Bone Conduction

Abstract

Bone conduction, which MeSH classifies as a form of hearing, is the transmission of sound to the inner ear through vibration of the skull, bypassing the outer- and middle-ear path that carries ordinary airborne sound. Any vibration applied to the head — a tuning fork on the mastoid, a transducer behind the ear, or one's larynx — sets the temporal bone and cochlear fluids in motion, exciting the same sensory cells that air-conducted sound reaches through the eardrum. Because the two routes end at a common organ, comparing them localises where hearing fails: a loss that spares bone conduction lies in the conductive apparatus, whereas one depressing both lies in the cochlea or nerve. This article sets out the pathways to the cochlea, the audiometric logic of the air–bone gap, the occlusion effect, and the devices that use it.

Keywords: bone conduction, air conduction, cochlea

What Bone Conduction Is

Bone conduction is the delivery of acoustic energy to the inner ear by mechanical vibration of the skull rather than by an airborne pressure wave travelling through the ear canal and middle ear. The ordinary route to hearing — air conduction — collects sound at the pinna, funnels it down the ear canal to the tympanic membrane, and relays it through the ossicular chain to the oval window of the cochlea. Bone conduction short-circuits this chain: a vibrating source in contact with the head sets the temporal bone oscillating, and that oscillation is communicated directly to the cochlear fluids and sensory structures embedded within it (#ref-stenfelt-2005). The crucial fact is that both routes converge on the same cochlea, so once vibration reaches the inner ear the two are, from the sensory cells onward, indistinguishable (Figure 1).

Figure 1

The phenomenon has been known for centuries through the simple observation that a tuning fork pressed to the skull is heard even when the ears are plugged, but its quantitative study began with Georg von Békésy, whose psychophysical experiments separated the air- and bone-conducted components of hearing and established the mechanics of the travelling wave the two routes share (#ref-bekesy-1960). Békésy's cancellation experiments — in which an air-conducted tone was adjusted to null a bone-conducted one — showed that the two stimuli ultimately drive the same structure, since one can annul the other, and framed the modern understanding that bone conduction is not a separate sense but an alternative input to ordinary hearing.

Because bone conduction reports the state of the cochlea independently of the conductive apparatus, it became the foundation of diagnostic audiology. If the outer or middle ear is damaged, air conduction suffers but bone conduction does not; if the cochlea or auditory nerve is damaged, both routes suffer together. The entire logic of localising a hearing loss, developed in the sections below, rests on this independence, and so does the design of devices that restore hearing by driving the bone route when the air route cannot be used (#ref-reinfeldt-2015).

Pathways to the Cochlea

Bone-conducted sound does not reach the cochlea by a single mechanism. When the skull vibrates, energy arrives at the inner ear through several parallel physical pathways that sum to the total response, and the balance among them changes with frequency. Stenfelt and Goode's synthesis of the experimental literature enumerated five principal contributors and quantified their relative importance across the audible range (#ref-stenfelt-2005).

First, skull vibration radiates sound into the ear canal: the walls of the cartilaginous canal move, generating an airborne pressure that then follows the ordinary air-conduction route through the eardrum. This component is substantial at low frequencies and is the one most altered when the canal is blocked. Second, the inertia of the middle-ear ossicles contributes: because the malleus, incus, and stapes have mass, they lag behind the vibrating temporal bone, and the relative motion between ossicles and skull drives the stapes in the oval window much as air conduction does. Third, and dominant across the speech range, is the inertia of the cochlear fluids: the fluid columns inside the cochlea resist the acceleration of the surrounding bony walls, producing a pressure difference across the cochlear partition that is the single largest source of bone-conduction excitation at mid frequencies (#ref-stenfelt-2011).

The remaining two pathways are the compression and expansion of the cochlear walls — the bony capsule is alternately squeezed and stretched by the passing vibration, distorting the fluid-filled spaces and displacing the partition (sometimes called the cochlear-distortion or compression component) — and pressure transmitted through the skull contents, the soft tissue and cerebrospinal fluid, which can couple to the cochlea through its fluid connections to the cranial cavity. Modern experimental work has refined the picture: direct measurements of promontory motion and intracranial pressure during bone stimulation show how the stimulation site and the way the transducer is coupled to the head redistribute energy among these routes (#ref-dobrev-2019), and finite-element models of the whole head now simulate the power transmitted to each cochlea from any point on the skull (#ref-chang-2018). The relative weighting of the five pathways across frequency is summarised in Table 1, and the demonstration below lets that weighting be explored directly.

Clinical Assessment: Tuning-Fork Tests and Audiometry

The diagnostic power of bone conduction follows from its independence of the conductive apparatus, and it is harnessed first by the classical tuning-fork tests and then, quantitatively, by pure-tone audiometry. In the Rinne test, a vibrating fork is held first at the mastoid (bone conduction) and then beside the ear canal (air conduction); in a normal ear, air conduction is heard as louder and longer, because the intact middle ear amplifies the airborne signal. When bone conduction is heard as the louder of the two — a negative Rinne — the middle-ear amplifier is failing, signalling a conductive loss. The Weber test places the fork on the midline of the skull: the tone lateralises toward a conductively impaired ear (which is shielded from masking background noise and so hears the bone signal more clearly) and away from a sensorineural one. These bedside tests are quick and informative but imperfect; their accuracy against audiometry is modest, and they screen rather than quantify (#ref-boatman-2007).

Pure-tone audiometry makes the comparison precise. Separate thresholds are measured for air conduction, through headphones, and for bone conduction, through a vibrator placed on the mastoid or forehead, at each test frequency. The air–bone gap — the amount by which the air-conduction threshold exceeds the bone-conduction threshold — is the quantity that localises the lesion. A large gap with normal bone-conduction thresholds means the cochlea is healthy but the sound is not reaching it efficiently: a conductive hearing loss. Elevated thresholds on both routes with little or no gap means the fault lies in the cochlea or nerve: a sensorineural hearing loss. A loss showing both an air–bone gap and depressed bone conduction is mixed.

One complication makes bone-conduction audiometry subtler than it first appears: a vibrator on one mastoid stimulates both cochleae, because the skull transmits the vibration across to the opposite side with very little loss. This transcranial attenuation — the reduction in signal between the two cochleae — is small for bone conduction, often only a few decibels, so a bone-conduction threshold measured on one side may actually reflect the better cochlea on the other. Stenfelt's measurements quantified transcranial attenuation for stimulation at the mastoid and at the bone-conduction hearing-aid position, providing the values clinicians use to decide when masking of the non-test ear is required (#ref-stenfelt-2012). The demonstration below works through the air–bone gap and its interpretation.

The Occlusion Effect and Hearing One's Own Voice

Blocking the ear canal changes bone-conduction hearing in a specific and measurable way: low-frequency bone-conducted tones become louder. This is the occlusion effect. When the canal is open, part of the sound generated by skull vibration — the ear-canal radiation pathway of Table 1 — escapes out of the canal; when the canal is sealed by a finger, an earplug, or an earmould, that low-frequency energy is trapped and its pressure at the eardrum rises, improving the bone-conduction threshold below about 1 kHz by as much as 10–20 dB. Stenfelt and Reinfeldt modelled the effect quantitatively, relating the measured threshold shift to the change in ear-canal acoustics and the compliance of the canal walls (#ref-stenfelt-2007), and later experimental work has mapped how the size of the effect depends on where the skull is stimulated and how completely the canal is occluded (#ref-wang-2022).

The occlusion effect is the key to a universal everyday experience: the strangeness of one's own recorded voice. When we speak, we hear ourselves by two routes at once — the air-conducted sound that travels from the mouth to the ear, and the bone-conducted sound that the vibrating larynx and vocal tract transmit through the skull to the cochlea. The bone-conducted component is especially rich in low frequencies, so our internal experience of our own voice is bassier and fuller than the purely air-conducted version that a microphone captures and a recording plays back. Reinfeldt and colleagues measured the air- and bone-conducted contributions to hearing one's own voice during phonation and quantified how much of the self-heard signal is carried by bone (#ref-reinfeldt-2010). A recording removes the bone route entirely, which is why the playback sounds thinner, higher, and unfamiliar — it is, quite literally, the first time we hear our voice the way others always have. The demonstration below shows how occluding the canal reshapes the bone-conduction threshold across frequency.

Clinical Applications: Devices and Third-Window Lesions

Because bone conduction reaches a healthy cochlea without using the middle ear, it offers a route to hearing when the conductive apparatus cannot be used — a blocked or malformed ear canal, a chronically draining middle ear, or an absent ossicular chain. The modern realisation of this idea is the bone-anchored hearing aid. Håkansson and colleagues established the design of a percutaneous device in which a titanium fixture is osseointegrated into the skull behind the ear and a sound processor clips onto an abutment, driving the bone directly rather than through skin and soft tissue, and characterised its electroacoustic performance (#ref-hakansson-1985). The surgical approach was pioneered clinically by Tjellström, who implanted and followed the first bone-anchored hearing aids and documented the long-term stability of the osseointegrated titanium fixtures that make direct bone drive possible (#ref-tjellstrom-1994). Later generations of transcutaneous and active implants, which drive the bone through intact skin or an implanted transducer, extended the approach while addressing the skin-care and attenuation limitations of the percutaneous design (#ref-reinfeldt-2015; #ref-ellsperman-2021).

Bone conduction also figures in the diagnosis of a class of inner-ear disorders in which it is pathologically enhanced. A healthy cochlea is enclosed in bone with two mobile windows — the oval and round windows — but a defect in the bony wall creates a third window that abnormally changes how pressure moves through the labyrinth. In superior canal dehiscence syndrome, described by Minor, a gap in the bone overlying the superior semicircular canal opens such a third window; among its signs is a lowering of bone-conduction thresholds — the ear becomes supranormally sensitive to bone-conducted sound, so that patients may hear their own eye movements or footsteps, and audiometry shows a low-frequency air–bone gap produced not by a conductive loss but by improved bone conduction (#ref-minor-1998). The two decades of work since have established the third-window mechanism as the unifying account of the syndrome's auditory and vestibular signs (#ref-ward-2017).

Worked Example

Bone-conduction audiometry is read through the air–bone gap, the difference between the air- and bone-conduction thresholds at a given frequency:

ABG = AC_threshold − BC_threshold

where both thresholds are in decibels of hearing level (dB HL). Consider a right ear tested at 1 kHz with an air-conduction threshold of 55 dB HL and a bone-conduction threshold of 20 dB HL:

- ABG = 55 − 20 = 35 dB

A gap this large, standing on a bone-conduction threshold that is itself near normal (≤ 25 dB HL), is the signature of a conductive loss: the cochlea hears well when driven directly through bone, but airborne sound is losing 35 dB somewhere in the outer or middle ear. Contrast a second ear with an air-conduction threshold of 55 dB HL and a bone-conduction threshold of 50 dB HL:

- ABG = 55 − 50 = 5 dB

Here the two routes agree and both are depressed; the negligible gap places the fault in the cochlea or nerve — a sensorineural loss. The same 55 dB air-conduction threshold thus carries opposite diagnoses depending entirely on the bone-conduction value, which is why bone conduction is indispensable.

The occlusion effect can be quantified from the same kind of threshold pair. It is the improvement in the bone-conduction threshold when the ear canal is sealed, measured at a low frequency where the effect is strong. Suppose that at 250 Hz a listener's bone-conduction threshold is 10 dB HL with the canal open and −8 dB HL with the canal occluded:

- OE = BC_open − BC_occluded = 10 − (−8) = 18 dB

The 18 dB gain confirms a robust occlusion effect in the low frequencies, where trapped ear-canal energy adds to the bone-conducted signal; repeated at 2 kHz the same measurement would yield a gain near zero, because the ear-canal radiation pathway contributes little there. The demonstrations let both the air–bone gap and the occlusion gain be varied directly.

Discussion

Bone conduction occupies an unusual place in the study of hearing: it is at once a second, everyday route to sound, a diagnostic instrument, and a window onto the mechanics of the cochlea. Its scientific value comes from the single fact that it shares an end organ with air conduction while bypassing everything upstream of the inner ear. That shared endpoint is what let Békésy use one route to cancel the other and so prove they drive a common structure (#ref-bekesy-1960), and it is what lets the clinic read the cochlea's health through the conductive apparatus's faults (#ref-stenfelt-2005). The air–bone gap is not merely a measurement convention but a direct expression of this architecture: it isolates the contribution of the middle ear by subtracting away the cochlea.

The multi-pathway character of bone conduction is its other enduring theme. Because vibration reaches the cochlea by five partly independent routes whose balance shifts with frequency, no single mechanism explains bone hearing, and apparent paradoxes — a canal that is blocked yet hears better, a dehiscence that lowers thresholds rather than raising them — resolve once the pathways are kept distinct (#ref-stenfelt-2011; #ref-minor-1998). This same complexity is why quantitative models matter: the finite-element and intracranial-pressure studies are attempts to predict, from the physics of a vibrating head, how energy is partitioned among the routes for any stimulation site (#ref-chang-2018; #ref-dobrev-2019). The clinical devices that drive the bone route and the disorders that enhance it are, in the end, applications of the same mechanics the pathway analysis describes.

Current Directions

Much of the current research front is device-driven. A recurring question is where on the head to apply the stimulus: coupling the transducer closer to the cochlea raises the energy delivered to the inner ear, and controlled measurements have begun to quantify the gain available from positions nearer the otic capsule than the conventional mastoid site (#ref-wils-2024). The same concern with stimulation geometry runs through the finite-element modelling of whole-head power transmission, which aims to turn device placement from empirical trial into prediction (#ref-chang-2018), and through the experimental mapping of promontory motion and intracranial pressure as functions of stimulation site and coupling (#ref-dobrev-2019).

A second, consumer-facing front is the bone-conduction headset, which leaves the ear canal open and so has made the perception of bone-conducted speech and music outside the clinic a practical research topic in its own right. Recent work has characterised how such headsets deliver sound and the fidelity limits that distinguish bone-conducted from air-conducted listening (#ref-surendran-2023), and how stimulation position and canal occlusion together shape what the listener perceives (#ref-wang-2022). Alongside these, the steady improvement of active transcutaneous implants continues to refine the trade-off between the efficiency of direct percutaneous drive and the skin-preserving comfort of transcutaneous coupling (#ref-reinfeldt-2015), a device landscape that recent reviews survey comprehensively (#ref-ellsperman-2021).

Common Misconceptions

Bone conduction is a different sense from ordinary hearing.

It is the same sense reached by a different route. Both air- and bone-conducted sound excite the identical cochlear receptors, which is precisely why an air-conducted tone can be used to cancel a bone-conducted one (Békésy, 1960).

Bone conduction reaches the cochlea by one mechanism.

At least five parallel pathways contribute — ear-canal radiation, ossicular inertia, cochlear-fluid inertia, cochlear-wall compression, and skull-content pressure — and their balance changes with frequency, with fluid inertia dominant across the speech range (Stenfelt & Goode, 2005).

An air–bone gap always means a conductive loss.

Usually, but not always. A third-window lesion such as superior canal dehiscence can produce a low-frequency air–bone gap by improving bone conduction rather than by impairing the middle ear (Minor, 1998).

A bone vibrator tests only the ear it is placed on.

The skull carries the vibration to both cochleae with only a few decibels of transcranial attenuation, so a bone-conduction threshold may reflect the opposite ear unless the non-test ear is masked (Stenfelt, 2012).

Glossary

Air conduction.

The ordinary route to hearing, in which airborne sound passes through the ear canal, eardrum, and ossicles to the cochlea; the comparison route against which bone conduction is read.

Air–bone gap (ABG).

The amount by which the air-conduction threshold exceeds the bone-conduction threshold at a frequency; a large gap with normal bone conduction indicates a conductive loss.

Audiometry.

The measurement of hearing thresholds; pure-tone audiometry measures separate air- and bone-conduction thresholds at each test frequency.

Bone-anchored hearing aid (BAHA).

A device that drives the skull directly through an osseointegrated titanium fixture, delivering sound by bone conduction when the air route cannot be used.

Cochlea.

The fluid-filled, spiral inner-ear organ whose sensory cells transduce vibration into neural signals; the shared endpoint of air and bone conduction.

Cochlear-fluid inertia.

The bone-conduction pathway in which the cochlear fluids resist acceleration of the bony walls, producing a pressure difference across the partition; dominant across the speech range.

Cochlear-wall compression.

The pathway in which the bony capsule is alternately squeezed and stretched, distorting the fluid spaces; sometimes called the cochlear-distortion component, emphasised at higher frequencies.

Conductive hearing loss.

A loss arising in the outer or middle ear, marked by an air–bone gap on a near-normal bone-conduction threshold.

Occlusion effect.

The improvement in low-frequency bone-conduction sensitivity when the ear canal is sealed, trapping sound radiated into the canal by skull vibration.

Ossicular inertia.

The pathway in which the mass of the middle-ear bones lags the vibrating skull, driving the stapes in the oval window.

Rinne test.

A tuning-fork test comparing air- and bone-conduction loudness at one ear; bone heard louder than air signals a conductive loss.

Sensorineural hearing loss.

A loss arising in the cochlea or auditory nerve, marked by depressed thresholds on both routes with little or no air–bone gap.

Superior canal dehiscence syndrome (SCDS).

A third-window disorder in which a gap in the bone over the superior semicircular canal lowers bone-conduction thresholds and produces sound- and pressure-induced vertigo.

Third window.

An abnormal opening in the bony labyrinth, additional to the oval and round windows, that alters pressure flow and can enhance bone conduction.

Transcranial attenuation.

The small reduction in a bone-conducted signal as it crosses the skull from one cochlea to the other; its small size is why masking is often needed in bone-conduction audiometry.

Weber test.

A tuning-fork test with the fork on the skull midline; the tone lateralises toward a conductive loss and away from a sensorineural one.

Key Researchers

Georg von Békésy

(1899–1972; Harvard University). Established the travelling-wave mechanics of the cochlea and the foundational psychophysics of bone-conducted hearing, including the cancellation experiments that separated the air- and bone-conduction components of one's own voice; awarded the 1961 Nobel Prize in Physiology or Medicine. [Wikipedia]

Bo Håkansson

(Chalmers University of Technology). Engineering originator of the bone-anchored hearing aid and of the transcutaneous bone-conduction implant, establishing the percutaneous titanium-transducer design and the electroacoustic characterisation of bone-conduction transducers. [ORCID]

Lloyd B. Minor

(Stanford University School of Medicine). Described superior canal dehiscence syndrome, relating sound- and pressure-induced vertigo and supernormal bone-conduction thresholds to a mobile third window in the bony labyrinth, and developed its surgical repair. [Wikipedia]

Sabine Reinfeldt

(Chalmers University of Technology). Quantified the human bone-conduction transmission chain and the perception of one's own voice by bone conduction, and co-developed the active transcutaneous bone-conduction implant. [ORCID]

Stefan Stenfelt

(Linköping University). Leading physiologist of bone-conduction hearing; his synthesis with Goode enumerated the five pathways to the cochlea and identified cochlear-fluid inertia as dominant, and his finite-element and transcranial-attenuation studies quantified how vibration reaches each cochlea. [ORCID]

Anders Tjellström

(University of Gothenburg / Sahlgrenska University Hospital). Clinical originator of the bone-anchored hearing aid; performed the first osseointegrated bone-conduction implant in 1977 and led the long-term clinical evaluation of the percutaneous titanium-abutment system. [Faculty page]

Frequently Asked Questions

What is bone conduction?

Bone conduction is the transmission of sound to the inner ear through vibration of the skull rather than through airborne sound in the ear canal. A vibrating source in contact with the head sets the temporal bone and cochlear fluids in motion, exciting the same sensory cells that ordinary air-conducted sound reaches through the eardrum.

How does bone conduction differ from air conduction?

Air conduction carries sound through the ear canal, eardrum, and middle-ear bones to the cochlea; bone conduction bypasses all of these and vibrates the cochlea directly through the skull. Because both end at the same cochlea, comparing them reveals whether a hearing problem lies in the conductive apparatus or in the inner ear.

What are the pathways of bone conduction to the cochlea?

Vibration reaches the cochlea by at least five parallel routes: sound radiated into the ear canal, inertia of the middle-ear ossicles, inertia of the cochlear fluids, compression of the cochlear walls, and pressure transmitted through the skull contents. Cochlear-fluid inertia dominates across the speech range.

Why does bone conduction matter in a hearing test?

Bone conduction tests the cochlea independently of the outer and middle ear. If bone conduction is normal but air conduction is poor, leaving a large air-bone gap, the loss is conductive; if both are depressed together, the loss is sensorineural. Bone conduction is therefore what localises the lesion.

What is the occlusion effect?

The occlusion effect is the increase in low-frequency bone-conduction loudness when the ear canal is blocked. Sealing the canal traps the low-frequency sound that skull vibration radiates into it, raising the pressure at the eardrum and improving the bone-conduction threshold by as much as 10 to 20 dB below about 1 kHz.

Why does a recorded voice sound different from how the speaker hears it?

When a person speaks, they hear themselves by both air and bone conduction, and the bone-conducted component adds low-frequency richness that makes the voice sound fuller from the inside. A recording captures only the air-conducted sound, so playback sounds thinner and higher, the voice as other people always hear it.

What is a bone-anchored hearing aid?

It is a device that drives the skull directly, usually through a titanium fixture osseointegrated into the bone behind the ear, delivering sound by bone conduction. It is used when the ear canal or middle ear cannot carry airborne sound, such as in chronic ear disease or canal malformation.

What is superior canal dehiscence and how does it affect bone conduction?

Superior canal dehiscence is a gap in the bone over the superior semicircular canal that creates an abnormal third window in the inner ear. Among its effects is a lowering of bone-conduction thresholds, so the ear becomes supranormally sensitive to bone-conducted sound and audiometry can show a low-frequency air-bone gap without any conductive loss.

References

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