dental disorders
Evaluation of the Dental Patient
Physical Examination
A thorough inspection requires good illumination, a tongue blade, gloves, and a gauze pad. Complete or partial dentures are removed so that underlying soft tissues can be seen. Most physicians use a head-mounted light. However, because the light cannot be precisely aligned on the axis of vision, it is difficult to avoid shadowing in narrow areas. Better illumination results with a head-mounted convex mirror; the physician looks through a hole in the center of the mirror, so the illumination is always on-axis. The head mirror reflects light from a source (any incandescent light) placed behind the patient and slightly to one side and requires practice to use effectively. The examiner initially looks at the face for asymmetry, masses, and skin lesions. Slight facial asymmetry is universal, but more marked asymmetry may indicate an underlying disorder, either congenital or acquired (see table Some Disorders of the Oral Region by Predominant Site of Involvement ). Teeth are inspected for shape, alignment, defects, mobility, color, and presence of adherent plaque, materia alba (dead bacteria, food debris, desquamated epithelial cells), and calculus (tartar). Teeth are gently tapped with a tongue depressor or mirror handle to assess tenderness (percussion sensitivity). Tenderness to percussion suggests deep Caries (tooth decay) that has caused a necrotic pulp with periapical abscess or severe periodontal disease. Percussion sensitivity or pain on biting also can indicate an incomplete (green stick) fracture of a tooth. Percussion tenderness in multiple adjacent maxillary teeth may result from maxillary sinusitis. Tenderness to palpation around the apices of the teeth also may indicate an abscess. usually indicate severe Periodontitis but can be caused by Calculusis mineralized bacterial plaque—a concretion of bacteria, food residue, saliva, and mucus with calcium and phosphate salts. After a tooth is cleaned, a mucopolysaccharide coating (pellicle) is deposited almost immediately. After about 24 hours, bacterial colonization turns the pellicle into plaque. After about 72 hours, the plaque starts calcifying, becoming calculus. When present, calculus is deposited most heavily on the lingual (inner, or tongue) surfaces of the mandibular anterior teeth near the submandibular and sublingual duct orifices (Wharton ducts) and on the buccal (cheek) surfaces of the maxillary molars near the parotid duct orifices (Stensen ducts). Caries (tooth decay) first appears as white spots/defects in the tooth enamel due to demineralization. Caries progression results in a cavitated brown lesion. Remineralization of a white spot results in repair of the enamel defect. can result from gastric acid exposure due to severe Gastroesophageal Reflux Disease (GERD) (erosion), mechanical action (abrasion) due to Deformed teethmay indicate a developmental or endocrine disorder. In Down syndrome, teeth are small, sometimes with agenesis of lateral incisors or premolars and conically shaped mandibular incisors. In congenital syphilis, the incisors may be small at the incisal third, causing a pegged or screwdriver shape with a notch in the center of the incisal edge (Hutchinson incisors), and the 1st molar is small, with a small occlusal surface and roughened, lobulated, often hypoplastic enamel (mulberry molar). In ectodermal dysplasia, teeth are absent or conical, so that dentures may be needed from childhood. Dentinogenesis imperfecta, an autosomal dominant disorder, causes abnormal dentin that is dull bluish brown and opalescent and does not cushion the overlying enamel adequately. Such teeth cannot withstand occlusal stresses and rapidly become worn. People with pituitary dwarfism or with congenital hypoparathyroidism have small dental roots; people with gigantism have large ones. Acromegaly causes excess cementum in the roots as well as enlargement of the jaws, so teeth may become widely spaced. Acromegaly also can cause an open bite, a condition that occurs when the maxillary and mandibular incisors do not come into contact when the jaws are closed. Congenitally narrow lateral incisors occur in the absence of systemic disease. The most commonly congenitally absent teeth are the 3rd molars, followed in frequency by the maxillary lateral incisors and 2nd mandibular premolars. Defects in tooth colormust be differentiated from the darkening or yellowing that is caused by food pigments, aging, and, most prominently, smoking. A tooth may appear gray because of pulpal necrosis, usually due to extensive caries penetrating the pulp, or because of hemosiderin deposited in the dentin after trauma, with or without pulpal necrosis. Children’s teeth darken appreciably and permanently after even short-term use of tetracyclines by the mother during the 2nd half of pregnancy or by the child during odontogenesis (tooth development), specifically calcification of the crowns, which lasts until age 9. Tetracyclines rarely cause permanent discoloration of fully formed teeth in adults. However,minocyclinedarkens bone, which can be seen in the mouth when the overlying gingiva and mucosa are thin. Affected teeth fluoresce with distinctive colors under ultraviolet light corresponding to the specifictetracyclinetaken. In congenital porphyria, both the deciduous and permanent teeth may have red or brownish discoloration but always fluoresce red from the pigment deposited in the dentin. Congenital hyperbilirubinemia causes a yellowish tooth discoloration. Teeth can be whitened (see table Tooth-Whitening Procedures ). Defects in tooth enamelmay be caused by rickets, which results in a rough, irregular band in the enamel. Any prolonged febrile illness during odontogenesis can cause a permanent narrow zone of chalky, pitted enamel or simply white discoloration visible after the tooth erupts. Thus, the age at which the disease occurred and its duration can be estimated from the location and height of the band. Enamel pitting also occurs in tuberous sclerosis and Angelman syndrome. Amelogenesis imperfecta, an autosomal dominant disease, causes severe enamel hypoplasia. Chronic vomiting and esophageal reflux can decalcify the dental crowns, primarily the lingual surfaces of the maxillary anterior teeth. can result in widespread decalcification of teeth because the drug dissociates in saliva into a base and hydrochloric acid. Chronic use of methamphetamines induces Xerostomia , which markedly increases severe Swimmers who spend a lot of time in overchlorinated pools may lose enamel from the outer facial/buccal side of the teeth, especially the maxillary incisors, canines, and 1st premolars. If sodium carbonate has been added to the pool water to correct pH, brown calculus develops but can be removed by a dental cleaning. Fluorosisis mottled enamel that may develop in children who drink water containing>1 ppm of fluoride during tooth development. Fluorosis depends on the amount of fluoride ingested and the age of the child during exposure. Enamel changes range from irregular whitish opaque areas to severe brown discoloration of the entire crown with a roughened surface. Such teeth are highly resistant to dental caries. The lips are palpated. With the patient’s mouth open, the buccal mucosa and vestibules are examined with a tongue blade; then the hard and soft palates, uvula, and oropharynx are viewed. The patient is asked to extend the tongue as far as possible, exposing the dorsum, and to move the extended tongue as far as possible to each side, so that its posterolateral surfaces can be seen. If a patient does not extend the tongue far enough to expose the circumvallate papillae, the examiner grasps the tip of the tongue with a gauze pad and extends it. Then the tongue is raised to view the ventral surface and the floor of the mouth. The teeth and gingiva are viewed. An abnormal distribution of keratinized or nonkeratinized oral mucosa demands attention. Keratinized tissue that occurs in normally nonkeratinized areas appears white. This abnormal condition, called leukoplakia, requires a biopsy because it may be cancerous or precancerous. More ominous, however, are thinned areas of mucosa. These red areas, called erythroplakia, if present for at least 2 weeks, especially on the ventral tongue and floor of the mouth, suggest dysplasia, carcinoma in situ, or Oral Squamous Cell Carcinoma . With gloved hands, the examiner palpates the vestibules and the floor of the mouth, including the sublingual and submandibular glands. To make palpation more comfortable, the examiner asks the patient to relax the mouth, keeping it open just wide enough to allow access. The temporomandibular joint (TMJ) is assessed by looking for jaw deviation on opening and by palpating the head of the condyle anterior to the external auditory meatus. Examiners then place their little fingers into the external ear canals with the pads of the fingertips lightly pushing anteriorly while patients repeatedly open widely and then close. Patients also should be able to comfortably open wide enough to fit 3 of their fingers vertically between the incisors (typically 4 to 5 cm). Trismus, the inability to open the mouth, may indicate Overview of Temporomandibular Disorders (TMDs) (the most common cause), pericoronitis, systemic sclerosis, arthritis, ankylosis of the TMJ, dislocation of the temporomandibular disk, tetanus, or peritonsillar abscess. Unusually wide opening suggests subluxation or type III 