Bones - Chapter 6 - Mareib Human Anatomy and Physiology, 5th //6th ed. text.

Label the anatomical perspectives: dorsal, ventral, superior, inferior, lateral, medial,
anterior, and posterior. See pg. 14-17.

Bone Structure

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Structure of Bone (See page 177//180)

1. Epiphysis - the end of the bone which is covered distally by articular cartilage (hyaline)

and internally has spongy bone and the red marrow that makes blood cells.
It and the metaphysis, below, is covered thinly by compact bone tissue.
2. Metaphysis - region where the diaphysis joins the epiphysis. A line, the epiphyseal line,

is seen internally and externally. It represents the old epiphyseal plate closure. See
endochondral ossification, below.
3. Diaphysis - the shaft on the bone bone, made enirely of compact bone tissue.
4. Periosteum - a layer of fibrous/collagenous connective tissue which covers the bone.

This layer must be present and alive in order for bone repair to take place. It contains
blood vessels which penetrate the bone, bone cells, and fibroblasts which make the
collagen fibers imbedded in calcium phosphate matrix of bone. Examine a chicken
bone or ham bone carefully. Distinguish the epiphysis, diaphysis, articular cartilage
and periosteum. Break open the bone and observe the marrow cavities and the yellow
and red marrow. Observe the spongy bone inside the epiphyses. Take a chicken bone
and soak it in vinegar for 3-4 days (change the vinegar every 12 hours).

Spongy bone on left Compact bone on right.
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Bone Cells

1. Osteoprogenitor cells - They produce osteoblasts and are found in the inner

surface of the periosteum.
2. Osteoblasts - found in new bone and in mending bone. They deposit calcium

phosphate on collagen fibers produced by fibroblasts. Takes calcium from the
blood and deposits it in bone, indirectly assisted by the hormones calcitonin
and calciferol.

See http://www-medlib.med.utah.edu/WebPath/BONEHTML/BONE012.html
 

3. Osteocytes - as they mature the osteoblasts become osteocytes. The osteocytes

then become surrounded by a porous matrix of calcium phosphate. Canaliculi are
present which allow many thin cytoplasmic extensions of the different osteocytes to
touch each other and therefore transfer nutrients and wastes to and from the blood.
4. Osteoclasts -the term means "bone breaker." Probably, they develop from white

blood cells called monocytes. Under the influence of the hormone PTH, they break
down the calcium phosphate matrix and relay the calcium ions to blood. It is
thought that calcitonin, estrogen and testosterone inhibit osteoclasts. What
would be the effect of that? Osteoclasts are important in bone growth, maintenance,
and repair. Paget's disease weakens bone because of abnormally high resorption
by osteoclasts.

1. Intramembranous Ossification - bone is formed directly on or within fibrous

membranes which first contained mesenchyme cells which later matured into
osteoprogenitor cells. The "soft spots" in the baby's head are fontanels in which
intramembranous ossification occurs. The resulting bones are flat bones.
2. Endochondral ossification (See p. 181-183.//184-186) - bone formation from or within cartilage.

In a fetus, the long bones appear first as cartilage models.

1. Long bones are formed as hyaline cartilage models.
2. The center of the diaphyseal area ossifies first - the primary center of ossification.

The cartilage cells die and the cartilage matrix calcifies. A nutrient artery brings
osteoprogenitor cells. The fibrous layer, the perichondrium, around the cartilage
model becomes the periosteum. Spongy bone develops first, to be replaced by
compact bone.

1. The secondary center of ossification develops when arteries enter the epiphysis.
On either side of the secondary center are articular cartilage distal to the diaphysis,
and the epiphyseal plate cartilage proximal to the diaphysis.
2. When the epiphyseal plate cartilage disappears (closes), the bone has stopped

growing lengthwise.

Vitamins

Vitamin D or calcitriol (activated cholecalciferol) is a derivative of cholesterol
which is activated in the skin by violet light and in the kidneys. Vitamin D increases
absorption of calcium from the intestine and therefore more is deposited in the bones.
Rickets is a Vit. D deficiency disease in childhood which makes the legs bow
permanently. In adults, Vit. D deficiency causes a type of weakening of the bone
called osteomalacia.

In order to avoid acid rebound or getting "hooked" on Calcium-containing antacids,
an enteric coated pill containing Ca phosphate and Vit. D is recommended.

Vitamin C or ascorbic acid is needed to make collagen. Collagen is the foundation
fiber of connective tissues.

Scurvy is a deficiency disease for Vit. C. What would happen to a person with
scurvy? Check out the story of Andersonville, GA. civil war prison camp.
http://www.sinclair.edu/sec/his102/mcknight/bm06.htm

Vitamins A and B12 have roles in bone growth. Excess Vit. A causes bone hypertrophy.

Hormones

Calcitonin and Parathyroid hormone (PTH) form an antagonistic hormone system
that regulates content in the blood stream. Bone can be regarded as a
reservoir of  Ca⁺⁺. When calcium levels are too low, PTH raises them by stimulating
osteoclasts which pull  Ca⁺⁺  out of the bones. Calcitonin is thought to inhibit
osteoclasts therefore lowing blood calcium. See pg. 185//189.

Steroid hormones including testosterone and estrogen also encourage calcium to be
deposited and remain in bone. Males or females, respectively, who have deficiencies of
one of these hormones may suffer from a weakening of the bones called
osteoporosis. See pg. 190//193. Taking too much testosterone (weight lifters?) can cause
premature closure of the epiphyseal plate and therefore shorter stature. The active form of
vitamin D (calcitriol) is another steroid hormone which increases calcium
absorption by the small intestine.

Pituitary giants are people who have had an excessive secretion of human Growth
Stimulating Hormone (hGH) during childhood.

Consider the following risk factors for osteoporosis:

1. Age - decreased hGH, estrogen and testosterone.
2. Post-menopausal - decreased estrogen secretion by ovaries.
3. Hysterectomy that also took out the ovaries causes a dramatic decrease of estrogen.
4. Petite frame - load strenthenes bone, a lack of load weakens them.
6. Sedentary life style. Arthritis may make exercise painful. Again, load strengthens
bone. See the piezoelectric effect, above.
7. Calcium intake. Calcium intake should follow the recommended daily intake
(RDA) and it should be ideally comnbined with Vit. D.Too much calcium can
contribute to arteriosclerosis. Eating antacids is a poor way to add calcium to a diet.
Frequently raising your stomach pH contributes to the acid rebound phenonmenon.
The basic causes of osteoporosis are hormonal and physical.

Excessive hGH in adulthood causes increased growth in the diameter of fingers and
other long bones as well as an increase in the width of the mandible, a condition called
acromegaly. Pituitary dwarfs are affected by too little hGH in childhood.
Achondroplastic dwarfism is a inherited dominant genetic condition where there is
insufficient cartilage formed as a precursor to bone formation. They have normal
trunks but short legs and arms.

Bone Fracture Repair - Stages (See page 189//191.)

1. Hematoma formation - occurs as blood vessels are broken and blood,

dead cells and bone debris fill the fracture and push the periosteum outward.
White blood cells including macrophages (from monocytes) and neutrophils
migrate into the fracture to clean up the hematoma. The intact periosteum
provides the osteoprogenitor cells to repair the fracture.
 
2. Soft Callus Formation (3 weeks) - occurs when collagenous fibers and

cartilage form in the fracture. Osteoblasts begin to form spongy bone.

See http://www-medlib.med.utah.edu/WebPath/BONEHTML/BONE015.html
 

3. Hard Callus Formation (3 months) - occurs as the fibrocartilage and spongy bone

are resorbed by osteoclasts and compact bone is deposited by osteoblasts.
Eventually the bony callus is usually undetectable by palpation as the dead bone
is resorbed.

A second problem for geriatrics is an increase in bone matrix minerals relative to
their collagen content. As collagen content drops due to a reduction in protein
synthesis in senescent cells, the bones become brittle and also more susceptible to
fracture. Experiments with hGH on geriatrics show improvements in bone and
muscle strength.
 

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Fracture Types (See page 188//192.)

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Bone Types - see pg. 177.

1. Long Bones - described in the previous section, include phalanges, humerus, ulna,
femur.
2. Short bones -somewhat cubic, examples are tarsals and carpals.
3. Flat bones -hard and compact on the outside; found in the skull, sternum,
ribs and scapula.
4. Irregular bones - include sesamoid bones imbedded in tendons, e.g., the patella,
and wormian bones found between the skull bones.

Important Bone Markings and Processes

1. Canal, Fissure, Foramen - openings through which nerves or blood vessels pass.

2. Fossa - a depression

3. Meatus - a tube-like canal

4. Sinus - cavity

5. Head, Condyle - large rounded, articular processes

6. Facet - a flat articular surface

7. Trochanter - a large projection of the femur

8. Tubercle - a small, rounded process

9. Tuberosity - a roughened area

Study Questions
1. Describe the stages of bone fracture repair.
2. How is the femur you had 5 years ago different than the one you have today?
3. Describe three risk factors for osteoporosis.
 

 Email:jaliff @ gpc.edu