Download - Heritability of cephalometric and occlusal variables as assessed from siblings with overt malocclusions

Heritability of cephalometric and occlusal variables as assessed from siblings with overt malocclusions

Lisa King, DDS, MS," Edward F. Harris, PhD, b and Elizabeth A. Tolley, PhD ~ Memphis, Temz.

It has been thoroughly documented that measurements of the craniofacial complexes have moderate to high heritabilities--that they are primarily a consequence of "nature" rather than "nurture." In contrast, recent studies, which used twin and sibship analyses, have shown that malocclusions per se (i.e, measures of tooth position and dental interrelationships) have low heritabilities; malocclusions sensu stricto are primarily acquired (environmentally induced), not inherited. All such studies have, however, focused on persons not treated orthodontically. This can introduce selection bias since cases with moderate to severe malocclusions would have received treatment and, thus, be excluded from study. The present analysis addresses this issue of ascertainment bias by examining just that portion of the adolescent population receiving comprehensive orthodontics, initial treatment records of 104 pairs of siblings were studied, all of whom subsequently received full-banded treatment. In this selected series of overt malocclusions, heritability estimates for craniometric variables were significantly lower than in a comparable series o! adolescents with naturally occurring good occlusions, whereas heritability estimates for occlusal variations (e.g., rotations, crossbites, displacements) were significantly higher. This vindicates the clinical perception that siblings often present withsimilar malocclusions. We propose that the substantive measures of intersib similarity for occlusal traits reflect similar responses to environmental factors common to both siblings. That is, given genetically influenced facial types and growth patterns, siblings are likely to respond to environmental factors (e.g., reduced masticatory stress, chronic mouthbreathing) in similar fashions. Malocclusions appear to be acquired, but the fundamental genetic control of craniofacial form often diverts siblings into comparable physiologic responses leading to development of similar malocclusions. (AM J ORTHOD DENTOFAC ORTHOP 1993;104:121-31 .)

I t is a common perception among orthodontists that siblings often exhibit similar malocclusions. This clinical experience often leads to the inference that malocclusions are genetic in origin, that they are due primarily to "nature" rather than "nurture." Lund- strSm's celebrated study of malocclusion in twins' is often cited as confirmatory support of this viewpoint. Moreover, authors of most orthodontic textbooks state, generally unequivocally (albeit in the absence of much evidence), that most patients have malocclusions by virtue of their genetic predispositions.

On the other hand, several recent quantitative studies effectively reject the importance of genetics in the development of malocclusions. These studies, notably those by Corruccini and coworkers 2-s have used the contemporary analytic protocols for twin analysis of

"Kang 6'7 and ChristianY ~ Others provide complemen-

*Southwestern Medical Center, Dallas, Texas. t'Department of Orthodontics and Department of Pediatric Dentistry, College of Dentistry, University of Tennessee, Memphis. Tenn. 'Department of Biostatistics and Epidemiology, College of Graduate Itealth Sciences. University of Tennessee, Memphis, Tenn. Copyright �9 1993 by the American Association of Orthodontists. 0889-5406193/$1.00 + 0.10 8/1/35"013

tary evidence on the basis of sib analyses, x~-'~ A limi- tation of many of these studies is that they were nec- essarily based just on twins or siblings who did not

receive orthodontic treatment. Often, twins or siblings with extreme malocclusions were excluded because, at the time of the study, they had been treated and their pretreatment status was unknown to the investigator. Because treated cases and, thereby, twin pairs and sibships containing one or more treated patients were excluded from most studies, estimates of genetic and environmental contributions may have been affected by ascertainment bias.

We have been interested in assuaging these two observations: (1) the alleged phenotypic similarities of siblings presenting for comprehensive orthodontic treatment and (2) the potential biases imposed by deleting overt malocclusions from genetic analyses. In other words, whether the inferences based on clinical experience can be validated empirically. We report here on an assessment of skeletodental relationships in sibships, all of whom exhibited moderate to severe malocclusions that warranted comprehensive orthodontic treatment. The purposes of this study were (1) to estimate the

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122 King, Harris, and Tolley American Journal of Orthodontics and Dentofacial Orthopedics A!tgust. 1 9 9 3

'Normal'

Minor

Definite

Severe

Very Severe

�9 Treated Cases [ ] Population Distribution

Handicapping i |

0 10 20 30 40 P e r c e n t a g e

Fig. 1. Frequency distributions of severity of malocclusion as judged from treatment priority index in United States population of 12 to 17 year olds 2~ (t~) and this series of cases subsequently receiving comprehensive orthodontic treatment ('=). The labels used here (norma/through handicapping) are those applied by the epidemiologists.

Table I. Sample sizes by sex and Angle 's sagittal molar relationship

Sex 1 I II II1 Total

Male 28 46 7 81 Female 44 73 10 127

Total 72 119 17 208

genetic contribution to phenotypic similarities for skeletodental variables of siblings presenting for comprehensive orthodontic treatment (i.e., estimate heritabilities of skeletodental variables) and (2) to compare our estimates of heritability with those of a previous study of siblings not needing comprehensive orthodontic treatment, thereby assessing potential bias imposed by excluding overt malocclusions from genetic studies.

METHODS AND MATERIALS Sample selection

This was a cross-sectional study in which v,'e assessed the prctreatment records of 104 white sibling pairs. Subjects were selected by using three criteria: (I) both siblings rcquired comprehensive, full-banded orthodontic therapy, (2) both siblings had all four permanent canines at least partially erupted through the mucosa at examination, and (3) neither sibling had had prior treatment, such as serial extraction or functional appliances. All.subjects ',`.'ere adolescents at treatment, with a mean starting age of 13.5 years (SE = 2.21; range: 9 to 22 years). There were 15 male-male sibships, 51 male-female sibships, and 38 female-female sibships (Table 1). The sample

contained 72 Class 1, 119 Class II, and 17 Class III subjects. (In practice, sagittal molar relationships were measured on a continuous, millimetric scale-" rather than grouping by An- gle's classification.) Even though not every case in this series had extreme malocclusion, the modal condition was far more severe than in the population at large (Fig. !).

Cephalometric analysis

Each initial lateral cephalometric rocntgenogram was traced, and the landmarks were digitized (Fig. 2). Data files of the landmarks, stored as Cartesian coordinatesl were used to compute the cephalometric variables listed in Table II.

Cast analysis

Variables measured on the pretreatment dental study models are broadly divisible into t,,vo categories, (1) those that quantify arch size and shape and (2) those that assess tooth and intertooth relationships (Table II). The measurement tech- niques employed here have been published by Smith and Bailit'--" and Harris and Johnson. 2~

For ~ach person, the treatment priority index (TPI) was computed following the protocol of Kelly and Harvey.-" The TPI uses various occlusal components to evaluate the severity of the malocclusion. Although not comprehensive, it does provide one method of reducing a complex set of graded ocelusal relationships to a summary value.

Statistical analysis

Data `.vcre transferred to the mainframe computer (a VAX cluster) at the University of Tennessee `.,,'here analyses ',,,'ere performed with the Statistical Analysis System software.-" After exploratory data analysis, the generalized linear model

American Journal of Orthodontics and Dentofacial Orthopedics King, Harris, and Tolley 123 Volume 104, No. 2

T a b l e II. L i s t i n g o f h e r i t a b i l i t y e s t i m a t e s f o r the

c r a n i o f a c i a l , a r c h , a n d o c c l u s a l p a r a m e t e r s

]Standard j Heritability I error I

Craniofacial variable estimate of h" Model~

Craniofacial parameters Sella-gnathion distance 0.66* 0.17 3 Nasion-menton distance 0.79* 0.16 3 Sella-nasion distance 0.65* 0.18 2 Sella-A point distance 0.74* 0.17 2 Sella-B point distance 0.68* 0.17 3 SelIa-PNS distance 0.77* 0.17 4 Sella-gonion distance 0.47* 0.18 4 Nasion-ANS distance 0.5 i * 0.18 3 SNA angle 0.58* 0. ! 8 I SNB angle 0.55* 0.18 ! ANB angle 0.61" 0.18 3 SN-palatal plane angle 0.49* 0.18 1 Gonion-PNS distance 0.53* 0.18 4 Articlare-B point dis- 0.48* 0.18 3

lance Articulare-pogonion 0.39* 0.19 3

distance Gonion-pogonion dis- 0.50* 0 .18 3

tance SN-mandibular plane 0.53* 0.18 4

angle I It-mandibular plane 0.67* 0.17 4

angle AO-BO discrepancy 0.59* 0.18 4 Total height index 0.41' 0.19 4 Anterior height index 0.80* 0.16 I

Arch parameters MX 3-3 width 0.53* 0.18 2 MD 3-3 width 0.79* 0.16 I NIX 6-6 width 0.32 0.19 4 MD 6-6 width 0.77* 0.17 3 NIX arch length 0.73* 0.17 3

�9 MD arch length 0.60* 0.18 2 NIX arch shape 0.24 0.19 3 MD arch shape 0.27 O. 19 3 NIX arch ratio 0.33 0.19 I MD arch ratio 0.53* O. 18 3

Occlusal parameters Incisor overjet 0.58* 0.18 3 Incisor overbite 0.62* 0.18 1 IMPA 0.91" 0.16 1 lnterincisal angle 0.77* 0.17 3 Buccal segment relation- 0.46* 0.19 i

shi p (right side) Buccal segment relation- ,,0.50* 0.18 1

ship (left side) NIX incisor irregularity 0.37* O. 19 4 MD incisor irregularity 0.54* 0.18 l NIX crowding-spacing 0.35* 0.19 1 MD crowding-spacing 0.68* 0.17 1 Posterior crossbites 0.45* 0.19 4 NIX rotations 0.84* O. 16 I MD rotations 0.49* 0.18 1 NtX displacements 0.12 0.19 I MD displacements 0.52* 0.18 1 Treatment priority index 0.15 0.19 i

Fig. 2. Schematic of cephalogram identifying landmarks located on each tracing.

(GLM) procedure was used to assess each variable (k = 47) for age and sex effects and age-with-sex interaction. On the basis o f these results, response variables were analyzed with one of four GLM models: (I) no significant sex or age effect; (2) significant sex difference without an age effect; (3) significant age difference without a sex effect; or (4) significant age-with-sex interaction with or without significant main effects. These models permit the calculation o f intraclass correlation across the whole sample while controll ing for potential age and sex differences. Least square means (from type III or "partial sums o f squares ~') were obtained since they provide the most accurate est imates o f the class marginal means expected for a balanced design involving the class variable (sex) witti all covariates at their mean value.

Results o f these analyses were used to est imate between �9 sibship variance, the residual or within sibship variance, and

the in t r ac la s s correlation coefficient, r~. The statistical gcn-

*P < 0.05. "tOperational definitions have been published in Kelly and Harvey,"' Smith and Bailit,-" and Harris and Johnson. 2~ The four generalized linear models permit simultaneous analysis of the entire sample: (I .) no age or sex effect and no age-sex interaction, (2.) significant sex effect. (3.) significant age effect, and (4.) significant age and sex effect and significant interaction.

124 King, Harris, and Tolley American Journal of Orthodontics and Dentofacial Orthopedics August 1 9 9 3

Sella-Gnathion . . . . . .

Nasion-Menton

Sella-Nasion

Sella-A Point

Sella-B Point

Sella-PNS

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H e r i t a b i l i t y E s t i m a t e s

Fig. 3. Histogram of heritabilities (• for 21 of the facial size and form measurements in this series, and those reported by Harris and Johnson "~ derived from a series with generally good occlusions.

eralized linear models used here controlled for the fixed effects of age and sex and age-x-sex interaction where these effects had significant influences on a given variable. To estimate the variance components and intraclass correlation coefficient, we used Henderson's method 3, which uses the reduction sums of squares and estimates variance components by equat- ing each computed reduction to its expectation under the full model, z6'27 By using this method, we avoided bias ofestimates that can occur when data are unbalanced.

The heritability estinaate for each skeletodental variable was calculated from the intraclass correlation as h, 2 ~ 2r,. Theoretically, the genetic contribution to phenotypic similarities between first degree relatives (siblings) is limited by the intraclass correlation of 0.5, which indicates that siblings share half of their genes in common by descent3 s Therefore heritability estimates should fall within the range of 0 (no heritability) to I (complete genetic determination). However, estimates may exceed this range because of sampling fluc- tuation and/or environmental covariation (e.g., enhanced acquired similarity). Bias of heritability estimates as a result of

shared environmental factors (i.e., environmental covariance) is likely because the sample consists of siblings, and, generally, siblings share a common environment, r~ Consequently, these heritability estimates provide the upper limit of the heritability of skeletodental characteristics among persons with overt malocclusions. Given equal sibship sizes (k = 2 in this study)," the formula for the standard error of the h 2 estimate ~~ is the following:

,, , , , , ri1 ] where n. is the total number of siblings in the study, r, is the intraclass correlation coefficient, k is the number of siblings per sibship, and S is the number of sibships.

RESULTS H e r i t a b i l i t y e s t i m a t e s

The statistical general ized l inear models used here controlled for effects o f age and sex and age-x-sex

American Journal of Orthodontics and Dentofacial Orthopedics King, t larris, and Tolley 125 Volume 104, No. 2

MX Arch R a t i o ' ~ t t"

MD Arch Ratio ! t

MX 6-6 Width ~,#227//~ | 1

Y~Y//AY/~V'A~'//AP'//X,V/Xd MD 6-6 Width f

MX 3-3 Width

MD 3-3 Width ~/'///////Y/,~W///////Xd'//A

V//////.#'/f~P'/,#/~,~, MX Length I

I~I/I/)Z/Z//////J7,d MD Length I

~//'////, MX Shape ~////, | I

MD Shape ~ ' I

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0.00 0.25 0.50

I B Malocclusions [] Normal Occlusions t data unavailable

!

I

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0.75 1.00 1.25 1.50 1.75

Heritability Estimates

Fig. 4. Histogram of heritabilities (• SE) for arch size variables.

interaction where these had significant influences on a given variable.

For discussion purposes, we have grouped heritability estimates for the skeletodental variables into three general areas: craniofacial, arch, and occlusal variables. Heritability estimates for the 21 craniofacial variables are graphed in Fig. 3, and the numerical values are listed in Table II. Estimates ranged from 0.39 for articulare-pogonion to 0.80 for the anterior height index with a mean value of 0.59 for these craniofacial variables. For the 10 arch dimensions (Fig. 4), h z estimates ranged from 0.24 for maxillary shape index to 0.79 for mandibular intercanine width. Mean h ~ was 0.5 I. Her- itability estimates for the occlusal variables (Fig. 5) ranged from 0.15 for the TPI index to 0.91 for incisai mandibular plane angle with a mean value of 0.52.

Inspection of these three histograms (Figs. 3 to 5) does not suggest any particular difference in the magnitude of h z among the craniofacial, arch, or occlusal vari,'ibles. To test this impression, a Kruskal-Wallis one- way analysis of variance w a s u s e d . 32 The II value with 2 df was 1.82, which is not significant (0.50 > P > 0.30). In this series of overt malocclusions, then, there is no noteworthy difference between

" h z estimates of these three sorts of skeletodental variables.

Contrast with normative data Heritability is not only a property of a particular

phenotypic characteristic, but also a property of the population and environment from which the sample was obtained. ~3 ttarris and Johnson's 23 longitudinal analysis

of malocclusion used a very similar protocol to assess heritability in a sample of unselected cases from the Bolton-Brush studies. 34 Consequently, it was possible to pair the heritability estimates for 21 craniofacial variables from this study with those from their series of 14-year-old subjects who did not warrant comprehensive orthodontics. A goodness-of-fit chi square test was used to assess the departure from a chance 1 to 1 distribution. Sixteen of the 21 comparisons were lower in the present study (Fig. 3); the goodness-of-fit test yielded X 2 = 5.8 (1 df), which is statistically significant (P = 0.02).

The 6 arch and 14 occlusal variables available for comparison were combined. The goodness-of-fit test resulted in X 2 = 5.0, which achieves significance (P = 0.02, 1 df). Here, our series of adolescents needing treatment tend to have higher h z estimates than the

normative series.

DISCUSSION Clinical perceptions favor the idea that heredity

plays a major role in both craniofacial structure and ,tooth-based malocclusions. The unfounded conjecture of the inheritance of tooth size from one parent and jaw size of the other leading to malocclusions ~'36 is still a common clinical metaphor, but it is incompatible with the contemporary understanding of polygenic inheritance. Talbot ~7 provides an extensive review of the sources of this 19th century idea. This claim has been augmented (1) by the work of Stockard and Johnson, 3s which used inappropriate animal models in an attempt

126 King, Harris, and Tolley American Journal o f Orthodontics and Dentofacial Orthopedics August 1993

MD Displacements

MX Displacements

Mandibular Rotations ~:~//'~/~/~

Maxillary Rotations : §

Crossbites

MD Crowding/Spacing

MX Crowding/Spacing

Mandibular Irregularity

Maxillary Irregularity

Buccal Segment Relation

Inter-lncisal Angle- ~7////,~'~

IMPA

Incisor Overbite z////~;,/,~

Incisor Overjet

I Z

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~:y./,,~//////?/,y/~ I I

; ~ / / / / ~ / / / / / / / / / 4 r

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,

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Malocclusions I Normal Occ lus ions

I

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0.00 0.25 0.50 0.75 1.00 1.25 1.50 Heritability Estimates

Fig. 5. Histogram of heritabilities (___ SE) for occlusal variables.

1 1.75

to mimic admixture among human populations, (2) xe- nophobic fears of race-crossing, 39 and (3) the fact that these authors' misinterpretations frequently go unap- preciated in more recent texts despite evidence to the contrary. '~-43

The aim of the present study was to assess the perceptions of those who maintain that malocclusions are "genetic." An explicitly biased sample of overt malocclusions was used to determine whether these ex- tremes of the population distribution exhibit heritabilities different from.samples composed of persons with naturally occurring good occlusions. That is, the claim of strong family resemblances may simply reflect se- lective recollection of noteworthy cases; likewise, spe- cialists only treat cases with substantive malocclu- s ions - -a select group that may not be similar to the normative group. Genetic determination of malocclusions may have a real biologic basis; persons with overt malocclusions may express these disharmonies against a different genetic'background than other segments of the population, particularly those with naturally occurring sound occlusions.

The influence of genetics on facial features (i.e., craniofacial structure) is obvious in some families, 4J and familial resemblances for craniofacial structure have been documented in many studies. "''2''4'6''455 Fa- milial inheritance also has been illustrated by the "Haps- burg jaw," the mandibular prognathism present in the royal German family, 56 and across a spectrum of chro- mosomal anomalies. 57'58 Indeed, most reviews of the "genetics of malocclusion" actually focus on skeletal components of facial fom~, not on tooth and intertooth relationships. 43'59~2 At least in part, then, there is con- fusion in the literature as a result of extrapolation from data on facial form to untested issues of "crooked teeth" sensu stricto.

Studies which have focused specifically on tooth- based variables have shown that acquired, environmental factors account for virtually all of the observed variation.* In overview, measurements of tooth position, such as rotations, displacements, and buccal segment relation, are strongly influenced by environmental

*Re'fences 2-5, 17, 18, 40, 41, 63-66.

American Journal o f Orthodontics and Dentofacial Orthopedics King, Ilarris, and Tolley 127 Volume 104, No. 2

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Fig. 6. The epigenetic landscape (redrawn f romWaddington~) .

factors. In contrast, measures of arch size commonly exhibit statistically significant genetic components.

The message in these several studies is that cranio- . facial, bone-based dimensions and proportions are under moderately strong genetic control, whereas variables of tooth position are environmentally induced rather than inherited. This simple dichotomy is not sup- ported by the present study. Measures of craniofacial size and form have lower genetic components than an- ticipated, whereas occlusal, tooth-based variables have higher h 2 estimates. The net effect is that our results obscure the skeletal versus occlusal dichotomy observed in studies including only normal subjects.

Developmental scenario

On one hand, results of the present study substan- tiate the clinical perception that siblings tend to exhibit similar malocclusions. Sibling correlations for occlusal parameters were significantly higher in this series of overt malocclusions than in our prior study of only normal occlusions. 2~ On the other hand, analysis in itself does not provide an ,explanation of the apparent differences. We would, however, conjecture the following scenario: Malocclusion, both in terms of its prevalence and modal severity, has increased very rap- idly in industrialized countries, probably due in large part to increased allergens in the food and air with an industrialized lifestyle 67"7~ and decreased masticatory stress afforded by sophisticated food processing tech- niques. 7~'72 The collective influence of these forces on a person increases craniOfacial-skeletodental disharmonies, what is occasionally termed a decrease in mor- phologic integration. 64'7~ Put simply, the increased, dys-

trophic effects of the environment diminish the developmental harmony of the skeletodental complexes. Convincing evidence of this is available in studies of reduced masticatory stress in controlled animal studies, 63'64'74"77 reduced (inadequate) masticatory function during growth increases the occurrence and severity of malocclusions. There are now, as well, a number of clinical studies that extend this paradigm to the human c o n d i t i o n 4 , 7 2 , 7 8 . 8 1

Reduced morphologie integration can be tied to a related concept developed by Waddington. s2 To para- phrase his description, a�9 is genetically heterogeneous and it inhabits a heterogeneous environment; some children are intrinsically, more resistant to environmental stresses than others, and some grow up in a more supportive environment (e.g., better nutrition, more exercise, better health care). This produces a mul- tidimensional space of epigenetic environments. Pic- turing this as a landscape with ridges and valleys where time (growth) is one important dimension (Fig. 6), the development of a given child will proceed down one of several valle):s. With time, his genotype and the environment may divert the course of development "away from the valley floor, up the neighboring hillside, but there will be a tendency for the process to find its way back, not to the point from which it was dis- placed--the homeostatic equilibrium--but to some later position on the canalized pathway of change." If the insults to growth are severe enough, the child's course may even be diverted laterally into a different valley.

Because siblings share half their genes in common by descent and more are identical in kind, their geno-

128 King, ttarris, and Tolley

typic predispositions are quite similar. Likewise, broth- ers and sisters within a nuclear family share many environmental factors in common, including maternal effects, dietary and nutritional patterns, socioeconomic status, and pattems of illness. The combined effect of nature and nurture places siblings on very similar courses in Waddington's epigenetic landscape. We con- tend that this phenomenon of homeorrhesis s385 (i.e., stabilization of growth along a developmental pathway) explains our results that siblings possess similar kinds of malocclusions. Their shared genetic backgrounds and similar environments preferentially push them along similar pathways.

Given the preponderance of children with malocclusions in today's society, 24'~6's7 it is easy to overlook the fact that this is not a natural phenomenon; instead, it reflects the pandemic nature of the environmental stressors that put virtually all children at r isk) 89~ The nature of these stressors is still poorly understood, though chronic mouthbreathing and reduced masticatory stress are two common problems. The effect of these dystrophic stressors i~ to perturb the child's developmental pathway and, given shared genetic poten- tials and a shared environmental milieu, siblings are likely to be pushed into similar pathways and end up with comparable kinds of malocclusions though the genetic contribution per se may be low.

Heritability

The etiology of skeletal and dental malocclusion is most certainly "multifactorial" in the sense that many, diverse causes converge to produce the observed changes. Shared environments inflate heritability values computed from members of the same household, though there is no way to estimate the magnitude of this con- founding effect in a sibling model. Garn and coworkers 9t have examined the resemblances that occur through the process of living together and have termed these "cohabitational effects." Persons living together exhibit dimensional resemblances whether or not they are genetically related. Resemblances in stature and fatness have been documented between parents and their adopted children, as well as between adopted, biologically unrelated siblings. Other observations have been made between spouses' resemblance in age at death, cause of death, and specific disease procliv- ity. 92-96 This may not be so mysterious, since spouses tend to share similar intakes of salt, fat, sugar, alcoholic beverages, and cigarettes.

Manifestation of a malocclusion is the culmination of a hierarchy of subclinical molecular, biochemical, physiologic, and metabolic markers of risk. Any one of these can be.modified by the environment, which

American Journal of Orthodontics and Dentofacial Orthopedics

, August 1993

makes the clinical expression remote from gene action. This is the essence of why dentofacial structure is not suitable for analyses with Mendelian models. 62"97,9s

Heritability is a one-dimensional descriptive statistic that does not address the mode of inheritance of malocclusions. 98 The long-term goal should be to identify factors that affect the frequency and./or severity of the phenotype. 99'~~176 Calculation of heritability estimates is a preliminary step that should be followed by tests for causative agents. Within clinical orthodontics, the preliminary goal has been to define the relative contributions of genetics and the environment.

This goal has important implications. If dentofacial structure and malocclusion are primarily genetic, then treatment will always be palliative and, in severe cases, genetic counseling would be indicated. The search for control would ultimately focus on delineating the re- sponsible genes. Conversely, if components of dentofacial structure and malocclusion have trivial heritabilities, then the search needs to be directed at factors inducing malocclusion during growth and development. The goal would be to identify causes and formulate means of intercepting their negative influences. An appropriate analogy is the reduced caries incidence over the past few decades from fluoride treatments and pubhc water fluoridation programs.l~176

Overview

Many studies confirm the importance of genetics in craniofacial size and form. In contrast, few have specifically examined tooth-based malocclusions, and very few have included severe malocclusions. These overt cases are treated orthodontically, which excludes them from study, we have examined the pretreatment records of 104 sibling pairs, all of whom were treated subsequently. This selected po.rtion of the total spectrum yielded quite different estimates of sibling similarity: Cephalometric (bone-based) measures offacial structure have significantly lower h 2 estimates than are derived from samples with naturally occurring good occlusions, and, secondly, the occlusal, tooth-based variables exhibit significantly higher estimates. This essentially vindicates clinicians' experiences that siblings examined in the orthodontic setting do frequently present with very similar malocclusions.

We are indebted to Dr. James L. Vaden who so graciously provided the majority of sibling pairs used in this study.

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S Karger, 1948. 2. Corruccini RS, Potter RHY. Genetic analysis of occlusal vari-

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American Journal of Orthodontics and Dentofacial Orthopedics Kblg, Harris, and Tolley 1 29 Volume 104, No. 2

3. Potter RHY, Corruccini RS, Green LJ. Variance of occlusion traits in twins. J Craniofac Genet Dev Biol 1981;1:217-27.

4. Corruccini RS, Choudhury AFH. Dental occlusal variation among rural and urban Bengali youths. Hum Biol 1986;58: 61-6.

5. Sharma K, Corruccini R. Genetic basis of dental occlusal variations in Northwest Indian twins. Eur J Orthod 1986;8:91-7.

6. Kang KW, Lindeman JP, Christian JC, Nance WE, Norton JA. Sampling variances in twin sibling studies of man. Hum Hered 1974;24:363-72.

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American Journal of Orthodontics and Dentofacial Orthopedics King, Harris, and Tolley 131 Volume 104, No. 2

100. PotterRH. Atwinhalf-sib model for occlusion traits [Abstract]. J Dent Res 1990;69:338.

I01. Horowitz HS. The future of water fluoridation and other sys- temic fluorides. J Dent Res 1990;69:760-4.

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Reprint requests to: Dr. Edward F. Harris Department of Orthodontics College of Dentistry University of Tennessee 875 Union Ave. Memphis, TN 38163

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