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.

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