Stimulation of fracture-healing with systemic intermittent parathyroid hormone treatment.

Over the past several years, there has been an increasing interest in the biology of bone repair and potential technologies for enhancing fracture-healing. Part of this interest is derived from the growing age of the population and the recognition that increased age carries an increased risk of complications after fracture. Although use of locally implanted or injected growth factors has received the most attention, systemic treatments for the enhancement of bone repair, especially for situations in which bone repair may be diminished or delayed, are now under investigation.

Advanced glycation end products induce apoptosis in fibroblasts through activation of ROS, MAP kinases, and the FOXO1 transcription factor.

Advanced glycation end products (AGEs) are elevated in aged and diabetic individuals and are associated with pathological changes associated with both. Previously we demonstrated that the AGE N(epsilon)-(carboxymethyl)lysine (CML)-collagen induced fibroblast apoptosis through the cytoplasmic and mitochondrial pathways and the global induction of proapoptotic genes. In the present study we investigated upstream mechanisms of CML-collagen-induced apoptosis.