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Therefore, we propose that the role of IGF-1 in this process lies more on the maintenance of a normal pace of proliferation rather than in the initiation of cell division ( Cart igf-1r mutants compared to the global knockouts indicates that other cells such as osteoblasts ( The maturation of chondrocytes from a resting to a hypertrophic state is a critical event in regulating mineralization ( igf-1 knockout mouse indicates a role for IGF-1 in mineralization via regulation of chondrocyte differentiation ( igf-1 null animals, the switch from type II collagen to type X collagen expression during chondrocyte differentiation is perturbed as shown by an increased number of type II collagen-expressing prehypertrophic chondrocytes and persistent type II collagen expression in hypertrophic chondrocytes

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Evidence that intermittent treatment with parathyroid hormone increases bone formation in adult rats by activation of bone lining cells

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