Analysis of the vertical facial form in patients with severe hypodontia

Analysis of the Vertical Facial Form in PatientsWith Severe Hypodontia

N. BONDARETS1 AND FRASER MCDONALD2*1Department of Orthodontics, Institute for Advanced Dental Education,Ministry of Public Health, Moscow, Russia2Department of Orthodontics and Paediatric Dentistry, GKT School ofMedicine and Dentistry, Kings College, London SE1 9RT, United Kingdom

KEY WORDS hypodontia; facial growth; ectodermal dysplasia

ABSTRACT We examined the lateral cephalograms of Russian patientsin the following categories: control with acceptable occlusions (group 1);severe hypodontia with absence of six or more teeth (group 2); and severehypodontia associated with hypohidrotic ectodermal dysplasia (HED) (group3). Analysis was in a cross-sectional manner, comparing dimensions at thestart of the mixed dentition phase (age 6–10) and in the permanent dentition(age 12–18). The groups were matched for age and sex. Thirty-one hard- andsoft-tissue landmarks were traced, and 35 linear, 19 angular, and 7 ratioedmeasurements were taken and compared, using analysis of variance tocompare the means of each group.

A reduced anterior face height was found in groups 2 and 3 as a consequenceof a reduced anterior lower face height. In group 2 in the mixed dentition, theposterior face height was also reduced. The inclination of the mandible (,Se SGo Gn) was significantly reduced to 28.22° 6 0.71° in group 2 and to 24.07° 60.97° in group 3. The facial profile appeared flat or concave (,se pn pg wasincreased up to 8.42° 6 1.56° in children and 16.81° 6 2.18° in adolescents).The subnasion point was behind the aesthetic line (EL), and in group 2patients the naso-labial angle was obtuse when compared to nonaffectedpatients. In group 3 patients, the naso-labial angle became acute and lipswere protuberant and everted as a consequence of the reduced vertical height.Groups 2 and 3 have the typical facial characteristics unique to hypodontia,with reduced vertical dimensions as a consequence of limited alveolar bonegrowth. However, group 3 patients have a unique abnormal craniofacialdevelopment. Am J Phys Anthropol 111:177–184, 2000. r 2000 Wiley-Liss, Inc.

In this investigation we have defined se-vere hypodontia as the congenital absence ofsix or more permanent teeth, excluding thethird molars. The multiple absence of numer-ous teeth can occur either in isolation or inassociation with other clinical signs as asyndrome (oligodontia). The general conse-quences on long-term dental managementare often profound, requiring protracted careinvolving many dental specialties. It is recog-nized that certain patterns of hypodontiaare genetically determined, and the impor-tance of genetic specificity has been exam-

ined, with some groups identifying muta-tions in MSX1 as a cause of dental agenesis(Vastardis et al., 1996), while others havequestioned its role (Niemenen et al., 1995).Whatever the cause, it is believed that otherfeatures of dental development are affected,suggesting a more widespread effect of the

Grant sponsor: Royal Society, London.*Correspondence to: Dr. Fraser McDonald, Department of

Orthodontics, Floor 22, Guys Tower, St. Thomas St., KingsCollege, London SE1 9RT, United Kingdom. E-mail:[email protected]

Received 15 October 1998; accepted 12 September 1999.

AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 111:177–184 (2000)

r 2000 WILEY-LISS, INC.

abnormality. For example, it is known thattooth size varies in patients with oligodon-tia, with a general reduction in dental dimen-sions reflecting the generalized consequencesof this defect in development (Schalk-Vander Weide and Bosman, 1996). While theseeffects can be seen to be more widespreadthan the simple agenesis of tooth formation,it is unclear if the possible defects of thecondition can affect growth of the facialskeleton. The literature is very sparse onthis aspect of oligodontia (Bixler et al., 1988).

A significant clinical syndrome associatedwith severe hypodontia is ectodermal dyspla-sia or hypohydrotic ectodermal dysplasia(HED), where there is an abnormality of thedevelopment of ectodermal tissues. In thesecases, patients not only demonstrate a reduc-tion in the number of teeth, but also show areduction in the number of sweat glands andhave thin, sparse hair (Nakata et al., 1980).

In addition, it is well-known that thefacial skeleton varies not only between spe-cies but also between ethnic groups, and haschanged during evolution. Furthermore, thechanges of mandibular shape during evolu-tion are associated with a reduction in thenumber of teeth. While the overall reductionin facial skeletal dimensions is thought to bedue mainly to a change in the consistency ofour diet (Kaifu, 1997), the effects of geneinteractions between ethnic groups mustalso add to this evolutionary change, asdemonstrated in nonhuman primates (Ra-vosa, 1996). The general characteristics ofthe facial skeleton of extant monkeys showan increase in length of snout, an anteriorlytapering maxilla, and a large facial heightbelow the orbits (Benefit and McCrossin,1991).

Therefore, our aim was to examine thecross-sectional radiographic data of norma-tive Russian patients and to compare theseto patients with severe hypodontia in isola-tion and hypodontia in association with hy-pohidrotic ectodermal dysplasia. The spe-cific null hypothesis we wished to examinewas that there was no difference in thevertical facial skeleton in nonsyndromic andsyndromic patients when compared to unaf-fected Russian counterparts. We wished to

establish if the alveolar bone of the maxillaand mandible contributed significantly togrowth in the vertical dimension of thecraniofacial structures, and that as a conse-quence of a reduction in the number of teeth,there is also a reduction in facial height.

MATERIALS AND METHODS

Orthopantomogram radiographs of 1,516patients aged 6–18 years, presenting withmalocclusions, were used to establish theoccurrence of the condition of hypodontia.Lateral skull radiographs were taken beforeactive treatment of all patients, and theywere divided into:

Group 1. A clinically acceptable occlusion(class I) with no apparent abnor-mality of facial appearance, i.e.,class I or mild class II skeletalbase with a class I incisor relation-ship; the lips were on or close tothe E line (n 5 63; 31 in the mixeddentition, and 32 in the perma-nent dentition).

Group 2. An abnormal occlusion with six ormore congenitally absent missingteeth. The sweat gland functionwas established to be within nor-mal limits, and there appeared tobe normal hair distribution (n 585; 40 in the mixed dentition, and45 in the permanent dentition).Those patients with abnormalsweat gland function and a reduc-tion in hair were allocated to group3; they were diagnosed as havingsyndromic hypohidrotic ectoder-mal dysplasia.

Group 3. Severe hypodontia as part of hypo-hydrotic ectodermal dysplasia(n 5 34; 15 in the mixed dentition,and 19 in the permanent denti-tion).

Group 4. This group was examined to estab-lish the overall pattern of hypodon-tia in a Russian population. Inthis group, which consisted of1,516 orthopantomograms takenas a screen of patients attending aschool clinic, 256 patients (16.9%)had congenitally missing teeth.

178 N. BONDARETS AND F. MCDONALD

The patients of groups 2 and 3 werereferred to another specialist center for treat-ment.

Each group age varied in that in themixed dentition, the age spanned 6–10 years,and in the permanent dentition the age was12–18 years.

Thirty-one hard- and soft-tissue land-marks were identified and traced on eachcephalogram. This allowed analysis of 35linear, 19 angular, and 7 ratioed measure-ments (Bjork, 1947; Downs, 1948; Ricketts,1969; Biggerstaff et al., 1977). The specificanalysis is outlined in Figure 1, showing thedetailed labeling of points, while Table 1a,blists their definitions.

Analysis of variance with repeated mea-sures was used to compare the changes in across-sectional analysis between groups. Inaddition, each group was also comparedindependently, using multiple comparisons,with a Bonferroni correction for multipleStudent’s t-test (P , 0.01). This eliminatedthe findings by chance with multiple com-parisons (Bland, 1995).

RESULTS

Table 2 outlines the breakdown of teethwhich were absent, and clearly shows this tobe similar to reported Caucasian patterns ofabsence (Maklin et al., 1979). In the majorgroup of this study in which nonsyndromichypodontia patients were compared to ‘‘nor-mal’’ and ectodermal dysplasia patients, 182patients were identified who had completerecords, including lateral skull radiographs.

The typical lateral skull radiographs areshown of two patients who were clinicallydiagnosed with severe hypodontia. The first(age 21 years) has clinically diagnosed hy-podontia with the absence of 28 permanentteeth, but without any systemic defects (Fig.2a); the second case (age 23) has 29 missingteeth but has the clinical signs of syndromichypohidrotic ectodermal dysplasia (Fig. 2b).Notice in both cases the apparent lack ofalveolar bone, with a reduced lower faceheight.

One hundred and nineteen patients(7.85%) presented with severe hypodontia,with 34 (2.24%) of them diagnosed as suffer-ing from HED. Sixty-three patients were

used to compare with both groups as anonaffected group. Only the measurementswith significant differences are reportedhere; all data were compared (Tables 3–5).

The markedly decreased anterior faceheight (Se-Me) in hypodontia groups 2 and 3was mainly due to the significantly shorteranterior lower facial height (ANS-Me) (Table5). In the group 2 patients with mixed denti-tion, the posterior facial height (S-Go) alsodecreased (Table 3). The patients with HEDhad a reduced general facial divergence as aresult of the prevalent decrease of the ante-rior facial height (Se-Me) over the lack in theposterior facial height (SGo). In the period ofpermanent dentition, the posterior facialheight (S-Go) increased in the hypodontiagroups (2 and 3) and did not indicate anydeviation from normal development. Thetype of face was hypo-divergent due to aconsiderable decrease of the anterior facialheight. The inclination of the mandible (,SeS Go Gn) was significantly reduced up to28.22° 6 0.71° in hypodontia group 2 and24.07° 6 0.97° in HED group 3. The dimen-sions of the mid-face in group 2 were equalto those in the control group. While theanterior upper facial height (Se-ANS: Se-SpP) was initially reduced in the mixeddentition phase, following growth the valueapproximated that of nonaffected cases.

Craniofacial mid-face characteristics ofthe patients with hypohidrotic ectodermaldysplasia (group 3) displayed a lack of upperanterior (Se-ANS) and posterior (CRF-PSeS)facial heights (Table 4). The ratio betweentheir values (Se-ANS/CRF-PNS%) was closeto unity. There was no divergence of themiddle part of the facial skeleton; the cra-nial and spinal planes were almost parallel.The antero-posterior size of the maxilla (A’-M’, A’-PNS) was considerably smaller com-pared to the control group. The low value ofthe SSeA angle and posterior positioning ofthe maxilla were more severe cephalometriccharacteristics.

The prevalence of condylar growth andvertically insufficient height of the alveolarprocesses resulted in the anterior upwardmovement of the mandible. The ASeB anglesignificantly decreased in the period of mixeddentition, and had a negative value in the

179VERTICAL FACIAL GROWTH WITH HYPODONTIA

permanent dentition with severe hypodon-tia. These patients often demonstrated amandibular prognathism in relation to themaxillary deficit and a tendency towards aclass III malocclusion with anterior cross-bite. The values of the mandibular plane

inclination (,Se S Gn Go), Y-axis plane (,Se S Gn), lower gonial angle (,Se Go Gn),and Bjork’s sum angle (,Se S Ar 1 ,S ArGo 1 ,Ar Go Gn), ,Sp P MP, were muchsmaller compared to the control group. Thelower anterior facial height (, ANS-Xi-Pm,

Fig. 1. Diagrammatic representation of the points digitized on each lateral skull radiograph. Definedpoints are listed in Table 1.


ANS-Me) was also considerably reduced dueto deficiency in vertical dimension of thejaws. Defective alveolar bone growth wasrevealed in both jaws.

The posterior facial height (Ar-Go) wasshorter only in children with hypodontia(groups 2 and 3). In adolescents, this dimen-sion increased up to the average value. Theratio Ar-Go/ANS-Me% increased, resultingin hypo-divergence of the lower part of theface. The hard-tissue changes in facial mor-phology led to the typical ‘‘aged-face’’ appear-ance of the patients with severe hypodontia.A saddle-nose deformity with depressed rootand flat bridge is due to retroposition on thenasal bones in HED patients (group 3). Thedimension from the tip of the soft-tissuenose to the nasal plane (pn-Pn) and (Sn pn)angle were less than in the control group.

The facial profile was flat or concave (,sepn pg was increased up to 8.4 6 1.56 inchildren and 16.81 6 2.18 in adolescents).The retroposition of the upper jaw causedthe distal position of the subnasion point(Sn) in relation to EL. The naso-labial angle

TABLE 1. Names and definitions of landmarks andplanes in the maxilla and mandible

a. Pointname Definition

A Maxillary A point: the deepest part ofthe concavity of the maxillabeneath the anterior nasal spine.

A8 A point on the maxillary plane pro-jected perpendicular to the maxil-lary plane from the A point.

ANS Anterior nasal spine.Ar Articulare: a point where the poste-

rior outline of the condyle passesover the posterior and lower marginof the cranial base.

B Mandibular B point: deepest part ofthe mandibular alveolar concavity.

B8 A point of projection of a perpen-dicular from the mandibular planeof the B point.

Co Condylion: most posterior and supe-rior part of the condylar head.

CRF Cribriform: intersection of the greaterwings of the sphenoid bone and theanterior cranial base.

Go Gonion: the constructed most poste-rior and inferior point at the angleof the mandible.

Gn Gnathion: the most inferior point ofthe mandible midway between Pgand Me.

Li Most prominent point of the vermilionborder of the lower lip.

Ls Most prominent point of the vermilionborder of the upper lip.

Me Menton: the junction of the symphysiswith the mandibular border.

Or Orbitale: the most inferior anteriorpoint on the border of the orbit.

Pg Pogonion: the most anterior part ofthe bony chin.

pg Soft-tissue pogonion: the most ante-rior point on the tip of the chin.

Pm Pm point (Ricketts): anterior border ofsymphysis, halfway between B andPg.

Pn Pronasale: most prominent soft-tissuepoint on the tip of the nose.

PNS Posterior nasal spine.Po Porion: the superior border of the

bony external auditory meatus.Rhi Rhinion: tip of the nasal bone.S Sella: the central point of the sella

turcica.Se Sellion: the innermost point on the

concavity between the frontal andnasal bones. In younger patients,where the fronto-nasal suture isstill patent, it is the most anteriorpoint on the suture.

se Soft-tissue sellion, reflecting themaximum concavity of the nasalbones, representing the soft-tissueequivalent of point Se.

Sn Soft-tissue subnasale.Sto Stomion: the most anterior contact of

upper and lower lips.

TABLE 1. (continued)

b. Line andplane name Definition

EL Esthetic line joining the tip of thesoft-tissue profile of the nose to thesoft-tissue outline of the pogonion(pg).

J A line called the facial axis, joining Coto Pn.

J8 Perpendicular line reflecting midpointof J line onto mandibular plane.

M8 Posterior facial height: from PNS per-pendicular to maxillary plane toMP.

Mn Axis joining se to G.MP Mandibular plane: a line joining Go

with Me.

TABLE 2. Missing teeth

ToothPercent of

missing teeth1

Maxillary lateral incisors 13.54Mandibular second premolars 11.15Maxillary second premolars 10.64Mandibular central incisors 9.151 Of an analysis of 1,516 consecutive patients referred forassessment, 16.9% (256 patients) had at least one congenitallyabsent missing permanent tooth. Maxillary teeth accounted for51.35% of all absent teeth. There were no missing molars in thepermanent dentition in group 4.


was obtuse in group 2 patients when com-pared to nonaffected patients. In adoles-cents with HED, the naso-labial angle be-came acute, and the lips were protuberantand everted due to a markedly reducedvertical height of the lower face. The sulcussupramental was deeper than in nonaffectedpatients. The lips were behind the EL.

DISCUSSION

Although there is ample evidence that inanatomically modern humans, reduction inthe facial skeleton is thought to be a conse-

quence of changes in the consistency of thehuman diet (Kaifu, 1997), genetic phenom-ena unrelated to such an environmentalinfluence also have a role in the reduction infacial height. Our study design allows theinference that as-yet unknown geneticmechanisms may be present to bring aboutthe changes in the facial skeleton, just asknown genetic conditions also have specificimpacts on the facial skeleton.

As detailed earlier, it is now believed thatabsence of teeth can have a significant ge-netic basis. Two major types of HED arefound: the hypohidrotic and hidrotic types(Bergsma, 1973). In the former there issparseness of hair, absent or decreased sweatglands, and hypodontia; in the latter thereare abnormalities of hair and nails, butteeth and sweat glands are normal. Thesetwo types of syndrome differ in their mode ofinheritance: the hidrotic type is transmittedas an autosomal dominant trait, whereasthe HED syndrome is transmitted as anX-linked recessive trait. Carrier females ofsyndromic HED can show mild signs of thedisease such as sparse hair and patchyanhidrosis, together with an increased inci-dence of absence of teeth.

The prevalence of the absence of teeth hasbeen shown to be 5.7% in females and 3.1%in males aged between 11–14 years (Brook,1974). Further studies showed that whenhypodontia of teeth existed, 80% of affectedsubjects had one or two missing teeth, whileonly 5% had five or more missing teeth(Silverman and Ackerman, 1979). In af-fected syndromic HED patients, the averagenumber of missing teeth is reported to be23.7 (Crawford et al., 1991). The pattern ofhypodontia was similar to previous studiesin that the first molars and upper centralincisors were the teeth that were least af-fected by agenesis (Nakata et al., 1980).

In this study, we have demonstrated thatboth syndromic and nonsyndromic hypodon-tia cases are dependent on the teeth forgrowth in vertical height. Both the upperand lower facial heights were involved, andthe differences were most noticeable in themixed dentition when compared to unaffectedpatients. Here the overall facial height differedby 20.91 6 1.94 mm in the mixed dentition ofsyndromic patients. It also demonstrates that

Fig. 2. Typical radiographs of patients sufferingfrom HED. a: Clinically diagnosed hypodontia with theabsence of 28 permanent teeth (patient age, 21 years),but without any systemic defects. b: The second patient(age 23) has 29 missing teeth but has the clinical signs ofsyndromic hypohidrotic ectodermal dysplasia.


growth in craniofacial height appears to bedependent on the alveolar bone processes.

This finding is also in agreement withprevious work, which identified that facialheight and maxillary length were reduced.The patient’s profile was also found to be

flattened, with lips well behind the expectedprofile, although the E line was not used inthat study, in favor of the S-N-A point (Bix-ler et al., 1988).

However, in the case of syndromic HEDpatients, there appears to be a significant

TABLE 3. A comparison of nonsyndromic patients with control patients (group 2 and group 1)1

Cephalometric values

Mixed dentition Permanent dentition

D 6 SD P D 6 SD P

Se-Me 28.97 6 1.58 ,0.001S-Go 24.42 6 1.06 ,0.001S-Go/Se-Me% ratio 4.61 6 0.81 ,0.01ANS-Me 5.10 6 1.23 ,0.001 3.44 6 1.01 ,0.01Ar-Go 23.23 6 0.87 ,0.001Ar-Go/ANS-Me% ratio 5.13 6 2.04 ,0.05 9.53 6 1.68 ,0.001,ANS Xi Pm 24.13 6 0.77 ,0.001 26.60 6 0.77 ,0.001,SeS GoGn 25.96 6 1.16 ,0.001,Y-axis/,SeSGn/ 24.65 6 0.99 ,0.0011 D 6 SD, mean difference 6 standard deviation of the differences. P, probability. 2, a reduction in the dimension/angle; lack of minussign indicates an increase. For definitions of acronyms, see Table 1.

TABLE 4. A comparison of syndromic patients with control patients (group 3 and group 1)1



D 6 SD P D 6 SD P

Se-Me 220.91 6 1.94 ,0.001 27.94 6 1.41 ,0.001S-Go 29.28 6 1.40 ,0.001S-Go/Se-Me% ratio 5.61 6 1.25 ,0.001 6.82 6 1.14 ,0.001Se-ANS 28.53 6 0.92 ,0.001CRF-PNS 24.51 6 0.92 ,0.001CRF-PNS/Se-ANS% ratio 8.23 6 1.67 ,0.001 7.08 6 1.61 ,0.001ANS-Me 12.89 6 1.44 ,0.001 25.91 6 1.32 ,0.001Ar-Go 25.25 6 1.11 ,0.001Ar-Go/ANS-Me% ratio 11.62 6 2.28 ,0.001 11.40 6 2.43 ,0.001,ANS Xi Pm 28.66 6 1.15 ,0.001 26.81 6 1.10 ,0.001,SeS GnGo 27.86 6 1.48 ,0.001 210.10 6 1.34 ,0.001,Y-axis/SeSGn/ 27.75 6 1.04 ,0.001 28.42 6 1.11 ,0.001,SseA 27.47 6 1.09 ,0.001 27.37 6 1.17 ,0.001,SSeRhi 24.97 6 2.01 ,0.05 210.42 6 1.75 ,0.0011 D 6 SD, mean difference 6 standard deviation of the differences. P, probability. 2, a reduction in the dimension/angle; lack of minussign indicates an increase. For definitions of acronyms, see Table 1.

TABLE 5. A comparison of nonsyndromic patients with syndromic patients (group 2 and group 3)1



D 6 SD P D 6 SD P

Se-Me 211.94 6 1.84 ,0.001 24.74 6 1.41 ,0.01,SeS GoGn 25.41 6 1.15 ,0.01 24.15 6 1.20 ,0.01Se-ANS 25.69 6 0.88 ,0.001 23.01 6 0.94 ,0.01CRF.PMS/Se-ANS% ratio 5.99 6 1.72 ,0.01 5.80 6 1.60 ,0.01,SeSSpP 24.41 6 0.82 ,0.001 26.41 6 0.85 ,0.001,SseA 23.38 6 1.17 ,0.01Co-A 24.46 6 1.18 ,0.01A-PNS 22.84 6 0.75 ,0.01 23.29 6 0.82 ,0.01,Y-axis/SeSGn/ 26.58 6 0.87 ,0.001 23.77 6 1.02 ,0.01,Summ 26.02 6 1.34 ,0.001 24.37 6 1.43 ,0.01,se pn pg 26.20 6 1.57 ,0.01 216.75 6 4.85 ,0.01,SseRh 25.43 6 1.96 ,0.011 D 6 SD, mean difference 6 standard deviation of the differences. P, probability. 2, indicates a reduction in the dimension/angle; lackof minus sign indicates an increase. For definitions of acronyms, see Table 1.


reduction in forward growth of the nasalbones, with a typical ‘‘saddle-nosed defor-mity’’ and posterior positioning of the nasalbones. This seems to imply that some aspectof normal nasal growth and developmentappears deficient and that the control mecha-nisms of growth may be affected as a conse-quence of the underlying genetic basis ofthis disease. A candidate for causing thisdefect is the forward growth of the nose as aconsequence of deficient cartilaginous growthof the nasal septum (Wexler and Sarnat,1965). Furthermore, a possible hypothesis ofpartial penetration of the genetic disordercould be considered for the nonsyndromicHED patients. Analysis of this problem re-quires detailed pedigree analysis and exami-nation of the nuclear material of affectedindividuals.

CONCLUSIONS

Patients with severe hypodontia presentmany oral problems. Specific aspects arecommon to non-HED edentulous patients,and some are unique to the HED condition.The two groups often have typical craniofa-cial characteristics and decreased occlusalvertical dimension as a consequence of lim-ited alveolar bone. HED patients have aunique clinical problem expressed as abnor-mal craniofacial development and reducedmid-facial growth. This study presents thebaseline data for the treatment of childrenwith HED, showing their variations ingrowth and development. In addition, theevolutionary trend to decrease the size of thefacial skeleton is seen to be further ampli-fied by the absence of teeth.

ACKNOWLEDGMENT

N.B. was supported by the Royal Society,London.

LITERATURE CITED

Benefit BR, McCrossin ML. 1991. Ancestral facial mor-phology of Old World higher primates. Proc Natl AcadSci USA 88:5267–5271.

Bergsma D, editor. 1973. Birth defects: atlas and compen-dium. Baltimore: Williams and Wilkins.

Biggerstaff RH, Allen RC, Tuncay OC, Berkowitz J.1977. A vertical cephalometric analysis of the humancraniofacial complex. Am J Orthod 72:397–405.

Bixler D, Saksena SS, Ward RE. 1988. Characterizationof the face in hypohidrotic ectodermal dysplasia bycephalometric anthropometric analysis. Birth Defects24:197–203.

Bjork A. 1947. The face in profile. Svensk TandlakTidskr 40:55–66.

Bland M. 1995. An introduction to medical statistics,2nd ed. Oxford University Press.

Brook AH. 1974. Dental anomalies of number, form andsize: their prevalence in British schoolchildren. J IntAssoc Dent Child 5:37–53.

Burzynski NJ, Escobar VH. 1983. Classification andgenetics of numeric anomalies of dentition. BirthDefects 19:95–106.

Crawford PJM, Aldred MJ, Clarke A. 1991. Clinical andradiographic findings in X linked hypohidrotic ectoder-mal dysplasia. J Med Genet 28:181–185.

Downs WB. 1948. Variations of facial relationships;their significance in treatment and prognosis. Am JOrthod 34:812–840.

Kaifu Y. 1997. Changes in mandibular morphology fromthe Jomon to modern periods in eastern Japan. Am JPhys Anthropol 104:227–243.

Maklin M, Dummett CO, Weinberg R. 1979. A study ofoligodontia in a sample of New Orleans children. JDent Child 46:478–482.

Nakata M, Koshiba H, Eto K, Nance W. 1980. A geneticstudy of anodontia in X-linked hypohidrotic ectoder-mal dysplasia. Am J Hum Genet 32:908–919.

Niemenen P, Arte S, Pirinen S, Leltonen L, Thesleff I.1995. Gene defect in hypodontia: exclusion of MSX1and MSX2 as candidate genes. Hum Genet 96:305–308.

Ravosa MJ. 1996. Mandibular form and function inNorth American and European Adapidae and Omomy-idae. J Morphol 229:171–190.

Ricketts RM. 1969. The evolution of diagnosis to comput-erized cephalometrics. Am J Orthod 55:795–806.

Shapiro SD, Farrington FH. 1983. A potpourri of syn-dromes with anomalies of the dentition. Birth Defects19:129–140.

Schalk-Van der Weide Y, Bosman F. 1996. Tooth size inrelatives of individuals with ologodontia. Arch OralBiol 41:469–472.

Silverman NE, Ackerman JL. 1979. Oligodontia: a studyof its prevalence and variation in 4032 children. JDent Child 46:470–477.

Vastardis H, Karimbux N, Guthua SW, Seidman CE.1996. A human MSX1 homeodomain missense muta-tion causes selective tooth agenesis. Nat Genet 13:417–421.

Ward R, Bixler D. 1986. The distinctive facial features inhypohydrotic ectodermal dysplasia. Am J Hum Genet39:86 [abstract].

Wexler MR, Sarnat BG. 1965. Rabbit snout growth afterdislocation of nasal septum. Acta Otolaryngol (Stockh)81:305–313.


Analysis of the vertical facial form in patients with severe hypodontia

Documents

Transcript of Analysis of the vertical facial form in patients with severe hypodontia