Abstract
Investigations of age-related osteopenia increasingly suggest that, in addition to enhanced resorption, defective bone formation also contributes to bone loss and osteoporosis. Altered formation could explain why skeletal mass decreases in certain young adults who exhibit neither hypogonadism nor excess resorption (1–3). Such defective/diminished bone formation activity could putatively arise from decreased osteoblast number and/or function. Although there has been much study of osteoblast function and matrix production and mineralization, efforts have begun to examine the regulation of osteoblast progenitors and their maturation. Hormones and growth factors known to play a role in regulation of osteoblast function might also be expected to participate in regulation of osteoblast progenitor proliferation and differentiation. Such a role could signify pathogenetic as well as therapeutic importance for such regulatory factors.