Bone is a living, supportive connective tissue — constantly being built up and broken down by a small cast of specialized cells, and tightly regulated by hormones to keep blood calcium levels stable.

Bone Composition

Compact bone is built from osteon structures, which house the blood vessels and nerves running through the bone matrix. Spongy bone is made of a lattice of trabeculae, which is what gives bone its lighter weight without sacrificing much strength.

Bone Matrix

Both components matter: a bone matrix with plenty of minerals but no collagen is hard but brittle, while one with collagen but insufficient mineral is flexible but too soft to support weight.

Bone Cells

Diagram showing the relationship between osteoblasts (build bone), osteocytes (monitor bone), and osteoclasts (dissolve bone) in the bone remodeling cycle.

Clinical Conditions

Osteoporosis

Happens when osteoclast activity outpaces osteoblast activity, leaving bones progressively weaker. Normally osteoblast activity should stay ahead of osteoclast activity; osteoporosis is common in women after menopause, when a drop in estrogen removes some of the normal brake on osteoclasts.

Osteogenesis Imperfecta

Caused by reduced collagen production, leading to brittle bones. If the mineral matrix is still there but the collagen/protein fibers are missing, the bone loses its flexibility — it has no give left to absorb force before it snaps.

Rickets

Caused by a vitamin D₃ deficiency, leading to softer bones. Low blood calcium availability means osteoblasts have less calcium to work with during bone formation, so the resulting matrix ends up softer than it should be.

Hormonal Processes

Sex hormones (estrogen, testosterone, and progesterone) stimulate osteoblast activity, driving bone growth.

Calcitonin becomes active when blood calcium is high, and works by inhibiting osteoclast activity — it slows bone breakdown so less calcium is released.

Calcitriol is the active form of vitamin D₃ in the body. At normal blood calcium levels, it tells the small intestine to absorb more dietary calcium and tells the kidneys to reabsorb calcium that would otherwise be lost in urine. It also signals the parathyroid gland to stop producing PTH once calcium is back to normal.

Parathyroid hormone (PTH) is released when blood calcium is low. It signals osteoclasts to break down bone matrix and release calcium into the blood, and at low calcium levels it works synergistically with calcitriol to also pull more calcium in from the small intestine and kidneys.

Putting the loop together: low blood calcium → PTH released → kidneys release stored calcitriol → calcitriol increases intestinal and kidney calcium absorption → PTH also triggers osteoclasts to free up calcium from bone → blood calcium rises back to normal → calcitriol tells the parathyroid gland to stop making PTH.