Richard H. Osborne

Maternal smoking and tooth formation in the foetus. II. Tooth crown size in the permanent dentition

Altogether 2159 pregnancies among black and white Americans in the Collaborative Perinatal Study and dental casts from their children at the age of 6-12 years were studied to determine the effect of maternal smoking on permanent tooth crown dimensions. A trend of reduction, similar to that observed in the deciduous second molars, was found in the permanent first molars and also in the mesio-distal dimension of permanent incisors in relation to sex and race of the children and smoking habits of the mother. In terms of peak in their mitotic growth, the results can be interpreted to indicate a sensitive period of intra uterine development from the 24th to 28th gestational weeks. Comparisons of postnatal body size and differential correlation patterns in affected tooth dimensions with early postnatal body and head size between smokers and non-smokers, suggests that maternal smoking during pregnancy may have an effect on basic growth of the head and body and/or the developmental process that impacts tooth development at some specific sensitive period also during the postnatal formation of these tooth crowns.

Maternal and Gestational Influences on Deciduous and Permanent Tooth Size

Although there have been suggestions that prenatal factors could affect crown dimensions (Bailit and Sung, Archs Oral Biol 13:155-166, 1968; Cohen, Baum, Garn, Osario and Nagy, in: Orofacial Growth and Development, Dahlberg and Graber, eds., Mouton Publishers, The Hague, 1977, pp 119-126), limitations of sample size and investigative design restrict conclusions on the magnitude of the influences. However, using newly-acquired odontometric data on selected participants in the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke (NCPP), it is now possible to show systematic effects of three maternal and six developmental conditions on mesiodistal and buccolingual dimensions of both deciduous and permanent teeth. The basic sample consists of 870 white participants studied at the time of their seven-eightyear psychological examinations in 1972 and 1973. They were selected from six cooperating institutions from the Atlantic seaboard and the West Coast (Niswander and Gordon, The Women and Their Pregnancies, D.H.E.W., Washington, 1972). Diabetes, hypothyroidism, and hypertension were the three maternal conditions selected for exploration. Gestation length, birth weight, and birth length were among the fetal or developmental variables studied. The odontometric analyses primarily involved the permanent incisors, first molars and deciduous cheek teeth (dc through dm2). A group of clinically normal children was also included for comparison, since single-source odontometric standards for deciduous and permanent teeth did not exist at the time the project was conceived. Mean crown dimensions of the normal NCPP group proved to be virtually indistin-

Permanent tooth crown dimensions in prematurely born children

AIM The aim was to examine the effect of preterm birth on permanent tooth crown dimensions. MATERIALS AND METHODS The data consisted of 328 prematurely born white and black children and 1804 control children who participated in the cross-sectional study of the Collaborative Perinatal Project (USA) in the early 1960s and 1970s. The dental examinations were carried out in a standardized fashion at ages varying from 6 to 12 years in 95% of cases. Tooth crown size measurements were performed on the dental casts with an electronic measuring device and readout by two experienced observers according to precise definitions generally quoted in the anthropological and genetic literature. The preterm and control groups were divided by sex and race. RESULTS The results show both increased and decreased tooth crown dimensions in the prematurely born children. Significantly increased dimensions were found in the means of the intercuspal distances of the first permanent molars in the white boys and in the mesiodistal dimensions (MD) of the lower lateral incisors and the upper left first molar in the black girls. By contrast, there were decreased intercuspal distances, MD and labiolingual (LL) tooth crown dimensions in the white girls and black boys. The statistical method used was the Mann-Whitneys U-test (Willcoxon Rank-Sums test). CONCLUSIONS The findings partly support previous reports of decreased tooth crown dimensions in preterm infants, but the increased dimensions found in the preterm white boys and black girls differ from earlier reports. Our results indicate the importance of environmental factors including neonatal factors in determining permanent tooth crown dimensions. Growth patterns, the buffering capacity and the timing of sensitive moments in tooth crown volume gain may vary between the sexes and ethnic groups and the possible effect of the accelerated growth period in preterm infants (catch-up growth) may influence the determination of permanent tooth crown dimensions.

Tooth eruption symmetry in functional lateralities.

Dental casts and oral photographs from a cross-sectional sample of 2092 young North Americans with detailed information on functional lateralities (eyedness, handedness and footedness) were examined to compare the proportions of symmetrical and asymmetrical eruption of the antimeric (left-right, contralateral pair) permanent teeth using a four-grade eruption scale. The proportion of symmetrically erupting antimeric teeth was higher for some teeth in those with non-right-sidedness of the feet and eyes, but not significantly so in the case of handedness. Left-footedness was significantly (95% confidence interval) associated with an increased proportion of symmetrical pairs of the maxillary first molar and mandibular lateral incisor, and non-right-eyedness with an increased proportion of symmetrical eruption and left/right non-balanced proportions of asymmetrical eruption in maxillary central incisors. True right-sidedness (hand, foot and eye) was significantly (P< or =0.05) associated with advanced eruption of the left mandibular first molar. It is suggested that while the timing of antimeric tooth emergence and clinical eruption is primarily programmed before crown mineralization, starting approximately at the 30th gestational week in the case of first permanent molars, symmetrical/asymmetrical tooth emergence and eruption may provide information a posteriori on prenatal and early postnatal growth and development.

Maternal smoking and tooth formation in the foetus. III. Thin mandibular incisors and delayed motor development at 1 year of age

Dental casts from 2159 black and white Americans with detailed neurological data available from the Collaborative Perinatal Study were examined to investigate the relationship of maternal smoking during pregnancy and delayed motor development at 1 year of age to morphological traits in the dentition. Earlier results have indicated that maternal smoking during pregnancy may cause selected tooth size metric reductions in the deciduous dentition and at least in some of the permanent teeth with prenatal crown formation, these features being influenced by sex and race differences. The present results suggest that a thinning of the incisal parts of the permanent mandibular incisors is associated with heavy maternal smoking during pregnancy, and those white girls, in whom this dental variant is found, have probably experienced more severe central damage during the smoking sensitive gestational months, as is also seen in a delayed motor development at the age of 1 year.

Cancer and contagious disease in twins. Interrelation of host defense mechanisms

A co‐twin control method was utilized in a study of twin pairs with benign and malignant neoplastic disease and without neoplastic disease in relation to their contagious disease experience. These data were analyzed in respect to intrapair discordances for neoplastic disease and contagious disease. Relative birth weight and birth order also were analyzed in these twin pairs. In pairs discordant for cancer and contagious disease the member with malignant disease was most frequently the member who indicated having had clinical symptoms of a contagious disease not shared by his co‐twin. Also, the twin member with malignant disease was usually of heavier birth weight, and more frequently the first born member of the pair. These data suggest that there is an interrelationship between host defense mechanisms against cancer and viral infection and that prenatal and perinatal factors play a role in cancer resistance.

The 47,XYY-Male, Y-Chromosome and Tooth Size: A Preliminary Communication

Permanent teeth of 12 individuals with a 47,XYY chromosome constitution have been examined. The tooth sizes of 47,XYY males were found to be larger than those of control males and females. In many instances the differences were statistically significant. Using these results, it was possible to conclude that a factor or factors which influence excess growth of 47,XYY males probably are in effect during prenatal life, but without doubt must be in effect very early in postnatal life. The time period needed for the achievement of final excess growth is relatively short, in the case of first permanent molars probably only from 2 1/2 to 3 1/2 years. On the basis of the finding that the Y chromosome apparently carries genes affecting tooth sizes in normal males [1], it was suggested that gene products of the extra Y chromosome could cause the observed size difference between normal and 47,XYY males. The nature of the influence of one versus two Y chromosomes on growth was discussed in terms of the possible influence of the Y chromosome on the cell divisions within the developing tooth germ.

GENETIC STUDIES OF DISEASES ASSOCIATED WITH CHROMOSOMAL ABERRATIONS

The papers presented in this section have dealt with four quite distinct, but interrelated problem areas: first, the multiple causes of chromosomal changes, both oncogenic and nononcogenic viruses and radiation (Aula et al., 1968 Nasjleti & Spencer, 1968) ; second, the variety of chromosomal changes which can result from the action of anyone of these agents: polyploidy, endoreplication, fragmentation, ring forms, dicentrics, and rearrangements (Aula et al., 1968 Nasjileti & Spencer, 1968); third, the variety of disease entities which can result from these changes: congenital malformations and benign and malignant neoplastic disease; associated anemias and immunological irregularities were also discussed (Fialkow & Uchida, 1968; Bloom & Diamond, 1968); fourth, the familial incidence, or genetic susceptibility or resistance of the host to chromosomal changes or the disease processes associated with such changes (McCullough et aZ.,1968; Zellweger, 1968; Lynch et al., 1968). It is to this fourth area that I shall primarily address my remarks, and most particularly from the standpoint of cancer etiology. In doing this, however, my intention is to focus attention upon the actual unity of what I have designated as four separate problem areas. To investigate the possible role of the genetic or host factor in cancer etiology, it is usual to approach the problem as though a specified form of the disease, as listed in the Manual of Tumor Nomenclature (1953), constitutes a unique and completely delineated disease entity. It is also assumed that the disease process is in all probability initiated by the impact of a single environmental agent or event upon a specific, and relatively simple, genetic system. The results of studies based upon these simplifying propositions have been essentially negative, or at best inconclusive (McCullough et al., 1968), as might be anticipated from the multiple causes and effects of chromosomal changes ( A d a et al., 1968; Nasjleti & Spencer, 1968; Fialkow & Uchida, 1968; Bloom & Diamond, 1968). Investigations of quite a different type from those reported in this monograph may help to make this point clear. A major,milestone in cancer studies was recognition of the multiplicity of the disease and the variety of its histological types. Evidence has long been mounting, however, which clearly indicates that in studies of cancer etiology, some grouping of types on biological grounds is necessary, and that each form of the disease is not a unique entity, either in respect to the responsible causative agent or a host susceptibility factor. One example is the ABO blood group cancer association. Blood group A, for reasons still unknown, marks a genotype with a statistically increased susceptibility to neoplastic disease of the stomach (Aird et al., 1953), of the ovary (Osborne & DeGeorge, 1963), and of the salivary gland (Cameron, 1958; Osborne & DeGeorge, 1962). Three body sites and several histological types, both benign and malignant, are involved in the blood group association. This may be surprising to the hospital administrator for it cuts across the boundaries of three absolutely different services (Gastric, Gynecology, and Head and Neck), but there is a unifying biological element. The associated types are predominantly of glandular epithelium and all are characterized by atypical cell regeneration or metaplasia. Similarly, it is quite possible that in lymphatic leukemia, the genetic suscepti-