Mouth Opening and the Temporomandibular Joint

Cooking and cutlery both evolved after us; while our ancestors lived without tools or open fires, biting hard and opening the mouth wide were both advantageous.

A strong bite and a wide gape may seem to be conflicting ambitions. A firm bite, for instance, depends on a single, fused mandible, and on muscles inserting some way from the joint to gain greater leverage, as in humans. (In snakes, in contrast, each of the two halves of the mandible and the maxilla move independently from the skull and from each other, and their muscles insert close to the relevant joints, to give an enormous gape, but a weak bite.) An adequate gape is nevertheless achieved in most humans by subluxation. When the jaw is closed, the head of the mandible rests in the mandibular fossa in the temporal bone. But as the jaw opens, the head of the mandible is pulled out of the fossa by the lateral pterygoids (Figure 1.1). Rather than turning on its head, the mandible swivels on an axis which runs through the mandibular foramina (i.e. close to the insertion sites of temporalis and masseter).

Figure 1.1 (a) Mandible and muscle actions. (b) Mandibular movement for opening the mouth wide.

This shift in the axis of rotation allows both strong bite and wide gape: at the limit of closure, as the molars meet, the jaw is turning on the temporomandibular joint, and masseter and temporalis are working with leverage. But at the jaw’s widest opening, it turns about the muscles’ insertion sites; they are not so passively stretched, and the bones of the joint do not so impinge on one another.

Overenthusiastic openers of the mouth may sometimes find their jaw becomes stuck in subluxation (during assessment for anaesthesia, for example). The patient is left phonating like a distant gargle, with the mouth wide open; to return the jaw to its joint, it suffices to push firmly on the mandible’s molars posteriorly and inferiorly.

Gape may be reduced by abnormal skin around the mouth (e.g. scleroderma), by excessive tone in masseter (e.g. induced by a neighbouring abscess) or by disease in the temporomandibular joint itself (e.g. rheumatoid arthritis).

Mouth opening ability also depends on craniocervical flexion and extension. Head extension facilitates opening. Normal humans extend about 26° from the neutral position at the craniocervical junction to achieve maximal mouth opening. If cervical extension, from the neutral position, is prevented a subject can be expected to lose about one third of their normal interdental distance. Patients with poor craniocervical extension therefore suffer a ‘double whammy’ in terms of airway management.

The Oral Cavity and Oropharynx

The oral cavity is dominated by the tongue, and for anaesthetists, little else counts but its size. It may be swollen acutely (as in angioneurotic oedema) but is also susceptible to disproportionate enlargement by trisomy 21, myxoedema, acromegaly, tumours and glycogen storage diseases, among others.

Angioneurotic oedema can cause such swelling as to fill the entire pharynx, preventing both nasal and mouth breathing and making a front of neck airway necessary for survival. Less dramatically, a large tongue (relative to the submandibular space) can hinder direct laryngoscopy. That is, manoeuvred with reasonable force, the laryngoscope blade should squeeze the posterior tongue so as to achieve a direct view of the glottis. If the tongue is too large, or the jaw hypotrophied, it may not be possible directly to see the glottis over the compressed tongue.

Within the oral cavity, the tongue is like a thrust stage in a theatre. It is surrounded by two tiers of teeth (stalls and royal circle), and a series of wings and flies (Figure 1.2).

Figure 1.2 The mouth.

Each tooth consists of calcified dentine, cementum and enamel surrounding a cavity filled (if the tooth is alive) with vessels and nerves. Each tooth is held in its socket in the jaw by a periodontal ligament. If a tooth is inadvertently knocked out, the sooner it is returned to its socket the better. If the root is clean, the tooth can simply be put back in; if dirty, the root should first be rinsed with saline or whole milk. A dentist will then be able to splint the tooth in place. If a displaced tooth cannot be immediately replaced, whole milk is the best storage medium; a dental cavity exposed too long to saline, or worse water, dies. Calcification of the periodontal ligament is then inevitable, and the tooth will become brittle and discoloured, and may fracture, loosen or fall out again.

The stage’s side wings are formed by mucosal folds running over palatoglossal and palatopharyngeal muscles (from anterior posteriorly). Between the two folds on each side lie the tonsils (which may be invisible in adults, but in children may be so large as to meet, ‘kiss’, in the midline, hampering laryngoscopy). The glossopharyngeal nerve runs under the mucosa of the base of the palatoglossal arch (towards the posterior tongue) and can be blocked there. Just as in the theatre, so in the oral cavity: confusion surrounds the wings. Properly called the palatoglossal and palatopharyngeal arches, they are also commonly called fauces and pillars. They are all the same thing.

Access to the stage’s flies is controlled by the soft palate, a flap of soft tissue which can move up to separate the nasopharynx from the mouth and oropharynx (during swallowing), or move down to separate/shield the pharynx from the mouth (during chewing).

The soft tissues which surround the pharyngeal airway are themselves contained by bony structures (the maxilla, the mandible, the vertebrae and the base of the skull). When awake, tone in the pharyngeal musculature maintains airway patency. But once a patient is asleep, sedated or anaesthetised, muscular tone falls, and airway patency may depend on the relative sizes of these bones and of the soft tissues within them. Patients with more soft tissue, a shorter mandible or squatter cervical vertebrae may be at particular risk of obstructive sleep apnoea.