The body maintains a stable concentration of calcium in the blood and extracellular fluid through a tightly controlled process known as calcium homeostasis. This regulation is an ongoing feedback loop that ensures the amount of calcium available for immediate physiological use remains within a very narrow range, typically 8.8 to 10.4 milligrams per deciliter of blood. Precise control of this mineral is necessary for life, as even slight deviations from the normal range can have immediate and serious consequences for cellular function.
Essential Functions of Calcium
Calcium ions are involved in physiological processes beyond building strong bones and teeth. As an electrolyte, calcium carries an electrical charge that makes it indispensable for communication within the nervous system. When a nerve impulse arrives at a neuron, calcium influx triggers the release of neurotransmitters, allowing the signal to jump to the next cell.
Calcium is also essential for muscle function, as its release from internal stores initiates the contraction of skeletal, smooth, and cardiac muscles. Furthermore, it acts as a cofactor for many enzymes involved in biochemical reactions. For instance, the blood clotting cascade requires calcium ions to activate proteins that ultimately lead to clot formation and prevent excessive bleeding.
Key Hormones Maintaining Balance
Three primary chemical messengers regulate calcium concentration in the blood. Parathyroid Hormone (PTH) is produced by four small parathyroid glands located near the thyroid. PTH is secreted when receptors detect a fall in blood calcium levels, and its goal is to raise the concentration back to the normal set point.
Calcitriol, the active form of Vitamin D, is another hormone that increases blood calcium levels. Vitamin D is acquired through diet or sunlight, but it must be chemically modified first in the liver and then in the kidneys to become active calcitriol. This hormone specifically enhances the body’s ability to absorb calcium from consumed food.
The third major regulator is Calcitonin, produced by the parafollicular cells (C-cells) of the thyroid gland. Calcitonin is released when blood calcium levels become too high, and it decreases the concentration by opposing the actions of PTH. However, its role is considered less significant than PTH and Calcitriol, as abnormal calcitonin levels often cause few or no adverse symptoms.
The Organ Systems of Calcium Homeostasis
The hormones act upon three main target sites—the bone, the kidneys, and the small intestine. Bone functions as the body’s major calcium reservoir, holding over 99% of the body’s total calcium in the mineral matrix known as hydroxyapatite. When blood calcium drops, PTH stimulates specialized cells called osteoclasts to break down bone tissue, a process called bone resorption. This action releases stored calcium ions directly into the bloodstream.
The kidneys conserve the mineral and activate hormones. When PTH is released, it signals the kidney tubules to increase calcium reabsorption, ensuring less calcium is lost in the urine and more is returned to the blood. PTH also stimulates an enzyme in the kidneys that performs the final step in converting inactive Vitamin D into Calcitriol.
Calcitriol travels to the small intestine, the only source of new calcium intake from the external environment. Here, Calcitriol increases the efficiency of calcium absorption from digested food, boosting the total amount entering the circulation. Conversely, when blood calcium levels are elevated, Calcitonin acts primarily on the bone to inhibit osteoclast activity, slowing the release of calcium and promoting its deposition into bone. This coordinated action ensures blood calcium is kept within the narrow, life-sustaining range.
Conditions Resulting from Dysregulation
When calcium homeostasis fails, two main conditions result: hypocalcemia (low blood calcium) and hypercalcemia (high blood calcium). Hypocalcemia often results from a deficiency in Parathyroid Hormone (hypoparathyroidism), which can occur following damage to the parathyroid glands during neck surgery. Without sufficient PTH, the body cannot effectively mobilize calcium from the bone, reabsorb it in the kidneys, or activate Calcitriol, leading to a drop in circulating calcium.
Symptoms of hypocalcemia are primarily neuromuscular, as low calcium increases the excitability of nerve and muscle cells. Patients may experience paresthesias (numbness or tingling), especially around the mouth and extremities. More severe manifestations include painful muscle spasms (tetany), seizures, or cardiac rhythm abnormalities.
Hypercalcemia is most frequently caused by primary hyperparathyroidism, where the parathyroid glands produce too much PTH independently of the body’s need. Certain types of cancer can also cause hypercalcemia by releasing substances that mimic PTH. The excess calcium affects various organs, leading to non-specific symptoms that develop slowly.
The classic symptoms of hypercalcemia involve the central nervous system, gastrointestinal tract, and kidneys, often summarized as “moans, stones, groans, and psychic overtones.”
Symptoms of Hypercalcemia
- Moans and psychic overtones: Fatigue, muscle weakness, and confusion.
- Stones: Excess calcium precipitates in the kidneys, leading to the formation of kidney stones or permanent kidney damage.
- Groans: Common gastrointestinal issues such as constipation, nausea, and abdominal pain.