Enamel Hypoplasia and Dental Caries in Very-Low Birthweight Children

Enamelhypoplasia and dental caries in very-low birthweight children: a case-controlled, longitudinal study

P.Y. Lai, MDSc, FRACDSW. Kim Seow, MDSc, DDSc, PhD, FRACDS D.I. Tudehope, MBBS,FRACP Yvonne Rogers

Abstract laryngoscopy and intubation during the neonatal period.~2-13 This longitudinal study investigated the sequelae of enameldefects in a groupof 25 white, very-low birthweight The clinical implications of the high prevalence of (VLBW),preterm children (mean birthweight 969 +__ enamel hypoplasia in preterm children have not been g, meangestational age 27 +__ 1.9 weeks). Twenty-five well explored. In particular, the effects of enamel hypoplasia on the development of dental decay in race-, age-, and sex-matched,full-term normalbirthweight 3,16 (NBW)control children born at the same hospital, were preterm children are unclear. A few studies have selected randomlyfrom hospital records. The children were suggested that LBWpredisposes a child to increased examinedat approximate ages of 30, 44, and 52 months. dental caries but the relative importance of enamel At all examinations, VLBWchildren had significantly hypoplasia comparedwith other caries risk factors is higher prevalence of enamel hypoplasia than did the NBW unknown. To the authors’ knowledge, longitudinal children. At the last recall examination, 96%of VLBW studies to examine the sequelae of enamel defects in group, and 45%of the NBWgroup had at least one tooth VLBWchildren have not been done before. with enameldefect, with a meanof 7.6 ~ 4.9 affected teeth The aim of our investigation was to study a cohort per VLBWchild, and only 1.0 +__1.3 affected teeth per con- of VLBWchildren and a matched, control group of full- trol child (P < 0.001). A significant association of enamel term children longitudinally to determine whether defects with dental caries was observed only in the VLBW enamel hypoplasia seen in VLBWchildren predisposes group on the second and third examinations (P < 0.001). them to increased dental caries risk. The defect identified to be most significantly associated with dental caries was a variant showingboth enamelhy- Subjects and methods poplasiaand opacity. In spite of a high prevalenceof enamel The subjects were preterm, VLBWchildren cared for defects, the overall prevalenceof dental caries in the VLBW at the Mater Mothers’ Hospital27, TM All VLBWchildren children was not significantly different from that of NBW born between 1989 and 1992 were sent letters of invi- controls at all three examinations(P > 0.1). Other caries tation to participate. risk factors such as levels 0fStreptococcusmutans infec- For each VLBWsubject included in the study, a full- tion,fluoride supplementation,plaque scores, toothbrushing term, normal birthweight (NBW) control patient frequency, and daily sugar exposures were examined but matched for sex, and born at approximately the same none was found to be related significantly to development time at the same hospital, was selected at randomfrom of dental caries. (Pediatr Dent19:42~49, 1997) hospital records and invited to participate in the study. The consent rate for participation in the study was revious investigations on the dental complica- 97%in the group of patients whocould be contacted. p tions of preterm and low birthweight children The subjects were examined at the pediatric dental have all been cross-sectional.1-1s In these studies, clinic at the University Dental School. Signed informed a high prevalence of developmental enamel defects had consent was obtained from the parents. been found, with the highest frequency of more than The socioeconomic status of the subjects was as- 70%in very-low birthweight (< 1500 g, VLBW)chil- sumed based on the parents’ occupations and suburb dren, and lower frequency of approximately 40%in the of residence29, 20 Medicalperinatal and neonatal histo- low birthweight groups (1500-2000 g, LBW).1-11 The ries were obtained from hospital records. Relevant etiological factors associated with these defects include postnatal histories were obtained from the parents. systemic metabolic changes associated with prematu- Dental histories, including past dental treatment, fluo- rity 1-11 as well as local traumatic forces resulting from ride supplementation, and residence in towns with

42 American Academy of Pediatric Dentistry Pediatric Dentistry - 19:1, 1997 TABLE 1. DEMOGRAPHICDATA OF SUBIECTS IN STUDY. fluoridated water, oral hygiene habits, and frequency VLBW NBW of daily of toothbrushing 25) 25) P-value were obtained from the parents. Boys 12 12 NS" A three-day (including Girls 13 13 NS" weekend day) diet history MeanBirthweight (g) +_ 969 + 218 3418 + 415 P < 0.001 form2~ was issued to each Range (g) (652-1410) (2810-4110) t = 25.7, df = 44 patient, and the parents MeanGestational Age (wks) ._+ 27 + 1.9 40 + 1.2 P < 0.001 were requested to fill in de- Range (wks) (24-29) (37-42) t = 34.2, df = 44 tails of all foods and drinks SocioeconomicStatus ° consumed during and be- I (high) 12 8 NS tween meals. II (middle) 3 2 NS° The teeth were dried III (low) 8 10 NS" with gauze, and examined Unclassified 2 5 NS° MeanAge at Exam(month __+ SD) for enamel opacity, enamel Exam I 27.5 + 4.6 32.3 + 2.8 NS~ hypoplasia, and dental car- Exam II 41.4 + 6.5 46.2 + 3.6 NS+ ies. The modified DDE(De- Exam III 51.5 + 4.9 52,5 ± 4.2 NSt velopmental Defects of Enamel) Index 26 was used to ¯ Chi-squaretests. chart enamel defects. In t Student’st-test. brief, enamel hypoplasia

TABLE 2. PREVALENCEOF VARIOUS TYPES OF ENAMEL DEFECTS IN THE VLBW AND NBWCHILDREN

Exam I Exam II ExamIII VLBW NBW VLBW NBW VLBW NBW Total no. of children 25 25 19 11 24 20 No. (%) of children affected with Enamel hypoplasia 17 (68) 1 (4) 10 (53) 0 16 (67) 2 (10) (P-value) P < 0,001, X2 = 19.5, df = 1 P < 0.001, odds ratio = 0 P < 0.001, X2 = 12.2, df = 1 Enamel opacities 12 (48) 7 (28) 14 (74) 5 (46) 19 (79) 6 (30) (P-value) NS NS P < 0.001, Z2 = 8.8, df = 1 Hypoplasia with opacity 0 2 (8) 3 (16) 2 (18) 13 (54) 2 (10) (P-value) NS NS P < 0.005, Z2 = 7.6, df = 1 Total No. (%) affected children 22 (88) 10 (40) 18 (95) 6 (54) 23 (96) 9 (45) (P-value) P < 0.001, X2=10.5, df = 1 P < 0.029, X2 = 4.7, df = 1 P < 0.001, X2 = 11.8, df = 1

Total no. of teeth 377 476 392 220 479 399 No. (%) of teeth affected with Enamel hypoplasia 43 (11) 4 (1) 36 (9) 0 51 (11) 5 (1) (P-value) P < 0.001, X2 = 43.1, df = 1 P < 0.001, odds ratio = 0 P < 0.001, Z2 = 30.6, df = 1 Enamel opacity 24 (6) 9 (2) 48 (12) 9 (4) 88 (18) 12 (3) (P-value) P < 0.001, X2 = 10.2, df =1 P < 0.001, %2= 10.1, df = 1 P < 0.001, Z2 = 49.1, df = 1 Hypoplasia with opacity 0 3 (1) 6 (2) 3 (1) 49 (10) 3 (1) (P-value) NS NS NS NS P < 0.001, X2 = 33.4, df = 1 Total no. (%) affected teeth 67 (18) 16 (3) 90 (23) 12 (6) 188 (39) (P-value) P < 0.001, X2 = 48.1, df = 1 P < 0.001, Z2 =29.8, df= 1 P < 0.001,%2= 135.6, df = 1 Mean± SD affected teeth~child 2.6± 2.5 0.6 + 1.0 4.7 ± 4.1 1.1 + 1.2 7.8±4.8 1.0=1.3 (P-value) P < 0.001, t = 3.71, df = 48 P < 0.009, t = 2.8, df = 28 P< 0.001t=6.14, df=

PediatricDentistry - 19:1, 1997 AmericanAcademy of Pediatric Dentistry 43 was diagnosedif there was a deficiency of enamelin the bation for 2 days at 37°C, the strip was removed, air- form of pits, grooves, or other quantitative surface loss. dried, and the numberof Streptococcus mutans colonies Enamelopacity was diagnosed if there was a qualitative counted and graded against standards provided on the change in the translucency of enamel without loss of manufacturer’s charts. A score of 1 was given for enamel surface. Enamelopacity maybe white or stained. colony counts of <10~, 2 for counts of 10s-106, and 3 for Whenan enamel defect had both hypoplasia and opac- counts > 106. The second and third dental examinations ity, it was classified as a combinationdefect. The crite- were performed approximately 9 months and 18 ria of Radike~3 were used to diagnose dental caries. Only monthsafter the first one. lesions with frank cavitation were scored as carious. surfaces of each tooth were examined, and the sever- Statistical analysis ity and extent of each defect recorded. The student’s t-test, chi-square test, or Fisher’s ex- The percentages of teeth affected by enamel hypo- act test, was used for statistical analysis of the data plasia and by dental caries were computed by divid- where appropriate. ing the number of affected teeth by the total number of teeth present. Results A plaque score was obtained from each subject us- ing24, the modified plaque score of Loe and Silness. Demographyof subjects In brief, plaque was noted to be either present (score Table 1 shows the demography of subjects in the of 1) or absent (score of 0) on the facial, lingual, study. There was a total of 25 in each group of VLBW mesial surfaces of the following maxillary teeth: left and full-term control children. There were 12 boys and central incisor, left first molar, right second molar and 13 girls in each group. The mean birthweight and ges- the following mandibular teeth: right central incisor, tational age for the VLBWgroup was 969 + 218g and right first molar, and left second molar. This modified 27 + 1.9 weeks, and 3418 _+ 415 and 40 + 1.2 weeks for scoring system is simple and practical for use in young the NBWgroup. children. A percentage score was computed by divid- As shownin Table 1, there were no significant dif- ing the obtained score by the maximumpossible score. ferences in the distribution of SESbetween the VLBW The maximumscore was altered accordingly if one or and NBWgroups. moreof the index teeth used for scoring were absent. The mean ages (months) of preterm children at ex- The dental examinations were performed by a single aminationsI, II, and III were 27.5 + 4.6, 41.4 + 6.5, and examiner (PYL). Intra-examiner consistency of the ex- 51.5 + 4.9 respectively, and those for control children amination technique was demonstrated by comparing were 32.3 + 2.8, 46.2 + 3.6, and 52.5 + 4.2, respectively. the results of plaque scores, enameldefects, and caries Differences in the corresponding mean ages betweenthe examination of three VLBWchildren three times on VLBWand control groups were not significant (P > 0.1). three different occasions. The kappa statistic 24 value Prevalenceof enameldefects in VLBW was 0.7, which indicated good consistency. and NBWchildren Streptococcus mutans infection in each patient was assessed using Dentocult TM Strip mutans kits (Orion Table 2 shows the prevalence of enamel defects in Diagnostica, Espoo, Finland).27 A treated plastic strip the VLBWand NBWgroups. The percentage of NBW supplied by the manufacturer was inserted into the children showingat least one type of enamel defect was mouth, and turned five times on each side to contact 40%at exam I, 54%at examII, and 45%at exam III. the tongue. The strip was then removed and placed in In contrast, the percentage of VLBWchildren show- a vial containing bacterial culture medium.After incu- ing at least one type of enamel defect was 88%at exam

ExamI ExamII Exa~nIII VLBW NBW VLBW NBW VLBW NBW 25) (N = 25) (N = I9) (N = (~ = 24) (N = Meanage + SD(months) 27.5 + 4.6 32.3 + 2.8 41.4 + 6.5 46.2 + 3.6 51.5 + 4.9 52.5 + 4.2 No. (%) caries-free children 25 (100%) 24 (96%) 14 (78%) 10 (91%) 17 (71%) 16 (80%) Meanno. of decayed teeth (dt) per child 0 0.04_+ 0 0.58 + 2.0 0.45 + 0.8 0.42 + 1.1 1.15 + 2.2 Meanno. of filled teeth (ft) per child 0 0 0 0.42 + 1.1 0.25 + 0.6 Mean dmft + SD 0 0 + 0.2 0.6 + 1.4 0.5 + 1.5 0.8 + 1.5 1.4 + 3.2 Student’st tests indicatedthat differencesin meandraft betweenthe VLBWand NBW groups were nonsignificant at all dentalexaminations.

44 AmericanAcademy of PediatricDentistry PediatricDentistry - 19:1,1997 Teeth Affected Number[%1 Dental Caries Dental Dental Enamel Caries Caries Defects Present Absent Total P-value" Exam I Present 0 67 (19) 67 (19) VLBW NS Absent 0 290 (81) 290 (81) Total 0 357 (100) 357 (100)

NBW Present 0 16 (4) 16 (4) NS Absent 1 (0.2) 423 (96) 424 (96) Total 1 (0.2) 439 (99) 440 (100)

Exam II Present 10 (3) 78 (21) 88 (24) VLBW P < 0.001, Absent 1 (0.3) 283 (76) 284 (76) X2 = 24.7 Total 11 (3) 361 (97) 372 (100) df = 1

NBW Present 0 12 (6) 12 (6) NS Absent 5 (2) 203 (92) 208 (94) Total 5 (2.3) 215 (98) 220 (100)

Exam III Present 16 (3) 169 (35) 185 (38) VLBW P < 0.001 Absent 4 (1) 290 (61) 294 (62) X2 = 13.3 Total 20 (4) 459 (96) 479 (100) df = 1

NBW Present 1 (0.3) 19 (5) 20 (5) NS Absent 27 (7) 352 (88) 379 (95) Total 28 (7) 371 (93) 399 (100) ¯ P-valueswere calculated using the chi-squaretest. NS= Notsignificant.

I (P < 0.001), 95%at examII (P < 0.029), and 96%at the NBWgroup had a mean dmft of 1.4 + 3.2 compared [I! (P < 0.001). with 0.8 + 1.5 in the VLBWgroup. This difference was In relation to the total number of teeth present at not significant (P > 0.1). each examination (Table 2), in the NBWcontrol chil- Distribution of enameldefects and dental caries dren, the percentage of teeth showing at least one type of enamel defect was 3% at exam I, 6% at exam II, and The distributions of teeth affected by enamel defects 5% at exam III. In contrast, the figures for the VLBW and dental caries are shown in Fig 1. In the VLBW group were 18% at exam I (P < 0.001), 23% at exam group, the most commonprimary tooth series affected (P < 0.009), and 39%at exam III (P < 0.001). by enamel defects are, in order of decreasing prevalence, second molars (52%), first molars (43%), incisors Prevalence of dental caries in VLBWand NBW (31%), and canines (31%). With regard to dental caries, children the most common primary tooth groups affected are, Table 3 shows the prevalence of dental caries in the in order of decreasing prevalence, second molars (14%), VLBWand NBWcontrol groups of children. In Exam first molars (3%), incisors (1%), and canines (1%). I, all but one child in the NBWgroup were caries-free. In contrast, in the case of NBWchildren, enamel At exams II and III, more children were caries-free in defects were most commonly observed in the canines the NBWgroup than in the VLBWgroup, but the re- (13%), followed by the incisors (4%) and second sults were not statistically significant. The mean num- lars (4%) in decreasing order. Dental caries in this ber of decayed, missing and filled teeth (dmft) in- group was most commonin the first molars (15%), fol- creased with increasing ages of the children. At the last lowed in fairly even distribution by the second molars recall at mean age of approximately 52 weeks of age, (8%), canines (5%), and incisors (4%).

PediatricDentistry - 19:1, 1997 AmericanAcademy of Pediatric Dentistry 45 Associationof dental caries TABLE5. THEASSOCIATION DEvarious TYPesDE ENAMEL DEEEcTS TO DENTAL cArIEs with enamel defects ~n NBwAND VLBw chILDren (At exam III The number of enamel defects Teeth Affected with and without dental caries Caries Caries was analyzed to determine their Present Absent Total association. The results, as shown Enamel Defects No. (%) No. (%) No. (%) P-value" in Table 4, indicated that in the NBW case of the VLBWgroup, there None 27 (7) 352 (88) 379 (95) were strong associations between Hypoplasia 1 (0) 4 (1) 5 (1) NS enamel defects and dental caries Opacities 0 (0) 12 (3) 12 (3) NS only at exam II (P < 0.001) and Hypoplasia with opacity 0 (0) 3 (1) 3 (1) NS examIII (P < 0.001). In contrast, Total 28 (7) 371 (93) 399 (100) the case of the NBWcontrol children, there were no relationships VLBW between enamel defects and den- None 4 (1) 287 (60) 291 (61) tal caries at any examinations. Hypoplasia 0 (0) 51 (11) 51 (11) NS Opacities 4 (1) 84 (17) 88 (18) NS Type of enamel defects Hypoplasia with opacity 12 (2) 37 (8) 49 (10) P < 0.001, associated with dental caries X2=50.8, The data for this analysis were df=l taken from exam III. Table 5 Total 20 (4) 459 (96) 479(100) shows the different types of ¯ Usingchi-square tests. enamel defects associated with dental caries. In the VLBW F~°° group, only the type of defect ~ VLBW charted as "hypoplasia with opacity" was significantly associated with dental caries (P < 0.001). This type defect was most commonly found in the primary molars, and involved loss of full thickness of the enamel in the cuspal-occlusal regions. Dental caries was diag- 40~ nosed if these defects appeared soft to probing. Factors influencing dental caries Factors other than enamel hypoplasia that may in- fluence dental caries in the VLBWand NBWchildren 0 2nd molars Ist molars canines were examined also (Table 6). These include Streptococ- cus mutans scores, plaque scores, daily brushing frequency, fluoride exposure, and daily sugar intake. Re- gression tests indicated that none of the factors showed 100 significant association with dental caries (P > 0.1). In addition, the socioeconomic status of the children Control also was analyzed with respect to their dental caries status (Table 7). In the VLBWgroup, four of seven (57%) children with dental caries had high socioeconomic status (SES), compared to only one of five (20%) of the NBWgroup. However, these results did not ~ 40 reach statistical significance (P > 0.1). Discussion In this study, the prevalence of enamel defects of 0 2ad molars Ist molls c~inl~es Incisors 96% found in VLBWchildren was very high compared with our previous investigations, TM which showed ~ En. Defoot~ ~ Csrle~ prevalences of approximately 50-70%. The main rea- Fig 1. Distributionsof enamel(En) hypoplasiaand dental son for this could be that most of the subjects in this caries in pretermand control children. Thedata were study had extremely low birthweights of < 1000 g, obtainedfrom the final examinationat meanage of 51.5 whereas those of the previous studies were < 1500 g. + 5.1 monthsfor the VLBWchildren and52.5 + 4.2 The greater systemic derangement associated with the monthsfor the control children. extremely low birthweight, together with greater need

46 AmericanAcademy of Pediatric Dentistry PediatricDentistry - 19:1, 1997 TABLE6. FACTORSINFLUENCIN( DENTAL CARIES tion is that these enamel defects pre- dispose affected children to increased Numberof Children (%) caries risk, but no definitive longitu- VLBW NBW dinal data were previously available. Caries Caries Caries Caries An early report by Rosenzweig and ~ Present Free Present Free Sahar suggested that preterm children Strep. Mutans Score with enamel hypoplasia had increased 0 4 (24) 13 (76) 0 10 (100) dental caries. Also, Fadavi et al. 16, in a 1 0 (0) 3 (100) 0 1 (100) study on inner-city, black preterm 2 3 (75) 1 (25) 3 (100) 0 children reported a higher prevalence 3 0 1 (100) 1 (100) 0 of dental caries compared with full- term children. However, in that study, Plaque Score the employment of low birthweight 0-25% 5 (33) 10 (67) 0 13 (100) subjects from inner city population More than 25-50% 2 (25) 6 (27) 3 (33) 6 (67) groups with underlying high dental More than 50-75% 1 (100) 0 1 (50) 1 (50) caries rates associated with other so- More than 75% 0 0 0 l (100) cial factors may have introduced con- Brushing History founding variables not related to pre- (mean frequency~day) maturity and low birthweight. In 28 Less than i 0 2 (100) 0 0 contrast, Curzonet al., in a cross-sec- I to less than 2 1 (10) 9 (90) 4 (29) 10 (71) tional study on a small group of 2 to less than 3 6 (46) 7 (54) 0 10 (100) preterm children, reported that they 3 and more 0 0 1 (100) 0 did not have a higher rate of dental caries than those born full-term. Fluoride Exposure" We hypothesized that a case-con- Yes 5 (33) 10 (67) 1 (17) 5 (83) trolled, longitudinal study designed to No 2 (20) 8 (80) 4 (21) 15 (79) monitor the sequelae of the enamel defects would provide clearer infor- Sugar Intake mation on the role of these defects in (meandaily frequency) the development of dental caries. De- I to less than 2 0 5 (100) 0 2 (100) spite the fact that some children did 2 to less than 3 3 (50) 3 (50) 0 3 (!00) not attend all the examinations, our 3 to less than 4 3 (38) 5 (62) 1 (33) 2 (67) results showed a strong association of 4 to less than 5 0 2 (100) 0 1 (100) some enamel defects with dental car- Chi-squaretests showedno signficant differences between caries-present and caries- ies in the latter two recall examina- free children in both VLBWand NBW groups. tions in the VLBWgroup, but not in ¯ Fluorideexposure indicates history of residingin townwith fluoridatedwater or has usedfluoride supplements. the NBWcontrol children. The defects most significantly associated with caries were usually severe TABLE7. SOClOECONOMLCSTATUS (SES) ANDDENTAL CAr~ES IN VLBWAND NBW CHILDREN and involved loss of entire enamel thickness Numberof Children (%) in the cuspal-occlusal VLBW NBW regions of the first and Caries Present Caries Free Caries Present Caries Free second primary molars. n (%) N (%) N(%) ~ (%) These lesions became SES carious (soft to prob- I [high] 4 (16) 8 (32) 1 (4) 7 (28) ing) very soon after II [middle] 0 (0) 3 (12) 0 (0) 2 (8) emergence of the teeth. III [low] 1 (4) 7 (28) 3 (12) 7 (28) As the defects usually Unclassified 2 (8) 0 (0) 1 (4) 4 (16) show opacity around Chi-squaretests indicated that differencesin the percentageof caries-presentand caries-free children the areas of enamel between the VLBWand NBWgroups were nonsignificant. loss, they were desig- nated as "hypoplasia for prolonged endotracheal intubation are likely etiologi- with opacity". Our finding that this is the most com- cal factors in the high prevalence of enamel hypoplasia. mon type of enamel defect associated with decay con- The results of our longitudinal study have provided curs with previous investigations of other pediatric insight into the sequelae of the high prevalence of populations.29, 30 Other developmental enamel defects enamel hypoplasia found in VLBWchildren. Specula- such as pits, grooves and shallow areas of enamel loss

PediatricDentistry - 19:1, 1997 AmericanAcademy of Pediatric Dentistry 47 were not associated significantly with dental caries. 2. Only one type of severe enamel hypoplasia in- In this study, the overall susceptibility to dental car- volving full thickness loss of enamel, and com- ies of all the children was low. At the mean age of ap- monly found in newly erupted primary molars, proximately 4 years, the mean number of dmft in the was strongly associated with dental decay. preterm and control groups was 0.8 + 1.5 and 1.4 + 3.2, 3. Mild enamel defects did not increase caries respectively, compared with an overall mean of 1.7 for prevalence in the group of white, predomi- all 4-year-olds in the country in general. 31 Thus, the nantly, middle- and upper-class VLBWchildren VLBWchildren did not appear to be more predisposed compared to matched, full-term controls. to dental decay than the control children. At the third Dr. Lai was a postgraduatestudent in pediatric dentistry, Univer- examination, at an approximate age of 5 years, the NBW sity of Queensland Dental School at the time of study. Dr. control children, in fact, had a higher mean number of Tudehopeis director of perinatology, and Ms. Rogersis research decayed teeth per child than did the VLBWgroup. The officer, Mater Mothers’Hospital, SouthBrisbane, Australia. Dr. reason for the lack of increased risk to dental caries, in Seowis associate professor in pediatric dentistry, University of QueenslandDental School, Turbot St., Brisbane 4000, Australia. spite of a high prevalence of enamel hypoplasia in the Tel +61-7-3365-8061Fax: +61-7-3365-8199.Please direct all corre- VLBWgroup may be that most of the enamel defects were spondence to Dr. Seow. of the types that were not likely to become carious within the period of study. The only enamel defect found to be This study was funded in part by the Australian Dental Research FundInc. significantly associated with dental caries was a form of severe enamel hypoplasia that was found in only 10% of 1. Grahnen H, Larsson PG: Enameldefects in the deciduous the VLBWteeth. dentition of prematurely-born children. Odontol Revy 32-34 9:193-204,1958. Previous clinical studies have generally shownthat 2. GrahnenH, Sjolin S, StenstromA: Mineralization defects of detectable salivary levels of Steptococcus mutans in young primary teeth in children born preterm. Scand J Dent Res children are associated with dental caries, although the 8:396-400,1974. results are not always consistent 3s, probably due to rela- 3. Rosenzweig KA, Sahar M: Enamel hypoplasia and dental tively low sensitivity of the detection tests available. caries in the primary dentition of prematuri. Br Dent J 113:279-80,1962. Other risk factors associated with dental caries such as 4. FunakoshiY, KushidaY, HiedaT: Dental observation of low poor oral hygiene, and increased frequency of sugar birth-weight infants. Pediatr Dent3:21-25, 1981. exposure have also been shown to be significant risk fac- 5. Mellander M, Noren JG, Freden A, Kjellmer I: tors in caries development.32-34 In addition, low socioeco- Mineralisation defects in deciduous teeth of low birth nomic status, 36, particularly in relation to the mother’s weight infants. Acta Paed Scand 71:727-33, 1982. 32 6. Johnsen D, Krejci C, Hack M, Fanaroff A: Distribution of educational level, and characterized by lower levels of enameldefects and the association with respiratory distress oral hygiene and more cariogenic diet, is associated with in very low birthweight infants. J DentRes 3:59-64, 1984. increased caries risk. However, in our study, none of 7. Fearne JM, Bryan EM, Elliman AM, Brook AH, Williams these showed significant trends in the association with DM:Enamel defects in the primary dentition of children born weighingless than 2000g. Br Dent J 168:433-37,1990. dental caries. One reason for this may be the relatively 8. SeowWK, Brown JP, TudehopeDI, O’Callaghan M: Defects small number of subjects in the study. Another possibil- in the primary dentition of children born prematurely with ity may be "halo" as well as "hard" effects of increased very low birth weight and neonatal rickets. Pediatr Dent oral hygiene caused by enrollment in the study, result- 6:88-92, 1984. ing in reduction in plaque and oral bacterial counts. 9. Seow WK,Humphrys C, Tudehope DI: Increased prevalence of developmentaldental defects in low-birth-weight However, these effects would be observed to the same children: a controlled study. Pediatr Dent 9:221-25, 1987. extent in both the V-LBWand control groups. 10. SeowWK, Masel JP, Weir C, TudehopeDI: Mineral defi- As in other industrialized societies, differences in ciency in the pathogenesis of enamel hypoplasia in premao health36 practices among the different SES classes turely-born, very low birthweight children. Pediatr Dent would also be found in the Australian population. It 11:297-302,1989. 11. Seow WK:Enamel hypoplasia in low birthweight prema- was, therefore, not surprising, that in the control group, turely-born children. In: Recent Contributions to the Study the majority of children with dental caries was found on Enamel Developmental Defects. GoodmanAH, Capasso to have low SES. In contrast, the majority of children L, Eds. J Paleopathology MonographicPublications, 1992, with dental caries in the VLBWgroup was found to pp 321-30. have high SES, indicating that perhaps, caries risk fac- 12. Seow WK,Brown JP, TudehopeDI, O’Callaghan M: Devel- opmentaldefects in the primarydentition of very low birth tors other than the usual were operating in this group weight infants: adverse effects of laryngoscopyand pro- of children. It is likely that in the VLBWchildren, the longed endotracheal intubation. Pediatr Dent6:28-31, 1984. presence of the severe type of enamel defects predis- 13. Seow WK,Brown JP, TudehopeDI, O’Callaghan M: Effect poses even the high SES groups to increased caries risk of neonatal laryngoscopy and endotracheal intubation on palatal symmetryin two-to-five year old children. Pediatr despite their better health practices. Dent 7:30-36, 1985. 14. Seow WK,Humphrys C, MahanondaR, Tudehope Dh Den- Conclusions tal eruption in low birthweight, prematurely-bornchildren: 1. VLBWpreterm children showed a higher preva- a controlled study. Pediatr Dent10:39-42, 1988. lence of enamel defects than NBWcontrols. 15. Pimlott JFL, HowleyTP, Nikiforuk G, Fitzhardinge PM:

48 AmericanAcademy of Pediatric Dentistry PediatricDentistry - 19:1, 1997 Enamel defects in prematurely-born, low birthweight in- children and adolescents: II. Evaluation of oral hygiene; III fants. Pediatr Dent 7:218-23, 1985. Clinical applications. Pediatr Dent 4:64-72, 1982. 16. Fadavi S, Adeni S, Dziedzic K, Punwani I, Vidyasagar D: 26. Landis JR, Koch GG: The measurement of observer agree- The oral effects of orotrachael intubation in prematurely ment for categorical data. Biometrics 33:159-74, 1977. born preschoolers. ADSCJ Dent Child 59:420-24, 1992. 27. Jensen B, Bratthall D: A new method for the estimation of 17. Tudehope DI, Masel J, Mohay H, O’Callaghan M, Burns Y, mutans streptococci in human saliva. J Dent Res 68:468-71, Rogers Y, Williams G: Neonatal cranial ultrasonography as 1989. predictor of 2-year outcome of very low birthweight infants. 28. Curzon MEJ, O’Sullivan E, Ryan S, DrummondBK: Dental Aust Pediatr J 25:66-71, 1989. caries, enamel defects in primary teeth, and osteopenia of 18. O’Callaghan M, Burns Y, Gray P, Harvey JM, Mohay H, prematurity. Caries Res 25:236 (abs #84), 1991. Rogers Y, Tudehope DI: Extremely low birthweight and 29. Pascoe L, Seow WK: Dental caries and enamel hypoplasia control infants at 2 years corrected age: a comparison of in Australian aboriginal children. Pediatr Dent 16:194-99, intellectual abilities, motor performance, grow’ohand health. 1994. Early HumanDev 40:115-25, 1995. 30. Duray SM: Deciduous enamel defects and caries suscepti- 19. Harth SC, Thong YH: Sociodemographic and motivational bility in a prehistoric Ohio population. AmJ Phys Anthropol characteristics of parents who volunteer their children for 81:27-43, 1990. clinical research: a controlled study. Br MedJ 300:1372-75, 31. Australian Commonwealth Department of Health: Dental 1990. health of children in Australia 1977-1986. Canberra: Austra- 20. Seow WK, Hymphrys C, Powell RN: The use of fluoride lian government publishing service, 1987, pp 115. supplements in a non-fluoridated city in Australia in 1985. 32. Hallonsten AL, Wendt LK, Majare I, Birkhed D, Hakasson CommDent Health 4:86-94, 1987. C, Lindvall AM, Edwardsson S, Koch G: Dental caries and 21. Hallett KB, Radford DJ, Seow WK:Oral health of children prolonged breast-feeding in 18-month-old Swedish chil- with congenital cardiac disease: a controlled study. Pediatr dren. Int J Paediatr Dent 5:149-55, 1995. Dent 14:224-30, 1992. 33. Alaluusua S, Renkonen OV: Streptococcus mutans estab- 22. Federation Dentaire Internationale Commission on Oral lishment and dental caries experience in children from 2 to Health Research and Epidemiology: A review of Develop- 4 years old. Scand J Dent Res 91:453-57, 1983. mental Defects of Enamel (DDEIndex ). Int Dent J 42:411- 34. Kohler B, Andreen I, Jonsson B: The earlier the colonization 26, 1992. by mutans streptococci, the higher the caries prevalence at 23. Radike AW:Criteria for diagnosis of dental caries. In: Pro- 4 years of age. Oral Microbiol Immunol3:14-17, 1988. ceedings of Conference on the Clinical Testing of Cariostatic 35. Schroder U, WidenheimJ, Peyron M, Hagg E: Prediction of Agents. Oct 14-16, 1968. Chicago: American Dental Asso- caries in one-and-half year-old children. SwedDent J 18:95- ciation, 1972. 104, 1994. 24. L6e H, Silness P: Periodontal disease in pregnancy. Preva- 36. Crall JJ, Edelstein B, Tinanoff N: Relationship of microbio- lence and severity. Acta Odontol Scand 21:533-38, 1963. logical, social and environmental variables to caries status 25. Wei SHY, Lang KP: Periodontal epidemiological indices for in young children. Pediatr Dent 12:233-36, 1990.

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