10.19 : Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.

Hypocalcemia, a condition characterized by abnormally low calcium levels, can adversely affect different body systems, including circulation, muscles, nerves, and bone. Without adequate calcium, blood has difficulty coagulating, the heart may skip beats or stop beating altogether, muscles may have problems contracting, nerves may have difficulty functioning, and bones may become brittle. The causes of hypocalcemia can range from hormonal imbalances to an improper diet and treatments vary according to the cause.

Conversely, in hypercalcemia, a condition characterized by abnormally high calcium levels, the nervous system is underactive, resulting in lethargy, sluggish reflexes, constipation and loss of appetite, confusion, and in severe cases, coma.

Pathways in Calcium Homeostasis

The body regulates calcium homeostasis with two pathways; one is signaled to turn on when blood calcium levels drop below normal levels, and one is signaled to turn on when blood calcium levels are too high.

Calcium is a chemical element that cannot be produced by any biological processes. The only way it can enter the body is through the diet. The bones act as a storage site for calcium: The body deposits calcium in the bones when blood levels are too high, and it releases calcium from the bones when blood levels are too low. This process is regulated by PTH, vitamin D, and calcitonin.

Cells of the parathyroid gland have plasma membrane receptors for calcium. When calcium is not bound to these receptors, the cells release PTH, which stimulates osteoclast proliferation and resorption of bone by osteoclasts. This demineralization process releases calcium into the blood. PTH also promotes the reabsorption of calcium from the urine by the kidneys so that the calcium returns to the blood. Finally, PTH stimulates the synthesis of vitamin D, which stimulates calcium absorption from any digested food in the small intestine.

When all these processes return blood calcium levels to normal, the calcium binds with the receptors on the surface of the cells of the parathyroid glands, and this cycle of events is turned off.

When blood levels of calcium are too high, the thyroid gland is stimulated to release calcitonin, which inhibits osteoclast activity and stimulates calcium uptake by the bones. It also decreases the reabsorption of calcium by the kidneys. All of these actions lower blood levels of calcium. When blood calcium levels return to normal, the thyroid gland stops secreting calcitonin.

This text is adapted from Openstax, Anatomy and Physiology 2e, Section 6.7: Calcium homeostasis: Interactions of skeletal systems and other organ systems.