involved in the hearing loss (V). Although TNF-α, TNF receptor 1 and receptor 2 were observed in the vibrated cochlea, the expression of TNF receptor 2 was more prominent in the cochlea. The combination of TNF-α with TNF receptor 2 is capable of activating Jun N-terminal kinases (JNK) and nuclear factor (NF)-κB (Goeddel 1999). The activation of JNK and NF-κB has the function of an anti-apoptotic agent (Goeddel 1999, Watanabe et al. 2002, Biswas et al. 2003). On contrary, the activation of TNF receptor 1 induces apoptosis (Ashkenazi et al. 1998, Goeddel 1999). When both receptors are expressed, the activation of TNF receptor 2 enhances the effects of receptor 1 activation. The final fate of the cells should be related to the expression ratio of both receptors. Shear stress inhibits TNF-α induced apoptosis by activating phosphatidylinositol 3 (PI3)-kinase and inhibiting Caspase-3 (Pavalko et al. 2002).
Vibration induced VEGF and VEGF R2 expression in the cochlea, but not VEGF R1.
Our results confirm the biological significance of a previous in vitro study, which indicated that in vascular endothelial cells high shear stress induced an increase in VEGF R2 expression. This up-regulation reached its maximum and was in a linear gradient to the stress strength within a range of 2 to 40 dyne/cm2 (Abumiya et al. 2001).
The authors interpreted that an increase in the shear stress in the vasculature by post-ischemic reperfusion stimulates VEGF R2 expression, resulting in an increase in vascular permeability and leading to neo-vascularisation. After myocardial infarction the newly formed myofibroblasts express VEGF and VEGF R2 that seem to play a significant role in tissue repair/remodelling (Chintalgattu et al. 2003). When the cochlea is exposed to mechanical vibration, a shear stress is increased in the various cell types of the cochlea with concomitant increase of expression of VEGF and VEGF R2. Thus, VEGF may contribute to tissue remodelling and angiogenesis at the site of damage in an autocrine manner and may be important in preventing further damage to the cochlea.
The mostly enhanced expression was located in the spiral ganglion cells, stereocilia, supporting cells, the internal sulcus cells and epithelial cells of the lateral wall of the scala tympani. The spiral ganglion may be repaired under assistance of VEGF because both VEGF and VEGF R2 were expressed there.
Seki et al. (2001) suggested that the pathophysiology underlying vibration-induced hearing loss is an increase in porosity of the blood vessels in stria vascularis and degenerative changes in the intermediate cells of stria vascularis. The exact mechanism is being investigated. Vibration damage seem to cause upregulation of TNF and TNFα-receptors in spiral ganglion cells, and may cause necrosis and apoptosis, which leads to nerve degeneration.
7 CONCLUSION
The pathophysiological effects of vibration were studied.
(I) In the cross-sectional study, the prevalence of VWF was reduced and incidence was very low. The results in the cohort study indicated that in spite of a low prevalence of VWF (8%), sensorineural symptoms as numbness increased. Numbness was exposure-independent. Musculoskeletal disorders in the cohort study were more prominent on the right upper extremity, which carries the weight of the chain saw.
Vibration contributed to the development of musculoskeletal disorders in the upper extremity of forestry workers.
(II) Two tools have been constructed from mechanoreceptor- specific threshold shifts and threshold changes to assess tactile sensory function in the hands of forestry workers. Four patterns of threshold shift could be identified. The most common pattern in this group of subjects involved both hands and both median and/or ulnar sensory nerve pathways. Statistically significant positive threshold changes (i.e., reductions in sensitivity) were recorded in a majority of the hands over a five-year period. The threshold shift metric is closely associated with the tactile sensory changes.
(III) 27 out of 106 of forestry workers suffered from TN. TN-patients had poorer postural stability. In TN patients the activation or control of proprioceptive afferent endings may be faulty and may lead to inadequate postural reflexes. Vestibulospinal reflexes converge with proprioceptive input. There may be a mismatch of the impulses in the central control mechanisms.
(IV) In the animal model of the inner ear high frequency vibration causes more injury than low frequency vibration. The vibration can be exactly dosed and the responses evaluated with ABR.
(V) In vibration induced hearing loss it seems that shear stress may be the key factor for up-regulation of TNF-α, VEGF, TNF R1, TNF R2 and VEGF R2. The function of TNF-α is two-way, it can induce both cell damage and protection against apoptosis. The function of VEGF is to repair some of the damages to the cochlear cells.
In the future, an approach should be taken to evaluate the role of biomechanical risk factors in connection with hand-arm vibration exposure. Neurological examination may require ENMG, VPT and quantitative sensory testing in the future. The validity of the specific VPT in forestry worker population must be verified.
The inner ear damage model may provide insight into vibration-induced damages in the hand-arm vibration syndrome. It may provide a new understanding of mechanisms leading to vibration-induced hearing loss and vibration-induced cellular damage. In the future, detailed mechanism of vibration induced SNHL and pathophysiological mechanisms leading to HAVS should be researched.
More studies are needed for estimating the dose response relationship of vibration and SNHL in this model. Additional studies on upregulation of cytokines involved in the apoptotic pathway, in addition to TNF-α, are suggested. Also, the studies with the electron microscopy, magnetic resonance imaging and atomic force microscopy are needed to evaluate structural changes in cellular and molecular level in the inner ear.
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