Like other forms of connective tissue, the bone is composed of cells and fibers. Unlike the other types of connective tissue, however, the bone has higher amounts of calcium deposits, making it harder. This unyielding structure of bone enables it to perform its functions of support and protection.
The physical properties of bone are nothing short of amazing. Aside from maintaining great strength, bone is also capable of some degree of elasticity while being surprisingly lightweight. From its gross structure to microscopic levels, bone construction was designed for great strength while maintaining a great economy for material and weight.
However, despite its apparent toughness, bone is a living structure. It responds to metabolic and nutritional changes as well as endocrine influences. Bone undergoes constant reorganization while maintaining a certain degree of hardness necessary for its supportive and protective functions.
Parathyroid Hormones
Parathyroid hormone is responsible for controlling the extracellular calcium and phosphate concentrations. It does so by regulating intestinal reabsorption, renal excretion and the exchange between the extracellular fluid and the bone.
Parathyroid hormones are produced by the parathyroid glands located posterior to the thyroid gland. Normally, humans possess four parathyroid glands but in some cases, there could be as many as six. Removal of half the number of parathyroid glands may not affect the normal physiology much. However, the removal of three out of four of the normal glands may result in transient hypothyroidism. This means that even if only one of the parathyroid glands remain, it can compensate for the loss of the other three glands.
Parathyroid hormone acts on bone to elevate the levels of calcium in circulation in two ways:
- One is a rapid phase that calls on bone cells or osteocytes and proceeds in a matter of minutes to several hours. Existing osteocytes in the bone matrix pump calcium ions from the bone fluid into the extracellular fluid, increasing the circulating calcium ions in circulation.
- Another mechanism is slower and is dependent on the activation of osteoclasts. This mechanism could take days to weeks because osteoclasts are not directly stimulated by parathyroid hormone. Instead, they receive signals from the osteocytes to increase bone resorption.
Bone Disease in Hyperparathyroidism
Normally, there is a strict balance maintained between bone deposition by osteoblasts and bone resorption by the osteoclasts. Even in mild hyperparathyroidism, the activity of osteoblasts can compensate for the slight increase in bone resorption caused by activated osteoclasts. However, in severe hyperparathyroidism, bone resorption far outweighs the formation of new bone and the bone may be eaten away entirely. It is for this reason that bone fractures are commonly the reason a hyperparathyroid patient seeks medical help.
In cases of extremely high levels of parathyroid hormone, radiographs of bones reveal extensive decalcification and large punched-out areas filled with osteoclasts in the form of giant cell osteoclast "tumors". This means that the bone structure is extremely weakened by excessive resorption that even slight trauma can result in multiple fractures. The cystic bone disease of hyperparathyroidism is called osteitis fibrosa cystica.
Primary hyperparathyroidism is caused by an abnormality in the parathyroid glands themselves. Usually, the increased activity of the parathyroid glands are caused by tumors, which actively secrete parathyroid hormone. These tumors are more common in women than in men.
Secondary hyperparathyroidism, on the other hand, occurs as a compensatory mechanism for low calcium levels. This then signals the parathyroid glands to increase secretion of parathyroid hormone to replenish the depleted calcium ion in the circulation with calcium derived from deposits in the bone. Secondary hyperparathyroidism can be caused by vitamin D deficiency or chronic renal disease, in which the kidneys are too damaged to produce the active form of vitamin D in sufficient amounts.
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