Like many hearing care providers, we frequently see patients who present non-otic tinnitus and temporomandibular joint disorders (TMJD). It is reported that 60-70% of the general population has at least one sign of TMJD (joint noises, orofacial pain, and restricted jaw function)¹ and that 10-14% of adults have prolonged spontaneous tinnitus.²

Among this group, there are many patients who have non-otic tinnitus without any detectable ear/nerve disorder or without any temporal relationship between such disorders and tinnitus.³ Additionally, tinnitus is significantly more prevalent in the TMJD patients than in the healthy-patients control groups⁴ and sometimes the TMJD treatment ameliorates otologic symptoms.⁵

Nevertheless, few solid theories have been reported in the literature regarding the TMJD-tinnitus association. In the past, most authors suggested that TMJD-related otologic problems—particularly tinnitus—were caused by middle-ear structural involvement. In 1934, Costen⁶ considered the condylus dislocation as the ground of tinnitus in TMJD-patients, because of the compression of the chorda tympani and the Eustachian tube with the erosion of glenoid fossa roof. After about 30 years, Dolowitz⁷ and later Arlen⁸ supported the uncoordination of masticatory muscles as the cause of a generalized spasm of the middle-ear muscles and consequent tinnitus. At the same time, Pinto⁹ proposed that, in TMJD patients with abnormal masticatory muscles tone, the disco-malleolar ligament (described as the “tiny ligament”) could cause tinnitus through a mechanical tension on the malleus.

Recently, the central neural basis of TMJD-related tinnitus has been speculated. According to Vass,¹⁰ trigeminal nerve irritation induced by the TMJD can disturb the normal inner-ear vascular tone causing some otologic disturbances such as tinnitus.

According to the central neural theories proposed by Levine¹¹ and Henry,¹² the authors recently proposed “The Double Hit Hypothesis”.¹³ This proposes that TMJD could irritate the auricolo-temporal nerve (ATN), triggering a somatosensory pathway-induced disinhibition of the dorsal cochlear nucleus (DCN) activity in the auditory pathway. Signals from chronically stimulated DCNs—activating specific cortical neuronal networks—could yield plastic neural changes resulting in tinnitus.

Serotonin exerts major modulatory effects on sensory systems, and 5-HT dysfunction is implicated in a number of clinically-relevant conditions, including anxiety¹⁴ and the generation and chronicization of tinnitus.¹⁵ A genetically serotoninergic reduction could promote plastic changes underlying tinnitus that might be described as “tinnitus memory circuits” through diminished filtering of incoming signals (Figure 1).¹³

FIGURE 1. “The Double Hit Hypothesis.” 1) Signal generation: Neuroanatomical basis of auditory and somatosensory convergence; 2) Signal elaboration: 5-HT and “tinnitus memory circuits.” (Key: TMJD=temporomandibular joint disorders; ATN=auriculo-temporal nerve; DCN=dorsal cochlear nucleus; MSN=medullary somatosensory nuclei; 5-HT=serotonin; 5-HTT=serotonin transporter gene.)

Discussion
Tinnitus with no detectable ear/nerve disorder requires a thorough examination of current health and non-otic causes of tinnitus. According to our hypothesis, a TMJD-tinnitus management needs a “double hit strategy” under the umbrella of a multidisciplinary team: 1) Treatment for TMJD; 2) In selected patients, complementary therapies could be aimed at decreasing the activation of “tinnitus memory circuits,” modulating the serotoninergic neurotransmission.

More than 70 years after it was first described,⁶ every facet of the TMJD-tinnitus continues to evoke controversy. Any contribution to understand the pathogenesis of the controversial association between TMJD and tinnitus is to be welcomed.

Correspondence can be addressed to HR or Manuele Casale, MD, email: m.casale@unicampus.it.

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