1. Both hypo and hyper- thyroidism (Not parathyrodism) during childhood can caus

Question

1. Both hypo and hyper- thyroidism (Not parathyrodism) during childhood can cause short structure at adulthood. How is that possible?

2. Estrogen has a stronger effect on bone and cartilage than does testosterone. Also, Females enter puberty 2-3 years earlier than males. How do these two factors account for general defferences in height between males and females?

3. Do you predict that hyperpituitarism causing elevated GH secretion during childhood could affect adult height? Why or why not; and how so?

4. Would you expect a healthy person with well-functioning parathyroid glands and normal vitamin D levels to be hypocalcemic if they have a short-term dietary deficiency?

E.

1. Folate is required for proper mitosis. Could a folate deficiency affect skin and or bone repair? If not, why not? If so, how and why?

2.Vitamin C is required for collagen production. Could a vitamin C deficiency affect skin and / or bone production, maintenance and repair? If not why not? If so, why?

3.Cartilage does not heal as easily as do many other tissues. Why might that be?

4. Why must cartilage die before blood vessles move into a bone that is developing via endochondral ossification?

5.Bone marrow transplants for blood deseases often use blood taken from pelvic bone (ilium) of the donor. What is a benefit of sampling from the ilium rather than the shaft of the femur?

6.Bob the osteocyte lives in of lacunae closest to the central canal of his osteon. Across the next lamella, moving out toward the outer border of his osteon, lives Pam the osteocyte. Continuing to move outward, we find Paul in the next layer, then Tom in the next. Tom lives in the layer of lacunae adjacent to the outermost lamella of the osteon.

i) Draw an osteon, label lacunae, canaliculi, central canal, lamellae. Now draw more bone around it, indicating how blood supply reaches the central canal.

ii) Do Bob, Pam, Paul and tom live in compact or spongy bone? Explain:

iii) How do these bone cells get nutrients?

iv) Might these bone cells physically contact each other? Explain:

v) Draw a close-up of these cells and the wedge of the osteon that they live in. Be sure to include the cells' extentions and where those are. Draw some glucose molecules, indicating where the glucose came from and how they are able to get to each cell.

7. Sam, Harry and Ted live in a trabecula. Sam on the outside layer, Harry in the middle, and Ted on the inside.

i) Compare and contrast how these cells get nutrients with how Bob etc get nutrients.

ii) Do Sam, Harry and Ted live in a compact or spongy bone?

8. Osteoarthritis is a disease marked by loss/ breakdown of articular cartilages. Even though excercising these joints can be painful, low-impact exercise of the joints can help prevent or slow the progression of the desease. Why/ How?

9. Marjorie has been experiencing pain in her shoulder. During a consult with a physical therapist, Marjorie reveals that she has had no memorable injuries to the joint ( or significant injuries anywhere). She maintains a very low level of physical activity, making no specific effort to excercise. Marjorie assumes it is bursitis; but, after thorough examination, the PT tells Marjorie that her shoulder is depressed: scapula is literally sagging down, pulling on tendons and ligaments, and causing discomfort. PT assures Marjorie that exercises designed to strengthen the shoulder muscles should alleviate her pain.

i) Is the PT full of it or on to something (ie, is this possible)? Explain:

ii) What type of joint is, and types of movement allowed by, shoulder?

iii) Name three muscles the PT might target for strengthening.

Explanation / Answer

Question 1

Answer

The thyroid hormones produce its actions by binding to thyroid hormone receptors (TR)

These are two types THR and THR . These are Present in thyroid cells called thyrocytes. These receptors (THR- and THR-) also present in Osteoblasts, Chondrocytes and Osteoclasts.

Abnormal functioning of THR- leads to retardation of growth, delayed bone age, distubances in mineralization of bone and reduces the bone marrow density. Chondrification and bone mineralization are regulated by T3. In hyperthyroidism T3 actvate and releases IL-6 and IL-8, increases the effects of IL-1 and IL-6,that is synthesis of osteocalcin, increased proliferation, differentiation and apoptosis of osteoblast cells.

TSH is act as negative regulator of bone turnover and it leads to enhanced bone remodeling and osteoporosis.

          Hyperthyroidism in childhood produces premature accumulation of growth plates and leads to short stature. The balance between bone formation and bone destruction is disturbed.

Hypothyroidism in childhood can also result in growth retardation or may cause growth arrest; endochondral ossification is disturbed, and increased short stature.

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