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.