Occupational Noise Exposure in the Pediatric Dental Setting.

Purpose: To evaluate the noise levels recorded in a hospital-based pediatric dental clinic and evaluate the occupational exposure personnel have to potentially hazardous levels of noise. Methods: A SoundAdvisor™ Sound Level Meter Model 831C was used to gather 19 days of background sound data (equivalent continuous sound levels, measured as LAeq) in the open bay, quiet room, sedation suite, and operating room settings. A Spartan™ Wireless Noise Dosimeter Model 730 (Larson Davis) was utilized to capture data about personal noise exposure of pediatric dental residents over 81 clinic sessions. Personal noise exposure was compared to the Occupational Safety and Health Administration (OSHA) stand- ard. Results: Background A-weighted sound pressure level was significantly less for the open bay than in the operating room, quiet room, and oral sedation setting (P<0.05), while the operating room was significantly less than the oral sedation setting (P=0.038). Personal LAeq was significantly less for the open bay than the quiet room (P=0.007) and oral sedation settings (P=0.007). There was a significantly larger percentage of time above 80 dBA captured in the oral sedation suite compared to the open bay (P=0.010) or operating room (P=0.023). Conclusions: Daily occupational noise exposure did not exceed the thresholds set forth by OSHA. Sedation and quiet room treatment settings were noted to be the loudest pediatric dental clinical environments.

Impaired Glutamate Receptor Function Underlies Early Activity Loss of Ipsilesional Motor Cortex after Closed-Head Mild Traumatic Brain Injury.

Although mild traumatic brain injury (mTBI) accounts for the majority of TBI patients, the effects and cellular and molecular mechanisms of mTBI on cortical neural circuits are still not well understood. Given the transient and non-specific functional deficits after mTBI, it is important to understand whether mTBI causes functional deficits of the brain and the underlying mechanism, particularly during the early stage after injury. Here, we used in vivo optogenetic motor mapping to determine longitudinal changes in cortical motor map and in vitro calcium imaging to study how changes in cortical excitability and calcium signals may contribute to the motor deficits in a closed-head mTBI model. In channelrhodopsin 2 (ChR2)-expressing transgenic mice, we recorded electromyograms (EMGs) from bicep muscles induced by scanning blue laser on the motor cortex. There were significant decreases in the size and response amplitude of motor maps of the injured cortex at 2 h post-mTBI, but an increase in motor map size of the contralateral cortex in 12 h post-mTBI, both of which recovered to baseline level in 24 h. Calcium imaging of cortical slices prepared from green fluorescent calmodulin proteins-expressing transgenic mice showed a lower amplitude, but longer duration, of calcium transients of the injured cortex in 2 h post-mTBI. Blockade of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid or N-methyl-d-aspartate receptors resulted in smaller amplitude of calcium transients, suggesting impaired function of both receptor types. Imaging of calcium transients evoked by glutamate uncaging revealed reduced response amplitudes and longer duration in 2, 12, and 24 h after mTBI. Higher percentages of neurons of the injured cortex had a longer latency period after uncaging than that of the uninjured neurons. The results suggest that impaired glutamate neurotransmission contributes to functional deficits of the motor cortex in vivo, which supports enhancing glutamate neurotransmission as a potential therapeutic approach for the treatment of mTBI.