Parathyroid hormone (PTH) governs one of the body’s most tightly controlled processes: maintaining stable levels of calcium in the bloodstream. This hormone is fundamental for life, ensuring calcium is available for bone structure, nerve signaling, muscle contraction, and heart function. Produced by small glands in the neck, PTH acts as a rapid-response system to prevent calcium levels from dropping below a healthy range.
The Parathyroid Glands: Source and Trigger
The parathyroid glands are typically four tiny, round structures, each about the size of a grain of rice, nestled on the posterior surface of the thyroid gland in the neck. These glands are distinct from the thyroid and are solely responsible for synthesizing and secreting PTH. Specialized cells within these glands constantly monitor the concentration of calcium circulating in the blood.
The release of PTH operates based on a negative feedback loop. When blood calcium levels begin to fall, specialized calcium-sensing receptors on the parathyroid cells detect this change immediately. This drop in calcium triggers PTH secretion, causing the glands to release the hormone into the bloodstream. PTH then travels to distant organs to restore calcium levels to normal, which signals the parathyroid glands to slow or stop further PTH production.
PTH’s Central Role in Calcium Homeostasis
Parathyroid hormone acts simultaneously on three target organs—the bones, kidneys, and small intestine—to elevate calcium concentrations in the blood. The hormone’s primary goal is to restore calcium balance, even if it means “borrowing” the mineral from the skeleton, the body’s largest reservoir. PTH achieves this balance through direct action on the bone and kidneys, and an indirect effect involving Vitamin D on the intestine.
Action on Bone
Bone tissue serves as the body’s vast mineral bank, storing about 99% of total body calcium. PTH signals the body to make a withdrawal from this bank by stimulating bone resorption. Specifically, PTH binds to osteoblasts, the cells responsible for building bone, and prompts them to release a signaling molecule called RANKL.
RANKL signals the osteoclasts, which are the cells responsible for dissolving bone tissue. Increased osteoclast activity breaks down the bone matrix, liberating stored calcium and phosphate directly into the bloodstream. While short-term PTH release maintains blood calcium, chronically high levels can lead to a net loss of bone density over time.
Action on Kidneys
Parathyroid hormone executes a crucial “saving” strategy within the kidneys to minimize calcium loss in the urine. It acts on the kidney tubules, increasing the reabsorption of calcium back into the blood from the filtered fluid. This action ensures that less calcium is excreted, thereby conserving the existing supply.
Simultaneously, PTH promotes the excretion of phosphate into the urine, which is equally important for raising free calcium levels in the blood. High phosphate concentrations can bind to calcium, forming insoluble salts that remove usable calcium from circulation. By reducing phosphate reabsorption in the kidneys, PTH ensures that the calcium released from the bone remains available and active in the bloodstream.
Indirect Action via Vitamin D
The third way PTH boosts blood calcium is by ensuring the body can properly absorb the mineral from consumed food. In the kidneys, PTH stimulates the activity of the enzyme 1-alpha-hydroxylase. This enzyme converts the inactive form of Vitamin D into its biologically active form, calcitriol.
Calcitriol then travels to the small intestine, where it enhances the absorption of dietary calcium across the intestinal lining. Without this PTH-driven activation, even a calcium-rich diet would be poorly utilized by the body. This indirect action is a slower but sustained mechanism for long-term calcium maintenance.
Health Implications of PTH Imbalance
When the delicate balance of PTH secretion is disrupted, it can lead to two major clinical conditions with widespread effects on the body’s systems. These imbalances typically result from issues with the parathyroid glands or conditions that alter mineral levels. The resulting symptoms are a direct consequence of either too much or too little calcium circulating in the blood.
Hyperparathyroidism occurs when there is an overproduction of PTH, often due to a benign tumor on a parathyroid gland. The excess hormone leads to persistently high blood calcium levels, known as hypercalcemia. Chronic hypercalcemia can cause generalized fatigue, muscle weakness, excessive urination, and increases the risk of developing kidney stones. Continuous “borrowing” of calcium from the skeleton compromises bone health, leading to osteoporosis and an increased risk of fractures.
Conversely, hypoparathyroidism results from insufficient PTH production, most often caused by accidental damage to the glands during neck surgery. This lack of PTH causes blood calcium to drop to low levels, a state called hypocalcemia. Symptoms often involve neuromuscular excitability, including muscle cramps, spasms, and tingling or numbness, particularly in the fingers, toes, and around the mouth. In severe, untreated cases, hypocalcemia can trigger tetany, characterized by sustained, involuntary muscle contractions.