PEDIATRIC DENTISTRY/Copvnpht C> 1991 b\The American Academy of Pediatric Dentistry

Volume 13. Number 3

Natal primary molar: case reportGerald W. Friend, DDS, MS Harry H. Mincer, DDS, MS, PhDKenneth R. Carruth, DDS, MS James E. Jones, DMD, MSc, MSD

AbstractThe case of an immature natal maxillary first primary

molar is reported. Natal molars are rare occurrences, thepresent instance being only the eighteenth reported case.Clinical and histologic examination revealed that the toothwas rootless, incompletely mineralized, and acutely inflamed.Subsequent radiographs showed that the tooth was actuallythe primary first molar.

Review of LiteratureAccording to Bodenhoff (1960), 85% of natal or neo-

natal teeth are mandibular incisors, 11% are maxillaryincisors, and 3% are mandibular cuspids or molars.Only 1% are maxillary cuspids or molars. Similarly,Kates et al. (1984), in a study of 18,155 infants, reportedthat all of 61 observed natal or neonatal teeth weremandibular central incisors. Among the 38 infants soaffected, 61% had a pair of teeth.

Posterior teeth erupting during the perinatal periodare decidedly rare. Brandt et al. (1983) found 16 cases ofmolars in the newborn in the then extant literature andadded a case of their own. Thirteen were classified asnatal teeth, and three as neonatal teeth. For one, the timeof eruption was not specified.

The present report is a clinical and histological de-scription of a natal maxillary primary molar.

Case ReportThe infant was a two-day-old, healthy, full term

black male born from an uncomplicated pregnancy anddelivery. Maternal medical and social histories disclosedno significant information. Intraoral examination re-vealed a pale, globular toothlike structure on the max-illary left alveolar ridge (Fig 1). The specimen measured0.75 x 0.5 x 0.5 cm and had a somewhat flattened occlusalsurface, except for three shallow cusps which appearedto be calcified only on the tips. The remainder of thespecimen apparently was unmineralized, and the cen-tral fossa area of the occlusal surface was compressibleby probing with a blunt instrument. The tooth was

rootless and loosely attached near the cervical line tothe surface mucosa of the alveolar ridge.

Histomorphologically, the specimen showed thegeneral configuration of the crown of a primary molartooth. The cusp tips were comprised of regular tubulardentin which was thin-ner than normal (Fig 2,next page). Dentin thick-ness on the axial surfacesdecreased progressivelytoward the cervix. Theenamel, as evidenced byresidual matrix, was at-tenuated similarly. Thecentral fossa area be-tween the cusps con-tained a variable thick-ness of generally homo-geneous eosinophilicmaterial apparently rep-resenting uncalcified,a tubular osteodentin (Fig3, next page). Scatteredthrough this material were pyknotic or lytic nuclei. Inthis area enamel formation was not apparent, but theosteodentin was covered by primitive stratified squa-mous epithelium which varied in thickness and withinwhich were diffusely embedded large, eosinophilic,generally circular or polygonal, keratinaceous struc-tures. Pulp vasculature was dilated and hyperemic. Theodontoblast layer was reasonably well organized ex-cept in the central fossa area, where there was diffusepulp necrosis and infiltration with acute inflammatorycells consisting mainly of neutrophils. Also, at the cer-vical base, where the tooth had been joined to thealveolar crest, there was a thinner, fairly uniform bandof pulp necrosis. This was also infiltrated with neutro-phils, although less intensely than in the central fossaarea. Cementum was not identified.

Fig 1. Clinical photograph ofthe immature natal molar in the2-day-old infant.

PEDIATRIC DENTISTRY: MAY/JUNE, 1991 ~ VOLUME 13, NUMBER 3 173

Fig 2. Photomicrograph of immature natalmolar near cusp tip. In this area theodontoblast layer (O) of the pulp isrelatively well-formed and the dentin(D)shows regularity of tubules. An artefactspace (S) separates the residual enamelmatrix (E) from the underlying dentin.(Original magnification 100x).

Fig 3. Photomicrograph of immaturemolartooth inthe central fossa area of theocclusal surface. Thedentin(D) is atubularand contains degenerate nuclei. Noevidence of enamel formation isseen butthere is a covering of primitive stratifiedsquamousepithelium(E) containing manykeratinaceous structures (arrows). Thesubadjacent pulp (P) is acutely inflamed.(Original magnification 100x).

DiscussionThe reason usually given for eruption of teeth during

the perinatal period is superior placement of the toothgerm (Southam 1968; King and Lee 1989), but in mostcases specific pathogenetic factors cannot be identified.In some instances heredity seems to contribute. Masslerand Savara (1950) found first order relatives with natalor neonatal teeth in 10 of 24 cases. Also, because nataland neonatal teeth are often components of inheritedsyndromes with more serious manifestations, infantswith teeth at birth or shortly thereafter should be evalu-ated carefully (Chow 1980; Leung 1986; Darwish et al.1987). For example, pachyonychia congenita, a rarehereditary disorder characterized by nail hypertrophyand dyskeratoses of skin and mucosas, also will shownatal or neonatal teeth in a sizeable number of cases(Feinstein et al. 1988). Other congenital conditions as-sociated with premature teeth include Ellis-van Creveldsyndrome (Chow 1980), Pierre Robin anomaly,adrenogenital syndrome, cleft palate and rickets (Leung1986), Hallermann-Streiff syndrome (Chow 1980);craniofacial dysostosis (Ohishi et al. 1986), steatocystomamultiplex (King and Lee 1987), and patent ductus arte-riosus with lethal intestinal obstruction (Harris et al.1976). Also, natal teeth are among several structuraland metabolic defects reported in Japanese and Tai-wanese infants born to mothers who had ingested poly-chlorinated biphenyls (PCBs) in contaminated cookingoil (Rogan 1982; Miller 1985; Rogan et al 1988).

In the present case no underlying cause for the nataltooth was apparent. There was no evidence of heredi-tary influence, and pediatric follow-up examinations ofthe infant disclosed no other defects.

Histological examination of thespecimen showed that while calcifica-tion had begun on the cusps and axialsurfaces, the central fossa of theocclusal surface had not yet mineral-ized. Also possibly indicative ofhypocalcification was retention of theenamel matrix after decalcification ofthe specimen for histologic study(Southam 1968). According to the cri-teria established by Kraus and Jordan(1965) the degree of morpho-differ-entiation of this tooth was approxi-mately Stage XI for the maxillary firstprimary molar. This corresponds de-velopmentally to the maxillary firstprimary molar of a 28-week fetus.

Atubular osteodentin such as thatobserved in the occlusal central fossais equivalent to the irregular tertiarydentin deposited in response to unto-ward stimuli such as caries or attrition

(Southam 1968). This suggests that odontoblasts in thecentral fossa were exposed to the oral environmentbefore developing a covering of enamel and normaltubular dentin, and responded by depositing theatubular substance. Similar material found in the cervicalregion of other natal and neonatal teeth has been at-tributed to stimulation by movement of the teeth. It hasbeen further postulated that the mobility may causedegeneration of Hertwig's sheath thus preventing rootdevelopment and stabilization (Southam 1968).

Also attributed to premature eruption of the imma-ture tooth in this case was the primitive squamousepithelium covering the atubular dentin in the centralfossa area. The epithelium contained keratinaceousstructures reminiscent of the "ghost cells" seen in cal-cifying epithelial odontogenic cysts (Gorlin cysts) andin some odontomas (Shafer et al. 1983). We believe thataborted amelogenesis resulting from premature expo-sure to the oral environment resulted in metaplastictransformation of the normally columnar enamel epi-thelium to a stratified squamous configuration.

Dr. Friend is assistant professor, Dr. Carruth is associate professor,and Dr. Jones is professor and chairman, Department of PediatricDentistry, University of Tennessee, Memphis, TN. Dr. Mincer isprofessor, Department of Biologic and Diagnostic Sciences, Universityof Tennessee.

Reprint requests should be sent to Dr. Gerald W. Friend, Departmentof Pediatric Dentistry, University of Tennessee, 875 Union Ave.,Memphis, TN 38163.

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newborn. Pediatr Dent 5:210-13,1983.

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Chow MH: Natal and neonatal teeth. J Am Dent Assoc 100:215-16,1980.

Darwish S, Sastry KA, Ruprecht A: Natal teeth, bifid tongue, and deafmutism. J Oral Med 42:49-56, 1987.

Feinstein A, Friedman J, Schewach-Millet M: Pachyonychia congenita.J Am Acad Dermatol 19:705-11, 1988.

Harris DJ, Ashcraft KW, Beatty EC, Holder TM, Leonidas JC: Natalteeth, patent ductus arteriosus and intestinal pseudo obstruction:a lethal syndrome in’the newborn. Clin Genetics 9:479~82, 1976.

Kates GA, Needleman HL, Holmes LB: Natal and neonatal teeth: aclinical study. J Am Dent Assoc 109: 441-43, 1984.

King NM, Lee AMP: Natal teeth and steatocystoma multiplex: anewly recognized syndrome. J Craniofac Genet Dev Biol 7:311-17,1987.

King NM, Lee AMP: Prematurely erupted teeth in newborn infants. JPediatr 114:807-9, 1989.

Kraus BS, Jordan RE: The Human Dentition Before Birth. Philadel-phia: Lea and Febiger, 1965, pp. 69-80

Leung AKC: Natal Teeth. Am J Dis Child 140:249-51, 1986.Massler M, Savara BS: Natal and neonatal teeth: a review of twenty-

four cases reported in the literature. J Pediatr 36:349-59, 1950.Miller RW: Congenital PCB poisoning: a reevaluation. Environ Health

Perspect 60:211-14, 1985.Ohishi M, Murakami E, Haita T, Naruse T, Sugino M, Inomata H:

Hallermann-Streiff syndrome and its oral implications. ASDC JDent Child 53:32-37, 1986.

Rogan WJ: PCBs and cola-colored babies: Japan, 1968, and Taiwan,1979. Teratology 26:259~61, 1982.

Rogan WJ, Gladen BC, Hung KL, Koong SL, Shih LY, Taylor JS, WuYC, Yang D, Ragan NB, Hsu CC: Congenital poisoning by poly-chlorinated biphenyls and their contaminants in Taiwan. Science241:334-36, 1988.

Shafer WG, Hine MK, Levy BM: Cysts and tumors of odontogenicorigin. In A Textbook of Oral Pathology, 4th ed. Philadelphia: WBSaunders, 1983, pp. 258--317.

Southam JC: The structure of natal and neonatal t~eeth. Dent PractDent Rec 18:423-27, 1968.

The American Board of Pediatric DentistryIs Pleased To Announce the Following New Diplomates:

George Acs N Bronx, NYDeanna E. Aronoff N Pleasanton, CADonna J. Barefield ~ Dallas, TXJoel H. Berg - Houston, TXCharles M. Bordenca - Alabaster, ALGail E. Brossok N Farmington Hills, MILucy A. Chan-Wong ~ Roselle, NJAlice Chao - Murray Hill, NJGerald D. Cox N Martinez, GABarry J. Currey N Lubbock, TXSteven C. Demetriou ~ Tewksbury, MAV. Kayron Dube ~ Houston, TXNorman B. Farrar ~ APO New York, NYMichael L. Grimes ~ Monroeville, PARobert J. Henry ~ Gainesville, FLRandall W. Hollenberg ~ Katy; TXDonald V. Huebener - St. Louis, MOJeffrey P. Huston N Lodi, CAAlejandro J. Ibarra ~ CP 75230, MexicoAnthony A. Kamp N APO New York,NYConstance M. Killian ~ Doylestown, PAMark G. Koch ~ Fort Leonard Wood,MO

Daniel V. Launspach N Bakersfield,CARochelle Lopyan ~ Atlanta, GAOariona Lowe - Whittier, CAJeffrey C. Mabry ~ Beavercreek, OHB.J. Mistry ~ Tarrytown, NYElaine C. Nelson ~ FPO San Fran-cisco, CAMark L. Nelson ~ Bountiful, UTSteven J. Ni6thamer - PalmSprings, CAMartin J. Oakes ~ Fort Bragg, NCGustavo Pardo ~ Mexico DF,MexicoNeophytos L. Savide N PalosHeights, ILRandy G. Seely ~ Lewisville, TNSusan V. Seybold ~ Houston, TXHarry K. Sharp ~ Memphis, TNRonald L. Singer ~ Valencia, CAThomas C. Sorensen ~ Murray, UTGeorge P. Thomas ~ Silver Spring,MD

PEDIATRIC DENTISTRY: MAY/JUNE, 1991 -- VOLUME 13, NUMBER 3 175