- Email: [email protected]
A descriptive study of mandibular incisor alignment in untreated subjects
ORIGINAL ARTICLE
A descriptive study of mandibular incisor alignment in untreated subjects Susan Eslambolchi,a Donald G. Woodside,b and P. Emile Rossouwc Toronto, Ontario, Canada, and Dallas, Tex Introduction: The development of mandibular incisor crowding appears to be a continuous process throughout life, but more evidence is needed to understand why changes occur. Methods: In this study, we describe the longitudinal dental changes in untreated children (n ⫽ 15) who had records at 3 times and in an untreated adult group (n ⫽ 18) (parents) who had records for 2 times. The mean numbers of years between initial and final observations were 29.8 years for the children and 33.7 years for the parents. All subjects were participants in the original Burlington Growth Research Project at the University of Toronto. The following variables were measured to an accuracy of 0.01 mm: overjet, overbite, mandibular intercanine width, mandibular interfirst premolar width, mandibular intermolar width, mandibular arch length, Little’s incisor irregularity index, mandibular anterior space analysis, and Carey’s space analysis. Results: There were no statistically significant (P ⬎.01) differences between the sexes for the variables measured. Little’s irregularity index continued to increase in all groups (P ⬍.01), although this rate appeared to be lower in the parent group. Intercanine and interfirst premolar widths and arch lengths continued to decrease with age. Conclusions: These results underline the importance of studies showing that untreated dentitions change over time. Orthodontic patient education is imperative about retention protocols and late developmental crowding. (Am J Orthod Dentofacial Orthop 2008;133:343-53)
O
rthodontists have long been aware that posttreatment changes occur, but the etiology and mechanism of such changes have not been satisfactorily explained. Posttreatment changes can include changes in overjet, overbite, and interarch relationships, and the return of dental rotations. Probably the single most persistent, irritating, and recurring problem for both the patient and the clinician is mandibular incisor crowding. In general, posttreatment and postretention changes in orthodontically treated patients include decreases in arch length and arch width and increases in overbite, overjet, and mandibular incisor crowding.1-3 Sinclair and Little4 questioned whether mandibular incisor crowding occurs primarily as a result of orthodontic therapy or as part of the normal developmental process. Thus, they analyzed the maturation of untreated normal occlusions in a longitudinal study from ages 9 to 20. a
Private practice, Toronto, Ontario, Canada. Professor emeritus, Department of Orthodontics, University of Toronto, Toronto, Ontario, Canada. c Professor and chairman, Department of Orthodontics, Baylor College of Dentistry, Texas A&M University System Health Science Center, Dallas, Tex. Reprint requests to: P. Emile Rossouw, Department of Orthodontics, Baylor College of Dentistry, 3302 Gaston Ave, Dallas, TX 75246; e-mail, [email protected]. Submitted, March 2006; revised and accepted, April 2006. 0889-5406/$34.00 Copyright © 2008 by the American Association of Orthodontists. doi:10.1016/j.ajodo.2006.04.038 b
They concluded that mandibular incisor irregularity increased even in untreated occlusions. Over the years, various theories have evolved to explain why mandibular incisor irregularity increases with age. A popular hypothesis states that the third molars exert mesial pressure on the mandibular posterior teeth. Some studies have related mandibular incisor crowding to the third molars.5-10 However, other studies have shown no correlation between the mandibular third molars and late mandibular incisor crowding.11-14 Therefore, views are polarized about the role of the third molars in the etiology of late mandibular incisor crowding. Other hypotheses have been proposed to explain late mandibular incisor or developmental crowding. Maximum lip strength has been investigated.15,16 This factor could play an important role in developmental crowding. Unfortunately, it has been difficult to quantify the amount of lip pressure accurately; more research is needed in this area. Some studies have suggested that growth changes can lead to mandibular incisor crowding.17-19 However, Levin20 found no significant association between jaw growth and late mandibular incisor crowding. Tooth morphology and tooth size are other variables that have been studied. Fastlicht11 concluded that the larger the mesiodistal width of the mandibular incisors, the greater the crowding. Others have stated that the size and the 343
344 Eslambolchi, Woodside, and Rossouw
Table I.
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Sample characteristics
Sample Untreated children Untreated parents Total
Male
Female
Total
10 8 18
15 10 25
15 18 43
Table II. Ages of subjects (y): means and standard deviations Sample Untreated children Untreated parents
Mean age at TC1 or TP1
Mean age at TC2 or TP2
Mean age at TC3
13.1 ⫾ 2.2 36.1 ⫾ 3.3
19.3 ⫾ 1.4 69.4 ⫾ 3.7
42.9 ⫾ 2.7
Table III.
Time between visits (y): means and standard deviations Sample Untreated children Untreated parents
TC1 to TC2 or TP1 to TP2
TC2 to TC3
TC1 to TC3
6.7 ⫾ 1.4 33.7 ⫾ 1.6
23.1 ⫾ 1.1
29.8 ⫾ 2.9
shape of mandibular incisors do not significantly contribute to their alignment.21,22 Late mandibular incisor crowding can occur regardless of whether a person receives orthodontic treatment. Factors in late mandibular incisor crowding have been investigated; some are questionable, whereas others are more accepted. None has been proven at this time. Little23 stated that arch-length and arch-width reductions with concomitant crowding continue well into the 20s and 30s, but the rate of change seems to diminish after age 30. The purpose of this study was to describe the dental changes, specifically mandibular incisor irregularity, in 2 untreated groups of different ages to enhance our understanding of late mandibular incisor crowding. MATERIAL AND METHODS
The records of 33 subjects obtained from the Burlington Growth Centre at the Faculty of Dentistry, University of Toronto, fulfilled the inclusion criteria for this study. The Burlington Orthodontic Research Centre began in 1952.24,25 The inclusion criteria were mandibular teeth from canine to canine with no missing mandibular incisors, no orthodontic treatment after the last set of records in the original project, and no overt periodontal disease. Tables I through III describe the sample in more detail.
Fig 1. Width measurements: A, mandibular intercanine width; B, mandibular interfirst premolar width; C, mandibular intermolar width.
For the children, 3 sets of diagnostic casts were examined and labeled TC1 (child), TC2 (young adult), and TC3 (mature adult). The range of TC1 to TC3 for the untreated children was 25.3 to 38.2 years, with a mean of 29.8 years. For the parents, 2 sets of diagnostic casts were examined and labeled TP1 (mature adult) and TP2 (old adult). The range of TP1 to TP2 was 27.8 to 35.3 years, with a mean of 33.7 years. The following variables were measured on all casts. 1. Overjet: the distance in millimeters (parallel to the occlusal plane) from the most labial aspect of the maxillary central incisor to the most labial aspect of the mandibular central incisor. 2. Overbite: percentage of the mandibular central incisors overlapped by the maxillary central incisors. 3. Mandibular intercanine width: the distance in millimeters between cusp tips or estimated cusp tips in cases of wear facets (Fig 1). 4. Mandibular interfirst premolar width: the distance in millimeters between buccal cusp tips or estimated cusp tips in cases of wear facets (Fig 1). 5. Mandibular interfirst permanent molar width: the distance in millimeters from the buccal cusp tips of the mandibular permanent first molars in children and when present in the parents (Fig 1). 6. Mandibular arch length: the sum of the right and left distances in millimeters from mesial anatomic contact points of the first permanent molars to the contact point of the central incisors or the midpoint between the central incisors if spaced in children (Fig 2).
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
Fig 2. Mandibular arch length: A ⫹ B ⫽ arch length in children; C ⫹ D ⫽ arch length in parents.
Eslambolchi, Woodside, and Rossouw 345
Fig 4. Mandibular anterior crowding: P ⫹ Q ⫽ summed width of 6 anterior teeth.
Fig 3. Mandibular incisor irregularity: A ⫹ B ⫹ C ⫹ D ⫹ E ⫽ irregularity index.
7. Modified mandibular arch length: the sum of the right and left distances in millimeters from the buccal cusp tips of the first premolars to the contact point of the central incisors or to the midpoint between the central contacts, if spaced (Fig 2). The first premolars were selected because many parents had missing first permanent molars. 8. Mandibular incisor irregularity index26: the summed displacement of the anatomic contact points of the mandibular anterior teeth in millimeters (Fig 3). 9. Mandibular anterior space analysis: the sum of the mesiodistal widths of the mandibular teeth from canine to canine subtracted from the space available, which is measured from the contact
Fig 5. Total mandibular crowding: P ⫹ Q ⫹ R ⫹ S ⫽ summed width of right second molar to left second molar in children; A ⫹ B ⫽ summed width of right first premolar to left first premolar in parents.
point of the canine and the first premolar in millimeters (Fig 4). 10. Modified Carey’s space analysis: the mesiodistal widths of all teeth anterior to the mandibular second premolars subtracted from available linear arch length mesial to the mandibular second premolars in millimeters (Fig 5). The analysis was modified from the original analysis of Carey27 because many parents had missing first permanent molars.
346 Eslambolchi, Woodside, and Rossouw
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Fig 6. Changes in intercanine width in children and parents. *P ⬍.01, **P ⬍.001.
All measurements were made with a digital caliper (Mitutoyo, Aurora, Ill) with accuracy of 0.01 mm.
mine whether there were any systematic errors in the measurements.
Statistical analysis
RESULTS
Statistical analysis included descriptive statistics for the 2 groups (untreated children and parents). The following statistical tests were used: t test for paired groups to determine the significance of changes with time, Pearson product moment correlation coefficient to evaluate associations between variables, analysis of variance (ANOVA) to assess the differences between the sexes and the groups. Changes in subjects were calculated for each variable and divided by the time between measurements in years to give a rate of change for each subject. This removed the between-person variation from consideration. The significance level was established at P ⫽ .01. A correlation value (r) of 0.6 or better was considered clinically important if the probability value was less than or equal to .01. Measurement error was evaluated by random selection of 10 casts and remeasurement a week later (intraobserver error study [S.E.]). The same 10 casts were measured by another observer (D.W.) to assess interobserver measurement error. Pearson product moment correlation coefficients were calculated to assess examiner error. A 2-way ANOVA was used to deter-
The changes in the variables were studied longitudinally. A 2-way ANOVA was carried out to compare changes in males and females. In both children and parents, no statistically significant differences in the changes were observed in the sexes. Therefore, males and females were pooled. The mean change in overjet was not statistically significant both from TC1 to TC2 and TC2 to TC3 in the children. In the parent group, mean overjet showed a statistically significant increase from TP1 to TP2 (P ⫽ .003). The most frequent change was an increase of 0.5 mm in overjet. The mean change in overbite was not statistically significant both from TC1 to TC2 and from TC2 to TC3 in children. In the parent group, overbite increased slightly from TP1 to TP2 but not significantly. Mean mandibular intercanine width (Fig 6) decreased in children at a statistically significant rate both from TC1 to TC2 (P ⫽ .005) and from TC2 to TC3 (P ⫽ .006). The parents’ mean mandibular intercanine width also showed a statistically significant decrease from TP1 to TP2 (P ⫽
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
Eslambolchi, Woodside, and Rossouw 347
Fig 7. Changes in interfirst premolar width in children and parents: *P ⬍.01, **P ⬍.001.
.001). The most frequent change appeared to be a loss of 1.0 mm in intercanine width in both groups. Mean mandibular interfirst premolar width (Fig 7) decreased at statistically significant rates from TC1 to TC2 (P ⫽ .002) and from TC2 to TC3 (P ⫽ .001) in children. The parents’ mean mandibular interfirst premolar width also showed a statistically significant decrease from TP1 to TP2 (P ⫽ .01). As with intercanine width, the most frequent change was a loss of 1.0 mm in interfirst premolar width in both groups. Mean mandibular intermolar width decreased slightly from TC1 to TC2 in children, but this was not statistically significant. From TC2 to TC3, mean mandibular intermolar width increased slightly, but this was not significant. Intermolar width was not measured in parents because of many missing mandibular first molars in this group. The mean mandibular arch length decreased from TC1 to TC2 in children at a statistically significant rate (P ⫽ .0001). It continued to decrease significantly (P ⫽ .003) from TC2 to TC3. In the parent group, mean modified mandibular arch length decreased at a statistically significant rate (P ⫽ .0001) from TP1 to TP2. The most frequent changes were losses up to 2.0 mm in the children and 1.0 mm in the parents. In children, the mean index for mandibular incisor irregularity (Fig 8) increased significantly from TC1 to TC2 (P ⫽.0001) and from TC2 to TC3 (P ⫽ .0001). In the
parents, Little’s irregularity index continued to increase at a statistically significant rate from TP1 to TP2 (P ⫽ .002). In both groups, the most frequent change in the irregularity index was an increase of 2.0 to 4.0 mm. In children, the mean anterior space analysis value (Fig 9) changed at a statistically significant rate from TC1 to TC2 and from TC2 to TC3. From TC1 to TC2 and from TC2 to TC3, anterior spacing decreased (crowding increased) significantly (P ⫽ .0001). In the parents, this trend continued (anterior crowding increased) from TP1 to TP2 at a statistically significant rate (P ⫽ .0001). The most frequent change in children was an increase in anterior crowding of 1.0 to 2.0 mm; in the parent group, it was an increase of up to 1.0 mm of anterior crowding. In children, the mean Carey’s space analysis value changed at a statistically significant rate from TC1 to TC2 and from TC2 to TC3. From TC1 to TC2 and from TC2 to TC3, total spacing decreased (crowding increased) significantly (P ⫽ .0001). In parents, the same trend was observed. Mean total crowding increased from TP1 to TP2 at a statistically significant rate (P ⫽ .0001). The most frequent changes were increases in total crowding of 2.0 to 4.0 mm in children and up to 1.0 mm in parents. Tables IV and V show the means for the variables and their standard errors. These values are graphically presented in Figures 6 through 9.
348 Eslambolchi, Woodside, and Rossouw
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Fig 8. Combined changes in Little’s irregularity index in children and parents: *P ⬍.01, ***P ⬍.0001.
Fig 9. Changes in mandibular anterior crowding in children and parents: ***P ⬍.0001.
The mean annual changes in each variable are given for children and parents in Tables VI and VII. Comparisons of equality of the rates of change in children were made from TC1 to TC2 and from TC2 to
TC3. The 2 rates of change were compared to determine whether they differed at a statistically significant level. The following variables changed at a statistically significantly different rate from TC1 to TC2 compared
Eslambolchi, Woodside, and Rossouw 349
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
Table IV.
Means, standard deviations, and standard errors for children TC1
Age (y) Overjet (mm) Overbite (%) ICW (mm) IFPW (mm) IMW (mm) ARCHL (mm) LII (mm) ANTSP (mm) Carey (mm)
TC2
TC3
Mean
SD
SE
Mean
SD
SE
Mean
SD
SE
13.0 2.74 45.60 26.00 34.50 43.81 65.45 2.88 ⫺0.72 2.16
1.7 1.36 21.52 1.39 1.82 2.62 5.48 1.44 0.88 2.03
0.3 0.27 4.30 0.28 0.39 0.52 1.10 0.29 0.18 0.41
19.6 2.62 38.50 25.33 33.53 43.05 63.42 4.45 ⫺1.64 ⫺0.62
1.1 1.32 18.85 1.44 1.74 2.18 5.48 2.08 1.02 1.39
0.3 0.29 4.21 0.32 0.41 0.49 1.22 0.46 0.23 0.31
42.4 2.69 42.0 24.96 33.29 43.16 62.43 7.03 ⫺2.70 ⫺2.35
2.2 1.56 24.96 1.70 1.98 3.05 6.00 2.55 1.29 2.17
0.4 0.31 4.99 0.34 0.42 0.61 1.20 0.51 0.26 0.43
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis. Table V. Means, standard deviations, and standard errors for parents TP1
Age (y) Overjet (mm) Overbite (%) ICW (mm) IFPW (mm) ARCHL (mm) LII (mm) ANTSP (mm) Carey (mm)
TP2
Mean
SD
SE
Mean
SD
SE
36.1 2.93 38.13 24.99 33.52 40.28 5.36 ⫺1.76 ⫺1.82
3.3 2.30 16.72 1.79 2.64 2.55 2.70 0.96 1.71
0.8 0.58 4.18 0.42 0.62 0.60 0.64 0.23 0.40
69.4 3.41 39.12 24.17 32.70 39.38 6.80 ⫺2.68 ⫺2.71
3.7 2.50 15.54 2.11 2.22 2.15 2.55 0.99 1.76
0.9 0.61 3.77 0.50 0.52 0.51 0.60 0.23 0.41
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis.
with TC2 to TC3: overjet (P ⫽ .008), overbite (P ⫽ .003), intermolar width (P ⫽ .01), interfirst premolar width (P ⫽ .005), arch length (P ⫽ .0002), anterior space analysis (P ⫽ .004), and Carey’s space analysis (P ⫽ .0001). Intercanine width and Little’s irregularity index changed at slightly slower rates from TC2 to TC3 compared with TC1 to TC2, but these rates were not statistically significant at the .01 level. To investigate whether the rate of change in parents was slower, faster, or the same as the children, a modified t test was used. This test compared the rates of change from TP1 to TP2 with both TC1 to TC2 and TC2 to TC3 in children. The results indicated that overjet, overbite, and intercanine width changed at different rates in children from TC1 to TC2, compared with parents from TP1 to TP2, but the differences were not statistically significant. The following variables changed at significantly
Table VI.
Mean annual changes in children
Change in variable
Mean annual change
SE
P
Overjet TC1 to TC2 Overjet TC2 to TC3 Overjet TC1 to TC3 Overbite TC1 to TC2 Overbite TC2 to TC3 Overbite TC1 to TC3 ICW TC1 to TC2 ICW TC2 to TC3 ICW TC1 to TC3 IFPW TC1 to TC2 IFPW TC2 to TC3 IFPW TC1 to TC3 IMW TC1 to TC2 IMW TC2 to TC3 IMW TC1 to TC3 ARCHL TC1 to TC2 ARCHL TC2 to TC3 ARCHL TC1 to TC3 LII TC1 to TC2 LII TC2 to TC3 LII TC1 to TC3 ANTSP TC1 to TC2 ANTSP TC2 to TC3 ANTSP TC1 to TC3 Carey TC1 to TC2 Carey TC2 to TC3 Carey TC1 to TC3
⫺0.038 mm/y 0.008 mm/y ⫺0.001 mm/y ⫺1.505%/y 0.241%/y ⫺0.117%/y 0.090 mm/y 0.026 mm/y 0.035 mm/y 0.118 mm/y 0.023 mm/y 0.041 mm/y ⫺0.100 mm/y 0.001 mm/y ⫺0.023 mm/y ⫺0.278 mm/y ⫺0.059 mm/y ⫺0.102 mm/y 0.248 mm/y 0.128 mm/y 0.142 mm/y ⫺0.149 mm/y ⫺0.053 mm/y ⫺0.068 mm/y ⫺0.403 mm/y ⫺0.087 mm/y ⫺0.153 mm/y
0.022 mm 0.007 mm 0.006 mm 0.591% 0.133% 0.173% 0.028 mm 0.008 mm 0.008 mm 0.031 mm 0.005 mm 0.008 mm 0.039 mm 0.009 mm 0.012 mm 0.047 mm 0.013 mm 0.014 mm 0.048 mm 0.018 mm 0.016 mm 0.026 mm 0.007 mm 0.006 mm 0.054 mm 0.014 mm 0.013 mm
.11 .26 .82 .02 .09 .51 .005* .006* .0001* .002* .001* .0001* .02 .95 .07 .0001* .0003* .0001* .0001* .0001* .0001* .0001* .0001* .0001* .0001* .0001* .0001*
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis. *P ⬍.01.
slower rates in parents than in children: interfirst premolar width (P ⫽ .01), arch length (P ⫽ .0001), Little’s irregularity index (P ⫽ .0005), and anterior space analysis (P ⫽ .0002).
350 Eslambolchi, Woodside, and Rossouw
Table VII.
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Mean annual changes in parents
Change in variable
Mean annual change
SE
P
Overjet TP1 to TP2 Overbite TP1 to TP2 ICW TP1 to TP2 IFPW TP1 to TP2 ARCHL TP1 to TP2 LII TP1 to TP2 ANTSP TP1 to TP2 Carey TP1 to TP2
0.012 mm/y ⫺0.005%/y ⫺0.024 mm/y ⫺0.025 mm/y ⫺0.027 mm/y 0.043 mm/y ⫺0.027 mm/y ⫺0.027 mm/y
0.003 mm 0.056% 0.006 mm 0.009 mm 0.006 mm 0.012 mm 0.004 mm 0.005 mm
.003* .93 .001* .01* .0001* .002* .0001* .0001*
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis. *P ⬍.01.
When the children’s rate of change from TC2 to TC3 was compared with the parents’ rate of change from TP1 to TP2, there was more similarity in the rates. Overjet, overbite, intercanine width, interfirst premolar width, and arch length changed at rates that were not significant. However, the rates of change in Little’s irregularity index (P ⫽ .0004) and anterior space analysis (P ⫽ .005) were significantly slower in parents than in children. Pearson product moment correlation coefficients were calculated to determine whether there were any associations between the changes in the variables. The following correlations were found to be statistically significant. 1. In children from TC1 to TC2, change in intermolar width correlated with change in intercanine width (r ⫽ 0.75, P ⫽ .01). 2. In children from TC2 to TC3, change in Little’s irregularity index correlated with change in intercanine width (r ⫽ ⫺0.88, P ⫽ .001) and change in interfirst premolar width (r ⫽ 0.86, P ⫽ .003). 3. In children from TC1 to TC3, change in arch length correlated with change in Carey’s space analysis (r ⫽ 0.72, P ⫽ .002). 4. In parents from TP1 to TP2, change in Little’s irregularity index correlated with change in anterior space analysis (r ⫽ ⫺0.62, P ⫽ .006). In the children, there were statistically significant correlations between the TC1 and TC3 values in the following variables: intercanine width (r ⫽ 0.90, P ⫽ .001), interfirst premolar width (r ⫽ 0.93, P ⫽ .001), intermolar width (r ⫽ 0.94, P ⫽ .001), and arch length (r ⫽ 0.85, P ⫽ .0001). Final values for Little’s irregularity index, anterior space analysis, Carey’s space analysis, overbite, and overjet could not be
predicted from the initial values for these variables. On the other hand, in parents, all TP1 values for overjet, overbite, intercanine width, interfirst premolar width, arch length, Little’s irregularity index, anterior space analysis, and Carey’s space analysis correlated with TP2 values (r values ranged from 0.79 to 0.99, P ⫽ .0001). DISCUSSION
The subjects of this study were all selected from the Burlington Growth Centre. The most challenging aspect of any longitudinal study is the acquisition of many subjects with complete records. A larger sample size would have been ideal. However, it was still possible to make objective conclusions from this study. When Sinclair and Little4 compared 65 untreated normal occlusions from the Burlington Growth Centre with 30 first premolar extraction patients from Seattle, they reported that intercanine width decreased 3 times faster and incisor irregularity increased twice as fast in the treated group. There does not appear to be universal agreement about the effect of treatment on stability of the occlusion. From the most pessimistic3,28 to the most optimistic,29 where less than 10% relapse of the mandibular incisors occurred. A study, such as that by Sadowsky,30 fall somewhere in between. Our knowledge is enhanced with improvement in the study methodology which provides evidence about preventing relapse (Glenn et al,31 Franklin,32 and Buschang and Shulman33). Most long-term studies have included measurements of dental variables from early mixed dentition to early permanent dentition and early adulthood. In our study, we included these variables in subjects from their mid-30s to their late 60s (parents) and also in subjects from early permanent dentition to early adulthood and early 40s (children). Since there were no significant differences between the parents at TP1 and the children at TC3, it would be valid to use the results from the parents to predict what will eventually happen to the children’s dentition. Overjet in the children remained fairly stable. In the parents, there was a statistically significant increase. The most frequent finding was an increase of approximately 0.5 mm. Although this was statistically significant, clinically it might not be important. Overbite in children was also fairly stable. From early permanent to early adult dentition, there was a slight decrease; this agrees with the findings of Sinclair and Little.4 In both parents (TP1 to TP2) and children (TC2 to TC3), there was a slight increase in overbite. However, these changes were not significant in either group. Glenn et al31 also found overbite to be stable
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
during the postretention period. Little et al3 found a statistically significant increase in overbite during the postretention period for 65 first premolar extraction patients. The increase in overbite in that study was only 0.76 mm, which might not be clinically significant. Intercanine width decreased in both children and parents at statistically significant rates. This agrees with other postretention studies.3,4,23,28,32 The rate of decrease was not significantly slower in parents when compared with the children’s TC1 to TC2 or TC2 to TC3. Historically, there has been much interest in mandibular intercanine width. Because the canine is at the corner of the arch, any increase in canine width can dramatically increase the arch length. Often, this increase can convert extraction treatment into nonextraction treatment. A guiding principle commonly used in orthodontics is that the original canine width is inviolate. In theory, a patient having extraction treatment should be able to accommodate wider canine width, because the canines move posteriorly in a wider part of the arch. However, intercanine width decreases even in extraction patients whose original intercanine width was preserved.4 Questions regarding intercanine width and why it continues to decrease with age remain unanswered. Neuromusculature might play a role, but, unfortunately, many factors are not fully understood. Interfirst premolar width also decreased significantly in both children and parents. This decrease was significantly slower in parents when compared with children from TC1 to TC2. Most postretention studies did not examine interfirst premolar width, but Freeman34 also observed a statistically significant decrease in interfirst premolar width in both extraction and nonextraction Class II Division 1 patients. This is an important finding, since some malocclusions are treated by expansion in the premolar and canine area (arch development). Unless the arch is collapsed initially, or unless there is permanent retention, this might not be feasible, since there is gradual constriction in this area with age. Mandibular intermolar width remained relatively stable in children. This agrees with other studies.4,34 Steadman35 stated that, regardless of the changes in mandibular intermolar distance, the ultimate width is established by the balance of forces produced by muscles, function, and growth of the patient. Mandibular arch length decreased at a statistically significant rate in both groups. The rate of decrease was significantly slower in parents than the children from TC1 to TC2. A similar trend was observed in other studies.4,36 Mandibular incisor irregularity according to Little’s irregularity index was found to increase in both groups.
Eslambolchi, Woodside, and Rossouw 351
The rate of increase was significantly slower in parents when compared with children at both times. It appears that incisor irregularity is a continuing phenomenon well into the 20- to 40-year decades and probably beyond.23,33 This statement can now be supported by our findings. Incisor irregularity increased at a statistically significant rate up to age 70. Whether this finding is clinically important depends on each patient. Some patients are sensitive to even the slightest incisor irregularity. This is of concern if they have not been previously informed of posttreatment and postretention changes before treatment starts. Anterior spacing decreased (crowding increased) significantly in children and parents. The rate of change slowed significantly in parents when compared with children from TC1 to TC2 and TC2 to TC3. Crowding, arch length deficiency, and Little’s irregularity index are not equal terms. Little’s irregularity index measures the displaced contact points of the anterior teeth. Arch length deficiency is a clinical tool that represents the specific amount of space required for alignment of the teeth. In parents, there was a significant correlation between Little’s irregularity index and anterior space analysis. However, this relationship was not apparent in children. According to Carey’s space analysis, total spacing decreased (crowding increased) significantly in children and parents. The rate was not significantly slower in parents when compared with children in both time intervals. In children, the change in arch length correlated with the change in total spacing or crowding. Most postretention studies did not measure total spacing or crowding and concentrated on the anterior border of the dentition.28,30,31,36 It would be interesting to see whether future studies show the same trend as we found. Many parents had missing mandibular first molars. Since none of them had a mandibular removable retainer, the teeth anterior to the first molars tended to move distally into the extraction sites. As a result of this, some incisor irregularity was relieved. Little’s incisor irregularity decreased in 11.1% of the parents from TP1 to TP2. However, the modified Carey’s space analysis showed that, in all parents, total space decreased from TP1 to TP2. The similarity is interesting between parents at TP1 and children at TC3. Since there were no statistically significant differences between these groups at these ages, the changes in the various parameters were combined to produce a longitudinal picture of occlusal changes from adolescence to old age. The combined data illustrate that, for the most part, the deleterious changes in occlusion continue into old age. The rate of
352 Eslambolchi, Woodside, and Rossouw
change usually decreases after approximately age 40, but the changes continue with aging. All observed changes in children and parents fell within 1 SD above or below the mean. The changes that have been discussed essentially follow the same trends observed in previous studies. Stability appears to be multivariate. The lack of knowledge about all factors that lead to stability is apparent. As shown by this study, untreated subjects have instability with the same frequency as treated ones. The changes observed are part of a dynamic biologic process and could be another component of aging. Parker37 stated: “Teeth move as long as we live, just as surely as our hair color changes throughout our lives.” Another popular analogy is that of skin wrinkling with increasing age—thus “wrinkling of the teeth.” The problem of posttreatment stability of the mandibular incisors should be discussed with patients and parents during the initial consultation. They must be informed of the potential for change and be given some responsibility for monitoring long-term stability. Nanda and Burstone38 commented that retention is a continuation of treatment, and it requires the same analytical thinking necessary to establish specific treatment objectives at the beginning of orthodontic treatment. A retention regimen must be developed for each patient, whether with fixed retention or removable retainers; compliance with the retention protocol is imperative and dictates whether a future orthodontic therapy phase is an option. Patients can be told that, since teeth continue to move throughout one’s life, they could become irregular as time progresses. Also, since currently no dental cast variables can assist the orthodontist in predicting who will have more incisor irregularity, the patient can either have a retainer indefinitely or face the possibility of a short orthodontic treatment revision phase to align the incisors later, without a retainer. It is, however, imperative to fully describe late developmental incisor crowding to all patients during the initial consultation. CONCLUSIONS
This study supports the hypothesis that mandibular incisor irregularity occurs well into the seventh decade. The following conclusions were made. 1. Treated and untreated subjects have similar longterm changes. 2. There were no statistically significant differences in the variables studied between the sexes. 3. In children from TC1 to TC2, TC2 to TC3, and TC1 to TC3, the following variables decreased at statistically significant rates: intercanine width,
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
4.
5.
6.
7.
8. 9.
10.
interfirst premolar width, arch length, anterior space, and total space. Little’s irregularity index increased at a statistically significant rate. In parents from TP1 to TP2, the following variables decreased at statistically significant rates: intercanine width, interfirst premolar width, arch length, anterior space, and total space. Little’s irregularity index and overjet increased at statistically significant rates. In children, the rates of change were slower from TC2 to TC3 compared with TC1 to TC2 for all variables except for Little’s irregularity index and intercanine width. In parents, the rates of change were slower when compared with children’s TC1 to TC2 for all variables except overjet, overbite, intercanine width, and Carey’s space analysis. Parents’ rates of change were slower than children’s TC2 to TC3 only for Little’s irregularity index and anterior space analysis. In children, changes in Little’s irregularity index correlated with changes in intercanine and interfirst premolar width from TC2 to TC3. In parents, changes in Little’s irregularity index correlated with changes in anterior space analysis. In children, initial irregularity values did not correlate with final irregularity values, but, in parents, there was correlation between initial and final incisor irregularity. Late developmental crowding continues throughout life, although the rate seems to decrease with age.
REFERENCES 1. Shapiro PA. Mandibular dental arch form and dimension. Am J Orthod 1974;66:58-70. 2. Gardner SD, Chaconas SJ. Posttreatment and postretention changes following orthodontic therapy. Angle Orthod 1976;46: 151-61. 3. Little RM, Wallen TR, Riedel RA. Stability and relapse of mandibular anterior alignment-first premolar extraction cases treated by traditional edgewise orthodontics. Am J Orthod 1981;80:349-65. 4. Sinclair PM, Little RM. Maturation of untreated normal occlusions. Am J Orthod 1983;83:114-23. 5. Bergstrom K, Jensen R. Responsibility of the third molar for secondary crowding. Dent Abstr 1961;6:544. 6. Vego L. A longitudinal study of mandibular arch perimeter. Angle Orthod 1962;32:187-92. 7. Richardson ME. Late lower arch crowding: facial growth or forward drift? Eur J Orthod 1979;1:219-25. 8. Richardson ME. The role of the third molar in the cause of later lower arch crowding: a review. Am J Orthod Dentofacial Orthop 1989;95:79-83.
Eslambolchi, Woodside, and Rossouw 353
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
9. Richardson M, Mills K. Late lower arch crowding: the effect of second molar extraction. Am J Orthod Dentofacial Orthop 1990;98:242-6. 10. Lindqvist B, Thilander B. Extraction of third molars in cases of anticipated crowding in the lower jaw. Am J Orthod 1982;81: 130-9. 11. Fastlicht J. Crowding of mandibular incisors. Am J Orthod 1970;58:156-63. 12. Solomon AG. The role of mandibular third molars in the aetiology of mandibular incisor crowding and changing growth patterns in the dentofacial complex [thesis]. Toronto, Ontario, Canada: University of Toronto; 1973. 13. Kaplan RG. Mandibular third molars and postretention crowding. Am J Orthod 1974;66:411-30. 14. Southard TE, Southard KA, Weeda LW. Mesial force from unerupted third molars. Am J Orthod Dentofacial Orthop 1991; 99:220-5. 15. Posen AL. The influence of maximum perioral and tongue force on the incisor teeth. Angle Orthod 1972;42:285-309. 16. Thüer U, Ingervall B. Pressure from the lips on the teeth and malocclusion. Am J Orthod Dentofacial Orthop 1986;90:234-42. 17. Moore AW, Hopkins SC. Inadequacy of mandibular anchorage. Am J Orthod 1960;46:440-51. 18. Björk A. Prediction of mandibular growth rotation. Am J Orthod 1969;55:585-99. 19. Björk A, Skieller V. Facial development and tooth eruption: an implant study at the age of puberty. Am J Orthod 1972;62:339-83. 20. Levin PC. The role of differential horizontal jaw growth in the etiology of mandibular incisor crowding [thesis]. Toronto, Ontario, Canada: University of Toronto; 1975. 21. Puneky PJ, Sadowsky C, BeGole EA. Tooth morphology and lower incisor alignment many years after orthodontic therapy. Am J Orthod 1984;86:299-305. 22. Gilmore CA, Little RM. Mandibular incisor dimensions and crowding. Am J Orthod 1984;86:493-502. 23. Little RM. Stability and relapse of dental arch alignment. Br J Orthod 1990;17:235-41. 24. Popovich F, Grainger RM. One community’s orthodontic problem. In: Moyers RE, editor. Orthodontics in mid-century. Trans-
25.
26. 27. 28.
29.
30. 31.
32.
33.
34.
35. 36.
37. 38.
actions of a workshop in orthodontics, University of Michigan. St Louis: C. V. Mosby; 1958. p. 192-266. Harvold EP, Hatton ME. The Burlington Orthodontic Research Centre: a measure of its role in dental public health. J Canad Dent Assoc 1962;28:6-17. Little RM. The irregularity index: a quantitative score of mandibular anterior alignment. Am J Orthod 1975;68:554-63. Carey CW. Linear arch dimension and tooth size. Am J Orthod 1949;35:762-75. Little RM, Riedel RA, Årtun J. An evaluation of changes in mandibular anterior alignment from 10 to 20 years postretention. Am J Orthod Dentofacial Orthop 1988;93:423-8. Sandusky WC. A long-term postretention study of Tweed extraction treatment [thesis]. Memphis: University of Tennessee; 1983. Sadowsky C, Sakols EI. Long-term assessment of orthodontic relapse. Am J Orthod 1982;82:456-63. Glenn G, Sinclair PM, Alexander RG. Nonextraction orthodontic therapy: posttreatment dental and skeletal stability. Am J Orthod Dentofacial Orthop 1987;92:321-8. Franklin S. A longitudinal study of dental and skeletal parameters associated with stability of orthodontic treatment [thesis]. Toronto, Ontario, Canada University of Toronto; 1995. Buschang PH, Shulman JD. Incisor crowding in untreated persons 15-50 years of age: United States, 1988-1994. Angle Orthod 2003;73:502-8. Freeman BV. A comparison of post-retention mandibular incisor irregularity in treated Class II Division 1 malocclusions versus untreated Class I “normals” [thesis]. Toronto, Ontario, Canada: University of Toronto; 1993. Steadman SR. Changes of intermolar and intercuspid distances following orthodontic treatment. Angle Orthod 1961;31:207-15. Shields TE, Little RM, Chapko MK. Stability and relapse of mandibular anterior alignment: a cephalometric appraisal of first-premolar-extraction cases treated by traditional edgewise orthodontics. Am J Orthod 1985;87:27-38. Parker W. Retention—retainers may be forever. Am J Orthod Dentofacial Orthop 1989;95:505-13. Nanda R, Burstone CJ. Retention and stability in orthodontics. Philadelphia: W. B. Saunders; 1993. p.1-8.
A descriptive study of mandibular incisor alignment in untreated subjects Susan Eslambolchi,a Donald G. Woodside,b and P. Emile Rossouwc Toronto, Ontario, Canada, and Dallas, Tex Introduction: The development of mandibular incisor crowding appears to be a continuous process throughout life, but more evidence is needed to understand why changes occur. Methods: In this study, we describe the longitudinal dental changes in untreated children (n ⫽ 15) who had records at 3 times and in an untreated adult group (n ⫽ 18) (parents) who had records for 2 times. The mean numbers of years between initial and final observations were 29.8 years for the children and 33.7 years for the parents. All subjects were participants in the original Burlington Growth Research Project at the University of Toronto. The following variables were measured to an accuracy of 0.01 mm: overjet, overbite, mandibular intercanine width, mandibular interfirst premolar width, mandibular intermolar width, mandibular arch length, Little’s incisor irregularity index, mandibular anterior space analysis, and Carey’s space analysis. Results: There were no statistically significant (P ⬎.01) differences between the sexes for the variables measured. Little’s irregularity index continued to increase in all groups (P ⬍.01), although this rate appeared to be lower in the parent group. Intercanine and interfirst premolar widths and arch lengths continued to decrease with age. Conclusions: These results underline the importance of studies showing that untreated dentitions change over time. Orthodontic patient education is imperative about retention protocols and late developmental crowding. (Am J Orthod Dentofacial Orthop 2008;133:343-53)
O
rthodontists have long been aware that posttreatment changes occur, but the etiology and mechanism of such changes have not been satisfactorily explained. Posttreatment changes can include changes in overjet, overbite, and interarch relationships, and the return of dental rotations. Probably the single most persistent, irritating, and recurring problem for both the patient and the clinician is mandibular incisor crowding. In general, posttreatment and postretention changes in orthodontically treated patients include decreases in arch length and arch width and increases in overbite, overjet, and mandibular incisor crowding.1-3 Sinclair and Little4 questioned whether mandibular incisor crowding occurs primarily as a result of orthodontic therapy or as part of the normal developmental process. Thus, they analyzed the maturation of untreated normal occlusions in a longitudinal study from ages 9 to 20. a
Private practice, Toronto, Ontario, Canada. Professor emeritus, Department of Orthodontics, University of Toronto, Toronto, Ontario, Canada. c Professor and chairman, Department of Orthodontics, Baylor College of Dentistry, Texas A&M University System Health Science Center, Dallas, Tex. Reprint requests to: P. Emile Rossouw, Department of Orthodontics, Baylor College of Dentistry, 3302 Gaston Ave, Dallas, TX 75246; e-mail, [email protected]. Submitted, March 2006; revised and accepted, April 2006. 0889-5406/$34.00 Copyright © 2008 by the American Association of Orthodontists. doi:10.1016/j.ajodo.2006.04.038 b
They concluded that mandibular incisor irregularity increased even in untreated occlusions. Over the years, various theories have evolved to explain why mandibular incisor irregularity increases with age. A popular hypothesis states that the third molars exert mesial pressure on the mandibular posterior teeth. Some studies have related mandibular incisor crowding to the third molars.5-10 However, other studies have shown no correlation between the mandibular third molars and late mandibular incisor crowding.11-14 Therefore, views are polarized about the role of the third molars in the etiology of late mandibular incisor crowding. Other hypotheses have been proposed to explain late mandibular incisor or developmental crowding. Maximum lip strength has been investigated.15,16 This factor could play an important role in developmental crowding. Unfortunately, it has been difficult to quantify the amount of lip pressure accurately; more research is needed in this area. Some studies have suggested that growth changes can lead to mandibular incisor crowding.17-19 However, Levin20 found no significant association between jaw growth and late mandibular incisor crowding. Tooth morphology and tooth size are other variables that have been studied. Fastlicht11 concluded that the larger the mesiodistal width of the mandibular incisors, the greater the crowding. Others have stated that the size and the 343
344 Eslambolchi, Woodside, and Rossouw
Table I.
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Sample characteristics
Sample Untreated children Untreated parents Total
Male
Female
Total
10 8 18
15 10 25
15 18 43
Table II. Ages of subjects (y): means and standard deviations Sample Untreated children Untreated parents
Mean age at TC1 or TP1
Mean age at TC2 or TP2
Mean age at TC3
13.1 ⫾ 2.2 36.1 ⫾ 3.3
19.3 ⫾ 1.4 69.4 ⫾ 3.7
42.9 ⫾ 2.7
Table III.
Time between visits (y): means and standard deviations Sample Untreated children Untreated parents
TC1 to TC2 or TP1 to TP2
TC2 to TC3
TC1 to TC3
6.7 ⫾ 1.4 33.7 ⫾ 1.6
23.1 ⫾ 1.1
29.8 ⫾ 2.9
shape of mandibular incisors do not significantly contribute to their alignment.21,22 Late mandibular incisor crowding can occur regardless of whether a person receives orthodontic treatment. Factors in late mandibular incisor crowding have been investigated; some are questionable, whereas others are more accepted. None has been proven at this time. Little23 stated that arch-length and arch-width reductions with concomitant crowding continue well into the 20s and 30s, but the rate of change seems to diminish after age 30. The purpose of this study was to describe the dental changes, specifically mandibular incisor irregularity, in 2 untreated groups of different ages to enhance our understanding of late mandibular incisor crowding. MATERIAL AND METHODS
The records of 33 subjects obtained from the Burlington Growth Centre at the Faculty of Dentistry, University of Toronto, fulfilled the inclusion criteria for this study. The Burlington Orthodontic Research Centre began in 1952.24,25 The inclusion criteria were mandibular teeth from canine to canine with no missing mandibular incisors, no orthodontic treatment after the last set of records in the original project, and no overt periodontal disease. Tables I through III describe the sample in more detail.
Fig 1. Width measurements: A, mandibular intercanine width; B, mandibular interfirst premolar width; C, mandibular intermolar width.
For the children, 3 sets of diagnostic casts were examined and labeled TC1 (child), TC2 (young adult), and TC3 (mature adult). The range of TC1 to TC3 for the untreated children was 25.3 to 38.2 years, with a mean of 29.8 years. For the parents, 2 sets of diagnostic casts were examined and labeled TP1 (mature adult) and TP2 (old adult). The range of TP1 to TP2 was 27.8 to 35.3 years, with a mean of 33.7 years. The following variables were measured on all casts. 1. Overjet: the distance in millimeters (parallel to the occlusal plane) from the most labial aspect of the maxillary central incisor to the most labial aspect of the mandibular central incisor. 2. Overbite: percentage of the mandibular central incisors overlapped by the maxillary central incisors. 3. Mandibular intercanine width: the distance in millimeters between cusp tips or estimated cusp tips in cases of wear facets (Fig 1). 4. Mandibular interfirst premolar width: the distance in millimeters between buccal cusp tips or estimated cusp tips in cases of wear facets (Fig 1). 5. Mandibular interfirst permanent molar width: the distance in millimeters from the buccal cusp tips of the mandibular permanent first molars in children and when present in the parents (Fig 1). 6. Mandibular arch length: the sum of the right and left distances in millimeters from mesial anatomic contact points of the first permanent molars to the contact point of the central incisors or the midpoint between the central incisors if spaced in children (Fig 2).
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
Fig 2. Mandibular arch length: A ⫹ B ⫽ arch length in children; C ⫹ D ⫽ arch length in parents.
Eslambolchi, Woodside, and Rossouw 345
Fig 4. Mandibular anterior crowding: P ⫹ Q ⫽ summed width of 6 anterior teeth.
Fig 3. Mandibular incisor irregularity: A ⫹ B ⫹ C ⫹ D ⫹ E ⫽ irregularity index.
7. Modified mandibular arch length: the sum of the right and left distances in millimeters from the buccal cusp tips of the first premolars to the contact point of the central incisors or to the midpoint between the central contacts, if spaced (Fig 2). The first premolars were selected because many parents had missing first permanent molars. 8. Mandibular incisor irregularity index26: the summed displacement of the anatomic contact points of the mandibular anterior teeth in millimeters (Fig 3). 9. Mandibular anterior space analysis: the sum of the mesiodistal widths of the mandibular teeth from canine to canine subtracted from the space available, which is measured from the contact
Fig 5. Total mandibular crowding: P ⫹ Q ⫹ R ⫹ S ⫽ summed width of right second molar to left second molar in children; A ⫹ B ⫽ summed width of right first premolar to left first premolar in parents.
point of the canine and the first premolar in millimeters (Fig 4). 10. Modified Carey’s space analysis: the mesiodistal widths of all teeth anterior to the mandibular second premolars subtracted from available linear arch length mesial to the mandibular second premolars in millimeters (Fig 5). The analysis was modified from the original analysis of Carey27 because many parents had missing first permanent molars.
346 Eslambolchi, Woodside, and Rossouw
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Fig 6. Changes in intercanine width in children and parents. *P ⬍.01, **P ⬍.001.
All measurements were made with a digital caliper (Mitutoyo, Aurora, Ill) with accuracy of 0.01 mm.
mine whether there were any systematic errors in the measurements.
Statistical analysis
RESULTS
Statistical analysis included descriptive statistics for the 2 groups (untreated children and parents). The following statistical tests were used: t test for paired groups to determine the significance of changes with time, Pearson product moment correlation coefficient to evaluate associations between variables, analysis of variance (ANOVA) to assess the differences between the sexes and the groups. Changes in subjects were calculated for each variable and divided by the time between measurements in years to give a rate of change for each subject. This removed the between-person variation from consideration. The significance level was established at P ⫽ .01. A correlation value (r) of 0.6 or better was considered clinically important if the probability value was less than or equal to .01. Measurement error was evaluated by random selection of 10 casts and remeasurement a week later (intraobserver error study [S.E.]). The same 10 casts were measured by another observer (D.W.) to assess interobserver measurement error. Pearson product moment correlation coefficients were calculated to assess examiner error. A 2-way ANOVA was used to deter-
The changes in the variables were studied longitudinally. A 2-way ANOVA was carried out to compare changes in males and females. In both children and parents, no statistically significant differences in the changes were observed in the sexes. Therefore, males and females were pooled. The mean change in overjet was not statistically significant both from TC1 to TC2 and TC2 to TC3 in the children. In the parent group, mean overjet showed a statistically significant increase from TP1 to TP2 (P ⫽ .003). The most frequent change was an increase of 0.5 mm in overjet. The mean change in overbite was not statistically significant both from TC1 to TC2 and from TC2 to TC3 in children. In the parent group, overbite increased slightly from TP1 to TP2 but not significantly. Mean mandibular intercanine width (Fig 6) decreased in children at a statistically significant rate both from TC1 to TC2 (P ⫽ .005) and from TC2 to TC3 (P ⫽ .006). The parents’ mean mandibular intercanine width also showed a statistically significant decrease from TP1 to TP2 (P ⫽
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
Eslambolchi, Woodside, and Rossouw 347
Fig 7. Changes in interfirst premolar width in children and parents: *P ⬍.01, **P ⬍.001.
.001). The most frequent change appeared to be a loss of 1.0 mm in intercanine width in both groups. Mean mandibular interfirst premolar width (Fig 7) decreased at statistically significant rates from TC1 to TC2 (P ⫽ .002) and from TC2 to TC3 (P ⫽ .001) in children. The parents’ mean mandibular interfirst premolar width also showed a statistically significant decrease from TP1 to TP2 (P ⫽ .01). As with intercanine width, the most frequent change was a loss of 1.0 mm in interfirst premolar width in both groups. Mean mandibular intermolar width decreased slightly from TC1 to TC2 in children, but this was not statistically significant. From TC2 to TC3, mean mandibular intermolar width increased slightly, but this was not significant. Intermolar width was not measured in parents because of many missing mandibular first molars in this group. The mean mandibular arch length decreased from TC1 to TC2 in children at a statistically significant rate (P ⫽ .0001). It continued to decrease significantly (P ⫽ .003) from TC2 to TC3. In the parent group, mean modified mandibular arch length decreased at a statistically significant rate (P ⫽ .0001) from TP1 to TP2. The most frequent changes were losses up to 2.0 mm in the children and 1.0 mm in the parents. In children, the mean index for mandibular incisor irregularity (Fig 8) increased significantly from TC1 to TC2 (P ⫽.0001) and from TC2 to TC3 (P ⫽ .0001). In the
parents, Little’s irregularity index continued to increase at a statistically significant rate from TP1 to TP2 (P ⫽ .002). In both groups, the most frequent change in the irregularity index was an increase of 2.0 to 4.0 mm. In children, the mean anterior space analysis value (Fig 9) changed at a statistically significant rate from TC1 to TC2 and from TC2 to TC3. From TC1 to TC2 and from TC2 to TC3, anterior spacing decreased (crowding increased) significantly (P ⫽ .0001). In the parents, this trend continued (anterior crowding increased) from TP1 to TP2 at a statistically significant rate (P ⫽ .0001). The most frequent change in children was an increase in anterior crowding of 1.0 to 2.0 mm; in the parent group, it was an increase of up to 1.0 mm of anterior crowding. In children, the mean Carey’s space analysis value changed at a statistically significant rate from TC1 to TC2 and from TC2 to TC3. From TC1 to TC2 and from TC2 to TC3, total spacing decreased (crowding increased) significantly (P ⫽ .0001). In parents, the same trend was observed. Mean total crowding increased from TP1 to TP2 at a statistically significant rate (P ⫽ .0001). The most frequent changes were increases in total crowding of 2.0 to 4.0 mm in children and up to 1.0 mm in parents. Tables IV and V show the means for the variables and their standard errors. These values are graphically presented in Figures 6 through 9.
348 Eslambolchi, Woodside, and Rossouw
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Fig 8. Combined changes in Little’s irregularity index in children and parents: *P ⬍.01, ***P ⬍.0001.
Fig 9. Changes in mandibular anterior crowding in children and parents: ***P ⬍.0001.
The mean annual changes in each variable are given for children and parents in Tables VI and VII. Comparisons of equality of the rates of change in children were made from TC1 to TC2 and from TC2 to
TC3. The 2 rates of change were compared to determine whether they differed at a statistically significant level. The following variables changed at a statistically significantly different rate from TC1 to TC2 compared
Eslambolchi, Woodside, and Rossouw 349
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
Table IV.
Means, standard deviations, and standard errors for children TC1
Age (y) Overjet (mm) Overbite (%) ICW (mm) IFPW (mm) IMW (mm) ARCHL (mm) LII (mm) ANTSP (mm) Carey (mm)
TC2
TC3
Mean
SD
SE
Mean
SD
SE
Mean
SD
SE
13.0 2.74 45.60 26.00 34.50 43.81 65.45 2.88 ⫺0.72 2.16
1.7 1.36 21.52 1.39 1.82 2.62 5.48 1.44 0.88 2.03
0.3 0.27 4.30 0.28 0.39 0.52 1.10 0.29 0.18 0.41
19.6 2.62 38.50 25.33 33.53 43.05 63.42 4.45 ⫺1.64 ⫺0.62
1.1 1.32 18.85 1.44 1.74 2.18 5.48 2.08 1.02 1.39
0.3 0.29 4.21 0.32 0.41 0.49 1.22 0.46 0.23 0.31
42.4 2.69 42.0 24.96 33.29 43.16 62.43 7.03 ⫺2.70 ⫺2.35
2.2 1.56 24.96 1.70 1.98 3.05 6.00 2.55 1.29 2.17
0.4 0.31 4.99 0.34 0.42 0.61 1.20 0.51 0.26 0.43
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis. Table V. Means, standard deviations, and standard errors for parents TP1
Age (y) Overjet (mm) Overbite (%) ICW (mm) IFPW (mm) ARCHL (mm) LII (mm) ANTSP (mm) Carey (mm)
TP2
Mean
SD
SE
Mean
SD
SE
36.1 2.93 38.13 24.99 33.52 40.28 5.36 ⫺1.76 ⫺1.82
3.3 2.30 16.72 1.79 2.64 2.55 2.70 0.96 1.71
0.8 0.58 4.18 0.42 0.62 0.60 0.64 0.23 0.40
69.4 3.41 39.12 24.17 32.70 39.38 6.80 ⫺2.68 ⫺2.71
3.7 2.50 15.54 2.11 2.22 2.15 2.55 0.99 1.76
0.9 0.61 3.77 0.50 0.52 0.51 0.60 0.23 0.41
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis.
with TC2 to TC3: overjet (P ⫽ .008), overbite (P ⫽ .003), intermolar width (P ⫽ .01), interfirst premolar width (P ⫽ .005), arch length (P ⫽ .0002), anterior space analysis (P ⫽ .004), and Carey’s space analysis (P ⫽ .0001). Intercanine width and Little’s irregularity index changed at slightly slower rates from TC2 to TC3 compared with TC1 to TC2, but these rates were not statistically significant at the .01 level. To investigate whether the rate of change in parents was slower, faster, or the same as the children, a modified t test was used. This test compared the rates of change from TP1 to TP2 with both TC1 to TC2 and TC2 to TC3 in children. The results indicated that overjet, overbite, and intercanine width changed at different rates in children from TC1 to TC2, compared with parents from TP1 to TP2, but the differences were not statistically significant. The following variables changed at significantly
Table VI.
Mean annual changes in children
Change in variable
Mean annual change
SE
P
Overjet TC1 to TC2 Overjet TC2 to TC3 Overjet TC1 to TC3 Overbite TC1 to TC2 Overbite TC2 to TC3 Overbite TC1 to TC3 ICW TC1 to TC2 ICW TC2 to TC3 ICW TC1 to TC3 IFPW TC1 to TC2 IFPW TC2 to TC3 IFPW TC1 to TC3 IMW TC1 to TC2 IMW TC2 to TC3 IMW TC1 to TC3 ARCHL TC1 to TC2 ARCHL TC2 to TC3 ARCHL TC1 to TC3 LII TC1 to TC2 LII TC2 to TC3 LII TC1 to TC3 ANTSP TC1 to TC2 ANTSP TC2 to TC3 ANTSP TC1 to TC3 Carey TC1 to TC2 Carey TC2 to TC3 Carey TC1 to TC3
⫺0.038 mm/y 0.008 mm/y ⫺0.001 mm/y ⫺1.505%/y 0.241%/y ⫺0.117%/y 0.090 mm/y 0.026 mm/y 0.035 mm/y 0.118 mm/y 0.023 mm/y 0.041 mm/y ⫺0.100 mm/y 0.001 mm/y ⫺0.023 mm/y ⫺0.278 mm/y ⫺0.059 mm/y ⫺0.102 mm/y 0.248 mm/y 0.128 mm/y 0.142 mm/y ⫺0.149 mm/y ⫺0.053 mm/y ⫺0.068 mm/y ⫺0.403 mm/y ⫺0.087 mm/y ⫺0.153 mm/y
0.022 mm 0.007 mm 0.006 mm 0.591% 0.133% 0.173% 0.028 mm 0.008 mm 0.008 mm 0.031 mm 0.005 mm 0.008 mm 0.039 mm 0.009 mm 0.012 mm 0.047 mm 0.013 mm 0.014 mm 0.048 mm 0.018 mm 0.016 mm 0.026 mm 0.007 mm 0.006 mm 0.054 mm 0.014 mm 0.013 mm
.11 .26 .82 .02 .09 .51 .005* .006* .0001* .002* .001* .0001* .02 .95 .07 .0001* .0003* .0001* .0001* .0001* .0001* .0001* .0001* .0001* .0001* .0001* .0001*
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis. *P ⬍.01.
slower rates in parents than in children: interfirst premolar width (P ⫽ .01), arch length (P ⫽ .0001), Little’s irregularity index (P ⫽ .0005), and anterior space analysis (P ⫽ .0002).
350 Eslambolchi, Woodside, and Rossouw
Table VII.
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
Mean annual changes in parents
Change in variable
Mean annual change
SE
P
Overjet TP1 to TP2 Overbite TP1 to TP2 ICW TP1 to TP2 IFPW TP1 to TP2 ARCHL TP1 to TP2 LII TP1 to TP2 ANTSP TP1 to TP2 Carey TP1 to TP2
0.012 mm/y ⫺0.005%/y ⫺0.024 mm/y ⫺0.025 mm/y ⫺0.027 mm/y 0.043 mm/y ⫺0.027 mm/y ⫺0.027 mm/y
0.003 mm 0.056% 0.006 mm 0.009 mm 0.006 mm 0.012 mm 0.004 mm 0.005 mm
.003* .93 .001* .01* .0001* .002* .0001* .0001*
ICW, Mandibular intercanine width; IFPW, mandibular interfirst premolar width; IMW, mandibular intermolar width; ARCHL, mandibular arch length; LII, Little’s irregularity index; ANTSP, anterior space analysis; Carey, Carey’s space analysis. *P ⬍.01.
When the children’s rate of change from TC2 to TC3 was compared with the parents’ rate of change from TP1 to TP2, there was more similarity in the rates. Overjet, overbite, intercanine width, interfirst premolar width, and arch length changed at rates that were not significant. However, the rates of change in Little’s irregularity index (P ⫽ .0004) and anterior space analysis (P ⫽ .005) were significantly slower in parents than in children. Pearson product moment correlation coefficients were calculated to determine whether there were any associations between the changes in the variables. The following correlations were found to be statistically significant. 1. In children from TC1 to TC2, change in intermolar width correlated with change in intercanine width (r ⫽ 0.75, P ⫽ .01). 2. In children from TC2 to TC3, change in Little’s irregularity index correlated with change in intercanine width (r ⫽ ⫺0.88, P ⫽ .001) and change in interfirst premolar width (r ⫽ 0.86, P ⫽ .003). 3. In children from TC1 to TC3, change in arch length correlated with change in Carey’s space analysis (r ⫽ 0.72, P ⫽ .002). 4. In parents from TP1 to TP2, change in Little’s irregularity index correlated with change in anterior space analysis (r ⫽ ⫺0.62, P ⫽ .006). In the children, there were statistically significant correlations between the TC1 and TC3 values in the following variables: intercanine width (r ⫽ 0.90, P ⫽ .001), interfirst premolar width (r ⫽ 0.93, P ⫽ .001), intermolar width (r ⫽ 0.94, P ⫽ .001), and arch length (r ⫽ 0.85, P ⫽ .0001). Final values for Little’s irregularity index, anterior space analysis, Carey’s space analysis, overbite, and overjet could not be
predicted from the initial values for these variables. On the other hand, in parents, all TP1 values for overjet, overbite, intercanine width, interfirst premolar width, arch length, Little’s irregularity index, anterior space analysis, and Carey’s space analysis correlated with TP2 values (r values ranged from 0.79 to 0.99, P ⫽ .0001). DISCUSSION
The subjects of this study were all selected from the Burlington Growth Centre. The most challenging aspect of any longitudinal study is the acquisition of many subjects with complete records. A larger sample size would have been ideal. However, it was still possible to make objective conclusions from this study. When Sinclair and Little4 compared 65 untreated normal occlusions from the Burlington Growth Centre with 30 first premolar extraction patients from Seattle, they reported that intercanine width decreased 3 times faster and incisor irregularity increased twice as fast in the treated group. There does not appear to be universal agreement about the effect of treatment on stability of the occlusion. From the most pessimistic3,28 to the most optimistic,29 where less than 10% relapse of the mandibular incisors occurred. A study, such as that by Sadowsky,30 fall somewhere in between. Our knowledge is enhanced with improvement in the study methodology which provides evidence about preventing relapse (Glenn et al,31 Franklin,32 and Buschang and Shulman33). Most long-term studies have included measurements of dental variables from early mixed dentition to early permanent dentition and early adulthood. In our study, we included these variables in subjects from their mid-30s to their late 60s (parents) and also in subjects from early permanent dentition to early adulthood and early 40s (children). Since there were no significant differences between the parents at TP1 and the children at TC3, it would be valid to use the results from the parents to predict what will eventually happen to the children’s dentition. Overjet in the children remained fairly stable. In the parents, there was a statistically significant increase. The most frequent finding was an increase of approximately 0.5 mm. Although this was statistically significant, clinically it might not be important. Overbite in children was also fairly stable. From early permanent to early adult dentition, there was a slight decrease; this agrees with the findings of Sinclair and Little.4 In both parents (TP1 to TP2) and children (TC2 to TC3), there was a slight increase in overbite. However, these changes were not significant in either group. Glenn et al31 also found overbite to be stable
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
during the postretention period. Little et al3 found a statistically significant increase in overbite during the postretention period for 65 first premolar extraction patients. The increase in overbite in that study was only 0.76 mm, which might not be clinically significant. Intercanine width decreased in both children and parents at statistically significant rates. This agrees with other postretention studies.3,4,23,28,32 The rate of decrease was not significantly slower in parents when compared with the children’s TC1 to TC2 or TC2 to TC3. Historically, there has been much interest in mandibular intercanine width. Because the canine is at the corner of the arch, any increase in canine width can dramatically increase the arch length. Often, this increase can convert extraction treatment into nonextraction treatment. A guiding principle commonly used in orthodontics is that the original canine width is inviolate. In theory, a patient having extraction treatment should be able to accommodate wider canine width, because the canines move posteriorly in a wider part of the arch. However, intercanine width decreases even in extraction patients whose original intercanine width was preserved.4 Questions regarding intercanine width and why it continues to decrease with age remain unanswered. Neuromusculature might play a role, but, unfortunately, many factors are not fully understood. Interfirst premolar width also decreased significantly in both children and parents. This decrease was significantly slower in parents when compared with children from TC1 to TC2. Most postretention studies did not examine interfirst premolar width, but Freeman34 also observed a statistically significant decrease in interfirst premolar width in both extraction and nonextraction Class II Division 1 patients. This is an important finding, since some malocclusions are treated by expansion in the premolar and canine area (arch development). Unless the arch is collapsed initially, or unless there is permanent retention, this might not be feasible, since there is gradual constriction in this area with age. Mandibular intermolar width remained relatively stable in children. This agrees with other studies.4,34 Steadman35 stated that, regardless of the changes in mandibular intermolar distance, the ultimate width is established by the balance of forces produced by muscles, function, and growth of the patient. Mandibular arch length decreased at a statistically significant rate in both groups. The rate of decrease was significantly slower in parents than the children from TC1 to TC2. A similar trend was observed in other studies.4,36 Mandibular incisor irregularity according to Little’s irregularity index was found to increase in both groups.
Eslambolchi, Woodside, and Rossouw 351
The rate of increase was significantly slower in parents when compared with children at both times. It appears that incisor irregularity is a continuing phenomenon well into the 20- to 40-year decades and probably beyond.23,33 This statement can now be supported by our findings. Incisor irregularity increased at a statistically significant rate up to age 70. Whether this finding is clinically important depends on each patient. Some patients are sensitive to even the slightest incisor irregularity. This is of concern if they have not been previously informed of posttreatment and postretention changes before treatment starts. Anterior spacing decreased (crowding increased) significantly in children and parents. The rate of change slowed significantly in parents when compared with children from TC1 to TC2 and TC2 to TC3. Crowding, arch length deficiency, and Little’s irregularity index are not equal terms. Little’s irregularity index measures the displaced contact points of the anterior teeth. Arch length deficiency is a clinical tool that represents the specific amount of space required for alignment of the teeth. In parents, there was a significant correlation between Little’s irregularity index and anterior space analysis. However, this relationship was not apparent in children. According to Carey’s space analysis, total spacing decreased (crowding increased) significantly in children and parents. The rate was not significantly slower in parents when compared with children in both time intervals. In children, the change in arch length correlated with the change in total spacing or crowding. Most postretention studies did not measure total spacing or crowding and concentrated on the anterior border of the dentition.28,30,31,36 It would be interesting to see whether future studies show the same trend as we found. Many parents had missing mandibular first molars. Since none of them had a mandibular removable retainer, the teeth anterior to the first molars tended to move distally into the extraction sites. As a result of this, some incisor irregularity was relieved. Little’s incisor irregularity decreased in 11.1% of the parents from TP1 to TP2. However, the modified Carey’s space analysis showed that, in all parents, total space decreased from TP1 to TP2. The similarity is interesting between parents at TP1 and children at TC3. Since there were no statistically significant differences between these groups at these ages, the changes in the various parameters were combined to produce a longitudinal picture of occlusal changes from adolescence to old age. The combined data illustrate that, for the most part, the deleterious changes in occlusion continue into old age. The rate of
352 Eslambolchi, Woodside, and Rossouw
change usually decreases after approximately age 40, but the changes continue with aging. All observed changes in children and parents fell within 1 SD above or below the mean. The changes that have been discussed essentially follow the same trends observed in previous studies. Stability appears to be multivariate. The lack of knowledge about all factors that lead to stability is apparent. As shown by this study, untreated subjects have instability with the same frequency as treated ones. The changes observed are part of a dynamic biologic process and could be another component of aging. Parker37 stated: “Teeth move as long as we live, just as surely as our hair color changes throughout our lives.” Another popular analogy is that of skin wrinkling with increasing age—thus “wrinkling of the teeth.” The problem of posttreatment stability of the mandibular incisors should be discussed with patients and parents during the initial consultation. They must be informed of the potential for change and be given some responsibility for monitoring long-term stability. Nanda and Burstone38 commented that retention is a continuation of treatment, and it requires the same analytical thinking necessary to establish specific treatment objectives at the beginning of orthodontic treatment. A retention regimen must be developed for each patient, whether with fixed retention or removable retainers; compliance with the retention protocol is imperative and dictates whether a future orthodontic therapy phase is an option. Patients can be told that, since teeth continue to move throughout one’s life, they could become irregular as time progresses. Also, since currently no dental cast variables can assist the orthodontist in predicting who will have more incisor irregularity, the patient can either have a retainer indefinitely or face the possibility of a short orthodontic treatment revision phase to align the incisors later, without a retainer. It is, however, imperative to fully describe late developmental incisor crowding to all patients during the initial consultation. CONCLUSIONS
This study supports the hypothesis that mandibular incisor irregularity occurs well into the seventh decade. The following conclusions were made. 1. Treated and untreated subjects have similar longterm changes. 2. There were no statistically significant differences in the variables studied between the sexes. 3. In children from TC1 to TC2, TC2 to TC3, and TC1 to TC3, the following variables decreased at statistically significant rates: intercanine width,
American Journal of Orthodontics and Dentofacial Orthopedics March 2008
4.
5.
6.
7.
8. 9.
10.
interfirst premolar width, arch length, anterior space, and total space. Little’s irregularity index increased at a statistically significant rate. In parents from TP1 to TP2, the following variables decreased at statistically significant rates: intercanine width, interfirst premolar width, arch length, anterior space, and total space. Little’s irregularity index and overjet increased at statistically significant rates. In children, the rates of change were slower from TC2 to TC3 compared with TC1 to TC2 for all variables except for Little’s irregularity index and intercanine width. In parents, the rates of change were slower when compared with children’s TC1 to TC2 for all variables except overjet, overbite, intercanine width, and Carey’s space analysis. Parents’ rates of change were slower than children’s TC2 to TC3 only for Little’s irregularity index and anterior space analysis. In children, changes in Little’s irregularity index correlated with changes in intercanine and interfirst premolar width from TC2 to TC3. In parents, changes in Little’s irregularity index correlated with changes in anterior space analysis. In children, initial irregularity values did not correlate with final irregularity values, but, in parents, there was correlation between initial and final incisor irregularity. Late developmental crowding continues throughout life, although the rate seems to decrease with age.
REFERENCES 1. Shapiro PA. Mandibular dental arch form and dimension. Am J Orthod 1974;66:58-70. 2. Gardner SD, Chaconas SJ. Posttreatment and postretention changes following orthodontic therapy. Angle Orthod 1976;46: 151-61. 3. Little RM, Wallen TR, Riedel RA. Stability and relapse of mandibular anterior alignment-first premolar extraction cases treated by traditional edgewise orthodontics. Am J Orthod 1981;80:349-65. 4. Sinclair PM, Little RM. Maturation of untreated normal occlusions. Am J Orthod 1983;83:114-23. 5. Bergstrom K, Jensen R. Responsibility of the third molar for secondary crowding. Dent Abstr 1961;6:544. 6. Vego L. A longitudinal study of mandibular arch perimeter. Angle Orthod 1962;32:187-92. 7. Richardson ME. Late lower arch crowding: facial growth or forward drift? Eur J Orthod 1979;1:219-25. 8. Richardson ME. The role of the third molar in the cause of later lower arch crowding: a review. Am J Orthod Dentofacial Orthop 1989;95:79-83.
Eslambolchi, Woodside, and Rossouw 353
American Journal of Orthodontics and Dentofacial Orthopedics Volume 133, Number 3
9. Richardson M, Mills K. Late lower arch crowding: the effect of second molar extraction. Am J Orthod Dentofacial Orthop 1990;98:242-6. 10. Lindqvist B, Thilander B. Extraction of third molars in cases of anticipated crowding in the lower jaw. Am J Orthod 1982;81: 130-9. 11. Fastlicht J. Crowding of mandibular incisors. Am J Orthod 1970;58:156-63. 12. Solomon AG. The role of mandibular third molars in the aetiology of mandibular incisor crowding and changing growth patterns in the dentofacial complex [thesis]. Toronto, Ontario, Canada: University of Toronto; 1973. 13. Kaplan RG. Mandibular third molars and postretention crowding. Am J Orthod 1974;66:411-30. 14. Southard TE, Southard KA, Weeda LW. Mesial force from unerupted third molars. Am J Orthod Dentofacial Orthop 1991; 99:220-5. 15. Posen AL. The influence of maximum perioral and tongue force on the incisor teeth. Angle Orthod 1972;42:285-309. 16. Thüer U, Ingervall B. Pressure from the lips on the teeth and malocclusion. Am J Orthod Dentofacial Orthop 1986;90:234-42. 17. Moore AW, Hopkins SC. Inadequacy of mandibular anchorage. Am J Orthod 1960;46:440-51. 18. Björk A. Prediction of mandibular growth rotation. Am J Orthod 1969;55:585-99. 19. Björk A, Skieller V. Facial development and tooth eruption: an implant study at the age of puberty. Am J Orthod 1972;62:339-83. 20. Levin PC. The role of differential horizontal jaw growth in the etiology of mandibular incisor crowding [thesis]. Toronto, Ontario, Canada: University of Toronto; 1975. 21. Puneky PJ, Sadowsky C, BeGole EA. Tooth morphology and lower incisor alignment many years after orthodontic therapy. Am J Orthod 1984;86:299-305. 22. Gilmore CA, Little RM. Mandibular incisor dimensions and crowding. Am J Orthod 1984;86:493-502. 23. Little RM. Stability and relapse of dental arch alignment. Br J Orthod 1990;17:235-41. 24. Popovich F, Grainger RM. One community’s orthodontic problem. In: Moyers RE, editor. Orthodontics in mid-century. Trans-
25.
26. 27. 28.
29.
30. 31.
32.
33.
34.
35. 36.
37. 38.
actions of a workshop in orthodontics, University of Michigan. St Louis: C. V. Mosby; 1958. p. 192-266. Harvold EP, Hatton ME. The Burlington Orthodontic Research Centre: a measure of its role in dental public health. J Canad Dent Assoc 1962;28:6-17. Little RM. The irregularity index: a quantitative score of mandibular anterior alignment. Am J Orthod 1975;68:554-63. Carey CW. Linear arch dimension and tooth size. Am J Orthod 1949;35:762-75. Little RM, Riedel RA, Årtun J. An evaluation of changes in mandibular anterior alignment from 10 to 20 years postretention. Am J Orthod Dentofacial Orthop 1988;93:423-8. Sandusky WC. A long-term postretention study of Tweed extraction treatment [thesis]. Memphis: University of Tennessee; 1983. Sadowsky C, Sakols EI. Long-term assessment of orthodontic relapse. Am J Orthod 1982;82:456-63. Glenn G, Sinclair PM, Alexander RG. Nonextraction orthodontic therapy: posttreatment dental and skeletal stability. Am J Orthod Dentofacial Orthop 1987;92:321-8. Franklin S. A longitudinal study of dental and skeletal parameters associated with stability of orthodontic treatment [thesis]. Toronto, Ontario, Canada University of Toronto; 1995. Buschang PH, Shulman JD. Incisor crowding in untreated persons 15-50 years of age: United States, 1988-1994. Angle Orthod 2003;73:502-8. Freeman BV. A comparison of post-retention mandibular incisor irregularity in treated Class II Division 1 malocclusions versus untreated Class I “normals” [thesis]. Toronto, Ontario, Canada: University of Toronto; 1993. Steadman SR. Changes of intermolar and intercuspid distances following orthodontic treatment. Angle Orthod 1961;31:207-15. Shields TE, Little RM, Chapko MK. Stability and relapse of mandibular anterior alignment: a cephalometric appraisal of first-premolar-extraction cases treated by traditional edgewise orthodontics. Am J Orthod 1985;87:27-38. Parker W. Retention—retainers may be forever. Am J Orthod Dentofacial Orthop 1989;95:505-13. Nanda R, Burstone CJ. Retention and stability in orthodontics. Philadelphia: W. B. Saunders; 1993. p.1-8.