Bone tissue is a reservoir of calcium and phosphate. If blood calcium is low, the body breaks down mineralized bone to release calcium into the bloodstream. If blood calcium is high, the body removes calcium from the bloodstream and stores it in bone for future needs.

Both osteoblasts and osteoclasts are constantly at work on bone. A balance between building and chewing (osteoblasts and osteoclasts) is critical and is under hormonal control.

High blood calcium (hypercalcemia): If blood calcium is too high, it’s time to deposit the extra calcium in the “calcium bank” – bone. Calcitonin (CT), made by parafollicular cells in the thyroid gland, is secreted when blood calcium is too high. Calcitonin inhibits osteoclasts and their bone chewing, and slightly stimulates osteoblasts, allowing these bone builder cells to “get ahead” with bone building. In doing so, the osteoblasts absorb calcium from the bloodstream and deposit it as hydroxyapatite in bone, thereby lowering blood calcium levels back to normal.

Low blood calcium (hypocalcemia): If blood calcium falls too low, the body withdraws some from the bone “calcium bank.” Parathyroid hormone (PTH) is secreted from the parathyroid glands, a set of small, pea-shaped glands on posterior edges of the thyroid gland. PTH stimulates osteoclastic (chewing) activity. Osteoclasts break down the mineralized portion of bone [hydroxyapatite, Ca₁₀(PO₄)₆(OH)₂], releasing calcium into the bloodstream and raising the blood calcium level back to normal. There is also a slight inhibition of osteoblasts, which helps the osteoclasts release even more calcium into the bloodstream since the osteoblasts are not taking it back out.

In summary:

High blood Ca2⁺ → parafollicular cells in thyroid release calcitonin → calcitonin inhibits osteoclasts while osteoblasts keep depositing Ca₂⁺ in new bone → blood Ca₂⁺ goes down to normal → calcitonin release stops

Low blood Ca₂⁺ → parathyroid glands release parathyroid hormone (PTH) → PTH stimulates osteoclasts → osteoclasts chew more bone → Ca₂⁺ released from bone → blood Ca₂⁺ goes up to normal → PTH release stops

One additional consideration is the third hormone involved in blood calcium homeostasis, calcitriol, which is hormonally-active vitamin D. PTH stimulates the kidneys to release calcitriol, which increases calcium absorption (from food) in the digestive system. This, along with the PTH, helps increase blood calcium, restoring it to normal.

Bone Remodeling

In children, bone is undergoing several dynamic processes all at once. In addition to constant remodeling and being involved in calcium homeostasis as just described, children’s bones are rapidly growing, along with the rest of the body. Human growth hormone (hGH) drives new bone tissue formation and bone growth at the epiphyseal plates of long bones and at multiple ossification centers in other bones. Levels of hGH are high in childhood, gradually decrease after puberty, drop fairly precipitously to low levels in young adults, and stay low the rest of our lives. After epiphyseal plates close, excess hGH (as from a secretory tumor) will not cause bones to lengthen further, but will cause bones to enlarge and thicken.

Throughout our lifetimes, bone is constantly remodeled. The activity that predominates—osteoblastic or osteoclastic—determines whether there is a net gain or a net loss of bone. In addition to blood calcium levels, physical stress (absence, presence, degree) also determines which type of osteo- cells are the most active. In adolescent and adult bones (and somewhat less so in children’s bones), moderate “good” stress (weight-bearing exercise) stimulates osteoblastic activity which thickens and strengthens bone.

Weight-lifters and other athletes know well the effects of moderate stress on bone formation and use that to their advantage in training. On the other hand, one of the side effects of extended space travel is bone loss due to being in a “weightless” environment (very little to no physical stress on bones). Astronauts loose just over 1% of their bone mass per month spent in space. “Bad” stress (friction in joints as a result of articular cartilage loss) also results in bone formation, in the form of bone spicules (bone spurs). This new bone formation is responsible for the joint deformities commonly seen in severe osteoarthritis.

The constant, active remodeling of bone is also the reason bone can heal after a fracture. The periosteum is critically important to and very involved in the repair process (more detail on this if/when you take our Pathophysiology course, HTHS 2230).