Tooth formation begins during the sixth week of embryonic life and continues through the first 17 years of age. Tooth development begins in utero and continues until after the tooth erupts. Normally all 20 deciduous teeth have erupted by age 3 and have been shed by age 13. Permanent teeth, eventually totaling 32, begin to erupt by age 6 and have completely erupted by age 14, though third molars (wisdom teeth) may erupt later.

The erupted tooth consists of the visible crown covered with enamel and the root submerged below the gum line and covered with bonelike cementum. Dentin, a material that is denser than bone and exquisitely sensitive to pain, forms the majority of the tooth substance. Dentin surrounds a core of myxomatous pulp containing the vascular and nerve supply. The tooth is held firmly in the alveolar socket by the periodontium, supporting structures that consist of the gingivae, alveolar bone, cementum, and periodontal ligament. The periodontal ligament tenaciously binds the tooth’s cementum to the alveolar bone. Above this ligament is a collar of attached gingiva just below the crown. A few millimeters of unattached or free gingiva (1–3 mm) overlap the base of the crown, forming a shallow sulcus along the gum-tooth margin.

Dental Caries, Pulpal and Periapical Disease, and Complications

Dental caries begin asymptomatically as a destructive process of the hard surface of the tooth. Streptococcus mutans, principally, along with other bacteria colonize the organic buffering film on the tooth surface to produce plaque. If not removed by brushing or the natural cleaning action of saliva and oral soft tissues, bacterial acids demineralize the enamel. Fissures and pits on the occlusion surfaces are the most frequent sites of decay. Surfaces adjacent to tooth restorations and exposed roots are also vulnerable, particularly as teeth are retained in an aging population. Over time, dental caries extend to the underlying dentin, leading to cavitation of the enamel and ultimately penetration to the tooth pulp, producing acute pulpitis. At this early stage, when the pulp infection is limited, the tooth becomes sensitive to percussion and hot or cold, and pain resolves immediately when the irritating stimulus is removed. Should the infection spread throughout the pulp, irreversible pulpitis occurs, leading to pulp necrosis. At this late stage pain is severe and has a sharp or throbbing visceral quality that may be worse when the patient lies down. Once pulp necrosis is complete, pain may be constant or intermittent, but cold sensitivity is lost.

Treatment of caries involves removal of the softened and infected hard tissue; sealing the exposed dentin; and restoration of the tooth structure with silver amalgam, composite plastic, gold, or porcelain. Once irreversible pulpitis occurs, root canal therapy is necessary, and the contents of the pulp chamber and root canals are removed, followed by thorough cleaning, antisepsis, and filling with an inert material. Alternatively, the tooth may be extracted.

Pulpal infection, if it does not egress through the decayed enamel, leads to periapical abscess formation, which produces pain on chewing. If the infection is mild and chronic, a periapical granuloma or eventually a periapical cyst forms, either of which produces radiolucency at the root apex. When unchecked, a periapical abscess can erode into the alveolar bone producing osteomyelitis, penetrate and drain through the gingivae (parulis or gumboil), or track along deep fascial planes, producing a virulent cellulitis (Ludwig’s angina) involving the submandibular space and floor of the mouth (Chap. 157). Elderly patients, those with diabetes mellitus, and patients taking glucocorticoids may experience little or no pain and fever as these complications develop.

Periodontal Disease

Periodontal disease accounts for more tooth loss than caries, particularly in the elderly. Like dental caries, chronic infection of the gingiva and anchoring structures of the tooth begins with formation of bacterial plaque. The process begins invisibly above the gum line and in the gingival sulcus. Plaque, including mineralized plaque (calculus), is preventable by appropriate dental hygiene, including periodic professional cleaning. Left undisturbed, chronic inflammation ensues and produces a painless hyperemia of the free and attached gingivae (gingivitis) that typically bleeds with brushing. If ignored, severe periodontitis occurs, leading to deepening of the physiologic sulcus and destruction of the periodontal ligament. Pockets develop around the teeth and become filled with pus and debris. As the periodontium is destroyed, teeth loosen and exfoliate. Eventually there is resorption of the alveolar bone. A role for the chronic inflammation resulting from chronic periodontal disease in promoting coronary heart disease and stroke has been proposed. Epidemiologic studies demonstrate a moderate but significant association between chronic periodontal inflammation and atherogenesis, though a causal role remains unproven.

Acute and aggressive forms of periodontal disease are less common than the chronic forms described above. However, if the host is stressed or exposed to a new pathogen, rapidly progressive and destructive disease of the periodontal tissue can occur. A virulent example is acute necrotizing ulcerative gingivitis (ANUG), or Vincent’s infection, characterized as “trench mouth” during World War I. Stress, poor oral hygiene, and tobacco and alcohol use are risk factors. The presentation includes sudden gingival inflammation, ulceration, bleeding, interdental gingival necrosis, and fetid halitosis. Localized juvenile periodontitis, seen in adolescents, is particularly destructive and appears to be associated with impaired neutrophil chemotaxis. AIDS-related periodontitis resembles ANUG in some patients or a more destructive form of adult chronic periodontitis in others. It may also produce a gangrene-like destructive process of the oral soft tissues and bone that resembles noma, seen in severely malnourished children in developing nations.

Prevention of Tooth Decay and Periodontal Infection

Despite the reduced prevalence of dental caries and periodontal disease in the United States due in large part to water fluoridation and improved dental care, respectively, both diseases constitute a major public health problem worldwide and for certain groups. The internist should promote preventive dental care and hygiene as part of health maintenance. Special populations at high risk for dental caries and periodontal disease include those with xerostomia, diabetics, alcoholics, tobacco users, those with Down’s syndrome, and those with gingival hyperplasia. Furthermore, patients lacking dental care access (low socioeconomic status) and those with reduced ability to provide self-care (e.g., nursing home residents, those with dementia or upper extremity disability) suffer at a disproportionate rate. It is important to provide counseling regarding regular dental hygiene and professional cleaning, use of fluoride-containing toothpaste, professional fluoride treatments, and use of electric toothbrushes for patients with limited dexterity and to give instruction to caregivers for those unable to perform self-care. Internists caring for international students studying in the United States should be aware of the high prevalence of dental decay in this population. Cost, fear of dental care, and language and cultural differences may create barriers that prevent some from seeking preventive dental services.

Developmental and Systemic Disease Affecting the Teeth and Periodontium

Malocclusion is the most common developmental problem, which, in addition to a problem with cosmesis, can interfere with mastication unless corrected through orthodontic techniques. Impacted third molars are common and occasionally become infected. Acquired prognathism due to acromegaly may also lead to malocclusion, as may deformity of the maxilla and mandible due to Paget’s disease of the bone. Delayed tooth eruption, receding chin, and a protruding tongue are occasional features of cretinism and hypopituitarism. Congenital syphilis produces tapering, notched (Hutchinson’s) incisors and finely nodular (mulberry) molar crowns.

Enamel hypoplasia results in crown defects ranging from pits to deep fissures of primary or permanent teeth. Intrauterine infection (syphilis, rubella), vitamin deficiency (A, C, or D), disorders of calcium metabolism (malabsorption, vitamin D–resistant rickets, hypoparathyroidism), prematurity, high fever, or rare inherited defects (amelogenesis imperfecta) are all causes. Tetracycline, given in sufficiently high doses during the first 8 years, may produce enamel hypoplasia and discoloration. Exposure to endogenous pigments can discolor developing teeth: erythroblastosis fetalis (green or bluish-black), congenital liver disease (green or yellow-brown), and porphyria (red or brown that fluoresces with ultraviolet light). Mottled enamel occurs if excessive fluoride is ingested during development. Worn enamel is seen with age, bruxism, or excessive acid exposure (e.g., chronic gastric reflux or bulimia).

Premature tooth loss resulting from periodontitis is seen with cyclic neutropenia, Papillon-Lefèvre syndrome, Chédiak-Higashi syndrome, and leukemia. Rapid focal tooth loosening is most often due to infection, but rarer causes include histiocytosis X, Ewing’s sarcoma, osteosarcoma, or Burkitt’s lymphoma. Early loss of primary teeth is a feature of hypophosphatasia, a rare inborn error of metabolism.

Pregnancy may produce severe gingivitis and localized pyogenic granulomas. Severe periodontal disease occurs with Down’s syndrome and diabetes mellitus. Gingival hyperplasia may be caused by phenytoin, calcium channel blockers (e.g., nifedipine), and cyclosporine. Idiopathic familial gingival fibromatosis and several syndrome-related disorders appear similar. Removal of the medication often reverses the drug-induced form, though surgery may be needed to control both. Linear gingival erythema is variably seen in patients with advanced HIV infection and probably represents immune deficiency and decreased neutrophil activity. Diffuse or focal gingival swelling may be a feature of early or late acute myelomonocytic leukemia (AML) as well as of other lymphoproliferative disorders. A rare, but pathognomonic, sign of Wegener’s granulomatosis is a red-purplish, granular gingivitis (strawberry gums).

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