Introduction

Bone serves as a framework for the body and as a metabolic reserve of calcium and phosphate at times of mineral deficiency. It consists of cells from two distinct lineages, bone-forming osteoblasts and bone-resorbing osteoclasts, and the calcified extracellular matrix that these cells secrete and remodel.

Bone formation begins in the embryo, either via a cartilaginous intermediate, as in the case of the long bones, or via a membranous intermediate, as in the case of the flat bones of the skull. Continued production of cartilage at specialized sites on the long bones, termed growth plates, and the subsequent conversion of this cartilage into bone results in longitudinal postnatal growth. Skeletal growth and development is regulated by genetic, mechanical and hormonal mechanisms. In general, genetic influences dictate the basic structure of the skeleton, while responses to mechanical loading adjust the strength of particular bones to their functional environment.

Simultaneously, hormonal mechanisms coordinate the movement of calcium and phosphate to and from the skeleton, thereby enabling bone to act as a reservoir of these minerals at times of calcium stress (e.g., pregnancy and lactation). At the cellular level, bone growth is coordinated by an array of interacting cytokines and growth factors, which control bone cell division, maturation and activity.

Failure of the mechanisms controlling bone cell function, especially during bone turnover in adults, leads to bone loss, and this can produce clinical osteoporosis. Other skeletal disease states result from nutritional deficiency, e.g., rickets, or from genetic defects, e.g., osteopetrosis or osteogenesis imperfecta.

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