CELLS LEFT BEHIND
WHEN NEW CELLS FORM
• THIS LAYER ENLARGES AND THICKENS THE
EPIPHYSEAL PLATE MORE
• THE ENTIRE BONE LENGTHENS AS A RESULT
• AT THE SAME TIME, INVADING OSTEOBLASTS
SECRETE CALCIUM SALTS AND ACCUMULATE IN THE
EXTRACELLULAR MATRIX ADJACENT TO THE OLDEST
CARTILAGINOUS CELLS
• THE EXTRACELLULAR MATRIC CALCIFIES AND THE
CELLS BEGIN TO DIE
ZONE OF CALCIFIED CARTILAGE
• THIS IS A THIN LAYER
• IT IS COMPOSED OF DEAD CELLS AND CALCIFIED
EXTRACELLULAR MATRIX
• IN TIME, LARGE MULTINUCLEATED CELLS CALLED
OSTEOCLASTS BREAK DOWN THE CALCIFIED
MATRIX BY SECRETING AN ACID
• OSTEOCLASTS ALSO PHAGOCYTIZE COMPONENTS OF
THE BONY MATRIX
• AFTERWARDS, BONE BUILDING OSTEOBLASTS
INVADE THE REGION AND DEPOSIT BONE TISSUE
CONTINUED GROWTH
• BONES CONTINUE TO DEVELOP AFTER YOU ARE
•
•
•
BORN
BETWEEN EARLY CHILDHOOD AND LATE
ADOLESCENCE, BONE CELLS GRADUALLY REPLACE
THE CARTILAGE IN LONG BONES OF THE ARMS
AND LEGS
WHEN ALL THE CARTILAGE IN THE EPIPHYSEAL
PLATE IS REPLACED WITH BONE, A PERSON HAS
REACHED THEIR FULL HEIGHT
THE EPIPHYSEAL PLATES BECOME EPIPHYSEAL
LINES
OSSIFICATION TIMELINE
Age
Occurrence
3rd month of prenatal development
Ossification in long bones begins
4th month of prenatal development
Most primary ossification centers
have appeared in the diaphysis of
bones
Birth to 5 years old
Secondary ossification centers
appear in the epiphyses
5-12 years old (females)
5-14 years old (males)
Ossification rapidly spreads from
the ossification centers
15-18 years old (females)
17-20 years old (males)
Bones of upper limbs and scapulae
completely ossified
16-21 years old (females)
18-23 years old (males)
Bones of the lower limbs and hip
bones completely ossified
21-23 years old (females)
23-25 years old (males)
Bones of the sternum, clavicles, and
vertebrae completely ossified
By 23 years old (females)
By 25 years old (males)
Nearly all bones completely ossified
HOMEOSTASIS OF BONE TISSUE
• AFTER THE INTRAMEMBRANOUS AND ENDOCHONDRAL
BONES FORM, THE ACTIONS OF OSTEOCLASTS AND
OSTEOBLASTS CONTINUALLY REMODEL THEM
• BONE REMODELING OCCURS THROUGHOUT LIFE AS
OSTEOCLASTS RESORB BONE TISSUE AND OSTEOBLASTS
REPLACE THE BONE
• THE PROCESSES OF RESORPTION AND DEPOSITION OCCUR
ON THE SURFACES OF THE ENDOSTEUM AND PERIOSTEUM
• THE RATE OF BONE REMODELING IS NOT UNIFORM, SPONGY
BONE IS FASTER THAN COMPACT BONE
• THESE PROCESSES REPLACE 10% TO 20% OF THE SKELETON
EACH YEAR
FACTORS AFFECTING BONE
DEVELOPMENT, GROWTH & REPAIR
•NUTRITION
•EXPOSURE TO SUNLIGHT
•HORMONAL SECRETIONS
•PHYSICAL EXERCISE
NUTRITION FACTORS
• VITAMIN D IS NECESSARY FOR PROPER ABSORPTION OF
CALCIUM IN THE SMALL INTESTINE
• WITHOUT ENOUGH OF IT, THE BONE MATRIX SOFTENS AND
THEREBY DEFORMS THE BONE
• VITAMINS A AND C ARE ALSO REQUIRED
• VITAMIN A IS NECESSARY FOR OSTEOBLAST AND
OSTEOCLAST ACTIVITY DURING NORMAL DEVELOPMENT
• A LACK OF VITAMIN A MAY RETARD (SLOW) BONE
DEVELOPMENT
• VITAMIN C IS REQUIRED FOR COLLAGEN SYNTHESIS
• A DEFICIENCY PREVENTS OSTEOBLASTS FROM PRODUCING
ENOUGH COLLAGEN IN THE EXTRACELLULAR MATRIX OF THE
BONE TISSUE, AND AS A RESULT BONES BECOME
ABNORMALLY SLENDER AND FRAGILE.
HORMONAL FACTORS
• THE PITUITARY GLAND SECRETES GROWTH HORMONE, WHICH
STIMULATES DIVISION OF CARTILAGE CELLS IN THE
EPIPHYSEAL PLATES
• WITHOUT THIS HORMONE PITUITARY DWARFISM OCCURS
• IF TOO MUCH GROWTH HORMONE IS PRODUCED, THEN
PITUITARY GIGANTISM OCCURS
• THE THYROID HORMONE THYROXINE STIMULATES
REPLACEMENT OF CARTILAGE IN THE EPIPHYSEAL PLATES OF
LONG BONES WITH BONE TISSUE
• THIS HORMONE ALSO INCREASES CELLULAR METABOLISM,
INCLUDING STIMULATING OSTEOBLAST ACTIVITY
• THE PARATHYROID HORMONE STIMULATES AN INCREASE IN
THE NUMBER AND ACTIVITY OF OSTEOCLASTS, WHICH BREAK
DOWN BONE
HORMONAL FACTORS CONT.
• BOTH SEX HORMONES, TESTOSTERONE FOR MALES
AND ESTROGEN FOR FEMALES, PROMOTE FORMATION
OF BONE TISSUE
• AT PUBERTY, THESE HORMONES ARE ABUNDANT,
CAUSING THE LONG BONES TO GROW CONSIDERABLY
• SEX HORMONES ALSO STIMULATE OSSIFICATION OF
THE EPIPHYSEAL PLATES AND THUS, STOP BONE
LENGTHENING AT A RELATIVELY EARLY AGE
• ESTROGEN HAS A STRONGER AFFECT ON THE
EPIPHYSEAL PLATES AND, THUS FEMALES TYPICALLY
REACH THEIR MAXIMUM HEIGHTS SOONER THAN
MALES
PHYSICAL FACTORS
• PHYSICAL STRESS STIMULATE BONE GROWTH
• FOR EXAMPLE, WHEN SKELETAL MUSCLES CONTRACT,
THEY PULL AT THEIR ATTACHMENTS ON BONES, AND
THE RESULTING STRESS STIMULATES THE BONE
TISSUE TO THICKEN AND STRENGTHEN
(HYPERTROPHY)
• WITH A LACK OF EXERCISE, BONE TISSUE WASTES
BECOMING THINNER AND WEAKER (ATROPHY)
• THIS IS WHY THE BONES OF ATHLETES ARE USUALLY
STRONGER AND HEAVIER THAN THOSE OF NONATHLETES