Selective loss of unmyelinated nerve fibers after extracorporeal shockwave application to the musculoskeletal system.

Application of extracorporeal shockwaves (ESW) to the musculoskeletal system may induce long-term analgesia in the treatment of chronic tendinopathies of the shoulder, heel and elbow. However, the molecular and cellular mechanisms behind this phenomenon are largely unknown. Here we tested the hypothesis that long-term analgesia caused by ESW is due to selective loss of nerve fibers in peripheral nerves. To test this hypothesis in vivo, high-energy ESW were applied to the ventral side of the right distal femur of rabbits. After 6 weeks, the femoral and sciatic nerves were investigated at the light and electron microscopic level. Application of ESW resulted in a selective, substantial loss of unmyelinated nerve fibers within the femoral nerve of the treated hind limb, whereas the sciatic nerve of the treated hind limb remained unaffected. These data might indicate that alleviation of chronic pain by selective partial denervation may play an important role in the effects of clinical ESW application to the musculoskeletal system.

Neuron loss during early adulthood following prenatal low-dose X-irradiation in the mouse brain.

PURPOSE: Apart from subsequent cell death, little is known about long-term effects of a prenatal low-dose X-irradiation (PLDI) on nuclear (n) and mitochondrial (mt) DNA, and whether these effects are connected with reduced neuron numbers in the adult brain. MATERIALS AND METHODS: Pregnant mice were X-irradiated with 0, 10 or 50cGy at day 13 (E13) of pregnancy. One day after (E14), or postnatally at day 25 (P25) or P180, the brains of the offspring were analysed concerning the extent of nDNA repair, mt biogenesis, and the relative content of nDNA single strand breaks (SSB). Stereology was applied for evaluating neuronal loss. RESULTS: One day after irradiation no unrepaired SSB were detected. Significant results were mainly obtained for hippocampal pyramidal cells at P180, particularly cell loss following 50 cGy PLDI, increased SSB content and mt biogenesis (0 vs. 10cGy) but decreased mt biogenesis for 10 vs. 50 cGy. CONCLUSIONS: A hypothesis closely related to that regarding molecular events during aging is presented for explaining this second wave of cell death in adult mice following PLDI as a result of accumulated mtDNA damage caused by PLDI. A possible relation to the neurodegenerative hypothesis of schizophrenia is discussed.