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The skeleton comprises cartilage and bone and is a support for the insertion of muscles and tendons enabling movement, a shield for soft tissue organs, a site for storage of bone marrow, and a reserve pool of calcium, phosphate, and other ions. There are flat (eg, cranium, scapula, pelvis) and long (eg, humerus, femur, phalanges) bones. The outer surface of bone is enclosed in periosteum (a fibrous network of osteoblasts that synthesizes peripheral compact bone); endosteum lines its inner surface. The central portion of long bones is a hollow shaft of dense cortical bone termed the diaphysis; at both ends of many long bones are the metaphysis (composed of cortical and cancellous or trabecular bone), cartilaginous growth plate, and epiphysis.

Osteoblasts are bone-forming cells derived from stromal mesenchymal stem cells that secrete collagen types I and III and noncollagenous proteins that together form osteoid or bone matrix into which calcium and phosphate are deposited. Osteoclasts are bone resorbing cells that are derived from hematopoietic precursor cells. Bone modeling is the process by which the shape and size of a bone is determined and occurs only during intrauterine development and postnatal growth. Bone remodeling is a process in which formed bone is replaced by new bone and takes place throughout life.

Eighty percent of the skeleton is composed of cortical bone present in the cranium, scapula, mandible, ilium, and shafts of the long bones. Cancellous or trabecular bone is found in vertebrae, skull base, pelvis, and ends of the long bones. Since only 15% to 25% of trabecular bone is calcified, it has a large surface area and a high turnover rate and is particularly susceptible to disorders that affect bone mineralization. Intramembranous ossification is initiated by local condensation of mesenchymal stem cells that differentiate directly into osteoblasts. When intracellular levels of β-catenin are low, the mesenchymal stem cell evolves into a chondroblast. Longitudinal growth of bone is the result of chondrocyte proliferation in orderly columns within the cartilaginous growth plate (see eFig. 543.1). Resting or reserve cells at the most distal aspect of the growth plate differentiate into proliferating chondrocytes under stimulation by bone morphogenetic protein-6 and growth hormone. Locally synthesized insulin-like growth factor I(generated in response to growth hormone, thyroid and sex hormones) stimulates division of these chondrocytes and increase in the length of the cartilage growth plate and of the long bone. Proliferating chondrocytes mature into prehypertrophic chondrocytes, and these become hypertrophic chondrocytes that secrete collagen type X prior to their death. Endochondral bone develops as invading blood vessels bring with them chondroclasts, osteoclasts, and osteoblasts; chondroclasts reabsorb cartilage matrix and dying chondrocytes. Primary spongiosa of bone is formed and then replaced by mature bone. In addition to collagen type I, osteoblasts secrete many noncollagenous proteins (eg, bone-specific alkaline phosphatase, osteocalcin) into a matrix into which calcium and phosphate are deposited as hydroxyapatite. Osteoblasts have a life span of 3 months.

eFigure 543.1.

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