The first routine dental examination should take place by age 1 year or when the first tooth erupts. Subsequent evaluations should take place at 6-month intervals or whenever symptoms develop. For individuals who are at higher risk for dental disease from a variety of factors (eg, cariogenic diet, 3 or more carious lesions or restorations in the last 36 months, special health care needs, xerostomia), shorter intervals between evaluations may be needed. Examination of the mouth is part of every general physical examination. Oral findings in many systemic diseases are unique, sometimes pathognomonic, and may be the first sign of disease (see table Oral Findings in Systemic Disorders). Oral cancer may be detected at an early stage.
(See also Introduction to the Dental Patient.)
History in the Dental Patient
Important dental symptoms include bleeding, pain, malocclusion, new growths, numbness or paresthesias, and chewing problems (see table Some Oral Symptoms and Possible Causes); prolonged dental symptoms may decrease oral intake, leading to weight loss. General information includes use of alcohol or tobacco (both major risk factors for head and neck cancer) and systemic symptoms, such as fever and weight loss.
Some Oral Symptoms and Possible Causes
Symptom | Causes |
|---|---|
Bleeding or pain with brushing (common) | Acute necrotizing ulcerative gingivitis (rare) Gingivitis (most common) |
Ear pain, referred (fairly common) | Inflamed gingival flap around a partly erupted mandibular third molar (pericoronitis) Localized osteitis (dry socket) after lower molar extraction |
Face, head, or neck pain (uncommon, except with poorly fitting dental appliances or Temporomandibular disorders) | Eagle syndrome† Infection Occult lesions with low-grade anaerobic infections spreading to the bone Poorly fitting dental appliances Spasm of the masticatory muscles |
Facial numbness or paresthesias (uncommon, except with stroke) | Antrum or nasopharynx tumor Brain stem tumors Extraction of a mandibular molar causing damage to the inferior alveolar nerve‡ Oral tumor (rare) Stroke Viral infection (facial nerve palsy) |
Masticatory fatigue (rare, except with poorly fitting dentures) | Congenital muscular or neuromuscular disorder (in younger people) Myasthenia gravis (a cardinal symptom) Poorly occluding dentures (in older people) |
Masticatory pain or jaw claudication (rare) | |
Weight loss (fairly common) | Poorly fitting dental appliances Too loose, too few, or painful teeth |
* May first manifest as easily induced gingival hemorrhaging. | |
† Elongation of the styloid process or ossification of the stylohyoid ligament, causing pain when the head is turned. | |
‡ May cause paresthesia of the lower lip. | |
Physical Examination of the Dental Patient
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.
The face
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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).
Some Disorders of the Oral Region by Predominant Site of Involvement
Site | Disorder or Lesion | Description |
|---|---|---|
Lips | Actinic atrophy | Thin atrophic mucosa with erosive areas; predisposes to neoplasia |
Acute swelling | ||
Angular cheilitis (cheilosis) | Fissuring at corners of mouth, often with maceration | |
Cheilitis glandularis | Enlarged, nodular labial glands with inflamed, dilated secretory ducts; sometimes everted, hypertrophic lips | |
Cheilitis granulomatosa | Diffusely swollen lips, primarily the lower | |
Multiple bullae that rupture quickly, leaving hemorrhagic ulcers; includes Stevens-Johnson syndrome | ||
Exfoliative cheilitis | Chronic desquamation of superficial mucosal cells | |
A locally destructive epithelial tumor thought to be a form of squamous cell carcinoma that usually regresses spontaneously | ||
Brownish black melanin spots, with GI polyposis | ||
Secondary herpes simplex (cold sore) | Short-lived vesicle (≤ 1 day) followed by small painful ulcer (≤ 10 days) at the vermillion border (common) | |
Verruca vulgaris (wart) | Pebbly surface | |
Buccal mucosa | Aspirin burn | Painful white area; when wiped off, exposes an inflamed area |
Fordyce granules | Cream-colored macules about 1 mm in diameter; benign; aberrant sebaceous glands | |
Small ulcerated vesicles; coxsackievirus strain infection in young children; mild | ||
Vesicles in posterior of mouth | ||
Irritation fibroma | Smooth-surfaced, dome-shaped, sessile | |
Koplik spots | Tiny, grayish white macules with red margins near orifice of parotid duct; measles precursor | |
Linea alba | Thin white line, typically bilateral, on the level of the occlusal plane; benign | |
Smokeless tobacco lesion | White or gray corrugated; usually behind lower lip; a risk factor for oral cancer | |
Verrucous carcinoma | Slow-growing, exophytic, usually well-differentiated; at site of snuff application; metastasis unusual, occurs late | |
White sponge nevus | Thick white folds over most of buccal mucosa except gingivae; benign | |
Palate | Granulomatosis with polyangiitis (formerly Wegener granulomatosis) | Lethal midline granuloma, with bone destruction, sequestration, and perforation |
Petechiae at junction of hard and soft palate | ||
Red to purple painless macules progressing to painful papules | ||
Necrotizing sialometaplasia | Large, rapidly developing ulcer, often painless; appears grossly malignant; heals spontaneously in 1–3 months | |
Papillary inflammatory hyperplasia | Red, spongy tissue, succeeded by fibrous tissue folds; velvety texture; benign; occurs under poorly fitting dentures | |
Pipe smoker’s palate (nicotine stomatitis) | Red punctate areas are ducts of minor salivary glands, appearance is red spots surrounded by leukoplakia (often severe, usually benign) | |
Secondary herpes simplex | Small papules quickly coalescing into series of ulcers (uncommon) | |
Overgrowth of bone in midline; benign | ||
Tongue and floor of mouth | Ankyloglossia | Tongue unable to protrude; speech difficulty Pulling away of the gingiva by the lingual frenulum |
Benign lymphoepithelial cyst | Yellowish nodule on ventral part of tongue or anterior floor of mouth | |
Benign migratory glossitis (geographic tongue, erythema migrans) | Changing patterns of hyperkeratosis and erythema on dorsum and edges; desquamated filiform papillae in irregular circinate pattern, often with an inflamed center and a white or yellow border | |
Dermoid cyst | Swelling in floor of mouth | |
Enlargement of tongue (macroglossia) | Localized or generalized depending on how many teeth are missing; adjacent teeth may indent tongue; posterior enlargement associated with obstructive sleep apnea and snoring | |
Fissured (scrotal) tongue | Deep furrows in lateral and dorsal areas | |
Glossitis | Red, painful tongue; often secondary to another condition, allergic, or idiopathic | |
Dark, elongated filiform papillae | ||
Linea alba | Thin white line on edges of tongue, usually bilateral | |
Lingual thyroid nodule | Smooth-surfaced nodular mass of thyroid tissue follicles, on the far posterior dorsum of tongue, usually at the midline | |
Painful, tender swelling under the tongue resulting from odontogenic infection; can compromise the airway by forcing the tongue superiorly and posteriorly | ||
Median rhomboid glossitis | Red (usually) patch in midline of tongue, without papillae; asymptomatic | |
Neurilemoma | Persistent swelling, sometimes at site of prior trauma; can be painful | |
Smooth, pale tongue, often with glossodynia or glossopyrosis | ||
Ranula | Large mucocele penetrating the mylohyoid muscle; may plunge deep into the neck; swollen floor of mouth | |
Thyroglossal duct cyst | Midline swelling that moves upward when tongue protrudes | |
Ulcers on dorsum (firm), cervical adenopathy | ||
Salivary glands | Benign lymphoepithelial lesion (Mikulicz disease) | Unilateral or bilateral enlargement of salivary glands; often with dry mouth and eyes |
Swelling, often painful; benign | ||
Swelling (eg, of floor of mouth) that increases at mealtime or with ingestion of sour or bitter foods | ||
Systemic disease causing dry mucous membranes | ||
Dry mouth; usually secondary to medications | ||
Various | Widespread ulcerating vesicular lesions; always present on gingiva; other locations may be involved; usually in young children | |
Multiple oral ulcers similar to those of aphthous stomatitis | ||
Canker sores, recurrent aphthous stomatitis | Small painful ulcers (canker sores) or large, painful scarring ulcers (recurrent aphthous stomatitis) | |
Bullae that rupture quickly, leaving ulcers; ocular lesions develop after oral lesions; found on alveolar mucosa and vestibules | ||
Sexually transmitted warts forming cauliflower-like clumps | ||
Dyskeratosis | Occurs with erythroplakia (red), leukoplakia (white patch on mucous membrane that does not rub off), and mixed red and white lesions; precancerous | |
Purple to dark-red lesions, similar to port wine stain; benign | ||
Localized dilated blood vessels | ||
Lacy pattern (Wickham striae), sometimes erosive; may become malignant; most common on buccal mucosa, lateral tongue | ||
Localized swelling or discoloration; benign; most common on tongue | ||
Mucocele (mucous retention cyst) | Soft nodule resulting from traumatized salivary gland; if superficial, covered by thin epithelium; appears bluish; most common on lips and floor of mouth | |
Noma | Small vesicle or ulcer that rapidly enlarges and becomes necrotic | |
Small yellow or hemorrhagic tense bullae; may last several days before rupture; most common on vestibules and alveolar mucosa | ||
Bullae that rupture quickly, leaving ulcers; can be fatal without treatment | ||
Chancre (red papule rapidly developing into a painless ulcer with a serosanguineous crust), mucous patch, gumma |
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The teeth
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.
Loose teeth usually indicate severe periodontal disease but can be caused by bruxism (clenching or grinding of teeth) or trauma that damages periodontal tissues. Rarely, teeth become loose when alveolar bone is eroded by an underlying mass (eg, ameloblastoma, eosinophilic granuloma). A tumor or systemic cause of alveolar bone loss (eg, diabetes mellitus, hyperparathyroidism, osteoporosis, Cushing syndrome) is suspected when teeth are loose and heavy plaque and calculus are absent.
Calculus is 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 lesion. Remineralization of a white spot, which usually employs fluoride or calcium phosphate compounds, results in repair of the enamel defect.
Wear of teeth can result from gastric acid exposure due to severe gastroesophageal reflux (erosion), mechanical action (attrition or abrasion) due to bruxism or a porcelain crown rubbing against opposing enamel (porcelain is harder than enamel), or aging. Wear makes chewing less effective and causes noncarious teeth to become sensitive when the eroding enamel exposes the underlying dentin. Dentin is sensitive to touch and to temperature changes. A dentist can desensitize such teeth or restore the dental anatomy by placing crowns or onlays over badly worn teeth. In minor cases of root sensitivity, the exposed root may be desensitized by fluoride, silver diamine fluoride or potassium nitrate application, or dentin-bonding agents.
Deformed teeth may 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 first 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 growth hormone deficiency or with congenital hypoparathyroidism have small dental roots; people with gigantism have large roots. 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 third molars, followed in frequency by the maxillary lateral incisors and second mandibular premolars.
Defects in tooth color must 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 second 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, minocycline darkens 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 specific tetracycline taken.
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).
Tooth-Whitening Procedures
Done By | Ingredients | Comments |
|---|---|---|
Dentist | ||
In office | Concentrated hydrogen peroxide is applied to teeth, which is exposed to a light or laser | Very effective Gingiva, skin, and eyes must be protected |
Patient | ||
At home | 10% carbamide peroxide (becomes 3.5% hydrogen peroxide when applied) and a thickening agent containing copolymers of acrylic acid cross-linked with a polyalkenyl polyether are added to a custom-made tray | Very effective |
Patient (OTC products) | ||
Commercial whitening strips | Composed of carbamide peroxide | Very effective |
Whitening toothpaste | Usually contain carbamide or hydrogen peroxide | Moderately effective |
Paint-on whitening | Usually composed of titanium dioxide | Not very effective |
Defects in tooth enamel may 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 complex and Angelman syndrome. Amelogenesis imperfecta, an autosomal dominant disease, causes severe enamel hypoplasia. Chronic vomiting and gastroesophageal reflux can decalcify the dental crowns, primarily the lingual surfaces of the maxillary anterior teeth.
Chronic snorting of cocaine 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 tooth decay and periodontal inflammation (“meth mouth”).
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 first 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.
Fluorosis is enamel discoloration that may develop in children who drink water containing > 1.5 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 mouth and oral cavity
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 cancer.
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
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 temporomandibular disease (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 Ehlers-Danlos syndrome.
Testing in the Dental Patient
For a new patient or for someone who requires extensive care, the dentist takes a full mouth x-ray series. This series consists of 14 to 16 periapical films to show the roots and bone plus 4 bite-wing films to detect early caries between posterior teeth. Modern techniques reduce radiation exposure to a near-negligible level.
Patients at high risk of caries (ie, those who have had caries detected during the clinical examination, have many restorations, or have recurrent caries on teeth previously restored) should undergo bite-wing x-rays every 6 to 12 months. Otherwise, bite-wings are indicated every 2 to 3 years.
A panoramic x-ray can yield useful information about tooth development, cysts or tumors of the jaws, supernumerary or congenitally absent teeth, third molar impaction, Eagle syndrome (less frequently), and carotid plaques.
