A new descriptive index, the HHI (hypocalcification-hypoplasia index), is described for comparing enamel defects in groups of people. The index was used in a study completed in 1986, in which 1251 11-year-old children from different ethnic groups resident in South Africa were examined: 210 rural black, 203 urban black, 206 urban colored, 426 urban Indian, and 206 urban white. The index can be used as a screening examination, and the results from these different ethnic groups are presented.TS2016.http://journals.sagepub.com/doi/abs/10.1177/08959374890030021001?journalCode=adr

Cleaton-Jones, P. E.

Hargreaves, J. A.

Williams, S. D. L.

English

Wits Institutional Repository on DSPACE

HYPOCALCIFICATION ANDHYPOPLASIA IN PERMANENT TEETH OFCHILDREN FROM DIFFERENT ETHNICGROUPS IN SOUTH AFRICA ASSESSEDWITH A NEW INDEXJ.A. HARGREAVES1, P.E. CLEATON-JONES2, AND S.D.L. WILLIAMS2faculty of Dentistry, The University of Alberta, Edmonton, AB, Canada; and 2MRC/University of theWitwatersrand, Dental Research Institute, Johannesburg, South AfricaAdv Dent Res 3(2):126-131, September, 1989ABSTRACTAnew descriptive index, the HHI (hypocalrification-hypoplasia index), is described for comparing enameldefects in groups of people. The index was used in a study completed in 1986, in which 1251 11-year-old children from different ethnic groups resident in South Africa were examined: 210 rural black, 203 urbanblack, 206 urban colored, 426 urban Indian, and 206 urban white. The index can be used as a screeningexamination, and the results from these different ethnic groups are presented.INTRODUCTIONIn assessments of dental diseases or conditions inchildren, the development of the teeth with defectscaused by illness or trauma, or from general meta-bolic conditions, including nutrition, is of impor-tance. Mellanby (1934), in defining her index ofhypoplasia, related her findings to vitamin D and nu-tritional deficiencies. These studies have been takenfurther in recent years with the work of Nikiforukand Fraser (1979) and Pimlott et al. (1985), who ex-amined enamel defects in primary and permanentteeth of premature and low-birth-weight children.Enamel opacities and hypoplasia have been shownto occur with excessive fluoride ingestion (enamelfluorosis) [Dean (1934, 1942); Thylstrup and Fejer-skov (1978); and Horowitz et al (1984)]. Russell (1961),Iizuka and Yasaki (1976), and Murray and Shaw (1979),among others, have examined the differential diag-nosis of fluoride and non-fluoride enamel defects.Trauma to the primary teeth has been documentedPresented at the Symposium and Workshop on DevelopmentalDefects of Enamel, February 23-25, 1988, Rotorua, New Zealand,sponsored by Colgate-Palmolive (NZ) Ltd., the New Zealand Den-tal Research Foundation, and the Medical Research Council of NewZealand126in the possible disturbance of the developing per-manent teeth, resulting in localized hypoplasia or hy-pocalcification (Andreasen and Ravn, 1973; Hargreaveset al, 1981).Cutress and Suckling (1982) gave an overview ofindices that had been developed for the assessmentof non-carious defects of enamel, and the Commis-sion on Oral Health, Research and Epidemiology ofthe FDI suggested an index of enamel defects, theDDE index (1982). Results from studies which usedthis index have been given recently (Dummer et al,1986; Suckling and Thurley, 1984; Suckling et al, 1985,1987). Based on these studies, and on concerns raisedfor examination of enamel defects, a new descriptiveindex was developed and used in a study of differentethnic groups in South Africa.MATERIALS AND METHODSIn 1986, 1251 11-year-old children from differentethnic groups resident in South Africa were exam-ined — 210 rural black, 203 urban black, 206 urbancolored, 426 urban Indian, and 206 urban white. Theurban children all lived within the Greater Johannes***burg metropolitan area, and all communities sharedthe same piped water supply (0.3 ppm fluoride), whilerural black children were in five villages in the Ge-Vol. 3 No. 2 HYPOCALCIF1CATION-HYPOPLAS1A INDEXHypocalcification/Hypoplasia Index127Classification03C0(/)Db75c3c0)08DescriptionNo Hypoplasia or HypocalcificationHypocalcification in incisa! or occlusal half oftooth crownHypocalcification in cervical half of tooth crownHypoplasia in incisal or occlusal half oftooth crownHypoplasia in cervical half of tooth crownHypocalcification < V2 facial surface of atooth crownHypocalcification > Vfe facial surface of a toothcrown or involving more than one surface ofa toothHypoplasia < V4 facial surface of a tooth crownHypoplasia > V2 facial surface of a tooth crownor involving more than one surface of a toothHypocalcification/Hypoplasia not included in theabove, e.g. diffuse hypoplasia restricted to asingle surface other than facialAnteriorTeethPosteriorTeethlukspan district of Bophuthatswana some 350 km westof Johannesburg. Here, all the borehole water wassampled, and fluoride levels ranged from 0.18 to 0.35ppm, which were within the same range when com-pared with findings obtained in another survey somesix years earlier. Dental caries, enamel defects, heightand weight, and details of each child's diet were re-corded. The nutritional and caries data will be re-ported elsewhere. The reason 11-year-olds wereselected is that this was a base-line age group being128 HARGREAVES et al. Adv Dent Res SeptemberTABLE 1HHI: CHILDREN 11 YEARS OF AGEnChildren Showing any Sign of Hypocalcificationor Hypoplasia of Enamel% of childrenwith hypocalcification/hypoplasia% of childrenwith >4 teeth involvedRural blackUrban blackUrban coloredUrban IndianUrban white21020320642620612519.519.716.08.28.74.57.06.31.93.0used in a series of longitudinal assessments by theauthors (Cleaton-Jones and Hargreaves, 1988).Enamel defects were assessed by use of the newindex, the HHI (hypocalcification-hypoplasia index),which is described in the Fig. The index was appliedto each erupted permanent tooth and recorded enameldefects as either linear or as general (diffuse). In theformat described, the recorders found no difficulty ininterpreting or applying the criteria.The teeth were examined under either natural lightor with anglepoise lamps with 60-watt bulbs, de-pending on field conditions, and after the teeth wereair-dried but not cleaned. Replaceable sickle probeswere used, as previously described by Cleaton-Joneset al. (1989), to facilitate tactile detection of surfacedefects of the enamel.When any doubt occurred about the presence orabsence of a defect, the tooth surface was recordedas normal.RESULTSOf the children seen, the urban black and the urbancolored children were most commonly affected byenamel defects and had prevalence levels approxi-mately twice those in the other groups. In the differ-ent racial/ethnic groups, from 1.9 to 7.0% of childrenhad more than four teeth with defects (Table 1). Thepercentages of teeth affected by each of the nine cat-egories of HHI by ethnic group are shown in Table2; since little variation was seen in homologous teeth,the data for the homologies have been combined. Themost common lesions found were linear hypocalci-fications or hypoplasias of the incisal or occlusal halfof the tooth crowns (categories 1 and 3).The percentage of total teeth involved in any of theethnic groups was less than 5%, but up to 13.4% ofspecific teeth were affected. For example, maxillarycentral incisors showed the most enamel defects (Ta-ble 3).DISCUSSIONThe index was found to be easy to use and allowedfor a rapid assessment of the children. As a screeningtool, it can give an assessment of the number of chil-dren who have hypocalcified or hypoplastic teeth. Inthis study with the five different ethnic groups, theurban black and urban colored children had the mostdefects compared with the number of children af-fected; both of these groups had approximately twiceas many children with defects compared with the otherthree groups. When the index was used to examinethe teeth involved by category, the rural black, urbanblack, and urban colored had the highest percentageof teeth with hypocalcification or hypoplasia; thefindings are based only on the teeth erupted. A fur-ther evaluation, examining the specific teeth groupedin homologous pairs, showed the urban black andurban colored to have the highest percentage of teethaffected in the maxilla, with over 13% of the centralincisor teeth involved, and in the mandible the ruralblack and urban black had the most teeth involved.No consistency of defects in the maxilla and the man-dible is shown, particularly the findings in the groupof colored children.The 11-year-old children examined in this study area key group in current longitudinal assessments bythe authors, but because not all permanent teeth areerupted in all children, a slight increase in teeth af-fected may be shown during future longitudinalstudies with these same children. If only the anteriorteeth and the first molars are assessed, all of theseteeth being erupted in all children, again no obviouspattern is shown. For example, in the urban coloredgroup, a higher involvement of maxillary anterior andfirst molar teeth is shown when compared with themandibular teeth, although in all racial groups themaxillary teeth are more commonly involved than themandibular teeth. An examination of the categoriesof the HHI for the urban black and urban coloredchildren shows that enamel hypocalcification or hy-poplasia of the incisal or occlusal third of a tooth wasVol. 3 No. 2 HYPOCALCIF1CATION-HYPOPLASIA INDEX 129TABLE 2HHI CATEGORIES FOR 1251 CHILDREN AGED 11 YEARSCategories of HHI123456789All categoriesRural blackn = 2100.610.651.050.070.020.020.000.390.002.81PercentageUrban blackn = 2031.570.040.560.270.480.120.000.320.003.36of Teeth InvolvedUrban coloredn = 2061.270.030.260.000.690.240.000.030.032.55by Category andUban Indiann = 4260.460.060.070.080.580.010.030.050.001.34Ethnic GroupUrban whiten = 2060.520.030.070.000.310.120.030.420.001.50All childrenn = 12510.890.160.400.080.420.100.010.240.012.31the most dominant condition found with the maxil-lary incisors, the most common teeth involved. Theseteeth commenced development during the first yearof life, and the position of enamel defects on the in-cisal portions involved the first areas of enamel to beformed.These findings suggest, specifically if hypoplasiawas present, that the most vulnerable time for thedevelopment of enamel defects in these communitiesis during the first year of life.None of the children resided in an optimum fluo-ride region (all had water supplies of less than 0.35ppm F), and fluorosis was not considered to be oneof the contributing factors.The children in the white and Indian communitiesresided in areas with good food availability and hous-ing — conditions typical of European and NorthAmerican residential areas. The rural black childrenlived in the homeland region of Bophuthatswana andmaintained many of their traditional customs, inclu-ding housing and diet. Many of these children werebreast-fed for at least one year (Richardson et al., 1981).The colored and black urban dwellers were essen-tially those with standardized sub-economic housingwith some overcrowding. Food conditions, with manyof their cultural traditions abandoned as they settledin urban regions close to the cities, had deteriorated.It is these two groups that showed the greatest num-ber of enamel defects in their permanent dentition.The index used, the HHI, was developed to makecomparisons among children of different ethnic groupsin South Africa, and direct comparison with otherindices is not possible.Many other results in the literature include the pos-sibility of fluoride involvement (fluorosis), which isnot a factor with this group of children. Wilson andCleaton-Jones (1978), in examining enamel defects andinfectious exanthemata, found no correlation be-tween defects and the onset time of the illness. Suck-ling et al. (1987), in a study of more than 1000 NewZealand children, reviewed the literature of etiolog-ical factors that could influence the prevalence of de-velopmental defects of enamel. They highlighted theinfluence of fluoride. Despite extensive statisticaltesting, positive and strong associations were few.Their study illustrated the difficulty of establishingan etiology of enamel defects, even when medicaland dental histories were available. Pimlott et al. (1985)speculated that the high prevalence of enamel hy-pocalcification in permanent teeth of premature andlow-birth-weight infants is the result of metabolicstresses during the first few months post-term.In the present study, the position of enamel defectsupports an early onset age for the majority of defectsfound. Pimlott et al. (1985) described a much higherinvolvement of maxillary than of mandibular teeth;this relationship was also observed in the present in-vestigation and has been reported by other workers(Grahnen et al., 1969, 1974; Funakoshi et al., 1981;Johnsen et al., 1984; Dummer et al., 1986). No satis-factory explanation for the greater involvement ofmaxillary teeth than of mandibular teeth has beenreported. Thylstrup and Fejerskov (1978) have relatedfluoride defects to the thickness of enamel in differenttooth types, and this may be a possible reason formaxillary incisors having more defects than mandib-ular incisors. Localized enamel and dentin defects inparticular permanent teeth, following trauma or peri-apical infection in the primary tooth predecessor, are,however, well-documented (Hargreaves et al., 1981).Defects in enamel from areas with high fluoride levelsin the drinking water are also well-documented andhave recently been reported by Horowitz et al. (1984)in their assessments of dental fluorosis using a newfluorosis index. The mechanisms of fluoride in pro-ducing all types of enamel defects are not completelyunderstood, nor are studies available that fully ad-dress them.230 HARGREAVES et al. Adv Dent Res September 1989TABLE 3HHI: CHILDREN AGED 11 YEARSMaxillary Teeth1234567TotalMandibular Teeth1234567TotalRural blackn = 2106.24.82.22.21.93.11.23.13.63.32.42.72.72.90.52.6Percentage ofUrban blackn = 20313.17.73.03.00.52.80.34.34.63.43.02.71.11.90.02.4Homologous ToothUrban coloredn = 20613.08.50.50.50.35.80.04.11.40.90.70.00.33.60.31.0Types InvolvedUrban Indiann = 4264.11.61.01.30.61.60.41.51.61.81.40.90.81.20.51.2by Ethnic GroupUrban whiten = 2065.11.91.41.40.71.40.01.71.20.70.51.91.42.70.01.2All childrenn = 12518.34.91.61.70.82.90.42.92.52.01.61.61.42.50.21.7It was not the purpose of this study to examinemedical records of the children or to relate defects tospecific early nutritional deficiencies. It is clear thatdifferent patterns of dental defects of enamel are beingfound from these investigations, but firm etiologicalfactors have not been detailed nor discrepancies re-solved.The need for further study in different communi-ties to record numbers of people and individual teethaffected by enamel defects is apparent. Additionalstudies could give indications for further research toimprove our understanding of the cause and possibleprevention of enamel defects in developing and de-veloped communities.The results presented in this paper add to this bodyof information, and the HHI could be useful in allow-ing comparisons to be made within and among pop-ulation groups.REFERENCESANDREASEN, J.O. and RAVN, JJ. (1973): Enamel Changes inPermanent Teeth After Trauma to Their Primary Predecessors,Scand J Dent Res 81:203-209.CLEATON-JONES, P. and HARGREAVES, J.A. 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Hypocalcification and hypoplasia in permanent teeth of children from different ethnic groups in South Africa assessed with a new index

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Hypocalcification and hypoplasia in permanent teeth of children from different ethnic groups in South Africa assessed with a new index

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