Vitamin D deficiency accounts for the most common nutritional deficiency among children and adults. Osteomalacia describes a disorder of “bone softening” in adults that is usually due to prolonged deficiencies of vitamin D. This results in abnormal osteoid mineralization. In contrast, rickets describes deficient mineralization at the cartilage of growth plates in children.

Several cell types constitute bone and participate in the coordinated process of bone remodeling. Osteoclasts (bone-resorbing cells) are responsible for breaking down bone by secreting collagenase. Osteoblasts are responsible for depositing the osteoid matrix, a collagen scaffold in which inorganic salts are deposited to form mineralized bone. This intricate process is directly and indirectly influenced by hormonal signals, namely parathyroid hormone (PTH) and calcitonin, both of which act in response to serum levels of calcium.

In processes that decrease the amount of vitamin D or its bioproducts, normal serum calcium will be maintained by mobilizing calcium from the bones. Specifically, PTH will be secreted by the parathyroid glands in response to this hypocalcemia from vitamin D deficiency and will attempt to bring the body back to normal serum calcium levels. Bones are the primary target to recruit calcium, and by extracting calcium from the bones, osteomalacia will ensue. Therefore, in adults, processes that disrupt vitamin D metabolism and its production are at risk for eventually developing osteomalacia and its clinical manifestations.