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Teeth Ronald J. Billings, DDS, MSD; Robert J. Berkowitz, DDS; and Gene Watson, DDS, PhD ABSTRACT. Common environmental chemicals, Teeth are most susceptible to developmental distur- drugs, or physical agents can adversely affect human bances during the mineralization phase of tooth for- teeth during their embryonic development and after their mation. In general, the permanent dentition is more eruption into the oral cavity. One of the more common susceptible to disturbances in mineralization by en- elemental toxicants is lead. Teeth are known to accumu- vironmental toxicants and drugs than is the primary late lead during their development. Both animal and dentition, most likely as a consequence of its later human studies have shown that teeth with high lead levels are generally more susceptible to dental caries. development. As such, this review focuses on some Similarly, although inorganic fluorides have long been of the more commonly observed developmental dis- recognized for their potential to prevent dental caries, turbances of the permanent dentition that result from exposure to excessive amounts of fluoride when enamel excess exposure to various environmental chemicals is forming often leads to a type of enamel hypoplasia and drugs and touches on other, somewhat contro- referred to as dental fluorosis or mottled enamel. Tera- versial, toxicants that may adversely affect the child togenic agents, such as tetracyclines, a class of antibiotic as a whole as well as the dentition. Damage to the drugs commonly administered to infants and children, teeth from orofacial trauma is also reviewed for its will often result in the discoloration of tooth enamel impact on the dentition of both children and adoles- when prescribed during tooth development. It has re- cents. cently been suggested that childhood exposure to passive smoking increases the risk for dental caries. Environmen- tal tobacco smoke has previously been linked to peri- ENVIRONMENTAL CHEMICALS odontal disease in adults. However, this is the first report Lead of an association between passive tobacco smoke and It has long been known that lead crosses the pla- increased susceptibility to dental caries. Last, an often- centa and has the potential to affect the development overlooked source of damage to teeth among all age of different organ systems,1,2 including teeth,3–7 and groups after their eruption into the oral cavity is physical trauma from a variety of sources, especially sports-re- its accumulation in developing teeth has provided a 8,9 lated injuries. Epidemiologic data suggest that up to one useful record of both fetal and long-term uptake third of all dental injuries are sports related. Pediatrics for the study of neuropsychological effect of uniden- 2004;113:1120–1127; environmental chemicals, drugs, tified childhood exposure to lead.10,11 Although physical agents, tooth development, teeth, dental caries. clear, unequivocal evidence of a cause-and-effect re- lationship between embryonic and early childhood ABBREVIATIONS. ETS, environmental tobacco smoke; PAH, exposure to lead and enhanced susceptibility to den- polyhalogenated aromatic hydrocarbon; PCB, polychlorinated bi- tal caries is lacking, the preponderance of epidemio- phenyl; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin. logic data, combined with data from animal studies, are suggestive of such a relationship. Bowen12 de- scribed several potential mechanisms on how pre- umans have 2 sets of teeth: the primary, or eruptive exposure to lead could enhance caries risk. deciduous, dentition followed by the perma- However, a dose–response relationship between nent dentition. Primary tooth formation and H preeruptive exposure to lead and dental caries has development usually begins, on average, between never been determined. Lead has also been shown to the 13th and 16th weeks of gestation for incisors and accumulate in teeth posteruptively.3,13 Although a between the 14th and 24th weeks for canines and number of ecological and cross-sectional studies con- molars. Mineralization of the enamel surface is usu- ducted in the 1960s and 1970s implicated posterup- ally complete by the end of the first year of life and tive exposure to lead as a risk factor for caries, the root development by 12 to 18 months after eruption. data are not clear that posteruptive exposure to lead The permanent dentition begins to form in utero, and has a direct effect on caries susceptibility.14 A more mineralization is usually complete by age 4 or 5 and recent study of the association of dental caries and root development by 2 to 3 years after eruption. blood lead levels in children 5 to 17 years of age showed that a 5-␮g/dL change in blood lead level From the Eastman Department of Dentistry, University of Rochester, School was associated with an increased risk for caries and of Medicine and Dentistry, Rochester, New York. that Ͼ2 million excess cases of dental caries in US Received for publication Oct 7, 2003; accepted Oct 20, 2003. children may be attributable to environmental lead Reprint requests to (R.J.B.) Eastman Department of Dentistry, University of exposure or factors that are linked to lead expo- Rochester, School of Medicine and Dentistry, 625 Elmwood Ave, Rochester, 15 NY 14620. E-mail: [email protected] sure. However, as the data were cross-sectional in PEDIATRICS (ISSN 0031 4005). Copyright © 2004 by the American Acad- nature, no temporal or causal relationship could be emy of Pediatrics. established. In a study specifically designed to exam- 1120 PEDIATRICS Vol.Downloaded 113 No. 4 from April www.aappublications.org/news 2004 by guest on September 29, 2021 ine the temporal association between lead exposure more related to posteruptive forces, then a similar and caries, second- and fifth-grade children who pattern of caries susceptibility in the permanent den- were known to have blood levels up to 45 ␮g/dL tition should be observed. These findings are clearly (mean: 10.7 ␮g/dL) as toddlers were not shown to be provocative and beg for aggressive studies that will at greater risk for caries than children who had little elucidate the causative role of ETS on the oral health or no lead exposure.16 As noted by the authors, how- of children and adolescents. Other studies that ever, the study had limited statistical power to detect clearly need to be undertaken revolve around poten- a clinically relevant odds ratio. tial mechanisms underlying tobacco’s cariogenic po- Other ways in which lead could have an impact on tential. For example, 1 in vitro study suggested that caries risk revolves around its effect on salivary tobacco may have an effect on the growth of oral gland development and function. Work by Watson et cariogenic streptococci.31 However, the study in- al17 reported significantly diminished salivary flow volved only smokeless tobacco products, and, as the rates and subsequent high caries levels in the off- authors noted, growth of cariogenic organisms may spring of laboratory rats whose dams were exposed have been attributable entirely to the manufacturer’s to 34 ppm lead in the drinking water during preg- added sugar and not to natural tobacco sugar. No nancy and during lactation. These observations are reported studies have investigated a potential rela- currently being followed up in an ongoing clinical tionship between tobacco in other forms, eg, smoked study of caries risk resulting from environmental tobacco, whether active or passive, and growth of lead exposure in a birth cohort of 245 Cincinnati cariogenic oral flora. Clearly, much work remains to children who have been participants in the Cincin- be undertaken in this area. nati Lead Study since late 1979. This group of black and white Appalachian children is arguably the most Mercury well-described longitudinal cohort ever studied for Although the toxic properties of mercury have prenatal and postnatal lead exposure, with peak been well understood for many years, there is no blood levels ranging from 5 to Ͼ809 ␮g/dL.18,19 A known association between mercury and tooth de- major goal of this study is to measure potential con- velopment or between mercury and dental health. founding factors, including dietary habits, oral hy- Mercury is an integral component of dental amal- giene, and socioeconomic status, and to assess the gam, a mixture of mercury, tin, silver, zinc, and influence of these on any observed association be- copper for use as a restorative material in the treat- tween dental caries and lead exposure. If a causal ment of dental caries. The major concern with mer- relationship between environmental lead and dental cury, as used in dentistry, has been the observation caries is supported, then more aggressive measures that mercury vapor is released from amalgam resto- for caries prevention could be targeted toward chil- rations,32–35 and some observers have contended that dren with high blood lead levels. exposure to mercury from dental amalgam often ex- ceeds the sum of exposure from all other sources.36 Tobacco As 1 of the potential sequelae from mercury toxicity Several recent studies have reported on the ad- is neurologic damage, studies in both humans and verse impact of both smoked and smokeless tobacco animals have attempted to provide evidence of a on the oral health of children, adolescents,20–22 relationship between mercury released from dental and adults.23–26 Investigators have specifically linked amalgam and various neurologic disorders, in par- cigarette smoking with periodontal disease in ticular multiple sclerosis.37 To date, no credible evi- adults,25,27,28 and a relationship between environ- dence has been forthcoming on any ill effects from mental tobacco smoke (ETS) and periodontal health the small amount of mercury released by dental in adults has been reported.28 Conversely, only a few amalgams,38,39 including multiple sclerosis.40,41 Both studies on the effect of active or passive smoking on the American Dental Association and the US Public oral health, including dental caries and periodontal Health Service have conducted exhaustive reviews of disease, in children have been reported.

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