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Two nasal foreign bodies were discovered by a dental practitioner on a routine radiographic examination of a 15-year-old autistic patient. Going over past radiographs, one of the nasal foreign bodies was detected in a radiograph performed 2 years previously. No nasal complaints or other clues to the problem were apparent. The patient was referred to the emergency room, and the foreign bodies were removed by an Ear Nose and Throat specialist, under general anesthesia. This paper reviews the diagnosis and treatment of nasal foreign bodies, and highlights the important role of the dental practitioner in the proper detection and diagnosis, prompt referral for management, and reduction in related complications. [ABSTRACT FROM AUTHOR]

The author discusses the profound connection between dentistry and otolaryngology (ENT), highlighting how issues in one can significantly impact the other. He discusses the possible causes of earaches, the important role of the oral microbiome in overall health, and benefits of collaboration between dental practitioners and ENT specialists.

Objective: The aim of this study was to document sensory changes in the supraorbital, infraorbital, and mental nerve distributions following acute and chronic maxillary and frontal sinusitis. Method and Materials: Seven patients with a total of 14 infected sinuses were included in the study. Neurosensory function was evaluated by measuring the electrical detection threshold for large myelinated nerve fibers and heat detection thresholds for the assessment of the thin unmyelinated nerve fibers. The sensory tests were conducted in the infraorbital, supraorbital, and mental dermatomes. Patient evaluation included clinical examination and computerized tomographic imaging of the sinuses. Sinusitis symptoms of 1 month or less were considered acute, and symptoms that persisted for more than 3 months were considered chronic. Detection thresholds in 8 healthy volunteers served as controls. Results: Eight acute and 6 chronic sinusitis cases were diagnosed. Acute sinusitis produced bilateral large myelinated fiber hypersensitivity (electrical) relative to healthy controls, with no significant change in the thin unmyelinated nerve fiber detection threshold (thermal). Chronic sinusitis resulted in large myelinated fiber hyposensitivity and thin myelinated fiber bilateral hyposensitivity, as compared to healthy controls. Conclusions: This study concurs with previous studies in finding that early inflammatory neuritis can produce large myelinated nerve fiber hypersensitivity, while long-lasting processes, presumably accompanied with early nerve damage, may result in hyposensitivity. [ABSTRACT FROM AUTHOR]

Background: Exposure to high-intensity noise causes little, if any, reduction in vestibular function in normal animals as shown by short-latency vestibular evoked potentials (VsEPs)., Objective: To investigate the effect of noise exposure on VsEPs following fenestration of the horizontal semicircular canal., Design and Methods: Psammomys obesus (fat sand rat) underwent labyrinthectomy in 1 ear, while the lateral semicircular canal in the other ear was fenestrated. Control VsEPs to linear acceleration (approximately 3g; rise time, approximately 1-2 milliseconds) were recorded immediately after the operation. The experimental group animals were then subjected to loud white noise (113-dB sound pressure level) for 1 hour. Immediately after the noise exposure in the experimental group animals, VsEPs were once more recorded., Results: The VsEPs in the experimental group animals were significantly reduced immediately following the noise exposure, while there was no change in the recordings from the control group animals (fenestrated but not noise exposed; noise exposed but not fenestrated), even though the noise exposure induced a mean 47-dB threshold elevation of the auditory brainstem response., Conclusions: The presence of the fenestration caused the vestibular end organs to become vulnerable to noise exposure. The fenestration may create a pathway enabling pressure release through the vestibular end organs during noise exposure, thus increasing the possibility of damage to the vestibular end organs. This did not occur in the intact, nonfenestrated animals.