The present study examined the relationship between TMD symptoms and signs and mouth opening, gender, aural symptoms, temporomandibular joint pain, temporomandibular joint ankylosis, bruxism and hearing loss.
We found that 73.3% of the young Greek adult population examined in this study had TMD symptoms and signs. This finding is consistent with previous studies involving college students [12, 16]. Compared to previous studies on young populations, the present population had fewer subjects with mild TMD (31.76%) and more with moderate (40%) and severe TMD (28.2%).
We found that mouth opening differed, according to TMD severity, and the least opening was observed in the severe TMD group. Interestingly, we found that while mouth opening was less in severe TMD subjects (44.43 mm) compared to non-TMD subjects (46.45 mm), it was greater in severe TMD subjects than moderate TMD ones (44.08 mm). It has already been reported that joint hypermobility is often present in TMD patients . Mouth opening cannot be used as a sole criterion of TMD presence and the range of mouth opening found in our population could be considered as functional. Nevertheless, for the needs of our study, we compared the values found for each stratification group even of considered normal.
Ethnicity is believed to affect the degree of mouth opening [12, 17]. The present study is the first focused on a young Greek adult population. The overall mean mouth opening recorded was 45.09 mm. The only previous study of a Greek population took place in 1989 and involved participants aged between 18 and 70 years. The average maximum mouth opening was 52.85 mm for males and 48.34 mm for females . Studies of other ethnicities found that the average mouth opening was 49.10 mm in Chinese (51.11 mm for those aged 20-30 years) , 49.8 mm in Americans aged 16-70 years , 47.1 mm in Nepalese population aged 18-68 years , 50.77 mm in French aged 18-84 years , and 55.9 mm in Swedes aged 18-25 years . It ranged between 41-43 mm in Irish  and 35-61 mm in Croatians .
We found that TMD was more prevalent and severe in women than men. This observation is consistent with previous studies, as it has been reported that women present an increased risk of 1.5-2 or 2-9 times compared to men to develop TMD .
The current study found that pain in the temporomandibular joint was the most common symptom (27.05%) of TMD as reported elsewhere . Temporomandibular joint pain is caused by the pathological contraction of the masticatory muscles which stimulates extravascular production of inflammation associated substances around the temporomandibular joint . The incidence of pain in the present study is in accordance with the theory that TMD is more prevalent in early adulthood .
Joint sounds are regarded as the commonest sign of TMD (13.5%) , and are more frequent and severe in older populations. Joint sounds, such as clicks and friction, indicate temporomandibular joint derangement or joint disk displacements.
We found that bruxism was present in 27.02% of those with TMD and in none of the non-TMD subjects. Others reported that bruxism was present in 7.4%-27.2% of TMD subjects . Bruxism, as clenching or grinding, may be a source or a perpetuating factor for TMD. Some investigators reported that non-TMD and TMD patients have different electromyographic patterns  while others failed to find a difference .
Head and neck ache may be of neurological, vascular, muscular, ligamental or bony origin. The temporomandibular joint has muscular and ligamentary connections to the cervical region forming a functional complex. Headache is regarded as the most common symptom (22%) of TMD patients , while 55% of chronic headache patients referred to a neurologist had signs or symptoms of TMD . The muscles of the neck and trunk are reported to have a greater electromyographic activity in TMD subjects  sensitizing the sympathetic nerves of the autonomous nervous system and leading to headache via the trigeminal nerve.
We found that TMD severity is correlated with the number of aural symptoms. Costen, in 1934, firstly associated aural and craniosinusal symptoms with TMD, and named it Costen's or Otognathic Syndrome . There are four main theories concerning the co-existence of aural and temporomandibular joint dysfunction symptoms. The first one suggests that disposition of the joint disk during jaw movement increases pressure in the Eustachian tube, the ear structures, the auriculotemporal and masseteric nerve and some branches of the deep posterior temporal nerve. The auriculotemporal nerve innervates the TMJ, the tympanic membrane, the anterosuperior part of the external ear and the tragus, and its stimulation gives the sense of otalgia . We observed that 10.8% of TMD subjects reported ear pain, and that 75% of those TMD subjects had severe TMD. A number of series report ear pain in 35% of TMD patients , while 70% of temporomandibular joint pain cases are described as otalgia particularly during acute or subacute inflammation of the temporomandibular joint . Additionally, we found that the rarely investigated symptom of ear itching was more common in TMD than non-TMD subjects, as reported elsewhere .
The second theory involves the tiny ligament called the discomalleolar or Pinto's ligament, which originates from the anterior malleolar process, passes through the petrotympanic fissure and inserts in the medial and posterosuperior part of the articular capsule and the disk [34, 35]. In displacement of the temporomandibular joint disk, the discomalleolar ligament can lead to traction of the malleus , the ossicular chain and the tympanic membrane . Furthermore, in disk displacement, the intralaminal vascular tissue moves forward and is trapped between the head of the condyle and the roof of the fossa, leading to oedema, leakage and fibrosis . The petrotympanic fissure plays an important role in hosting the anterior malleolar ligament, the anterior tympanic artery and the chorda tympani nerve. Additionally, the petrotympanic fissure brings in contact the temporomandibular joint with the middle ear. Thus, beginning from the joint capsule, inflammation can spread to the origin of the levator and the tensor palatini muscles, and finally to the cul-de-sac over the vulnerable isthmus of the Eustachian tube, causing obstruction of the tube. A closed Eustachian tube may be responsible for the feeling of ear fullness, otalgia and serous otitis media . This fissure's length and position may influence the development of otalgia, tinnitus, hearing loss and vertigo .
The third theory proposes that common innervation of the tensor veli palatini, tensor tympani, masseter, temporalis and pterygoid muscles by the motor nucleus of the trigeminal nerve is the underlying cause of the aural symptomatology in TMD patients . Tensor tympani, tensor veli palatini and stapedial muscles are called auditory muscles, while the tensor veli palatini and the tensor tympani muscles are also called accessory mastication muscles . Strong sounds cause stapedial muscle contraction, which improves auditory discrimination , while tensor tympani muscle plays a role in the discrimination of low tones. Tensor tympani muscle also contracts in strong sounds, protecting from sound trauma, and vocalization, chewing, swallowing and facial muscle contraction . Malcontraction of the tensor tympani muscle pulls the ossicular chain medially in the middle ear and thus may alter the aural conductive system  causing hyperacousia or hypoacousia even with normal audiometric values . It has also been shown that the tensor tympani muscle is dysfunctional in TMD patients, leading to subjective hearing loss . The tensor tympani and stapedial are antagonistic muscles, and with the tympanic membrane are responsible for the appropriate balance and function of the ossicular chain in the middle ear (malleus, incus and stapes). If the tensor tympani or stapedial contract inappropriately, then the perilymphatic and endolymphatic pressures in the inner ear are changed via the oval window, causing vestibular and cochlear impulse imbalance . Changes in endolymph pressure affect the hair cells of the inner ear, which also results in aural symptoms. Electromyographical studies show that the tensor tympani and tensor and tensor veli palatini work simultaneously during swallowing, leading to ventilation of the Eustachian tube  raising the intratympanic pressure. The Eustachian tube is actively opened by the tensor palatini and passively opened by the levator palatini muscle. In TMD, the tensor tympani muscle is hypertonic, impeding this normal mechanism. Such a pathological state may lead to hypoacusia, tinnitius, vertigo, otalgia, otic fullness sensation and otitis media [9, 44]. Additionally, TMD patients cannot open their mouths wide to yawn, which leads to poor Eustachian tube function as well . One study reported that ear fullness was experienced by 13.5% of TMD and 4.7% of non-TMD patients [RR = 2.87], while in other series involving older populations the relative risk ratio was 14.0 . Objective tinnitus is caused by the palatine and middle ear myoclonus producing rhythmic movement of the tympanic membrane to the tension of the stapedial and tensor tympani muscle. Tinnitus related to TMD is thought to be produced by the lateral pterygoid muscles and the discomalleolar ligament .
Furthermore, every movement of the neck or jaw exerts tension on the carotid sheath, increasing the endolymphatic pressure of the hair cells in the cochlea via impedance of the saccus endolymphaticus' pressure-regulating mechanism, causing tinnitus and vertigo . In bruxism and TMD, the tensor veli palatini dysfunctions and may change the position of tympanic membrane and malleus due to its anatomic association with the tensor tympani . Thus, the velopharyngeal, neck and face movements play a major role in otic-TMD symptomatology .
The results of a previous study suggested that TMD peripherally sensitizes the V and VII pairs, leading to tonic spasm of these middle ear muscles. This process may cause low tones hearing loss. We found that severe TMD was associated with low tones hearing loss, while moderate TMD correlated with median tones hearing loss. Furthermore, the degree of hearing loss increased with TMD severity. In a study of 44 TMD patients, ear fullness was recorded in 13.6%, vertigo in 13.6% and hearing loss in 6.8% of the subjects. In that same study, audiometry revealed a sensorineural hearing loss in only one subject, at 28-30 dB . Other studies reported no difference in audiographic findings between TMD and non-TMD patients , and that hearing loss was not correlated to TMD severity . It has also been previously reported that TMD symptoms are more common in subjects who present with sudden sensorineural hearing loss .
Finally, the fourth theory proposes that psychosocial disorders are responsible for the co-existence of aural symptoms in TMD patients .
The limitation of our study is the absence of clinical diagnosis of TMD. No clinical examination or other laboratory findings confirmed or rejected each participant's score according to his anamnestic questionnaire. The tool employed only describes signs and symptoms of TMD which may not be seen as a synonym of TMD presence. Thus, many volunteers of this study could not be diagnosed as TMD patients. For the convenience of the results' interpretation we stratified our subjects in four TMD severity groups referring to the number of TMD signs and symptoms. Nevertheless, the results of several studies based on such data verify the utility of evaluation via only an anamnestic questionnaire [12, 28].