Masseter Muscle in Tinnitus: Botulinum Toxin Review

The scoping review by Gardellin, D’Angelo, and Spadotto identified only four studies that met their strict criteria for investigating Botulinum Toxin Type A (BoNT/A) for tinnitus related to jaw muscle tension. A fifth study was added from a manual search. This small body of evidence highlights a significant gap: despite strong anatomical reasoning, clinical proof for this potential treatment remains sparse.

### The Anatomical Rationale for Targeting Jaw Muscles

The core hypothesis driving this research is the concept of somatosensory tinnitus. In this subtype, input from the head, neck, and jaw muscles—the craniocervical system—can directly influence the perception of sound in the brain’s auditory pathways. The masseter muscle, a primary jaw-clenching muscle, has dense neural connections to brainstem areas that process both sound and facial sensation.

When the masseter is chronically overactive, often due to bruxism (teeth grinding) or temporomandibular disorders (TMD), it may send a constant stream of abnormal signals into these central circuits. The theory suggests this “noise” from the jaw could amplify or even trigger the perception of tinnitus in susceptible individuals. This mechanistic link explains why some people can temporarily alter their tinnitus by clenching their jaw or moving their neck.

### What the Scoping Review Actually Found

The researchers conducted a systematic scoping review, searching major medical databases up to May 2026. Their goal was to map all available evidence on BoNT/A for tinnitus and on the relationship between masticatory (chewing) dysfunction and tinnitus. The yield was strikingly low.

Only four studies fully met their inclusion criteria. Three addressed BoNT/A and tinnitus directly, while one examined tinnitus and masticatory dysfunction. The authors also included an additional 2024 report by Ranoux and Levine, identified outside the main search. This report documented tinnitus improvement in patients following BoNT/A injections in the periauricular (around the ear) and splenius capitis (neck) muscles. Notably, the same clinical protocol suggested masseter or temporalis (temple) injections as an alternative potential site.

The scarcity of high-quality studies underscores a critical point: the path from plausible mechanism to proven treatment is long and requires rigorous validation.

### Botulinum Toxin: A Hypothetical Tool, Not a Proven Cure

Botulinum Toxin Type A is well-established in clinical practice for treating conditions of muscle hyperactivity, such as cervical dystonia and chronic migraine. Its mechanism—temporarily blocking the release of neurotransmitters that cause muscle contraction—makes it a logical candidate for testing the masseter-tinnitus hypothesis. By relaxing an overactive masseter, BoNT/A could theoretically reduce the aberrant somatosensory input thought to be driving the tinnitus signal.

However, the review authors are emphatic that this remains a theory awaiting confirmation. The existing evidence is deemed insufficient to support its use as a standard treatment. They explicitly state that any application of BoNT/A for tinnitus at this stage should be considered **experimental**. It should only be approached within a multidisciplinary framework involving audiologists, neurologists, and orofacial pain specialists, and must include standardized methods to measure tinnitus outcomes.

### Implications for Patients and Clinical Practice

For individuals whose tinnitus is clearly modulated by jaw movement or clenching, this review offers a scientifically coherent explanation for their experience. It validates that the connection is real and rooted in neuroanatomy. It may guide a more comprehensive assessment, potentially including evaluation for TMD or bruxism by a dentist or specialist.

However, the primary practical implication is one of caution. Patients seeking new treatments should understand that BoNT/A injections for tinnitus are not a mainstream or evidence-backed option. The authors call for prospective, controlled trials to definitively test the hypothesis. Such trials would need to carefully select patients with confirmed somatosensory tinnitus and compare BoNT/A injections against a placebo or sham procedure.

This research intersects with broader themes in hearing health, particularly the relationship between somatic systems and auditory perception. For instance, the principle of cervical stimulation influencing hearing disorders shares a similar neurophysiological basis. Furthermore, the significant stress and anxiety often associated with chronic tinnitus, detailed in articles on tinnitus and mental health, highlight why finding targeted treatments for specific subtypes is so important. The potential role of muscle tension also relates to conditions like migraine-related auditory dysfunction, where sensory integration is often disrupted.

### The Need for Targeted Trials and Precise Patient Selection

The clear message from Gardellin and colleagues is that the field must move from theoretical support to empirical proof. Future research must prioritize clear definitions of the somatosensory tinnitus subtype and use consistent, validated tools to measure changes in tinnitus loudness, annoyance, and impact on quality of life. Identifying which patients are most likely to benefit—perhaps those with clear jaw-related triggers—is essential.

Until such data is available, BoNT/A for tinnitus resides firmly in the domain of experimental hypothesis. It represents a promising avenue for a specific patient subgroup, but one that remains unpaved with clinical evidence.

**Source Paper:** Gardellin J, D’Angelo M, Spadotto L. Botulinum Toxin for Somatosensory Tinnitus: A Scoping Review. *Toxins*. 2026;18(7):310. doi:10.3390/toxins18070310.