The injury to the sensory and suppo

The injury to the sensory and supporting cells is evident following the exposure and
the degeneration or loss of these cells will continue for some time after the exposure
has ceased. As the hair cells degenerate they are replaced by expansion of the
surrounding Deiters’ and pillar supporting cells which form a “phalangeal scar” in the
surface or reticular lamina of the organ of Corti.
More recently attention has centred on pathological changes in the lateral wall tissues
of the cochlea as well as the fibrocytes in the spiral limbus, a region medial to the
sensory cells of the organ of Corti. There is evidence of swelling and atrophy of the
stria vascularis, loss of the fibrocytes within the spiral ligament and the spiral limbus.
7, 9 Interestingly, all these structures are involved in the maintenance of the ionic
composition of the cochlear fluids, particularly endolymph, suggesting some more
generalised disturbance of ion homeostasis may occur as a consequence of the
cochlear injury. Injury to the lateral wall and supporting tissues is now recognised as a more significant cochlear pathology following noise exposure than previously
realised.
Changes occur in the central auditory nuclei which more likely are secondary to the
peripheral injury (eg. Zhang and Kaltenbach10). However, some studies have
suggested that the functional and structural alterations in the central nuclei and
auditory cortex may be more extensive than can be expected by the degree of
peripheral injury (eg Ryan et al.11). Cochlear injury and auditory function after noise
exposure may also be modified by further noise exposure in the post-noise period.12
Relationship to hearing loss—There is good evidence that cochlear hair cell loss or
permanent stereocilia abnormalities on surviving hair cells are correlated with the
permanent hearing loss. However, there may be some functional change without
significant sensory cell loss, although this may well be correlated with subtle sensory
cell injury or other changes in the cochlea, such as to lateral wall tissues and neurons.
Recent evidence 8 of continuing neuronal degeneration following noise exposure but
in the absence of hair cell loss and changes in auditory thresholds indicates that there may be subtle cochlear injuries that are not manifest as changes in thresholds, a routine clinical test of auditory function.
Temporary hearing loss has been shown to be correlated with reversible changes to
stereocilia stiffness and swelling of the primary type I afferent neurons 14, and may
also correlate to structural or molecular changes to the transduction channels (tip
links). Significant metabolic and molecular changes are also observed in the cochlea
following acute noise exposures that may represent a responsiveness of the cochlea to noise exposure, and it is not unreasonable to assume that not all the hearing loss is going to be correlated to structural abnormalities. Indeed it is becoming more
apparent that the acute hearing loss may occur without any evidence of overt
structural changes and may thus represent an adaptation to the noise exposure.
Mechanisms—There have been substantial advances in our understanding of the
mechanisms of the cochlear injury following noise exposure. Some injury to the organ
of Corti, including the more subtle pathologies such as stereocilia fracture and loss,
from high intensities and impulse noise exposures is a consequence of direct mechanical damage.
However, there is good evidence that the hair cell injury from lower level and chronic
exposures has a more metabolic genesis and most likely is due to oxidative stress and the excessive production of Reactive Oxygen Species (ROS) and free radicals.6, 16 These free radicals are molecules with an unpaired electron and in excessive amounts interact with other stable molecules, such as proteins, DNA and lipids, to cause cellular damage and degeneration. ROS may include oxygen free radicals, such as superoxide, which may be produced in the cochlea from excessive mitochondrial activity in hair cells and changes in cochlear blood flow (see Henderson et al.6 for more detail). These interact with hair cell molecules to cause cellular degeneration leading to cell loss.
There is strong evidence for an increase in various ROS molecules after noise
exposure and treatment of the cochlea with free radical scavengers or antioxidants or
block of oxidative enzymes can reduce the amount of cochlear injury.
The neuronal injury is likely the consequence of glutamate excitotoxicity. Glutamate
is the main neurotransmitter at the IHC/primary afferent neuron synapse. Excessive
release of glutamate during noise exposure, possibly coupled with poor clearance of
glutamate in the synaptic region by surrounding supporting cells, leads to prolonged
stimulation of the afferent synapse, neuronal swelling and degeneration. This effect
on the afferent terminals and the subsequent hearing loss can be blocked by glutamate receptor antagonists 14 (Gordon and Thorne unpublished observations), supporting an excitotoxic mechanism for the neuronal noise-induced injury. Oxidative stress may also be a cause or contributor to the neuronal injury 6.
Degeneration of cochlear tissues results from a combination of necrotic and apoptotic
processes.6, 17 Activation of a variety of apoptotic triggers have been identified in
cochlear tissues following noise exposure and this may also be a consequence of
increased intracellular calcium associated with the uptake or release in hair cells
during the chronic hair cell stimulation.
The mechanism of the changes to the stria vascularis, the spiral ligament and spiral
limbus have not been established. As these areas are involved in ion homeostasis, the structural and degenerative changes may be a consequence of a metabolically-induced abnormality in ion handling by these tissues. During sound stimulation there is a movement of potassium ions from endolymph, through the hair cells and into the
extracellular space. This potassium is removed from the extracellular space by the
epithelial supporting cells in the organ of Corti and the fibrocytes of the lateral and
medial wall tissues to be recycled back to the stria vascularis.
During noise exposure there may be excessive release of potassium into the
extracellular space which may not be removed adequately leading to the oedema and
degeneration observed in these supporting tissues. It is true that the functional
consequences of the changes in the stria vascularis and fibrocytes are not well
established.7 However, the cochlea may cope adequately with this lateral wall
degeneration whilst performing in quiet but there may be a more significant effect
during physiological noise exposure if the recycling pathway for potassium and other
metabolites has been impaired by the noise-induced degeneration of these supporting
structures. This has yet to be established.

Hasil (Bahasa Indonesia) 1:

Cedera pada sel sensoris dan penunjang jelas mengikuti pemaparan dandegenerasi atau kehilangan sel-sel ini akan terus selama beberapa waktu setelah eksposurtelah berhenti. Sebagai merosot sel-sel rambut mereka digantikan oleh perluasansekitar Deiters' dan pilar penyangga sel-sel yang membentuk "phalangeal bekas luka" dipermukaan atau retikuler lamina organ dari Corti.Baru-baru ini perhatian telah berpusat pada perubahan patologis dalam jaringan dinding lateralkoklea serta fibrocytes dalam spiral limbus, suatu medial ke wilayahIndra sel-sel organ dari Corti. Ada bukti dari pembengkakan dan atrofistria vascularis, hilangnya fibrocytes dalam ligamentum spiral dan spiral limbus.7, 9 Menariknya, Semua struktur ini terlibat dalam pemeliharaan ionikKomposisi cairan koklea, terutama endolymph, menyarankan beberapa lagimenghindari gangguan homeostasis ion merupakan kontributor dapat terjadi sebagai consequence darikoklea cedera. Cedera dinding lateral dan jaringan penyokong sekarang diakui sebagai patologi koklea lebih signifikan setelah terpapar kebisingan dari sebelumnyamenyadari.Perubahan terjadi di pusat inti pendengaran yang lebih kemungkinan besar sekunderperifer cedera (misalnya. Zhang dan Kaltenbach10). Namun, beberapa studi telahmenyarankan bahwa perubahan-perubahan struktural dan fungsional di pusat inti dankorteks pendengaran mungkin lebih luas daripada yang dapat diharapkan oleh tingkatcedera perifer (misalnya Ryan et al.11). Koklea cedera dan fungsi pendengaran setelah kebisinganpaparan juga dimodifikasi oleh paparan kebisingan lebih lanjut dalam suara pasca period.12Hubungan dengan pendengaran — ada bukti baik itu koklea sel rambut rontok ataukelainan permanen stereocilia sel-sel rambut untuk bertahan hidup berkorelasi denganpendengaran. Namun, mungkin ada beberapa perubahan fungsional tanpakehilangan sel sensorik yang signifikan, walaupun ini mungkin baik berkorelasi dengan halus sensoriksel cedera atau perubahan lain dalam koklea, seperti ke lateral dinding jaringan dan neuron.Bukti baru 8 melanjutkan saraf degenerasi setelah terpapar kebisingan tetapidalam ketiadaan sel rambut rontok dan perubahan ambang batas pendengaran menunjukkan bahwa mungkin ada cedera koklea halus yang tidak nyata sebagai perubahan ambang batas, uji klinis rutin fungsi pendengaran.Sementara pendengaran telah terbukti berkorelasi dengan perubahan reversibelstereocilia kekakuan dan pembengkakan dasar tipe I aferen neuron 14, dan mungkinjuga berkorelasi untuk perubahan struktural atau molekul transduksi saluran (tiplink). Perubahan metabolik dan molekul yang signifikan juga diamati dalam kokleamengikuti akut kebisingan eksposur yang mungkin mewakili respon dari koklea ke paparan kebisingan, dan tidak masuk akal untuk berasumsi bahwa tidak semua kehilangan pendengaran akan berkorelasi untuk kelainan struktural. Memang hal ini menjadi lebihapparent that the acute hearing loss may occur without any evidence of overtstructural changes and may thus represent an adaptation to the noise exposure.Mechanisms—There have been substantial advances in our understanding of themechanisms of the cochlear injury following noise exposure. Some injury to the organof Corti, including the more subtle pathologies such as stereocilia fracture and loss,from high intensities and impulse noise exposures is a consequence of direct mechanical damage.However, there is good evidence that the hair cell injury from lower level and chronicexposures has a more metabolic genesis and most likely is due to oxidative stress and the excessive production of Reactive Oxygen Species (ROS) and free radicals.6, 16 These free radicals are molecules with an unpaired electron and in excessive amounts interact with other stable molecules, such as proteins, DNA and lipids, to cause cellular damage and degeneration. ROS may include oxygen free radicals, such as superoxide, which may be produced in the cochlea from excessive mitochondrial activity in hair cells and changes in cochlear blood flow (see Henderson et al.6 for more detail). These interact with hair cell molecules to cause cellular degeneration leading to cell loss.There is strong evidence for an increase in various ROS molecules after noiseexposure and treatment of the cochlea with free radical scavengers or antioxidants orblock of oxidative enzymes can reduce the amount of cochlear injury.The neuronal injury is likely the consequence of glutamate excitotoxicity. Glutamateis the main neurotransmitter at the IHC/primary afferent neuron synapse. Excessiverelease of glutamate during noise exposure, possibly coupled with poor clearance ofglutamate in the synaptic region by surrounding supporting cells, leads to prolongedstimulation of the afferent synapse, neuronal swelling and degeneration. This effecton the afferent terminals and the subsequent hearing loss can be blocked by glutamate receptor antagonists 14 (Gordon and Thorne unpublished observations), supporting an excitotoxic mechanism for the neuronal noise-induced injury. Oxidative stress may also be a cause or contributor to the neuronal injury 6.Degeneration of cochlear tissues results from a combination of necrotic and apoptoticprocesses.6, 17 Activation of a variety of apoptotic triggers have been identified incochlear tissues following noise exposure and this may also be a consequence ofincreased intracellular calcium associated with the uptake or release in hair cellsduring the chronic hair cell stimulation.The mechanism of the changes to the stria vascularis, the spiral ligament and spirallimbus have not been established. As these areas are involved in ion homeostasis, the structural and degenerative changes may be a consequence of a metabolically-induced abnormality in ion handling by these tissues. During sound stimulation there is a movement of potassium ions from endolymph, through the hair cells and into theextracellular space. This potassium is removed from the extracellular space by theepithelial supporting cells in the organ of Corti and the fibrocytes of the lateral andmedial wall tissues to be recycled back to the stria vascularis.During noise exposure there may be excessive release of potassium into theextracellular space which may not be removed adequately leading to the oedema anddegeneration observed in these supporting tissues. It is true that the functionalconsequences of the changes in the stria vascularis and fibrocytes are not wellestablished.7 However, the cochlea may cope adequately with this lateral walldegeneration whilst performing in quiet but there may be a more significant effectduring physiological noise exposure if the recycling pathway for potassium and othermetabolites has been impaired by the noise-induced degeneration of these supportingstructures. This has yet to be established.