Fahim Khan

Bone Short Answer Questions: Answer 2/3 or all 3 for extra credit.

1. A postmenopausal woman slips while stepping off a curb, falls, and 
cracks her pelvic bone. During diagnosis, the physician begins to 
consider the possibility of osteoporosis. What are the symptoms and risk 
factors of osteoporosis? What diagnostic procedures would the physician 
order to verify the diagnosis of osteoporosis? If the diagnosis is 
verified, what treatment will the physician initiate? 
2. Describe how calcium homeostasis is regulated by calcitriol, 
calcitonin and parathyroid hormone.
3. Compare the structure and functions of spongy and compact bone. 
Compare the mechanisms of intramembranous ossification and endochondrial 
ossification. 

1. Osteoporosis causes bone to become abnormally porous (collagen and calcium is

lost) and this decrease in mass and density makes the bone weaker than normal. The bone
easily fractures or, in areas like the spine, may compress (leading to a hump or scoliosis).
There aren’t really any symptoms, other than something overt like a bone fracture, but
there are several well-defined risk factors.
For example, osteoporosis commonly affects postmenopausal women because the
female body stops producing estrogen, since the menstrual cycle ceases as ovaries stop
releasing eggs; estrogen production is directly related with calcium absorption in bones.
Most women who get osteoporosis are either white or Asian, and usually over 70 since
the process of bone loss is gradual and doesn’t manifest as a serious problem until around
30% of bone mass loss at age 70 – and, in fact, the longer you live the worse your bones
get (also, entering menopause earlier means more bone damage due to estrogen
deprivation occurring earlier).
Not only elderly white/Asian women get osteoporosis though, as other risk factors
for it include long periods of inactivity due to injury (or laziness), smoking, eating
disorders, certain medications e.g. anticonvulsants, overconsumption of alcohol, too
much protein in diet, too little calcium in diet, and lack of sunlight (required for the body
to make vitamin D, which itself aids in calcium absorption).
A physician could verify that a person has osteoporosis by performing a bone
density scan (usually dual­energy X­ray absorptiometry or DEXA, with low absorption 
meaning low density; other options are ultrasound, or normal X­rays). A blood or urine
test for chemical markers that may point to occurrence of bone formation also works.
Treatments for osteoporosis involves avoiding its preventable risk factors
(exercise, end smoking/alcohol/coffee addiction, get enough calcium and vitamin D).
Also, estrogen hormone replacement therapy (HRT) for menopausal women, selective 
estrogen receptor modulator (SERM) therapy (similar to HRT therapy without increased 
risk of breast cancer, though it may increase chances of dangerous blood clots), 
biophosphinates that slow down bone destruction rate, calcitonin to increase bone 
turnover rate (so that bones don’t have a chance to become brittle), calcitriol (a vitamin­D 
replacement used against postmenopausal osteoporosis), or teriparatides to promote bone 
formation.

2. Calcitriol is activated vitamin D and its role is to increase calcium absorption by

stimulating intestines, and decrease calcium and phosphate excretion (reduces urinary
secretion). It also promotes osteoclast activity, which results in destruction of bone. All
three processes of course increase blood calcium concentration.
Calcitonin (secreted by C cells in thyroid) reduces calcium when there is too
much by quickly (in 15 minutes) reducing osteoclast activity by up to 70%, and
increasing osteoblast number and acitivity. The osteoblasts create new bone,
incorporating calcium into their structure.
Parathyroid hormone (PTH) secreted by parathyroid glands increases blood
calcium level by promoting osteoclast production and activity, while reducing osteoblast
bone formation, reducing calcium secretion and increasing phosphate secretion (which
controls bone destruction) in urine. PTH also plays a crucial part in the formation of
calcitriol.
The interaction of these three hormones prevent hypercalcemia and hypocalcemia.

3. Compact bones are solid bones that sandwich spongy bones (AKA diploe) –
because of this, compact bones are divided into inner and outer varieties (inner side
facing a body cavity). Spongy bones are mostly hollow, with crisscrossing struts called
trabeculae that are spread throughout for strength. The hollow structure of spongy bone
allows them to act as “shock absorbers” that dissipates damage to the outer compact bone
so that the inner compact bone isn’t damaged (which would probably result in wounding
vital organs and also open up the body to the outside). Compact and spongy bones are
found in flat bones, such as those found in the sternum or cranium.
The two types of bone formation – intramembranous (IM here for convenience)
and endochondrial (EC, for convenience) ossification – correspond to different bone
types. IM ossification results in flat bones, while EC ossification results in mostly long
bones.
IM ossification starts out with the mesenchyme – undifferentiated progenitor cells
that are part of the embryonic mesoderm – “congealing” into strands (since the IC matrix
is gel-like) into the precursors of spongy bone – a network of trabeculae. Osteoblasts
form uncalcified osteoid tissue on the trabeculae, and then calcium phosphate crystallizes
the structured matrix formed, with some of the osteoblasts getting trapped within and
becoming osteocytes. Osteoblasts on the surface form compact bone while osteoclasts in
the network carve out hollow marrow spaces.
EC ossification means bone forming within cartilage. The bone sort of grows out,
so that by looking at a piece of long bone, the diaphysis would be the origin of growth
while the epiphyses are the latest growths. The diaphysis was originally cartilage
(chondrocytes) which became ossification centers (first steps in making bone), and the
outer membrane (the perichondrium) produce a bony collar. This new structure prevents
diffusion of nutrients into inside so chondrocytes inside die and the resulting hollow
space becomes the marrow or medullary cavity. A periosteal bud forms around the bony
collar and produces osteogenic cells that go into the marrow and become osteoblasts, and
these start depositing osteoid tissue which calcify into trabeculae (not unlike IM
ossification here). Osteoclasts are also in the cavity, enlarging it. The bone gets larger and
larger, and secondary ossification centers at the two tips of the bone not covered by the
periosteum form the articular cartilage.