Transcript No Slide Title

Intramembranous Ossification
• Produces flat bones of skull and clavicle.
• Note the periosteum and osteoblasts.
7-1
Endochondral Ossification
7-2
Endochondral Ossification
• Bone develops from pre-existing model
– perichondrium and hyaline cartilage
• Most bones develop this process
• Formation of primary ossification center
and marrow cavity in shaft of model
– bony collar developed by osteoblasts
– chondrocytes swell and die
– stem cells give rise to osteoblasts and
clasts
– bone laid down and marrow cavity created 7-3
Primary Ossification Center and
Primary Marrow Cavity
7-4
Endochondral Ossification
• Secondary ossification centers and
marrow cavities form in ends of bone
– same process
• Cartilage remains as articular cartilage
and epiphyseal (growth) plates
– growth plates provide for increase in
length of bone during childhood and
adolescence
– by early twenties, growth plates are gone
and primary and secondary marrow
cavities united
7-5
Secondary Ossification Centers
and Secondary Marrow Cavities
7-6
Fetal Skeleton at 12 Weeks
7-7
Bone Growth and Remodeling
• Bones increase in length
– interstitial growth of epiphyseal plate
– epiphyseal line is left behind when cartilage gone
• Bones increase in width = appositional growth
– osteoblasts lay down matrix in layers on outer
surface and osteoclasts dissolve bone on inner
surface
• Bones remodeled throughout life
– Wolff’s law of bone = architecture of bone
determined by mechanical stresses
• action of osteoblasts and osteoclasts
– greater density and mass of bone in athletes or
manual worker is an adaptation to stress
7-8
Dwarfism
• Achondroplastic
– long bones stop
growing in childhood
• normal torso, short limbs
– spontaneous mutation
during DNA replication
– failure of cartilage
growth
• Pituitary
– lack of growth hormone
– normal proportions with
short stature
7-9
Mineral Resorption from Bone
• Bone dissolved and minerals released into
blood
– performed by osteoclasts
– hydrochloric acid (pH 4) dissolves bone minerals
– enzyme (acid phosphatase) digests the collagen
7-10
Calcium and Phosphate
• Phosphate is component of DNA, RNA,
ATP, phospholipids, and pH buffers
• Calcium needed in neurons, muscle
contraction, blood clotting and exocytosis
7-11
Ion Imbalances
• Changes in calcium can be serious
– hypocalcemia is deficiency of blood calcium
• causes excitability of nervous system if too low
– muscle spasms, tremors or tetany ~6 mg/dL
– laryngospasm and suffocation ~4 mg/dL
• with less calcium, sodium channels open more easily,
sodium enters cell and excites neuron
– hypercalcemia is excess of blood calcium
• binding to cell surface makes sodium channels less likely to
open, depressing nervous system
– muscle weakness and sluggish reflexes, cardiac arrest ~12
mg/dL
• Calcium homeostasis depends on calcitriol,
calcitonin and PTH regulation
7-12
Carpopedal Spasm
• Hypocalcemia demonstrated by muscle spasm
of hands and feet.
7-13
Hormonal Control of Calcium Balance
• Calcitriol, PTH and calcitonin maintain
normal blood calcium concentration.
7-14
Calcitriol (Activated Vitamin D)
• Produced by the following process
– UV radiation and epidermal keratinocytes convert
precursor to vitamin D3
– liver converts it to calcidiol
– kidney converts that to calcitriol (vitamin D)
• Calcitriol behaves as a hormone that raises
blood calcium concentration
– increases intestinal absorption and absorption from
the skeleton
– increases stem cell differentiation into osteoclasts
– promotes urinary reabsorption of calcium ions
• Abnormal softness (rickets) in children and
(osteomalacia) in adults without vitamin D
7-15
Calcitonin
• Secreted (C cells of thyroid gland) when
calcium concentration rises too high
• Functions
– reduces osteoclast activity as much as 70%
– increases the number and activity of
osteoblasts
• Reduces bone loss in osteoporosis
7-16
Correction for Hypercalcemia
7-17
Parathyroid Hormone
• Glands on posterior surface of thyroid
• Released with low calcium blood levels
• Function = raise calcium blood level
– causes osteoblasts to release osteoclast-stimulating
factor increasing osteoclast population
– promotes calcium resorption by the kidneys
– promotes calcitriol synthesis in the kidneys
– inhibits collagen synthesis and bone deposition by
osteoblasts
7-18
Correction for Hypocalcemia
7-19
Other Factors Affecting Bone
• Hormones, vitamins and growth factors
• Growth rapid at puberty
– hormones stimulate osteogenic cells, chondrocytes
and matrix deposition in growth plate
– girls grow faster than boys and reach full height
earlier (estrogen stronger effect)
– males grow for a longer time and taller
• Growth stops (epiphyseal plate “closes”)
– teenage use of anabolic steroids = premature closure
of growth plate and short adult stature
7-20
Fractures and Their Repairs
7-21
Fractures and Their Repair
• Stress fracture caused by trauma
– car accident, fall, athletics, etc
• Pathological fracture in bone weakened
by disease
– bone cancer or osteoporosis
7-22
Healing of Fractures
7-23
Healing of Fractures
• Normally 8 - 12 weeks (longer in elderly)
• Stages of healing
– fracture hematoma (1) - clot forms, then
osteogenic cells form granulation tissue
– soft callus (2)
• fibroblasts produce fibers and fibrocartilage
– hard callus (3)
• osteoblasts produce a bony collar in 6 weeks
– remodeling (4) in 3 to 4 months
• spongy bone replaced by compact bone
7-24
Osteoporosis
• Bones lose mass and become brittle (loss
of organic matrix and minerals)
– risk of fracture of hip, wrist and vertebral
column
• Postmenopausal white women at greatest
risk
– by age 70, average loss is 30% of bone mass
– black women rarely suffer symptoms
7-25
Osteoporosis
• Estrogen maintains density in both sexes
(inhibits resorption)
– testes and adrenals produce estrogen in men
– rapid loss after menopause, if body fat too low or
with disuse during immobilizaton
• Treatment
– ERT slows bone resorption, but increases risk
breast cancer, stroke and heart disease
– PTH slows bone loss if given daily injection
– best treatment is prevention -- exercise and
calcium intake (1000 mg/day) between ages 25
and 40
– calcitonin
7-26
Spinal Osteoporosis
7-27