ALTERATIONS IN TOOTH COLOR Intrinsic Staining (Figs. 14-1 through 14-4) Alteration in tooth color, from the usual whitish appearance, is indicative of a genetic or acquired abnormality. Genetic processes that alter tooth color include amelogeneis and dentinogenesis imperfecta and dentin dysplasia. Acquired alterations in tooth color result from intrinsic or extrinsic processes. Intrinsically stained teeth are caused by loss of tooth vitality, the intake of drugs (i.e., teteracycline) and chemicals (excess fluoride), and certain disease states (hepatitis, biliary disease, erythroblastosis fetalis, porphyria) that occur during periods of tooth development. Extrinsic processes that stain teeth result from dark substances becoming adherent to the external tooth surface (see Extrinsic Staining). Nonvital Teeth. (Figs. 14-1 and 14-2) A nonvital tooth can be discolored yellow-brown to brown-gray from loss of pulpal fluids and the darkening of dentin. Many times these teeth have concurrent signs of caries, restorations, fractured incisal edges or vertical fracture lines. A large amalgam restoration may contribute to the gray-blue hue seen. Alternately, nonvital teeth can darken from the extravasation of pulpal blood into the dentin as the result of trauma or the accumulation of blood in the teeth at the time of nonvitality. This situation usually produces a pink to purple tooth in which the neck of the crown is more discolored than the incisal edge. A discolored nonvital, pink tooth has been called the "pink tooth of Mummery". Lepromatous leprosy has also been reported to cause rupture of pulpal blood vessels and pink teeth. Tetracycline Staining (Fig. 14-3) The tetracyclines are a group of bacteriostatic antibiotics that inhibit protein synthesis of certain bacteria. The drug is used in the treatment of skin and periodontal infections as well as chlamydial, certain rickettsial and penicillin-resistant gonococcal infections. Embryos, infants and children who receive tetracyclines are prone to develop varying degrees of permanent discoloration. This is more likely to occur during long-term use and repeated short term courses and is directly related to the total quantity of drug absorbed during embryogenesis and tooth development. Presence of tetracycline in the bloodstream promotes deposition of the drug in the developing enamel and dentin of teeth and bones as tetracycline-calcium-orthophosphate. The complex causes discoloration upon eruption and exposure to sun (ultraviolet) light. The discoloration is generalized and band-like if the drug was administered in courses; prolonged use produces a more homogeneous appearance. The discoloration appears light yellow with oxytetracycline (Terramycin), yellow with tetracycline (Achromycin), or green to dark gray with the synthetic tetracycline, minocycline. Chlortetracycline (Aureomycin), which is no longer available in oral form, was best known for its ability to produce gray-brown staining. Doxycycline and oxytetracycline appear to be the least discoloring. The diagnosis can be confirmed using an ultraviolet light which will make the teeth fluoresce. Adults who use tetracyclines chronically have been reported to acquire tetracycline staining. Accordingly, alternate antibiotics should be selected in children under age 8, and chronic use of tetracyclines should be avoided in adults if possible. Fluorosis (Fig. 14-4) Fluoride is a caries preventive chemical that has its greatest benefit when used at the appropriate concentration. Research has shown that the optimal fluoride concentration in the drinking water is between 0.7 and 1 part per million (ppm). At this level fluoride is incoportated into the enamel matrix adding hardness and caries resistance. At levels between 1.2 ppm and 4 ppm there is a increased risk of mild to severe fluorosis, respectively. Fluorosis is a disturbance of the developing enamel due to excess levels of fluoride in the blood and plasma. Blood levels are directly related to the level of fluoride ingested in water; excess levels can be acquired from well drinking water (endemic fluorosis) or excessive fluoride treatment and ingestion. At elevated fluoride levels, ameloblasts are affected during the apposition of enamel and produce deficient organic matrix. At high levels interference of the calcification process occurs. Mild fluorosis produces isolated, lusterless, whitish-opaque spots in the enamel. Their occurence near the incisal edge have been called "snow-capped". Moderate fluorosis is characterized by more generalized yellow to brown spots, whereas severe fluorosis has many symmetrically and bilaterally affected teeth with mottled and pitted enamel and brown and white spots. In the severe form, the morphology of the crown can be grossly altered. Extrinsic Staining (Figs. 14-5 through 14-8) Extrinsic stains result from the adherence of colored material or bacteria to the enamel of teeth. Most extrinsic stains tend to localize in the gingival third of the tooth above the gingival collar where bacteria accumulate and absorb the stain. Chromogenic bacteria can produce green to brown stains in this region from their interaction with ferric sulfide and iron in the saliva and gingival crevicular fluid. Fluids that contain color such as coffee, tea and chlorhexidine and inhaled tobacco smoke impart brown to black stain to teeth. These stains appear darkest in the gingival third of the tooth and develop as a result of frequent oral contact and enhanced contact by bacterial absorption. Amalgam restorations that leak into dentin produce blue-gray to black stain. This is most often apparent in the facial aspect of maxillary premolars that have a large class II restoration or a central incisor that has a lingually placed amalgam restoration. Along the gingival margin, stain should be distinguished from calculus and caries. Calculus adheres to the external surface of the tooth and appear greenish-black when subgingival or tan when supragingival. Caries can be dark like stain but causes loss of tooth structure, stain does not. Fig. 14-1. Intrinsic staining. Traumatic insult resulting in nonvitality evident by yellow-brown color, broken incisal edge and vertical fracture line. Fig. 14-2. Intrinsic staining - pink tooth of Mummery; nonvitality characterized by red-purple color from extravasated blood. Fig. 14-3. Intrinsic staining - Tetracycline staining; brown-gray band-like appearance. Fig. 14-4. Intrinsic staining - Fluorosis; characterized by generalized brown mottling and focal white spotting. Fig. 14-5. Extrinsic staining - chlorhexidine staining. Regions of plaque accumulation with greatest stain. Fig. 14-6. Extrinsic staining, marijuana staining. Fig. 14-7. Extrinsic staining, tobacco and coffee stains. Fig. 14-8. Extrinsic stain; applied with the holiday spirit (Courtesy Dr Dave Molina)