Dental caries
Dental caries, or cavities, are due to the destruction of the dental enamel and underlying tissues by organic acids. These acids are formed by bacteria growing in debris and food accumulated in pockets between the base of the teeth and the gum margins. Poor oral hygiene is the underlying predisposing circumstance. Malnutrition due to poverty, alcoholism, and malabsorption of vitamin D (rickets) or of proteins (as in celiac disease), initiate or aggravate caries. This periodontal infection ultimately leads to the invasion of the dental pulp, and the involvement of the nerve in the inflammation is the cause of toothache. An abscess may form at the apex of the tooth and extend into the jawbone, causing osteomyelitis (inflammation of the bone), or into the soft tissues around the roots of the teeth, causing cellulitis (inflammation of the soft tissues). Halitosis (foul breath) is due to the rotting debris in the pockets under the gum margins. Eventually the teeth loosen and fall out or need to be extracted. The resistance of the dental enamel to damage by organic acids is increased by fluoride, and in many countries this is incorporated into toothpaste formulas and is added to the water supplied to homes. In areas where these steps have been taken, the incidence of caries has dropped by more than 50 percent.
Pharyngitis
Inflammation of the posterior wall of the mouth and of the tonsils and adjoining tissue on each side of the oral pharynx is very common, especially in young persons. Such infections are due to bacteria of the streptococcal and staphylococcal species or from viral infections. In viral pharyngitis the tissue is usually less red and swollen than is true of streptococcal pharyngitis, and it is less often covered by a whitish exudate (protein-rich fluid). Other tonsillar tissue in the upper part of the pharynx and at the root of the tongue may be similarly involved. In diphtheritic pharyngitis, the membranous exudate is more diffuse than in other types of pharyngitis, it is tougher, and it extends over a much larger part of the mucous membrane of the mouth and nose. One of the complications of tonsillitis or pharyngitis may be a peritonsillar abscess, also called quinsy, adjacent to one tonsil; this appears as an extremely painful bulging of the mucosa in the area. Surgical incision and draining are sometimes necessary if antibiotics are not given promptly.
Congenital defects
Cleft lip, also known as harelip, is a congenital deformity in which the central to medial lip fails to fuse properly, resulting in a fissure in the lip beneath the nostrils. Other disorders are related to an abnormal position of the teeth and the jaws, resulting in inefficient chewing, and to the absence of one or more of the salivary glands, which may lessen the amount and quality of saliva that they produce. Neurological defects that provide inadequate stimulation to the muscles of the tongue and the pharynx can seriously impair chewing and even swallowing. Sensory-innervation defects may not allow the usual reflexes to mesh smoothly, or they may permit harmful ingestants to pass by undetected.
Salivary glands
The secretion of saliva is markedly diminished in states of anxiety and depression. The consequent dry mouth interferes with speech, which becomes thick and indistinct. In the absence of the cleansing action of saliva, food debris persists in the mouth and stagnates, especially around the base of the teeth. The debris is colonized by bacteria and causes foul breath (halitosis). In the absence of saliva, swallowing is impeded by the lack of lubrication for the chewing of food that is necessary to form a bolus. The condition is aggravated in states of anxiety and depression when drugs that have an anticholinergic-like activity (such as amitriptyline) are prescribed, because they further depress the production of saliva. The salivary glands are severely damaged and atrophy in a number of autoimmune disorders such as Sjögren disease and systemic lupus erythematosus. The damage occurs partly by the formation of immune complexes (antigen-antibody associations), which are precipitated in the gland and initiate the destruction. In these circumstances, the loss of saliva is permanent. Some symptomatic relief is obtained by the use of “artificial saliva,” methylcellulose mouthwashes containing herbal oils such as peppermint. As some of the salivary glands retain their function, they may be stimulated by chewing gum and by a parasympathomimetic agent such as bethanecol. The production of saliva may be also impaired by infiltration of the salivary glands by pathological lymphocytes, such as in leukemias and lymphomas. In the early stages of these diseases, the glands swell and become painful.
Excessive production of saliva may be apparent in conditions interfering with swallowing, as in Parkinson disease, or in pseudobulbar paralysis from blockage of small arteries to the midbrain regions. True salivary hypersecretion is seen in poisoning due to lead or mercury used in certain industrial processes and as a secondary response to painful conditions in the mouth, such as aphthous stomatitis (certain ulcers of the oral mucosa) and advanced dental caries.
Acute and painful swelling of salivary glands develops when salivary secretion is stimulated by the sight, smell, and taste of food but saliva is prohibited from flowing through an obstructed salivary duct. Swelling and pain subside between meals. Diagnosis can be confirmed by X ray. Persistent swellings may be due to infiltration by benign or malignant tumours or to infiltration by abnormal white blood cells, as in leukemia. The most common cause of acute salivary swelling is mumps.