Abstract
Human aging is a complex process which, as a result of multiple genetically programmed mechanisms as well as stochastic events, leads to accumulation of damaging alterations in vital cellular functions. A variety of in vitro studies indicate that aging is associated with an overall decline in protein synthesis and protein turnover as well as with an accumulation of damaged molecules (Glowacki 1999). With respect to bone turnover, several authors investigated the effects of age on generation, maturation, and function of osteoblasts in experimental animals as well as in humans. In rats, for example, a defect in maturation of preosteoblasts into osteoblasts was demonstrated, which led to a more than ten-fold decrease in the number of osteoblasts with age (Roholl et al. 1994). Quarto et al. (1995) determined the number of osteoprogenitor cells in bone marrow from adult and aged rats as well as their ability to differentiate and form bone. The number of adherent colony forming cells was significantly lower in marrow cells from aged rats than in those from adult rats.
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Pietschmann, P., Gruber, R., Peterlik, M. (2008). Pathophysiology and Aging of Bone. In: Grampp, S. (eds) Radiology of Osteoporosis. Medical Radiology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-68604-0_2
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