Mastication
All
muscles involved in the act of mastication are striated, that is, voluntary;
the neural regulation for the activity of the masticatory muscles originates in
the inferior medial portion of the motor cortex, whence projections pass via
the pyramidal tract to the pons to coordinate the motor nuclei of the nerves
supplying the muscles of mastication. The complex movements of these muscles
are centrally integrated, and coordination is aided by the impulses carrying sensation
from the teeth and mucosal surface of the mouth, as well as proprioception from
the muscles themselves. The proprioceptive pathways from the tooth sockets lead
to the principal mesencephalic sensory
nucleus (the only sensory root that has
its cells of origin within the central nervous system) and thence to the motor
nucleus, effecting control of the masticatory pressure and preventing the
breaking of teeth.
Mastication begins with the
cutting of the food by the incisor teeth and continues by bringing food in
position between the grinding surfaces of the molars and premolars. The
muscular forces of the tongue and cheek are also required in the act of
grinding and mastication. The mandible is alternately elevated (masseter,
temporal, internal pterygoid muscles) and depressed (digastric, mylohyoid,
geniohyoid), and moved forward (external pterygoid) and backward (lower fibers
of temporal) and from side to side (external pterygoid and elevators of the
opposite side). The strength with which this grinding is performed may be
appreciated by the fact that the molars have been shown to exert a biting force
as high as 270 pounds. The primary purpose of mastication is to facilitate
deglutition by reducing the size of the food particles and lubricating them with
saliva. How much chewing is required to accomplish this depends on the type of
food, the amount taken into the mouth at one time, the strength of the bite,
the intensity of hunger, and other factors. Ordinarily, by the time food is
swallowed, most of it has been reduced to particles less than 2 mm in diameter.
The largest particles usually do not exceed 12 mm. The nerve endings in the
mouth sense the size of the particles that form the bolus and determine when
the latter is ready to be swallowed. The efficiency of this function is such
that rarely does a bolus become lodged in the normal esophagus.
Mere facilitation of
swallowing is, however, not the only result of mastication. Thorough chewing
also aids digestion. The prolonged contact of tasty food with the oral mucosa
increases the cephalic (psychic) phase of gastric secretion, preparing the
stomach for further grinding and propulsion of food into the duodenum. The
greater the reduction in particulate size, the greater is the surface of
ingested food, and the more readily is it exposed to both salivary and gastric
enzymes. Reduction of particle size also facilitates gastric evacuation.
An important aspect of
thorough mastication relates to the salivary secretion that it stimulates.
Besides the diluting and lubricating effects of the saliva, its solvent action
improves the taste and thereby further enhances the cephalic phase of gastric
secretion. A copious flow permits more complete digestion of starches in the
stomach before the bolus is penetrated by the gastric acid, which inactivates
amylase (ptyalin). With diminished salivary secretion, termed xerostomia or
aptyalism, as occurs in conditions of dehydration or fever or in the
presence of Sjögren syndrome, all these effects are lost, and mastication is
rendered extremely difficult. Certain agents, such as quinine, sympatholytics,
and, particu- larly, anticholinergic drugs, inhibit salivary secretion and may
produce undesirable effects on digestion. The opposite disturbance, excessive
salivary secretion, called amylasemia (ptyalism) or sialorrhea, may
result from a local irritation (jagged edges of teeth, poorly fitting dentures,
dissimilar metals in fillings, lesions such as canker sores or stomatitis) or
as a reflex of visceral disease. When extreme, the loss of the secreted fluid
may lead to dehydration. Sialorrhea of a degree not clinically manifest has
been observed in association with gastric hypersecretion in ulcer patients.
The most common disturbance of
mastication probably is that resulting from the absence of teeth. Edentulous
individuals attempting to eat food that requires effective chewing may swallow
particles large enough to tax the triturating action of the stomach. The same
holds true for ill-fitting dentures. Thus, faulty mastication should be
seriously considered as a cause of indigestion in an edentulous patient.
Inadequate mastication resulting from poor dentition is typically a primary
reason for esophageal food impactions and tracheobronchial aspiration. Loss of
function of the buccinator and orbicularis oris muscles, as occurs in central
or peripheral paralysis of the facial nerve, usually results in the pocketing
of food between the teeth and the adjacent lips and cheek, and thereby
interferes with mastication on the affected side. Inability to chew food
thoroughly may be one of the early signs of myasthenia gravis. Mastication is
the initial step in propelling the food bolus to the pharynx for esophageal
transfer. With poor dentition, this step cannot be completed properly, and these
individuals can develop nutritional deficiencies, weight loss, and an overall
reduced quality of life.