Pathologies of the ear canal can cause hearing loss, recurrent infection, and complications including cranial nerve palsy and intracranial sepsis ( Ostrowski and Wiet, 1996). This leaves the outer ear, which is also indispensable for hearing, but is comparatively overlooked. Currently, the clinician’s arsenal is best equipped to treat middle ear disease, which consequently receives the lion’s share of clinical attention ( Cunningham and Tucci, 2017). However, there are limited options for treating sensorineural hearing loss with many potential treatments in the experimental phase ( Devare et al., 2018). Hearing loss is most commonly caused due to pathology in the inner ear, referred to as sensorineural hearing loss, which consequently receives the lion’s share of scientific research ( Cunningham and Tucci, 2017). Inset shows anterior, posterior, superior, and inferior axes as referred to in the text. The ear canal lumen varies in shape but typically has a pretympanic recess and meatal opening. The ear canal is enclosed in its inner two-thirds by a bony wall and its outer third by a cartilaginous wall, which is lined by hair-bearing skin. The inner ear (IE) includes the cochlea and semi-circular canals. The middle ear connects to the nasopharynx via the eustachian tube (ET).
The malleus inserts into the TM at the umbo. Schematic diagram of the three-part ear the external ear, which includes the pinna and ear canal the middle ear which includes the tympanic membrane (TM), middle ear cavity (MEC), and the ossicles. This intricate leverage mechanism corrects the impedance mismatch between gas and liquid allowing airborne sound waves to move hair cells in the fluid-filled cochlea, generating neural signals that are transmitted to the auditory cortex via the cochlear nerve. The middle ear ossicles connect the TM to the much smaller oval window of the inner ear. The pinna or auricle directs sound waves into the external auditory Meatus (EAM), which then funnels sound waves toward the ear drum or tympanic membrane (TM), causing it to displace and move the ossicular chain of bones in the air-filled middle ear. The mammalian ear is a crucial and fascinating sensory organ formed from the integration of three parts ( Figure 1).
That we can “hear” these waveforms involves a complex array of neurophysiological mechanisms which begin at the outer ear and end at the auditory cortex.
Sound is essentially a series of pressure waves in our airborne environment. Hearing places us within our external environment, allowing us to experience a multi-dimensional world, to listen and to communicate.
Together this knowledge allows clinical questions to be approached from a developmental biology perspective. Here we review our current understanding of ear canal development how this biological lumen is made what determines its location and how its structure is maintained throughout life. Recent studies have built on decades-old knowledge of ear canal development and suggest a novel multi-stage, complex and integrated system of development, helping to explain the mechanisms underlying congenital canal atresia and stenosis. Defects in development, or later blockages in the canal, lead to congenital or acquired conductive hearing loss. Unique anatomical adaptations, such as its migrating epithelium and cerumen glands, equip the ear canal for its function as both a conduit and a cul-de-sac. Within our complex hearing pathway, the ear canal is responsible for funneling sound waves toward the tympanic membrane (ear drum) and into the middle ear, and as such is a physical link between the tympanic membrane and the outside world. This review focuses on the often-neglected outer ear, specifically the external auditory meatus (EAM), or ear canal. The mammalian ear is made up of three parts (the outer, middle, and inner ear), which work together to transmit sound waves into neuronal signals perceived by our auditory cortex as sound.