ABSTRACT
Bone is composed of a highly specialized cell matrix that is made up primarily of osteoblasts, cells responsible for laying down new bone and increasing mineralization, and osteoclasts, which resorb mineralized bone. e bony matrix, or osteoid, is composed of type 1 collagen and noncollagenous proteins, primarily osteocalcin. Calcium and phosphate salts complex to increase the hardness of the bone; the serum levels of these essential minerals are regulated by vitamin D and parathyroid hormone (PTH).5 Bone mineralization begins before birth and continues throughout childhood and adolescence. Peak acquisition of bone mirrors the adolescent growth spurt, and bone formation exceeds resorption until the time of peak bone mass stage, which occurs sometime between 25 and 30 years old. In general, if vitamin D levels are decient during rapid skeletal growth as occurs in childhood, the clinical manifestation is of rickets, with cupping and widening of metaphyseal lines; however, this complication rarely occurs in CF even
in the presence of vitamin D deciency. If vitamin D de- ciency occurs following the completion of growth or aer closure of growth plates, osteopenia and osteomalacia are the norm, as demineralized osteoid replaces mineralized bone during remodeling.5 Age-related bone loss occurs in both sexes as part of the aging process, where bone resorption exceeds formation.
