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AN EVALUATION OF MANDIBULAR ANTERIOR CROWDING AS IT RELATES TO FACIAL DIVERGENCE IN TREATED AND UNTREATED SUBJECTS Avrum I. Goldberg, D.D.S. An Abstract Presented to the Graduate Faculty of Saint Louis University in Partial Fulfillment of the Requirements for the Degree of Master of Science in Dentistry (Research) 2012 ABSTRACT Purpose: To better understand the relationship between vertical facial growth and mandibular anterior crowding by evaluating untreated subjects cross-sectionally and treated subjects longitudinally. Methods: The sample consisted of 1) pre-treatment records of 75 untreated Class I Caucasian patients collected from the archives at Saint Louis University, and 2) post-treatment and post-retention records of 76 Caucasian patients, treated on an extraction basis to a Class I occlusion, collected from one private practice clinician. After digitization of models and cephalograms, two universal measures of crowding (II and TSALD) were related to four frequently used indices of divergence (MPA, PMA, PFH:AFH, LFH:AFH). Results: There were weak to moderately weak associations between facial divergence and crowding, subjects with greater divergence showed greater amounts of crowding than subjects with average amounts of divergence. Females, who were more hyperdivergent than males, also showed stronger relationships between divergence and crowding than males. There were moderate correlations between posterior face height and crowding in males; eruption of the lower incisors was moderately associated with crowding in females. Conclusions: Vertical growth and incisor 1 eruption, as well as facial divergence, are important determinants of malalignment. 2 AN EVALUATION OF MANDIBULAR ANTERIOR CROWDING AS IT RELATES TO FACIAL DIVERGENCE IN TREATED AND UNTREATED SUBJECTS Avrum I. Goldberg, D.D.S. A Thesis Presented to the Graduate Faculty of Saint Louis University in Partial Fulfillment of the Requirements for the Degree of Master of Science in Dentistry (Research) 2012 COMMITTEE IN CHARGE OF CANDIDACY: Professor Peter H. Buschang, Chairperson and Advisor Professor Rolf G. Behrents Associate Clinical Professor Donald R. Oliver i DEDICATION This work is dedicated to my wife Amy. You enrich my life every day, and without you this pursuit would not have been meaningful. Thank you for your sacrifices and unwavering support throughout my graduate education. To my parents, Debbie and Sheldon, and sister, Lisa, thank you for your love and support. To my father, thank you for introducing me to the profession of dentistry and encouraging me to pursue higher education. I also wish to dedicate this work to all those fulland part-time faculty, co-residents, and staff members who have contributed to my professional education and personal life. ii ACKNOWLEDGEMENTS This project could not have been completed without the help and support of the following individuals: Dr. Peter Buschang, your guidance and enthusiasm for research helped me turn the vision of this project into a reality. Thank you for your motivation throughout this project and constantly challenging me to think. Dr. Rolf Behrents, thank you for your contributions to my thesis and professional education. I am grateful for the opportunity to have continued my education at Saint Louis University. Dr. Donald Oliver, thank you for your attention to detail throughout my graduate education and revisions of my thesis. Your teachings will serve me well throughout my career. Dr. Jim Boley and Mrs. Sabrina Boley, for welcoming me into their practice and allowing the use of their long-term records. Without Dr. Boley’s efforts to collect long-term records of his patients, this thesis would not have been possible. It is both humbling and inspiring to witness such incredible long-term results. Mrs. Rita Bauer, who took the time to collaborate and help me obtain exceptional photographs for my thesis, even during a trip to the Swiss Alps. Dolphin Imaging™, particularly Barbara Brinker, Marcus O’Leary, and the programming department, who donated their time and services to create a custom model analysis for use in this study. My wife, Dr. Amy Mihaljevich, who helped pull cases, photograph models, and log data. Without her help this thesis would not have been completed within the rigors of our program. iii TABLE OF CONTENTS List of Tables............................................vi List of Figures.........................................viii CHAPTER 1: INTRODUCTION....................................1 CHAPTER 2: REVIEW OF THE LITERATURE Overview ..........................................3 Part I – Prevalence and incidence of crowding .....3 The scope of the problem....................3 Crowding in untreated individuals...........6 Crowding in treated individuals............11 Comparisons of crowding in treated and untreated individuals ..............16 Part II – Etiology of crowding ...................20 Treatment factors..........................20 Soft tissue treatment boundaries .......23 Non-treatment factors......................27 Susceptibilities .......................29 Race ...............................29 Sex ................................30 Age ................................31 Indirect causes ........................33 Tooth size and shape ...............33 Third molars .......................34 Periodontal and gingival fibers ....36 Anterior component of force ........38 Primary tooth loss, eruption sequence ..............42 Predisposing factors ...................44 Arch form ..........................44 Point-to-point contacts ............46 Facial divergence ......................48 Secular Trends .....................51 Dental eruption and instability ....53 Compensatory rotational changes ....64 Relations in the literature ........67 Cross-sectional studies ........67 Untreated samples...........67 Longitudinal studies ...........68 Untreated samples...........68 Treated samples.............71 Statement of Thesis ..............................73 References .......................................74 iv CHAPTER 3: JOURNAL ARTICLE Abstract .........................................93 Introduction .....................................94 Materials and Methods ............................98 Selection criteria ............................98 Cephalometric Analysis .......................100 Model Analysis ...............................101 Reliability of Measurements ..................103 Statistical Analysis .........................104 Results .........................................104 Untreated subjects ...........................104 Treated subjects .............................109 Discussion ......................................119 Untreated subjects ...........................120 Treated subjects .............................121 Summary and Conclusions .........................127 References ......................................128 Appendix A ..............................................135 Appendix B...............................................139 Vita Auctoris............................................141 v LIST OF TABLES Table 1.1: Crowding in untreated samples..................10 Table 1.2: Crowding in treated samples....................14 Table 1.3: Summarized data for treated and untreated samples .......................................16 Table 1.4: Summary of rates for arch perimeter and Incisor Irregularity change ...................18 Table 3.1: Age distribution in treated groups.............99 Table 3.2: Age distribution in untreated groups..........100 Table 3.3: Crowding in untreated groups..................105 Table 3.4: Comparison of T1 skeletal measures in untreated groups .............................107 Table 3.5: Comparison of T1 skeletal measures in untreated groups .............................107 Table 3.6: Correlation between T1 crowding and T1 skeletal measures in untreated groups ........108 Table 3.7: Crowding in treated groups....................109 Table 3.8: Comparison of T1 skeletal measures in treated groups ...............................111 Table 3.9: Comparison of T1 dental measures in treated groups ...............................111 Table 3.10: Comparison of skeletal changes in treated groups ...............................113 Table 3.11: Comparison of dental changes in treated groups ...............................113 Table 3.12: Correlation between T2 crowding and T1 skeletal measures .........................116 vi Table 3.13: Correlation between change in crowding and T1 skeletal measures .........................117 Table 3.14: Correlation between change in crowding and change in skeletal measures ..................118 Table A.1: Customized cephalometric analysis.............138 Table A.2: Customized model analysis.....................138 Table B.1: Method error study............................140 vii LIST OF FIGURES Figure 1.1: Relation between mandibular irregularity and age .......................................7 Figure 1.2: Relation between annual irregularity increase and age .......................................8 Figure 1.3: Changes in crowding with age in untreated subjects ......................................9 Figure 1.4: Changes in crowding with age in treated subjects .....................................13 Figure 1.5: Changes in crowding with age in treated and untreated subjects ...........................17 Figure 2.1: Soft tissue envelope (saggital view)..........24 Figure 2.2: Soft tissue envelope (frontal view)...........24 Figure 2.3: The progression of malalignment...............28 Figure 2.4: Anterior component of force (saggital view)...39 Figure 2.5: Anterior component of force (occlusal view)...40 Figure 2.6: Stability in relation to dental angulation to the mandibular plane .......................41 Figure 2.7: Maintenance of a functional occlusion.........55 Figure 2.8: Variations in growth rate.....................56 Figure 2.9: Velocity curves for tooth eruption............57 Figure 2.10: Relation between dentoalveolar height and facial height ...........................59 Figure 2.11: Cross-sectional views of the alveolus in short, normal, and long-faced individuals ...62 Figure 2.12: Comparison of divergence morphologies........64 Figure 2.13: Relation between facial divergence and tooth eruption ..............................67 viii Figure 2.14: Revised progression of malalignment.........126 Figure A.1: Customized cephalometric digitization regimen .....................................136 Figure A.2: Calculation of arch perimeter................137 Figure A.3: Calculation of intercanine width, intermolar width, and arch depth ............137 Figure A.4: Calculation of incisor irregularity..........137 ix CHAPTER 1: INTRODUCTION Although improved oral health, function, and social approval are benefits of orthodontic treatment, patients typically present to maximize facial and dental appearance.1-4 This is why dissatisfaction with crowding or irregular anterior teeth is often cited by patients as the reason for seeking treatment.5-7 This is significant because the most widespread malocclusion encountered by orthodontists is crowding. Still, it remains inconclusive as to why some develop crowding and others do not. Research derived from the University of Washington8,9 suggests that “[t]he only way to ensure continued satisfactory alignment post-treatment probably is by use of fixed or removable retainers for life.”10 This is important because long-term patient satisfaction with orthodontic treatment is partly associated with the stability of the final result.11,12 However, the use of permanent retention instills complacence in orthodontists and ownership is essentially transferred to the patient for permanency of the result. Therefore further research is important to understand those factors affecting stability and relapse, and adjust our tactics for treatment.13-15 1 Longitudinal studies have consistently shown that crowding increases over time.10,16-19 These increases are larger during adolescence and slow into adulthood,10,20,21 and are found to occur in both treated and untreated individuals.16,17 Therefore, it has been suggested that crowding may be the result of facial growth changes and not necessarily treatment-related relapse.17,20,22 Because the duration and extent of vertical growth is greater than for horizontal growth,1,17,23 vertical growth is suspected to play an important role in dentoalveolar compensations which could ultimately lead to instability and/or crowding of the teeth. It is the purpose of this study to determine whether differences in vertical growth proportions, as measured by various indices of facial divergence, relate to crowding in both treated and untreated subjects. More than seventy years ago Hellman (1940) stated that “We are in almost complete ignorance of the specific factors causing relapses and failures.” Today, we are still largely unaware of the causes of relapse. 2 CHAPTER 2: REVIEW OF THE LITERATURE OVERVIEW This section is divided into two parts. The first portion discusses crowding and various methods of measurement. This is followed by the presentation of data from various longitudinal studies on the prevalence and incidence of crowding among treated and untreated individuals. These groups are then compared, using relevant supportive literature. The second portion discusses treatment and physiological-related factors that may be involved in the development of crowding. These are introduced in an order that follows the development of crowding. The relation of facial divergence to crowding is presented last, as it is the factor of particular interest in this thesis. PART I – PREVALENCE AND INCIDENCE OF CROWDING THE SCOPE OF THE PROBLEM A lack of space for teeth within the dental arch can result in one of two outcomes: either tooth contact-point displacement, causing irregularity, or flaring of the anterior teeth, leading to protrusion.24,25 in treated and untreated cases. 3 Both can occur Because early studies consistently showed incisor crowding to be appreciably larger in the mandibular than the maxillary arch,24,25 the literature has tended to focus on the lower arch. Boundaries are more stringent in the mandible, as there is no opportunity for sutural expansion and lateral dental expansion provides only limited space gain.26 Incisor proclination can provide the largest opportunity for arch length increase;26 however, periodontal defects (i.e., recession and dehiscence) can be iatrogenically caused if teeth are moved out of their bony housing.27 Therefore, reduction of tooth structure within an arch, using either tooth extraction or interproximal reduction, may be necessary to manage extensive mandibular crowding. Mandibular crowding is typically measured in one of two ways. Tooth-size-arch-length discrepancy (TSALD) is a measure of how “crowded” the teeth are, and is the difference between the space available in the arch (the alveolar bone) and the amount of space required (the tooth structure present).28 This can involve the entire arch (Total TSALD or tTSALD), or the segment of the arch that includes the six anterior teeth (Anterior TSALD or aTSALD).29 A TSALD of 4 mm or less can typically be treated 4 without extractions, while 8 mm or more often requires extractions.30 Alternately, the Irregularity Index (II), devised by Little,31 is the sum of the contact point displacements of the anterior teeth, in millimeters. “crooked” the teeth are. It measures how This index is generally used in epidemiological studies because of its simplicity and efficiency. However it does not account for rotations or changes in inclination.32 An Irregularity Index less than 3.5 mm is considered acceptable, while more than 7 mm is considered clinically severe.31 Because these indices measure different aspects of malalignment, they are complementary to one another. A study by Harris and others33 compared aTSALD and II to determine whether they were related to one another. Based on 70 randomly selected cases, they found a statistically significant positive correlation (r=+0.53) that accounted for less than a third of the variation. Another study by Bernabé and Flores-Mir32 evaluated tTSALD and II in 200 randomly selected schoolchildren. Their correlation was also statistically significant (r=-0.68) but accounted for less than half of the variation. These studies suggest a more accurate relation between TSALD and II is gained by including more teeth in the space analysis. 5 However, the lack of a strong correlation indicates that both methods are necessary for a study evaluating crowding,33,34 as the use of either method alone could influence the results.17 CROWDING IN UNTREATED INDIVIDUALS In the 1960s the US Public Health Service conducted a large-scale survey to evaluate the level of malocclusion in the United States. This was conducted during the first National Health and Nutrition Examination Survey (NHANES I).35,36 In the late 1980s and early 1990s, statistical methods were used to collect a sample that would be representative of the three major racial groups in the US (whites, blacks, and Mexican-Americans). The NHANES III sample studied over 30,000 individuals collected between 1988 to 1994.37 Two papers in the orthodontic literature have presented tabulated NHANES III data showing differences in incisor irregularity due to age, sex, race, and various malocclusions and occlusal relations.30,38 Brunelle et al.38 found that a mean lower incisor irregularity of 1.6 mm for 8-11 year olds, 2.5 mm for 12-17 year olds, and 2.9 mm for 18-50 year olds. He also reported that 42.4% of 8-50 year olds had ideal alignment, 27.8% had mild irregularity, 15.1% had moderate irregularity, and 14.7% had severe to 6 extreme irregularity. However, percentages were not provided for irregularity based on discrete age groups. 1998, Proffit et al.30 provided more specific data In collection in terms of these percentages, based on ethnicity and age. The data showed that more than 20% of 8-11 year olds are affected by at least moderate lower crowding, and this worsens in adolescence (30% by 12-17 years). In adulthood (age 18+), about 40% have at least moderate crowding and only about a third have ideal (0-1 mm) irregularity. The trend for increased crowding with age is shown in Figure 1.1. Although these papers adequately described children in the mixed and early permanent dentition, they provided only a limited view of adult irregularity since their data was pooled. Figure 1.1. Relation between mandibular irregularity and age. Adapted from Proffit et al.30 7 In 2003, Buschang and Shulman20 compiled a more detailed breakdown of the original adult sample, based on a random sample of 9044 untreated adults collected from the NHANES III study. They showed a trend of increased incisor irregularity at increasing age grades, with significantly more irregularity in 30-40 year olds than 15-20 year olds. Increases in irregularity followed a curvilinear relationship, with annual changes decreasing over time (Figure 1.2). Most increases occurred during the teenage years and early twenties. Figure 1.2. Relation between annual irregularity increase and age. Adapted from Buschang and Shulman.20 Many longitudinal studies have also evaluated changes in untreated subjects. summarized in Table 1.1. Individual and combined data is Amalgamated data shows increases in TSALD and II of approximately 0.17 mm/yr and 0.09 mm/yr, respectively. When plotted (Figure 1.3), changes in TSALD 8 and II are shown to decrease over time, suggesting that a relation between age and crowding may be present. Figure 1.3. Changes in crowding with age in untreated subjects. 9 690 TOTAL - Angle Class NS I NS I I/II I/II I/II I NS I NS NS NS - 57% 49% 60% 44% 49% 52% 49% 57% 60% 57% 44% 50% 56% F F F F F F F F F F F F F Sex Sample features 17.82 13.0 13.1 13.1 13.3 13.9 14.3 16.9 18.0 19.3 21.0 22.8 25.6 36.1 T1 Age (yrs) 30.36 18.0 20.1 19.3 26.0 16.9 23.2 48.2 21.0 42.9 28.0 33.3 45.7 69.4 T2 Age (yrs) 12.54 5.0 7.0 6.2 12.7 3.0 8.9 31.3 3.0 23.6 7.0 10.5 20.1 33.3 Δ Age (yrs) +1.13 +0.70 +1.57 +0.47 +0.9 +1.59 +2.58 +1.44 Δ II (mm) -2.32 -2.78 -2.02 -1.29 -1.1 -2.06 -0.1 -1.73 -0.2 -0.22 -0.80 -0.89 -1.39 +0.09 10 Δ TSALD (mm) +0.10 +0.25 +0.16 +0.10 +0.05 +0.11 +0.04 Δ II/yr (mm/yr) *NS = not specified; II = Incisor Irregularity; TSALD = tooth-size-arch-length-discrepancy 51 65 25 32 46 44 53 46 25 46 144 30 18 Richardson, 1979 Sinclair & Little, 1983 Eslambolchi et al., 2008 Bishara et al., 1989 Carter & McNamara, 1998 Driscoll-Gilliland et al., 2001 Carter & McNamara, 1998 Richardson & Gormley, 1998 Eslambolchi et al., 2008 Richardson & Gormley, 1998 Bondevik, 1998 Bishara et al., 1994 Eslambolchi et al., 2008 UNTREATED N TABLE 1.1. Crowding in untreated samples -0.17 -0.46 -0.44 -0.16 -0.43 -0.12 -0.07 -0.03 -0.07 -0.03 -0.02 -0.04 -0.03 Δ TSALD/yr (mm/yr) CROWDING IN TREATED INDIVIDUALS A great deal of long-term data has been collected about crowding in treated subjects, much of which has been produced at the University of Washington under the guidance of Little. In 1981, Little et al.39 investigated long-term changes in mandibular crowding after orthodontic treatment. Records for 65 patients treated with first-premolar extractions were examined at 15 years (post-treatment) and 30 years (10 years post-retention). In the post-treatment period, irregularity increased from 1.73 mm to 4.63 mm (2.9 mm over 15 years); however, there was a great deal of variation in the sample. Satisfactory alignment (II < 3.5 mm) was found in less than 30% of the subjects post-retention. A follow-up study10 evaluated irregularity changes after the 10-year post-retention period, to determine if additional changes occurred with time. Thirty-one cases from the original study were further evaluated at 43 years, approximately 20 years post-retention. During the first follow-up period mandibular irregularity increased 3.59 mm over 15 years. This irregularity continued to increase with time, but to a much smaller extent during the second 11 follow-up period (0.77 mm over 13 years). Satisfactory alignment (<3.5mm) declined to 10% at 20 years. These two studies highlight the process of ongoing changes in the dentition after treatment. Changes may be due to treatment-related relapse or growth-related changes, which are confounded. However, because post-treatment records were collected a considerable period after treatment was discontinued (i.e., 10-20 years), it is unlikely that such changes were related to treatment alone. Because changes in irregularity diminished with time, this suggests that crowding could be related to facial growth, which also decreases over time. This has been discussed in other treated studies.21 Many other longitudinal studies have evaluated posttreatment dental changes in treated individuals. Amalgamated data shows increases in TSALD and II of approximately 0.12 mm/yr and 0.10 mm/yr, respectively (Table 1.2). When the data are plotted it appears that changes in crowding decrease over time (Figure 1.4). Although some studies show variations from this trend, treated patients generally appear to follow similar tendencies as untreated individuals. Therefore, research comparisons of crowding between treated and untreated groups is necessary and valuable. 12 Figure 1.4. Changes in crowding with age in treated subjects. 13 Dugoni et al, 1995 Ferris et al, 2005 Sadowsky et al, 1994 Paquette et al, 1992 Elms et al, 1996 Rossouw et al, 1999 Luppanapornlarp et al, 1993 Glenn et al, 1987 Moussa et al, 1995 Yavari et al, 2000 TOTAL EXTRACTION Haruki & Little, 1998 Paquette et al, 1992 Boese, 1980 Luppanapornlarp et al, 1993 Rossouw et al, 1999 Harris & Vaden, 1994 Little et al, 1981 Driscoll-Gilliland et al, 2001 Vaden et al, 1997 McReynolds & Little, 1990 McReynolds & Little, 1990 Little et al, 1988 Boley et al, 2003 Haruki & Little, 1998 Vaden et al, 1997 Little et al, 1988 Harris & Vaden, 1994 TOTAL NON-EXTRACTION I/II NS I/II NS I/II/III NS I/II 28 55 55 355 36 33 40 33 39 44 65 I/II/III I/II I/II NS I I/II I/II/III NS NS - 43 36 14 32 31 32 47 36 31 30 622 I/II NS I/II NS II - 29 25 20 22 30 42 49 NS 72% F 79% F 81% F NS NS - 75% F 79% F 81% F 63% F NS 63% F 51% F 62% F Comb PP Comb PP Comb PP - Comb Comb PP PP NS PP Comb Uni Comb Uni PP PP PP PP - 75% F 61% F 75% F Uni PP PP PP Uni PP NS NS 71% F NS - F F F F F F Site 54% F 68% 55% 73% 37% 81% 63% Sex Sample features Angle Class I/II I/II I/II NS II I/II/III N 14 15.5 15.5 16.3 21.6 30.4 32.2 17.4 15.3 15.3 15.3 15.2 14.9 15.1 15.2 14.8 14.4 14.4 14.5 14.8 15.7 16.5 14.62 14.8 13.6 13.7 13.9 14.2 14.5 14.5 PostTx Age (yrs) TABLE 1.2. Crowding in treated samples 30.4 31.6 32.0 30.5 43.3 36.2 29.3 31.9 29.8 21.6 28.9 20.9 21.7 30.1 30.2 30.6 28.8 20.1 26.6 22.0 28.2 26.14 30.1 27.9 24.3 28.6 28.7 23.1 21.9 PostRt Age (yrs) 14.9 16.1 15.7 8.9 12.9 4.1 11.9 16.7 14.5 6.3 13.7 6.0 6.6 14.9 15.4 16.2 14.4 5.6 11.8 6.3 11.7 11.52 15.3 14.3 10.6 14.7 14.5 8.6 7.4 Δ Age (yrs) +3.59 +0.7 +2.75 +0.81 +0.77 +0.34 +1.60 +2.6 +2.0 +0.58 +1.3 +1.2 +0.55 +2.9 +2.6 +1.53 +2.4 +0.62 +1.2 +0.8 0.0 +1.40 +3.1 +1.61 +1.11 +1.4 +3.0 +0.4 +1.4 Δ II (mm) +0.24 +0.04 +0.18 +0.09 +0.06 +0.08 +0.13 +0.16 +0.14 +0.09 +0.10 +0.2 +0.08 +0.19 +0.17 +0.09 +0.17 +0.11 +0.10 +0.13 0.0 +0.12 +0.20 +0.11 +0.10 +0.10 +0.20 +0.05 +0.19 Δ II/yr (mm/yr) -2.35 - - - -1.0 - -3.7 +0.5 - -1.90 -2.6 -1.81 +0.3 - Δ TSALD (mm) -0.17 - - - -0.09 - -0.24 +0.03 - -0.22 -0.17 -0.17 +0.02 - Δ TSALD/yr (mm/yr) I/II II - 604 125 334 189 1252 TOTAL (PP) TOTAL (Uni) TOTAL (Comb) TOTAL (NS) TOTAL (All) - 83% F 58% F - 69% F 63% F 83% F - 84% E 47% E - NS 56% E 84% E Ext - PP Comb - NS NS PP Site 16.7 14.6 19.2 15.5 16.9 21.5 31.1 19.9 17.9 14.7 14.2 PostTx Age (yrs) 27.4 29.5 34.2 27.9 29.4 37.2 45.1 36.3 47.4 21.5 30.3 PostRt Age (yrs) 10.7 14.9 15.0 12.4 12.5 15.6 14.0 16.4 29.5 6.7 16.1 Δ Age (yrs) +0.86 +2.78 +2.38 +1.45 +1.55 +0.85 +2.86 +1.68 +1.93 +1.28 +1.50 Δ II (mm) +0.08 +0.19 +0.16 +0.16 +0.12 +0.06 +0.20 +0.12 +0.07 +0.19 +0.09 Δ II/yr (mm/yr) -1.41 -1.38 -1.60 -1.42 -1.60 -1.60 - Δ TSALD (mm) -0.13 -0.09 -0.05 -0.10 -0.05 -0.05 - Δ TSALD/yr (mm/yr) 15 *Tx = treatment; Rt = retention; NS = not specified; II = Incisor Irregularity; TSALD = tooth-size-arch-lengthdiscrepancy; PP = Private practice; Uni = University setting; Comb = Combination of Private practice and University setting - I/II 45 78 275 88 13 I/II/III 51 Sex Sample features Angle Class I/II EXTRACTION/ NON-EXTRACTION Park et al, 2010 Rossouw et al, 1993 Carter & McNamara, 1998 Park et al, 2010 Artun et al, 1996 TOTAL N TABLE 1.2 (continued). Crowding in treated samples COMPARISONS OF CROWDING IN TREATED AND UNTREATED INDIVIDUALS As mentioned above, treated and untreated subjects follow a similar trend in terms of age-related crowding. Annualized changes in irregularity and TSALD are comparable in both groups (Table 1.3 and Figure 1.5), implying that post-treatment crowding is not necessarily related to treatment itself, but to normal physiological changes such as growth.17 Table 1.3. Summarized data for treated and untreated samples N Δ Age (yrs) Δ II (mm) Δ II/yr (mm/yr) Δ TSALD (mm) -1.39 -1.07 Δ TSALD/yr (mm/yr) -0.17 -0.13 TOTAL (UnTx) 690 12.5 +1.13 +0.09 TOTAL (All Tx) 1252 12.5 +1.55 +0.12 TOTAL (Non355 11.5 +1.40 +0.12 -1.37 -0.11 exo) TOTAL (Exo) 622 11.9 +1.60 +0.13 -1.40 -0.10 TOTAL (PP) 604 10.7 +0.86 +0.08 -1.41 -0.13 TOTAL (Uni) 125 14.9 +2.78 +0.19 -1.38 -0.09 TOTAL (Comb) 334 15.0 +2.38 +0.16 TOTAL (NS) 189 12.4 +1.45 +0.16 -1.60 -0.05 *Tx = treatment; Rt = retention; NS = not specified; II = Incisor Irregularity; TSALD = tooth-size-arch-length-discrepancy; PP = Private practice; Uni = University setting; Comb = Combination of Private practice and University setting; NS = Not specified 16 Figure 1.5. Changes in crowding with age in treated and untreated subjects. A study by Carter and McNamara16 evaluated changes in crowding among 82 treated and untreated subjects from the Michigan Growth Study. Three groups were compared, including an untreated sample followed from 14 to 48 years, an untreated adult sample followed from 32 to 45 years, and a treated sample followed from 18 to 47 years. Summarized changes in arch perimeter and irregularity are shown in Table 1.4. Although the untreated adult and treated sample sizes were small, and no statistical comparisons were made between groups, similar annualized perimeter loss and irregularity increases were found, except during puberty. In contrast, the untreated sample showed much higher rates of increase during puberty. Unfortunately, a treated pubertal group was not available for comparison. 17 Table 1.4. Summary of rates for arch perimeter (AP) and incisor irregularity (II) change Untreated (n=53) Δ AP (mm) Δ AP/year (mm/yr) Δ II (mm) Δ II/year (mm/yr) Untreated Adult (n=10) Treated (n=13) Pubertal Adult 1.29 2.06 0.51 1.60 0.40 0.07 0.04 0.05 0.47 1.59 0.48 1.93 0.16 0.05 0.04 0.07 *AP = arch perimeter, II = Incisor Irregularity A study by Driscoll-Gilliland et al.17 also compared treated and untreated patients to evaluate changes in growth and crowding during the late adolescent and early adulthood periods. Fourty-four untreated subjects from the Bolton Growth Study and 43 extraction patients treated in private practice were analyzed during adolescence and early adulthood. Superimpositions were used to measure skeletal and dental changes, while contact irregularity, space irregularity, and TSALD were measured from models. Due to age differences between the samples, annualized changes were used for comparison. Over time, both samples showed significant changes (1-1.5 mm) in contact irregularity, space irregularity, and TSALD. These changes were similar in treated and untreated individuals, except for TSALD which was significantly greater (0.10 mm) in the untreated 18 group. Thus, supporting the hypothesis that changes in crowding are generally similar, regardless of treatment. In a study by Jonsson and Magnusson,40 the prevalence of dental crowding and spacing was compared longitudinally among 58 treated and 250 untreated subjects, from 12 to 38 years. According to their findings, lower anterior crowding increased significantly among both treated and untreated subjects. No differences were found between groups at either time point. However, changes in crowding prevalence were significant between treated subjects and untreated subjects. This disparity related specifically to the non-extraction group, which increased 8.7% more than the untreated group. In adulthood, those treated on a non- extraction basis were 17.7% more likely to have crowding (≥2 mm) than those treated with extractions. This difference was significant. These three studies support other longitudinal data (Table 1.3 and Figure 1.5), showing that differences between treated and untreated groups are small. Any differences appear to be based more on the age period studied, and the amount of growth that occurred, than treatment itself. Although extraction of teeth during treatment may affect stability (as shown by Jonsson and Magnusson40), other articles have found no such differences. 19 PART II - ETIOLOGY OF CROWDING Determining the specific factors that contribute to crowding is challenging, as correlation coefficients are typically weak. Therefore, it seems reasonable to assume that crowding is the result of many interacting factors.39,41 Commonly reported factors are described below, under the headings of treatment factors and non-treatment factors. TREATMENT FACTORS Studies have examined an assortment of treatment variables in hopes of finding the cause(s) for relapse and crowding post-treatment. However, these factors fail to explain a significant amount of the variation in posttreatment crowding. Most studies have not been able to link treatment with post-treatment changes,42,43 while those that have were not related to post-retention crowding.23,39,44 Relationships between pre- and post-treatment dental characteristics with relapse do not appear to show consistent relations either.39,45 In the 1981 study by Little et al.39 mentioned previously, dental casts of 65 patients treated with first premolar extractions were investigated for potential causes of post-retention mandibular crowding. 20 A wide variation in crowding was found, and the researchers were unable to predict future crowding based on dental changes during treatment. Angle classification, sex, length of retention, and age also failed to explain changes in crowding. Significant, but weak to moderate correlations, were found between post-retention irregularity and post-treatment arch length decreases (r=0.52), changes in arch width (r=0.38), overjet (r=0.26), and overbite (r=0.46). They concluded that neither single nor multiple dental factors were able to accurately predict crowding after treatment. A follow-up study by Shields et al.23 evaluated cephalometric variables for 54 patients in relation to post-retention crowding using a comparable sample of first premolar extracted cases. Similar findings in terms of a lack of predictive ability for post-retention crowding was found for cephalometric changes during the treatment period. No cephalometric changes were able to significantly predict irregularity or arch length changes. Mellion41 also had similar findings in his Master’s thesis. Several commonly cited causes of relapse (treatment change in IMPA, axial inclination of the buccal teeth, irregularity, maxillary and mandibular intercanine width, maxillary growth, and differential mandibular growth) were evaluated, and five significant multiple 21 regression equations were found. Each of these equations showed low correlation coefficients (r=0.32-0.48), suggesting that alone or together, treatment factors are responsible for a relatively small portion of crowding. Other treatment related factors, such as extraction versus non-extraction,46-51 or timing of extraction,44,52 do not show a significant effect on long-term crowding, although Haruki and Little53 found a significant relation between serial extractions and improved long-term alignment. The experience of the clinician has also been implicated in affecting relapse. Although studies from the University of Washington10,19,50,53 and Saint Louis University46,47 show poor long-term success rates, the majority of published literature from cases treated in private practices shows more acceptable post-treatment stability.21,54,55 Based on amalgamated data from longitudinal studies (Table 1.2), subjects treated in a university setting show larger long-term changes in II (0.19 mm/year) than subjects treated in private practice (0.08 mm/year). Although variation exists from site to site and clinician to clinician, it is possible that relapse in university patients is higher because they may be treated by multiple practitioners.21 22 However, conventional wisdom tells us that maintenance of arch width, especially in the canine region,39,51,56-59 preservation of arch length,60 and control of incisor position23,61,62 are important factors in the long-term stability of treatment. Although these have become basic tenets for treatment, the correlations are no stronger than for other factors. These tenets are discussed below in relation to soft tissue treatment boundaries. SOFT TISSUE TREATMENT BOUNDARIES The shape of the arches and tooth positions can be defined relative to an envelope of muscular function. In 1949, Strang56 suggested that if muscular forces were violated by arch width increases at the canines or molars, orthodontic treatment would be unstable. He applied this concept of arch width maintenance in clinical practice, and found that his treated cases remained stable despite a lack of retention. The “equilibrium theory,” as described by Weinstein et al.,63 maintains that tooth position is dictated by a balance between the musculature of the lips and cheeks, and that of the tongue (Figure 2.1, 2.2). For that reason, displacement of teeth outside of this region might be expected to result in relapse back to the area of stability. 23 Figure 2.1. Soft tissue envelope (saggital view). Adapted from Profitt.64 Figure 2.2. Soft tissue envelope (frontal view). Adapted from Proffit.1 Various studies by Weinstein et al.63 show that tooth movements occur if this equilibrium is disrupted. For instance, in eight patients planned to receive orthodontic extraction of four bicuspids, two bicuspids were randomly assigned to receive a 2 mm thick gold onlay on either the buccal or lingual surface. These were compared to the other two bicuspids, which were undisturbed. After relief of the proximal and occlusal contacts, these teeth were allowed to move freely for eight weeks, and observed at weekly intervals. A mean movement of 0.48 mm was found for 24 onlayed teeth, while the control teeth remained relatively stable. Probably the best source on changes in intercanine width (ICW) after treatment is a meta-analysis by Burke et al.65 In this review they examined a total of 1,233 subjects drawn from 26 studies. at three time points: and long-term. Individuals were examined before treatment, after treatment, Mean changes in ICW ranged from +0.81 to +2.02 mm during treatment and -1.00 to -1.60 mm posttreatment (0.5 to 12 years post-retention). Although there were inconsistencies in retention protocol and follow-up duration between studies, increases in intercanine width during treatment were generally unstable in retention. They suggest that changes in intercanine width in the range of 1 mm are maintainable, while changes greater than 1 mm tend to return to pre-treatment values. One drawback of such a study is that there was no long-term control for comparison. Thus it is difficult to ascertain whether post-treatment changes are related to treatment or growth. Data for untreated individuals from the University of Michigan Growth Studies66 shows relatively mild decreases (0.33 mm) in ICW for males and larger decreases (1.73 mm) for females between 12 and 18 years. Other long-term untreated studies show various changes in ICW, ranging from 25 significant decreases of 1.04 mm from 13 to 43 years and 0.82 mm from 36 to 69 years,67 to non-significant increases of approximately 0.14 mm between 20 and 54 years.68 The variety of changes in ICW could be due to differences in sample size and demographics. The soft tissue equilibrium also applies to the anteroposterior dimension. As such, we would expect proclination or retroclination of the incisors to result in relapse. This is relevant because proclination could be an undesirable consequence of attempts to increase arch length. A study by Mills61 looked at deliberate proclination of the lower incisors during treatment to determine the long-term position of incisors after discontinuation of retention. A sample of 56 cases which had received a minimum of five degrees of incisor proclination relative to the mandibular plane (Go-Me), was compared to an untreated control group of 47 cases. Cases were divided into two groups based on proclination of less than 10 degrees (Group A, mean 7.23 degrees), and 10 degrees or more (Group B, mean 14.4 degrees). After one year post-retention, Group A retained 4.8 degrees of proclination and Group B retained 8.6 degrees of proclination. Although this study was limited by its short-term follow-up, it shows that at least some 26 retroclination occurs post-retention, while a limited amount of proclination may be stable post-treatment. NON-TREATMENT FACTORS As long as basic tenets of treatment are followed, treatment does not appear to greatly affect the amount of post-treatment relapse.15,55 This is supported by similar annual changes in crowding for both treated and untreated individuals. Therefore, non-treatment factors such as physiological changes must be the major players in crowding. Many biologic factors can contribute to the movement of teeth. As they move, adjacent contact areas may displace from one another, resulting in a shift of teeth into malalignment. Contributing factors can be categorized as susceptibilities, indirect causes, and predisposing factors. These variables are shown in diagrammatic form (Figure 2.3), and discussed in the text that follows. 27 Figure 2.3. 28 The progression of malalignment. SUSCEPTIBILITIES RACE A review of the National Health and Nutrition Survey III by Buschang and Shulman20 evaluated incisor irregularity among whites, blacks, and Mexican-Americans based on a sample of 9044 subjects. They found significant differences in mean irregularity between races, with Mexican-Americans having the largest irregularity (3.97 mm), followed by whites (3.77 mm), and then blacks (2.83 mm). As will be explained later, tooth size is a contributing factor to crowding. Therefore, racial variations in tooth size could also be an important contributor to crowding. A study by Smith et al.69 investigated tooth size variations among 180 pre-treatment casts divided equally between black, white, and MexicanAmerican subjects. Although there were no significant differences between black and Mexican-American subjects (other than for larger mandibular posterior teeth in blacks), whites had significantly smaller teeth than both groups. These ranged from 3.6-4.8 mm smaller for whites in the lower arch. Racial differences and individual variation in arch form are also evident.70-74 And as will be discussed later, 29 narrower arch widths appear to be a predisposing factor for crowding. Several studies have shown that whites have significantly smaller arch widths and larger arch depths than Israelis70 and Japanese,71 larger arch widths than Egyptians,72 and smaller arch widths but similar arch depths than Koreans.73 However, at the time this review was written no comparisons for arch sizes between blacks and Mexican-Americans could be found. This would be useful in explaining why these racial groups have similar tooth sizes, but blacks have less crowding. SEX Arch form is also affected by sex.75 On average, men are generally larger than women,76 and tend to have larger arches than females.66,68,77,78 teeth than women.69,79,80 Men also generally have larger For example, Smith et al.69 showed that mandibular arch lengths were significantly larger for males than females for anterior and posterior tooth widths. This amounted to a total tooth size excess in the lower arch of 3.0 mm for males. Similarly, Howe et al.80 demonstrated that males had 2.5-3.5 mm larger total tooth widths, and 0.1-0.6 mm larger individual tooth widths than females, for the mandibular arch. differences were not significant. 30 However, these Conflicting literature makes it difficult to determine whether one sex has more crowding than the other. Increased crowding in males16,34 and no sex differences17,18,48,67,81 have both been described. In a sample of 50 white subjects age 18-29, Shah34 found larger crowding in males than females (II 1.6 mm, TSALD 0.31 mm), although this did not reach significance (p=0.06). Similarly, Bernabé and Flores-Mir82 evaluated a sample of 200 randomly selected Peruvian schoolchildren between 12 and 16 years, and found higher TSALD and II in males; they also did not find significant differences between sexes. Extensive population data from the NHANES III study demonstrates that men have significantly more crowding than women (0.52 mm); males have 13% greater odds of having crowding.20 Therefore, if sexual differences exist they are likely small and can only be appreciated by using an extremely large sample. AGE Teeth aligned during orthodontic treatment frequently show crowding during the post-retention period, but irregularity is also present among untreated individuals. Horowitz and Hixon83 alluded to the possibility that orthodontics could temporarily alter the physiological 31 changes, which resume upon completion of treatment. This fosters the idea that crowding may be related to growth. Buschang and Shulman20 have shown that irregularity increases in a curvilinear fashion with age in untreated subjects (Figure 1.2). These increases are greatest during the adolescent period and slow after early adulthood. Other studies show similar trends. Park et al.84 investigated long-term post-treatment occlusal and arch changes and consistently found larger decreases in arch length (0.14 mm) and greater increases in mandibular irregularity (0.65 mm) and PAR index (1.06) for adolescents than for adults. Harris and Vaden54 found lower post- treatment increases in irregularity among adults (0.21 mm), although these differences were not significant. In addition, Little et al.10 reported that although the postretention Irregularity Index continued to increase over time, increases were lower during late adulthood, compared to early adulthood. Several other studies discuss the possibility of a relation between post-treatment crowding and growth.21,24,57,85,86 32 INDIRECT CAUSES TOOTH SIZE AND SHAPE Tooth size is determined by many factors, including genetics, sex, race, and secular trends,87 and it has been suggested that larger teeth are more likely to be crowded.32,87 In a study by Puri et al.,87 forty mandibular dental casts from untreated subjects were classified as normal (+3 to -3mm), crowded (<-3mm), or spaced (>+3mm) based on TSALD. Measurements for arch perimeter and mesiodistal tooth sizes were recorded. Tooth widths were summed for the total, anterior (2-2) and posterior (3-5) segments. Generally, all groups showed significant differences in size for individual teeth and each arch segment. They concluded that spaced arches had smaller teeth and crowded arches had larger teeth. A multivariate study by Bernabé and Flores-Mir32 also evaluated crowding and tooth morphology. Two-hundred untreated children age 12-16 were randomly selected. Subjects were classified as having no, mild, or moderate crowding based on TSALD. For each individual, mesiodistal (MD) and buccolingual (BL) widths were measured, and MD/BL ratios were calculated for each teeth. Statistically significant differences in MD, but not BL, tooth size were found between the three crowding groups. 33 The lower first and second premolars and the lower central incisor contributed most to these variations. Those with moderate crowding also had larger MD/BL crown proportions than those with no crowding. In contrast, diminutive or missing teeth should create space to resolve crowding. For example, Buschang and Shulman20 found significant reductions in irregularity, and decreases in the odds ratio, as the number of missing posterior teeth increased. Surprisingly, significant increases in crowding occurred when third molars were missing. THIRD MOLARS There has been much discussion in the literature in terms of a potential relation between crowding and third molars. A survey conducted by Laskin in 1971 found that 65% of orthodontists and oral surgeons believed that third molars could occasionally cause crowding.88 It was thought that the force of eruption of third molars may constitute a mesially directed “push” against the neighboring dentition, leading to a loss of arch length. There is some literature to support this concept.89-91 However, the great majority of research supports the idea that third molars have no significant effect upon 34 crowding.92-99 One of the most cited studies relating third molars with crowding is that of Kaplan.99 He investigated seventy-five orthodontically treated patients divided among three groups: those with bilaterally erupted (n=30), bilaterally impacted (n=20), and bilateral agenesis (n=25) of third molars. Model analysis and cephalometric superimpositions provided information on arch width, arch length, lower incisor irregularity, lower incisor rotations, incisor angulation and position, and molar position. Crowding increased in all groups, and no significant differences were found between groups for any measures, more than 9 years post-retention. An epidemiological study of 9044 individuals by Buschang and Shulman20 also showed that erupted third molars do not appear to affect crowding. In fact, there was a greater likelihood of crowding if the third molars were not present. In a prospective randomized controlled study, Harradine and others95 also could not find any significant statistical or clinical relationship between the presence of third molars and crowding. In their study, 164 adolescent patients (14.8 years of age) were randomized to have either removal or retention of third molars. 5.5 years, 47% of patients presented for follow-up. After 35 Dental casts were collected before and after treatment and changes in irregularity (II), intercanine width (ICW), and arch length were compared between the two groups. The removal group demonstrated 1.0 mm less arch length compared to the retained group; however, there were no statistical differences in ICW or II. They concluded that there was insufficient support for the removal of third molars in order to prevent crowding. PERIODONTAL AND GINGIVAL FIBERS Reitan100 was the first to relate periodontal fibers and orthodontic relapse. By studying relapse in dogs, he found alterations in the supracrestal periodontal fibers after tooth rotation. It was later shown by Edwards,101 using tattoo markings on the attached gingiva, that reorganization of the tissue did not occur during orthodontic treatment. The current thinking is that stretching of the transseptal fibers creates a tendency for relapse as they recoil after orthodontic completion.15 These fibers can take up to 232 days to remodel,100 thus leading credence to the circumferential supracrestal fiberotomy technique (CSF). In fact, a prospective evaluation of CSF showed that this procedure was effective in reducing rotational 36 relapse in cases with significant initial irregularity.102 However, the procedure is less effective in preventing relapse in the mandibular anterior region,102 suggesting that periodontal fiber relapse may play only a small part in mandibular anterior crowding. The periodontal fibers are also important for mesial migration of teeth, also known as approximal drift.103,104 A split-mouth study by Picton and Moss103 examined this process in nine adult macaca monkeys. In the treatment group, interproximal tissue was traumatized by either scraping or using a scalpel to cut it to the level of bone every two weeks. In the control group, the tissue was either left untraumatized or the papillae was removed. A diamond disc was used to create space between neighboring teeth, and this was reopened at two week intervals with further disking if it had closed. To measure the amount of migration, the distance between amalgam fillings placed in the cheek teeth was measured at each follow-up visit using occlusal radiographs. In cases with either no trauma or papillectomies, they found that teeth reapproximated, while in cases with trauma to the interproximal periodontium, the teeth showed a marked reduction in reapproximation. Differences in total drift and rates of drift (micrometers per week) were statistically significant. 37 No differences were found between the control or papillectomy, or scraping versus cutting groups. This study supports the contribution of transseptal fibers to mesial drift. ANTERIOR COMPONENT OF FORCE In 1923, Stallard speculated that the malalignment of teeth was related to drift of the buccal segments toward the front of the mouth.105 He felt that the force of occlusion was dispersed during chewing by mesial tipping of the posterior teeth. As these teeth incline further forward they create a force, directed through the interproximal contacts, toward the front of the mouth (Figure 2.4).94 It was suggested that this anterior component of force (ACF) could result in mesial drift and consequent malalignment of the teeth. Two studies by Southard and coworkers help to substantiate this proposition.94,106 In the first study,94 the anterior force generated at each interproximal contact was determined using a dental matrix strip that was placed interproximally and withdrawn. A single known axial force (20 lbs) at the left second molars was used for each individual, and this was repeated for 15 subjects during biting and at rest. They confirmed the existence of an anteriorly directed force that dissipates exponentially 38 toward the front of the mouth. This force was higher during biting than rest, did not progress past any open contacts, and was reduced after it passed the contact between the lateral incisor and the canine (Figure 2.5). The force was also found to cross the midline up to the contact of the contralateral canine in some cases. In the second study,106 three groups of five subjects were selected based on their initial irregularity index. Group A had <2 mm irregularity, Group B 2-4 mm, and Group C >4 mm. Interproximal force recordings were made for each of these subjects at rest and during biting, as in the previous study. Significant correlations were found between irregularity and both the ACF and resting interproximal forces. Thus, the ACF theory helps explain why decreases in arch length and increases in malalignment (especially at the lateral incisor/canine region) occur over time. Figure 2.4. Anterior component of force (saggital view). 39 Adapted from Southard et al.94 Figure 2.5. Anterior component of force (occlusal view). Adapted from Southard et al.106 In a recent thesis by Myser et al.,107 interproximal restorations were also found to increase the amount of crowding. This is thought to be due to the creation of a “tight” contact, which may also result in an anterior component of force. This may be related to age, as the number and extent of filled surfaces generally increases over time. Finally, Sanin and Savara108 suggested that the axial inclinations of the molars and incisors were major contributors to the development of crowding. Among 150 children examined at 8 and 14 years of age, those with the worst prognosis for alignment tended to have more upright lower incisors and more mesially inclined first molars (Figure 2.6). In contrast, children with the most favorable prognosis had labially inclined incisors and 40 distally inclined first molars. These angulations may help resist the ACF. Figure 2.6. Stability in relation to dental angulation to the mandibular plane. Adapted from Sanin and Savara.108 However, Picton and Moss109 could not find any relation between root angulation and the rate or amount of mesial drift. In their investigation, tooth movement was assessed over a period of six to eight weeks by measuring the distance between two amalgam fillings. They evaluated 70 pairs of cheek teeth in nine adult macaca monkeys. Root angulation was estimated by averaging the angle of the roots to the occlusal plane for each tooth. Three scenarios were compared: migration in normal occlusion, 41 migration in normal occlusion with interproximal tissue trauma, and migration without occlusal contact (i.e., opposing teeth extracted). When the data was compared, no discernable relationship could be found between root angulation and the direction or amount of migration. PRIMARY TOOTH LOSS, ERUPTION SEQUENCE Premature loss of a primary tooth can be cause for concern if space is not maintained.110-112 This is because teeth drift toward the front of the mouth due to the anterior component of force94 and transseptal fiber pull.103 As teeth move forward, arch length is lost and there may be insufficient space for the permanent dentition to erupt.1 Northway and coworkers111 assessed the consequences of early loss of primary molars in dental casts of 107 children, evaluated annually between 6 and 12 years of age. Children were classified into two groups: mutilated, based on either severe caries and/or early tooth loss; or control, based on restorations and/or lack of (or mild) caries. The mutilated group was further divided based on which primary teeth were affected. After analysis, a large difference was found in space loss between the mutilated and control groups, which was significant at all time 42 points. Compared to the controls, early loss of a first primary molar (D) resulted in 3.3 mm more space loss, loss of a second primary molar (E) resulted in 2.6 mm more loss, and loss of both the D and E resulted in 3.6 mm greater loss; severe caries resulted in 2.1 mm greater loss. No association was found between the age of tooth loss and the total amount of space lost, but in all groups the majority of space was lost during the first year. In addition, early loss of the E had a significant effect on the occlusion, often resulting in mesiocclusion. Studies such as this explain why space maintenance has become an established treatment guideline for any lapse in permanent tooth eruption of more than 6 months after the deciduous tooth has been lost.1,112 Eruption sequence may also contribute to crowding if it promotes a loss of arch length. Changes in eruption sequence can occur due to localized alterations in bone density, tissue thickness, primary tooth resorption rates, ankylosis, or early loss of primary teeth through caries or infection.111,113 Lo and Moyers113 found that 17 different eruption sequences could occur in the mandible: almost half of the time the premolars erupt before the second molars, in the sequence 3 4 5 7; but, just under 20% of the time, the second molars erupt prior to the second bicuspid as 43 3 4 7 5. If the second primary molar has already been lost, this can result in mesial movement of the first molar and a decrease in arch length.1 This limits the amount of space available for the eruption of the second premolar, resulting in posterior arch crowding. Because literature relating eruption sequence to crowding is sparse, a recent thesis by Lange114 evaluated this topic. In her study, the eruption sequence of canines and premolars was evaluated in 28 patients using panoramic radiographs and correlated to dental arch measures (intermolar width, arch depth, and TSALD). Although a relatively small sample was used, she found that the lower arch had a more variable eruption sequence than the upper arch, and that the sequence 4 3 5 was related to significantly more crowding (2.5 mm) than the sequence 3 4 5. PREDISPOSING FACTORS ARCH FORM Since the dimensions of the arch affect the amount of space for the teeth to align, variations in arch form might be expected to be associated with crowding.107,108 It is well established that decreases in mandibular arch length, width, and depth occur over time;54,75,84 however, it is 44 unknown whether crowding causes, or is the result of, these changes. Two studies support the notion that narrower arch widths predispose individuals to crowding. Howe and coworkers80 evaluated the contributions of tooth size and arch size to crowding. Fifty casts of patients with significant crowding were compared to 54 casts of patients without or with only minimal crowding. Measures of tooth size and arch width were made, while arch perimeter and area were estimated. Their results indicated no differences between crowded and uncrowded groups for individual or total tooth size, but significant differences for all arch dimensions (except arch perimeter in males). Similarly, Myser107 found that narrower intercanine arch widths related to post-retention crowding in 66 subjects evaluated 16 years post-treatment. Correlation coefficients were low between intercanine width and TSALD (r=0.275) but moderate between intercanine width and II (r=-0.371). Richardson,115 however, did not find a relation between crowding and intercanine arch width or skeletal jaw width among 55 individuals 13 to 18 years of age. Arch depth is also an important factor in crowding as shown by Bernabé and others.116 45 In their study, 300 randomly selected casts were divided into no (n=127), mild to moderate (≤5 mm) (n=122), and significant crowding (>5 mm)(n=51) groups. Measures for mesiodistal (MD) and buccolingual (BL) tooth width, tooth width ratio (MD/BL), intercanine width, intermolar width, and arch depth were made. After modeling with stepwise multiple discriminant analysis, eight variables were found to differentiate between the crowding groups. These included arch length; intermolar width; central incisor, lateral incisor, canine, second premolar, and first molar MD sizes; as well as canine MD/BL ratio. The total equation accounted for 51% of the variability in crowding. After arch depth was removed, the predictive ability of the equation dropped to 14%. Removal of intermolar width resulted in a further decrease to 8%. Thus, arch depth had the greatest ability to discriminate between the groups in this sample. POINT-TO-POINT CONTACTS Tooth contacts areas, or proximal contacts, are the areas where a tooth crown contacts a neighbouring tooth. This corresponds with the area of greatest surface contour, known as the height of contour.117 They start initially as point contacts, and as teeth move during function, undergo surface wear. As the contact size broadens, they become 46 contact areas.117 Contact areas are larger in the posterior due to more wear (due to heavier contacts) and also because the teeth are larger, with more surface area in contact. Begg118 and Corrucini119 showed that Australian aborigines have wear at the interproximal surfaces of their teeth, amounting to approximately 4-6 mm.119 Such wear is thought to stabilize the teeth and prevent the contacts from “slipping” past one another. Contacts may be between two convex surfaces, or between a concave and convex surface, as in worn aboriginal teeth. An investigation into the mechanics of crowding by Ihlow120 investigated these two contact types using a twodimensional plexiglass model representing 12 teeth of an arch. The arch model was compressed with a plexiglass rod affixed to weights, ranging from 1-5 Newtons, and the arch height was measured. averaged. This was repeated 15 times and Prior to weight application, both arch forms were similar, but after the addition of force the point contacts showed about twice as much displacement as the overlapping contacts. Although an in vitro study, this provides some credibility to the stabilizing nature of larger contacts. The concept of broad contacts has also been suggested by some clinicians who advocate reproximation of lower 47 anterior teeth toward the end of treatment to help prevent relapse.121 Alexander122 found that in Class I extraction cases followed from 15.2-32.2 years, individuals with interproximal reduction (IPR) of the lower incisors had 1.4 mm less irregularity at the end of treatment than those without IPR. Wang et al.123 also investigated the use of anterior tooth reproximation to reduce post-treatment crowding. One-hundred-and-twenty-nine patients with average age 13 years were divided into control (n=81) and experimental (n=48) groups. The experimental group received circumferential fiberotomy (CSF) on the anterior segments while the control group did not. Of those experimental patients, 23 had further treatment involving contact point reproximation. for up to two years. Hawley retainers were worn Two years after discontinuation of retention, dental casts were measured for crowding. They found that crowding was reduced by 21.6% in the experimental group, and that contact reproximation reduced crowding 6.56% more than CSF alone. FACIAL DIVERGENCE Vertical growth of the face is the result of many interacting components. Dental, skeletal, and soft tissue structures act in concert to affect development, and are 48 modifiable by environmental inputs.124 Adaptations have been linked to weak masticatory muscles, reduced orofacial airways,125-128 and/or variations in craniofacial anatomy.124,129,130 The vertical morphology of the skull may be described in terms of “facial divergence,”86,131 defined by the angle between the cranial base (sella-nasion) and the mandibular plane. This may be used to differentiate those who have small divergence (hypodivergence) from those with normal (normodivergence) or large divergence (hyperdivergence). In fact, Reidel132 classified SN-MP quantitatively based upon one standard deviation from the mean. However, sexual differences of the cranial base angle (N-S-Ba) suggest that the palatomandibular angle (PP-MP) may be a more reliable indicator of divergence.133,134 Other classification methods such as posterior to anterior facial height ratio (PFH:AFH),135 upper to lower face height ratio (UFH:LFH),136 and lower to total anterior face height (LFH:AFH)137 are also described in the literature. These ratios have been shown to relate significantly to angular measures (i.e., SN-MP and PP-MP), as well as to one another, ranging from low (r=0.143) to moderately high (r=0.873) correlations.138 49 The vertical pattern of growth is established at a young age and is surprisingly stable.133,135,139 For example, Bishara135 found approximately three-quarters (77%) of individuals maintained their vertical classification from 5 to 25.5 years. Jacob and Buschang138 had similar findings, with 75-86% of individuals maintaining the same classification from 10 to 15 years; however, 27-53% of individuals within a category may worsen. Of those that did not maintain their classification, it was exceedingly rare (< 3%) for an individual to change more than one category.135 Although the mandibular plane angle may increase in some individuals,140 a tendency toward mild closure is most common in all groups.133,141 Remodeling of the mandibular border tends to mask roughly half of any rotational changes.140 Of particular interest in this paper are those with a hyperdivergent facial type. These individuals are categorized from hypodivergent and normodivergent individuals by several phenotypic features, including a downward rotation of the posterior maxilla, backward inclination of the condylar head, short mandibular ramus, obtuse gonial angle, antegonial notching of the mandibular border, forward inclined symphysis, mandibular retrognathism, acute interincisal or intermolar angles, 50 long lower anterior face height, anterior open bite, straight mandibular canal curvature, and/or maxillary transverse deficiency.124,129,130,142 Hyperdivergence may relate to crowding by three potential relationships. They include secular trends, dentoalveolar instability, and compensatory rotational changes. These are discussed separately. SECULAR TRENDS Malocclusion is a modern phenomenon. Epidemiological studies have shown that early traditional populations generally had worn but acceptable occlusions, while a trend toward increased crowding and less tooth wear has occurred in modern civilizations.143,144 This shift mirrored urbanization, with soft diets consisting of processed foods, resulting in a decrease of masticatory forces.143,144 These changes have been swift, occurring within only a few generations.145 Begg118 thought that crowding in “preindustrial” populations (Australian aborigines) was alleviated by interproximal tooth wear through vigorous chewing of a hard diet. Forty years later, Begg’s sample was re-examined by Corrucini119 and the wear was found to be much lower, on the order of only a few millimeters per quadrant, an amount 51 Corrucini145 insufficient to compensate for crowding. theorized, based on comparisons of “preindustrial” and “industrial” groups among various ethnicities, that mastication is important for the development of muscle and bone mass of the face; a reduction of function could lead to craniofacial alterations, such as decreases in jaw size, and insufficient space for the teeth.143 This theory has been supported by various animal (primates,146-149 rats,150-157 ferrets,158 and minipigs159) and human145,160-164 studies. Changes in masticatory function have also been closely linked to skeletal divergence.160,165-176 Studies of “premodern” and “modern” Finnish skulls by Varrela160 have shown facial divergence to increase in recent years, theoretically due to a reduction in masticatory muscle strength associated with softer diets. Studies supporting this link have shown decreased bite force, reduced mechanical advantage (ratio of muscle length to lever length),171 reduced muscular efficiency, reduced muscle activity,172 and reduced muscle thickness and volume177 in hyperdivergent individuals. In fact, Garcia-Morales et al.171 showed that divergence accounted for almost a quarter (24.3%) of the morphological variance in function. Specifically, the importance of masseteric muscle function is supported by the literature.178,179 52 Increases in mandibular plane angle and other hyperdivergent features have been produced experimentally by resection of the masseteric muscles in Wistar rats.180 Finally, the significance of muscular development and function on skeletal divergence can be observed in nature. Individuals with muscular disorders such as Duchenne and myotonic muscular dystrophy,181 cerebral palsy,182,183 and spinal muscular atrophy168 show increased divergence, maxillary transverse deficiency, long lower anterior face heights, posterior tooth eruption, anterior open bites, and increased crowding. Because secular trends involve increases in both crowding and facial divergence, it is possible that they are related through the same environmental influences, such as musculoskeletal alterations. Although these trends are interesting from the viewpoint of studying changes in a population over time, they are less useful in studying associations at the level of the individual. DENTAL ERUPTION AND INSTABILITY During normal development, eruptive movements maintain teeth in a functional occlusion. This occlusion is a position of homeostasis between the forces of eruption and those that oppose it, such as biting and soft tissue forces 53 (i.e., lips, cheeks, tongue).184 Growth, especially pubertal spurts, creates space between the teeth and allows notable eruption to occur. For example, Buschang et al.185 found that dentoalveolar heights increased 2.1 to 4.2 mm (7.6-23.0%) from age 10 to 15 years, depending on the region. Peak eruption occurred at around 12 years.186 As growth slows into adulthood, teeth retain their eruptive potential and occlusal relations are maintained despite attritional tooth loss or further growth.184 A study by Slagsvold et al.184 investigated whether tooth eruption would occur if occlusal forces were removed. Pre-operative records (impressions, intraoral photographs, and lateral cephalograms) were collected for three adult cercopithecus monkeys, followed by cementation of a silver splint, meant to artificially create tooth separation in half of the mouth. After 8.5-11 months, splints were removed and progress records were collected. Final records were collected 2-3 months after splint removal. In all three monkeys, dental eruption re-established occlusion of the teeth (Figure 2.7). 54 Figure 2.7. Photographs showing maintenance of a functional occlusion. (A) initial, (B) after splint cementation, (C) 10.5 months later, (D) after splint removal, (E) 3 months later. Adapted from Slagsvold and Karlsen.184 This finding implies that even after growth levels subside, eruptive potential remains if teeth are taken out of occlusal contact. This eruptive potential is also obvious in humans when an antagonistic tooth is lost, and supraeruption of the opposing tooth occurs. Thus, eruption appears to maintain an efficient and functional chewing system. This notion has been described as the dentoalveolar compensatory mechanism by Solow187 and is supported by various articles.185,186,188 Nonetheless, Behrents,189 Bishara,190 and others191,192 have shown that facial growth continues far into adulthood, though at a slower rate, thus implying that facial dimensions are in no way static. These growth trends have been modeled by Björk and Helm193 (Figure 2.8). 55 Figure 2.8. Variations in growth rate. Adapted from Björk and Helm.193 Growth is particularly pronounced in the vertical dimension, which is the last dimension to be completed,10,16-21 increasing approximately two to four times as much as horizontal growth during the early adulthood period.24,25 Furthermore, growth continues longer in the mandible,194 because of the cephalocaudal gradient of growth.1 Therefore, one could expect that vertical changes in mandibular growth would have a significant effect on the dentition and that dental eruption could be related to the rate of vertical growth of the mandible. relation was found by Liu and Buschang.186 56 In fact, such a In a longitudinal study of 124 untreated females between 10 and 15 years of age, superimpositions of the cranial base and mandible were used to determine the amount of vertical mandibular growth and tooth eruption, respectively. Vertical mandibular growth and mandibular tooth eruption were found to have similar velocity curves, and mandibular molar and incisor eruption were found to be closely related to vertical mandibular displacement (Figure 2.9). In terms of dental compensations, 54% of the variation in lower molar eruption and 13% of the variation in lower incisor eruption were due to inferior growth displacement of the mandible. Figure 2.9. Velocity curves for tooth eruption between 10 and 15 years. (A) molar and (B) incisor; g = growth, e = eruption, L = lower, U = upper Adapted from Liu and Buschang.186 57 Having established that vertical growth and dental compensations are related, the next step is to look at variations in vertical growth. Discrepancies between anterior and posterior vertical growth bring about different facial proportions, known as facial divergence. The greater the divergence, the greater the space between the jaws anteriorly, and the further the incisors must travel to maintain occlusion.195 Thus dentoalveolar compensation would be greatest in hyperdivergent individuals and smallest in hypodivergent individuals.187 This relation is well established in the literature.134,180,195-198 Janson et al.195 evaluated the relationship between dentoalveolar height and facial divergence in 344 untreated Class I and II individuals at 12 years of age. Using the upper to lower anterior facial height ratio (UFH:LFH), subjects were classified as short, normal, or long facial types. Dentoalveolar heights were measured at the incisors and molars from the incisal or occlusal edges to the palatal and mandibular planes, and analyzed in relation to facial height. The alveolus was significantly larger in those with long lower facial heights and significantly smaller in those with short lower facial heights (Figure 2.10). Males also generally had greater dentoalveolar 58 heights than females. Moderate negative correlations were found between the facial height ratio and dentoalveolar heights, with larger coefficients for the upper (r=-0.43 (molar), r=-0.60 (incisor)) than the lower (r=-0.32 (molar), r=-0.49 (incisor)) dentition. Multiple regression revealed that the variation in lower face height was explained by 22% posterior and 41% anterior dentoalveolar compensation. These findings indicate that the vertical position of the incisors is more closely correlated to face height than the molars, especially for the upper arch. This data conflicts with other studies that show increased relation of the lower dentition to variations in facial height.185,196,197 This could be possible due to sampling, population characteristics, or the cross-sectional nature of this study. Figure 2.10. Relation between dentoalveolar height and facial height. UPDH = Upper posterior dental height; LPDH = Lower posterior dental height; UADH = Upper anterior dental height; LADH = Lower anterior dental height. Adapted from Janson et al.195 59 Enoki and coworkers134 also found significant positive correlations between lower anterior face height and dentoalveolar eruption. In their study, eighty 11-13 year old Class I skeletal individuals were divided into short, normal, and long lower face height groups based on the ratio of lower to anterior facial height (LFH:AFH). Dentoalveolar heights were measured from the incisors and molars to the palatal and mandibular planes, and these were analyzed in relation to lower anterior face height. Although there was a trend to increasing dentoalveolar heights with increasing lower anterior face height, significant differences were found only between the upper incisor region in long faced individuals, and the molar and lower incisor regions in short faced individuals. Correlations between lower face height and incisor heights were significant for all groups at the 0.001 level, while molar heights showed a trend toward significance. Interestingly, although the palatomandibular angle differed significantly between all groups (p<0.001), the mandibular plane angle showed no relations. Sampling, population characteristics, the cross-sectional nature of the study, and the lack of a large sample size may have resulted in a lack of significance between some groups in this study. 60 Beckmann et al.197 compared vertical dentoalveolar compensations between 460 untreated Caucasian adults with normal overbite divided into short, normal, and long lower anterior facial height groups. segregated by sex. These groups were also Dentoalveolar heights were measured from the midpoint of the base of the symphysis or hard palate to the incisal edge, using a line bisecting both the cementoenamel junction and the midpoint of the alveolus; while dentoalveolar width was measured perpendicular to the bisecting line, tangential to the incisor apices. In general, the researchers found significant differences in dentoalveolar heights and widths for both jaws; however, males did not show differences in arch depths. Incisor dentoalveolar heights showed strong correlations (r=0.70 and r=0.82, respectively) with lower face height, while dentoalveolar widths showed moderate to weak correlations (upper r=-0.25, lower r= -0.48). The palatomandibular angle differed significantly between the three groups, also having a high correlation to lower face height of r=0.78. This study supports a trend to shorter alveolar heights and greater widths in short-face individuals and larger heights and smaller widths in long-face individuals (Figure 2.11). 61 Figure 2.11. Cross-sectional views of the anterior alveolus in short, normal, and long-face individuals. Adapted from Beckmann et al.197 In a similar study by Kuitert et al.,196 vertical dentoalveolar compensations were compared between long and short face groups, separately for men and women. Records of 557 untreated Caucasian adults were collected and subdivided based on overbite (open, edge-edge, normal, deep) and lower anterior face height (short, normal, long). Similar to Beckmann’s study, measurements were then made for dentoalveolar heights and widths, except that widths were measured perpendicular to the bisecting line through either A point or B point and the lingual surface of the alveolus. In general, greater dentoalveolar heights and smaller dentoalveolar widths were found in the lower arch than the upper arch, regardless of facial type. The alveolus was also taller and narrower in individuals with longer face heights than in those with short face heights, 62 which were shorter and thicker. These differences all reached statistical significance at the p<.001 level. In both groups the lower incisor dentoalveolar heights explained 32-37% of the variation in overbite, while upper incisor dentoalveolar heights explained only 3-4% of the variation. This suggests that variations in the lower arch are more related to variations in facial height. Longitudinal evaluations of dentoalveolar changes in various facial divergence categories and studies utilizing measures of divergence other than anterior face height are lacking. However, the literature provides evidence of a relationship between dentoalveolar height and facial divergence, suggesting that the greater the facial height, the more the incisors erupt to compensate for changes in the occlusion. In addition, the greater the divergence, the greater the alveolus is in height and the thinner it is in width, especially in the lower arch. In summary, long- face (hyperdivergent) individuals demonstrate a tall and narrow dentoalveolar process with a steep mandibular plane angle, while short-face (hypodivergent) individuals, have a wider and shorter dentoalveolar process with a shallower mandibular plane angle. These morphologies are illustrated below in Figure 2.12. 63 Figure 2.12. Comparison of divergence morphologies. Adapted from Solow.187 In hyperdivergent individuals, dentoalveolar changes may be significant, and such variability in incisor position has been hypothesized to result in instability of the occlusion,22 potentially leading to crowding or irregularity.17,122 It is currently unknown whether such a tall and narrow alveolus provides less protection from functional and soft-tissue forces that could cause tooth movements. COMPENSATORY ROTATIONAL CHANGES As growth continues, the face can maintain or change its vertical proportions depending on whether the anterior 64 and posterior face grow equivalently or disproportionately. If the anterior and posterior face increase similarly, there is no rotational component. However, there is typically a discrepancy favoring the vertical growth of the condyle and ramus, as compared to vertical growth of the alveolus, and so the mandible frequently has a rotational component.199 These rotational tendencies can influence the direction of eruption of the teeth. Excessive posterior growth results in forward mandibular rotation, leading to a short facial type with greater molar eruption than incisor eruption. Insufficient posterior growth, however, results in backward mandibular rotation, leading to a long facial type with greater incisor eruption than molar eruption. As early as 1946, Tweed documented natural variations in mandibular incisor position associated with facial morphology.200 He found that displacements from an upright mandibular incisor position corresponded to differences in the mandibular plane angle, and recommended that for every degree the mandibular plane angle (FMA) exceeded the norm of 25 degrees, the lower incisors should be positioned a similar amount behind their norm of 90 degrees.201 This suggests that subjects with a hyperdivergent mandibular plane would have the lower incisors placed lingually to 65 their typical upright position. This would reduce the available arch length and contribute to dental crowding. Condylar growth direction also has a bearing on the direction of tooth eruption, as confirmed by Björk.202 This direction is unpredictable, varying as much as 42 degrees.192 By superimposing serial cephalograms he showed that condylar growth direction was related to anterior tooth position (Figure 2.13). Similar to Tweed’s observations, Björk and Skieller140 suggested that compensations in the direction of tooth eruption occur relative to rotational changes of the mandible. Individuals with average condylar growth direction showed a relatively stable position of the anterior teeth, while vertical and anterior condylar growth was related to forward eruption, and sagittal condylar growth was related to backward eruption. As such, individuals with hypodivergence should show increased protrusion of the incisors, while individuals with hyperdivergence should show a tendency towards retroclination. This relation is supported in the literature.77,203,204 Either extreme may relate to crowding. Those with an average mandibular plane should show less propensity to either trend, and should demonstrate less crowding. 66 Figure 2.13. Relation between facial divergence and tooth eruption. Adapted from Bjork.202 FACIAL DIVERGENCE AND CROWDING IN THE LITERATURE Although three potential relations between facial divergence and crowding have been provided, the literature relating divergence to crowding is sparse. Studies relating facial divergence to crowding are described below, and separated into cross-sectional and longitudinal studies as well as treated and untreated samples. CROSS-SECTIONAL STUDIES Untreated samples: A study by Nasby et al.204 evaluated differences in crowding between high and low divergence subjects. From a patient population of 150 high angle and 53 low angle subjects at the University of Minnesota, 20 subjects were randomly sorted to each group based upon mandibular plane to sella-nasion angle (±1 SD from Reidel’s mean). 67 Mean ages were 12.9 and 13.7 years, respectively. Models were analyzed for arch perimeter, arch depth, TSALD, and intermolar width; while cephalograms were used to compare lower incisor inclination. Although no statistical analyses were used, hyperdivergent subjects had an average of 1.5 mm more crowding than hypodivergent subjects. They also showed narrower intermolar widths (2.3mm less) and more upright incisors (5.9 degrees), both of which could contribute to crowding. However, the small sample size and lack of significance testing detract from the generalizability of the results. Insufficient details were provided as to the demographic composition of the sample. LONGITUDINAL STUDIES Untreated samples: Richardson24 evaluated the effect of facial morphology on lower arch crowding (TSALD) in 51 subjects evaluated at 13 (T1) and 18 years (T2). Lateral cephalograms were used to evaluate 11 linear and angular measures, and changes were assessed based on superimpositions. Model analysis included measures for both anterior and total TSALD. Total TSALD was significantly correlated with lower face height (r=-0.47) and PP-MPA (r=-0.61) in males at T1. Multiple regression for the pooled sample revealed a relation 68 between the T1 measurements and change in total TSALD for ramus height, mandibular body length, lower face height, and PP-MPA (R=0.60). Of these, PP-MPA contributed most to the regression formula. No significant relations were found for anterior TSALD and T1 measures. In terms of change in measures (T2-T1) and change in TSALD, significant relations were found only for anterior TSALD; these included gonial angle, PP-MPA, NSGn, and mandibular rotation (R=0.58). However, many variables were studied and so it is possible that some of the results (5%) could have been due to chance alone. Other shortcomings include a lack of description of the demographic and dental classification of the sample. Orthodontic treatment in the upper arch of some patients may have increased facial divergence via extrusion, thus confounding the results. Leighton and Hunter205 compared 88 individuals from the King’s College and the Burlington Growth Study at 8 (T1) and 14 years (T2). Subjects were segregated into spaced, moderately crowded (≤4 mm), and severely crowded (> 4mm) groups, and various skeletal measurements were evaluated at both time points. Allowances were made for magnification between the two samples. Significant differences were found for facial divergence between each of the crowding groups, including measures of SN-MP, SN-OP, and SN69 endognathion. Unfortunately, there was no discussion of the demographic breakdown of the sample, nor any description of how crowding was measured. Sakuda et al.24 evaluated 30 untreated subjects at ages 12 (T1), 14 (T2), and 17 (T3) to determine if crowding was related to changes in skeletal growth. Twenty-seven skeletal measures as well as dental irregularity (in both the anterior (3-3) and posterior (6-3) regions) were measured. In terms of the changes in anterior crowding and growth changes from T1-T3, facial divergence (PP-MPA and SN-MP) did not enter the multiple regression formula. However, multiple regression showed that facial divergence (PP-MPA) at T1 was significantly, but weakly, related to the change in anterior crowding for both the upper (r=+0.18) and lower (r=+0.24) arches. Using 25 sets of twins studied from age 12-15 to 23-26 years, Lundström203 evaluated the relationship between various skeletal and dental measures. Lateral cephalograms were superimposed and compared with an Adams blinkcomparator. No covariation was apparent between the direction of growth of gnathion or increases in lower crowding, although statistical analyses were not used. Unfortunately, this study also lacked a description of the 70 demographic composition and it was unclear how crowding was measured. Treated samples: Using 123 patients from the University of Washington, Fudalej and Årtun206 examined the association between posttreatment crowding and changes in facial divergence in various facial types. Subjects were segregated into short, average, and long facial heights based upon post-treatment SN-MP angle (≤28 o, 29o-37 o, and ≥37 o, respectively) and irregularity was measured for each group. Mean age was 15.8 years post-treatment (T1) and 31.9 years postretention (T2). No significant differences were found for irregularity or change in irregularity between the groups. However, moderate crowding (>5.0 mm) at T2 was found in 13.6% of hypodivergent, 28.6% of normodivergent, and 31.4% of hyperdivergent individuals. This was significant at the 0.05 level, supporting the idea of increased crowding with hyperdivergence. Although the groups were matched, they were heterogeneous (including various malocclusions and treatment types). In addition, irregularity was the only measure of crowding and the power to detect a difference of ≥1mm irregularity was just 62%. 71 Another study, by Zaher et al.,207 evaluated whether post-treatment changes varied between facial types in 66 Class II Division 1 subjects treated on a non-extraction basis. Cephalograms and models were collected pre- treatment (T1), post-treatment (T2), and a minimum of 2 years post-retention (T3). Subjects were classified as having either a short (n=20), average (n=26), or long face (n=20) based on posterior to anterior face height ratio (PFH:AFH), mandibular plane inclination to Frankfort horizontal (FMA), and mandibular plane inclination to sella-nasion (SN-MP). In case of disagreement between the measures, two clinicians evaluated Björk’s various facial structures to determine the appropriate category. No significant post-treatment skeletal changes occurred between groups, except for a significant decrease in the upper anterior facial height proportion. In terms of dental changes, there were no significant differences in arch widths or arch length over the post-treatment interval. Amounts and changes for total and anterior TSALD were not reported for either treatment or post-treatment intervals, therefore it is assumed that these measurements did not differ significantly between the three facial types. 72 STATEMENT OF THESIS Many studies have evaluated the causes of crowding, but it is presently unclear why some patients develop crowding and others do not. Comparisons of treated and untreated individuals show similar changes in terms of the amount and rate of crowding over time. growth as a potential causative factor. 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Dietary consistency and craniofacial development related to masticatory function in minipigs. J Craniofac Genet Dev Biol. 1997;17:96-102. 160. Varrela J. Dimensional variation of craniofacial structures in relation to changing masticatoryfunctional demands. Eur J Orthod. 1992;14:31-36. 161. Corruccini RS, Whitley LD. Occlusal variation in a rural Kentucky community. Am J Orthod. 1981;79:250262. 162. Corruccini RS, Potter RH. Genetic analysis of occlusal variation in twins. Am J Orthod. 1980;78:140-154. 163. Potter RH, Corruccini RS, Green LJ. Variance of occlusion traits in twins. J Craniofac Genet Dev Biol. 1981;1:217-227. 164. Corruccini RS, Kaul SS, Chopra SR, Karosas J, Larsen MD, Morrow C. Epidemiological survey of occlusion in North India. Br J Orthod. 1983;10:44-47. 88 165. Proffit WR, Fields HW. Occlusal forces in normal- and long-face children. J Dent Res. 1983;62:571-574. 166. Proffit WR, Fields HW, Nixon WL. Occlusal forces in normal- and long-face adults. 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Contributions of facial morphology, age, and gender to EMG activity under biting and resting conditions: a canonical correlation analysis. J Dent Res. 1995;74:1496-1500. 173. Ringqvist M. Isometric bite force and its relation to dimensions of the facial skeleton. Acta Odontol Scand. 1973;31:35-42. 174. Ingervall B, Helkimo E. Masticatory muscle force and facial morphology in man. Arch. Oral Biol. 1978;23:203-206. 175. Raadsheer MC, van Eijden TM, van Ginkel FC, PrahlAndersen B. Contribution of jaw muscle size and craniofacial morphology to human bite force magnitude. J Dent Res. 1999;78:31-42. 89 176. Kayukawa H. Malocclusion and masticatory muscle activity: a comparison of four types of malocclusion. J Clin Pediatr Dent. 1992;16:162-177. 177. Gionhaku N, Lowe AA. Relationship between jaw muscle volume and craniofacial form. J Dent Res. 1989;68:805809. 178. Haskell B, Day M, Tetz J. 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Angle Orthod. 1994;64:425-436. 92 CHAPTER 3: JOURNAL ARTICLE Abstract Purpose: To better understand the relationship between vertical facial growth and mandibular anterior crowding, this study evaluated untreated subjects crosssectionally and treated subjects longitudinally. Methods: The sample consisted of 1) pre-treatment records of 75 untreated Class I Caucasian patients collected from the archives at Saint Louis University, and 2) posttreatment and post-retention records of 76 Caucasian patients, treated on an extraction basis to a Class I occlusion, collected from one private practice clinician. After digitization of the models and cephalograms, two universal measures of crowding (II and TSALD) were related to four frequently used indices of divergence (MPA, PMA, PFH:AFH, LFH:AFH). Results: There were weak to moderately weak associations between facial divergence and crowding, subjects with greater divergence showed greater amounts of crowding than subjects with average amounts of divergence. Females, who were more hyperdivergent than males, also showed stronger relationships between divergence and crowding than males. There were moderate correlations between posterior face height and crowding in males; eruption of the lower incisors was moderately associated 93 with crowding in females. Conclusions: Vertical growth and incisor eruption, as well as facial divergence, are important determinants of malalignment. Introduction Although improved oral health, function, and social approval are all benefits of orthodontic treatment, patients typically present to maximize facial and dental appearance.1-4 This explains why dissatisfaction with crowding or irregular anterior teeth is often cited as the reason for seeking treatment.5-7 It is significant because the most widespread malocclusion encountered by orthodontists is crowding. It is presently unclear why some patients develop crowding and others do not. It has been suggested that “[t]he only way to ensure continued satisfactory alignment post-treatment probably is by use of fixed or removable retainers for life.”8 This is important because patient satisfaction with orthodontic treatment is partly associated with the stability of the final result.9,10 However, the use of permanent retention instills complacency among orthodontists and it essentially transfers ownership to the patient for permanency of the result. Additional research is needed to further 94 understand those factors affecting stability and relapse, and adjust our tactics for treatment.11-13 Previous studies have generally found weak associations between individual dental and/or skeletal factors and posttreatment relapse. For example, Little et al.14 found low to moderate correlations (r=0.26-0.52) between posttreatment dental changes and irregularity, while Shields et al.15 found weak correlations (r≤0.60) between irregularity and cephalometric variables. Other factors such as initial irregularity,14,16 incisor flaring during treatment,17 tooth proportions,18,19 the anterior component of force,20 horizontal mandibular growth,21,22 vertical dentoalveolar change,17 and intermolar angle21 also show weak correlations, ranging from 0.09-0.55. Although it is likely that many factors are responsible for crowding, with the exception of a few studies,23,24 multiple regression equations still explain only about half of the variation.21,25,19,26 Longitudinal studies have consistently shown that mandibular crowding increases over time.8,26-28,14 These increases are greatest during adolescence and slow during early adulthood.8,29,22 Since crowding occurs similarly in both treated and untreated individuals,26,27 it has been suggested that this may be the result of facial growth 95 changes and not necessarily treatment-related relapse.26,29,30 Because the duration and extent of vertical growth is greater than for horizontal growth,1,26,15 vertical growth is suspected to play an important role in dentoalveolar compensations, which could ultimately lead to crowding of the teeth. Several studies have examined the associations between crowding and vertical growth. For example, Driscoll-Gilliland et al.26 found that untreated individuals with more eruption of the lower incisors and greater vertical ramal growth had greater crowding. McReynolds and Little31 showed that greater crowding was associated with greater posterior face heights and increased upper anterior facial height. Others have demonstrated greater posttreatment mandibular irregularity in individuals with increased vertical dentoalveolar eruption.17,32 There have been only a few studies that have assessed the association between crowding and facial divergence. An association would be expected since increases in divergence allow greater space between the jaws, which could result in greater occlusal instability30 and greater crowding. Moreover, hyperdivergence results in retroclination of the incisors, which may cause crowding by reducing the arch length.33,34 Nasby et al.35 reported greater crowding and more upright incisors among hyperdivergent subjects, but 96 their sample was small and they did not test the association statistically. Leighton and Hunter36 also found significant differences in crowding related to the mandibular plane angle. Positive relationships between crowding and the palatomandibular plane angle (PMA) have also been reported.24,23 In the only long-term posttreatment study evaluating this relationship, Fudalej and Årtun37 found greater prevalence of postretention II (i.e., >5.0 mm) among hyperdivergent than hypodivergent patients. Importantly, there have also been studies that have evaluated, but did not find an association between crowding and facial divergence.38,39 It is the purpose of this study to determine whether differences in vertical facial growth, as measured by various indices of facial divergence, relate to crowding in both treated and untreated subjects. This association needs to be evaluated longitudinally because it allows us to study maturational changes without obscuring variability in growth timing among the sample.1 Furthermore, it is important to exclude hypodivergent subjects because they exhibit different dental compensatory patterns than hyperdivergent individuals;33 while open-bites and severe deep-bites must be excluded because altered anterior tooth 97 contact relations could distort the pattern of dental compensations. Materials and Methods Selection Criteria This study evaluated 1) a cross-sectional sample of 75 untreated adults, selected from the archives at the Center for Advanced Dental Education at Saint Louis University, and 2) a longitudinal sample of 76 treated subjects with long-term post-retention records, selected from one private practice clinician (JCB). The treated sample was selected based on: (1) Caucasian subjects 14-18 years of age posttreatment, (2) Class I molar occlusion at the completion of treatment, with extraction of four bicuspids during treatment, (3) lack of orthognathic surgery, syndromes, significant asymmetries, or hypodivergence, (4) fully erupted occlusion without missing (other than four bicuspids), impacted, supernumerary teeth, or excessive cuspal wear, (5) absence of open-bite or excessively deep-bite, (6) acceptable quality records post-treatment and post-retention, including panorex or full mouth series, lateral cephalograms, and models, (7) post-retention records at least 5 years post-treatment. 98 The final treated group included 76 subjects (30 males and 46 females). Their average post-treatment and post- retention ages were 15.4 years (interquartile range [IQR] 14.8-16.3 years) and 32.0 years (IQR 26.9-36.7 years), respectively. Males were significantly older (0.67 years) than females at T1 (Table 3.1). Table 3.1. Age distribution of males and females in treated groups Male (n=31) Female (n=44) Diff Median IQR Median IQR p Age at T1 15.92 15.08-16.58 15.25 14.83-15.71 0.018 Age at T2 33.17 27.50-39.67 30.92 26.79-35.46 0.326 Age diff (T2-T1) 16.83 10.75-23.08 15.50 11.50-19.71 0.469 †Bold data is significant at p<0.05 Prior to treatment, 17 of the males and 20 of the females had Class II malocclusions; at the completion of treatment all subjects had a Class I molar relationship. The patients were treated with edgewise mechanics according to the Tweed philosophy, using extractions to resolve crowding or incisor protrusion. Eighty-three percent of the patients received extraction of four first premolars, 5% had second premolars extracted, and the remainder had other extraction combinations. Treatment was followed by retention with a banded 3-to-3 retainer for 2-3 years. 99 The untreated sample was selected based on the same criteria as the longitudinal sample, except that they had to be 15-30 years of age, did not have previous orthodontic treatment or previous extractions of premolars, and had Class I molar relationships. The untreated group included 75 subjects (26 males and 49 females). The average age for the untreated subjects was 19.3 years (IQR 17.5-24.2 years). Females were significantly older than males (3.55 years) (Table 3.2). Table 3.2. Age distribution of males and females in untreated groups Male (n=26) Female (n=49) Diff Median IQR Median IQR p Age at T1 17.25 15.88-19.30 20.80 18.90-25.25 <0.001 †Bold data is significant at p<0.05 Cephalometric analysis Acceptable post-treatment cephalograms for treated and untreated groups were screened to exclude hypodivergent subjects. Using age and sex specific standards,40 subjects with MP-SN angles less than 1 standard deviation were excluded. Cephalograms were traced on 0.003” acetate paper using a 0.3 mm mechanical pencil. Fourteen cephalometric landmarks were identified, as defined by Riolo et al.40 100 The tracings were scanned at 300 dpi using a RICOH Aficio MP 5000 printer/scanner, and uploaded into Dolphin Imaging™ (Version 11.0). All cephalograms were digitized at 7x magnification to reduce error. Fifteen measurements were calculated using a custom analysis, including N-Me (Anterior Face Height), N-ANS (Upper Face Height), ANS-Me (Lower Face Height), S-Go (Posterior Face Height), Ar-Go (Ramus Height), L1-GoMe (IMPA), Overjet, Overbite, L1-Me (L1 dentoalveolar height), L1-MP (L1 dentoalveolar height), and L1-APg (L1 protrusion). This included four measures of divergence: SN-GoMe (MPA), PP-GoMe (PMA), LFH:AFH (lower anterior to total anterior face height ratio), and PFH:AFH (posterior to anterior face height ratio) (See Appendix A, Figure A.1). Cephalometric measurements and method error are shown in Appendix B, Table B.1. Model Analysis The models were screened to eliminate individuals with open-bite (<0 mm) or severe deep-bites (>5 mm). Photographs were used for the model analysis because they have been previously shown41 to provide measurements as reliable as those taken directly from study models. Photographs were taken using a Canon Rebel EOS SLR T2i 101 camera with 100 mm macro lens and MR-14x ring flash positioned 580 mm from the occlusal plane. A 100 mm ruler, placed at the level of the occlusal plane, was used for calibration. To reduce error in data collection, one trained assistant (AM) took all photographs using standardized procedures. Photographs were uploaded as a JPEG format into Dolphin Imaging™ (Version 11.0) for custom digitization. Twenty-one dental landmarks, as described by Moyers et al.42 were digitized at 3x magnification. Seven dental measurements, including two measures of crowding (TSALD and II), were calculated using a custom analysis (See Appendix A, Figures A.2-A.4), including: 1) Intercanine width (ICW), measured between cusp tips of the lower canines. 2) Intermolar width (IMW), measured between central pits of the lower first molars. 3) Arch depth (AD), the distance measured from the contact of the mandibular central incisors perpendicular to a line connecting the mesial contacts of the first molars. 4) Anterior tooth width (TW), the sum of the mesiodistal dimension of the lower teeth from canine to canine. 102 5) Anterior arch perimeter (AP), the sum of four arch segments, two for each quadrant. The posterior segment from the distal contact of the canine to the contact between the lateral incisor and canine, and from this to the contact between the lateral and central incisor. 6) Anterior tooth-size-arch-length-discrepancy (TSALD), the difference between AP and TW. 7) Little’s irregularity index (II), the sum, in millimeters, of the contact point displacements of the six anterior teeth. Model measurements and method error are shown in Appendix B, Table B.1. Reliability of Measurements To reduce measurement errors, all cephalograms were traced and digitized by one investigator (AG). Method error, which was determined based on 24 replicates and described with the Dahlberg statistic,43 ranged from 0.510.79 mm and 0.62-0.82 deg (with the exception of IMPA which was 1.38 deg) for the cephalometric measurements and from 0.09 to 0.46 mm for the model measurements (See Appendix B, Table B.1). Systematic errors, evaluated using the 103 Wilcoxon signed ranks test, were not statistically significant. Statistical Analysis Because the skewness and kurtosis statistics showed that many variables were not normally distributed, nonparametric statistics were utilized. Medians and interquartile ranges (IQR) were used to describe the variables. The Mann-Whitney’s U test was used to evaluate differences between males and females. Changes over time were evaluated using the Wilcoxon signed ranks test. Correlations were calculated using Spearman’s rho. The calculations were performed using SPSS Statistics software (version 17.0, SPSS, Chicago, Ill), with the significance level set at 0.05. Results Untreated subjects The untreated subjects displayed severe irregularity (8.50 mm) and minor TSALD (-3.40 mm), but there was a wide range of values (Table 3.3). No statistically significant sex differences were found for either measure of crowding. There was a moderately high correlation (r=-0.782) between irregularity and TSALD. 104 Table 3.3. Crowding in untreated groups T1 (n=75) Variable Median IQR II 8.50 6.20-10.90 TSALD -3.40 -5.60-2.30 †Bold data is significant at p<0.001; Data was pooled since no sex differences were found for II or TSALD In terms of the pretreatment skeletal measures, all linear dimensions were significantly larger in males than females (Table 3.4). Sex differences ranged from 2.0 mm for lower face height to 7.6 mm for posterior face height. Males also had significantly larger arch forms (Table 3.5). Intercanine widths were 1.45 mm larger, intermolar widths were 2.85 mm larger, and arches were 1.50 mm deeper in males than females. Both sexes showed greater variation in intermolar than intercanine width. No statistically significant sex differences were found for facial divergence, although females were generally more hyperdivergent. All measures of facial divergence showed highly significant (p<0.001), moderate to high, inter-correlations (r=0.658-0.921), except for LFH:AFH and PFH:AFH, which were not associated. MPA and PFH:AFH showed the highest correlation (r=-0.921). Correlations between crowding and measures of divergence were not statistically significant for the 105 pooled sample (Table 3.6). When the sexes were evaluated separately, males showed no significant associations for the four divergence measures; females showed a significant, but weak, correlation between PMA and irregularity (r=0.335, p=0.019). 106 Table 3.5. 107 Comparison of pre-treatment (T1) dental measures in male and female untreated groups Male (n=26) Female (n=49) Diff Variable Median IQR Median IQR p OB* 4.65 2.23-5.45 4.00 2.55-5.90 0.916 OJ* 2.70 1.98-3.90 3.40 2.25-4.25 0.200 L1-Apg* 2.30 1.20-5.05 2.60 0.75-4.10 0.771 IMPA 95.55 89.28-100.83 93.20 88.00-98.30 0.145 0.010 ICW 25.45 24.35-26.53 24.00 23.00-25.25 0.001 IMW 41.55 39.68-42.50 38.70 37.45-41.15 0.008 Arch depth -21.60 -22.93--20.53 -20.10 -21.65--18.60 II 8.50 6.03-11.85 8.50 6.45-10.25 0.668 TSALD -3.00 -5.68--1.28 -3.50 -5.45--2.30 0.504 †Bold data is significant at p<0.05, *indicates skewed/kurtotic data Comparison of pre-treatment (T1) skeletal measures in male and female untreated groups Male (n=26) Female (n=49) Diff Variable Median IQR Median IQR p <0.001 Na-Me (AFH)* 131.65 128.23-138.58 126.30 121.65-130.95 <0.001 Na-ANS (UFH)* 59.10 57.48-62.03 56.60 54.65-58.70 0.021 ANS-Me (LFH) 74.30 70.93-79.13 72.30 68.05-74.50 <0.001 S-Go (PFH) 88.55 82.78-91.03 81.00 78.85-84.35 0.001 Ar-Go (RH) 52.05 48.60-57.15 48.20 46.25-50.40 0.001 L1-MP 45.90 43.78-49.00 43.50 41.15-45.60 0.001 L1-Me 47.20 44.48-49.75 44.30 42.05-46.15 LFH:AFH 0.56 0.55-0.58 0.56 0.55-0.59 0.755 PFH:AFH 0.67 0.64-0.69 0.65 0.62-0.68 0.086 MPA 31.85 28.53-36.73 34.10 30.60-37.05 0.162 PMA 23.50 20.15-27.40 26.10 22.60-29.30 0.063 †Bold data is significant at p<0.05, *indicates skewed/kurtotic data Table 3.4. Variable AFH UFH LFH PFH RH L1-MP L1-Me LFH:AFH PFH:AFH MPA PMA r 0.311 0.179 0.319 0.495 0.517 0.343 0.242 0.174 0.168 0.061 0.027 108 T1 TSALD p r -0.309 0.125 -0.184 0.367 -0.298 0.139 -0.476 0.014 -0.400 0.043 -0.285 0.158 -0.195 0.340 -0.181 0.375 -0.175 0.393 -0.009 0.964 -0.061 0.766 MALE p 0.122 0.383 0.113 0.010 0.007 0.086 0.234 0.394 0.413 0.767 0.897 T1 II Table 3.6 (continued) r -0.148 -0.251 0.053 -0.270 -0.219 -0.005 -0.005 0.201 -0.188 0.185 0.335 T1 TSALD p r 0.337 0.018 0.165 0.256 0.216 0.136 0.247 0.087 0.099 0.500 0.092 0.528 0.136 0.350 0.038 0.793 0.042 0.776 -0.037 0.803 -0.036 0.808 FEMALE p 0.311 0.082 0.719 0.060 0.131 0.971 0.971 0.166 0.196 0.204 0.019 T1 II Correlations between T1 crowding and pre-treatment (T1) skeletal measures in untreated subjects (n=74) POOLED T1 II T1 TSALD Variable p p r r AFH 0.048 0.685 0.109 0.353 UFH -0.049 0.674 0.058 0.619 LFH 0.164 0.159 0.013 0.909 PFH -0.001 0.991 0.066 0.572 RH 0.008 0.946 -0.010 0.931 L1-MP 0.146 0.212 -0.022 0.849 L1-Me 0.149 0.351 0.029 0.808 LFH:AFH 0.193 0.097 -0.063 0.588 PFH:AFH 0.084 0.476 -0.012 0.920 MPA 0.155 0.184 -0.062 0.598 PMA 0.192 0.100 -0.070 0.552 †Bold data is significant at p<0.05 Table 3.6. Treated subjects After treatment (T1) both sexes showed minor irregularity (2.00 mm) and mild crowding (-0.20 mm) (Table 3.7). Over time, II increased 0.90 mm and TSALD increased 0.70 mm. Some individuals displayed almost no change in crowding, or even developed spacing. Post-retention (T2) irregularity (3.10 mm) and TSALD (-1.00 mm) were minimal. There were no sex differences in crowding. Irregularity and TSALD were not related at T1 (r=+0.097, p=0.435); they were moderately correlated at T2 (r=-0.612, p<0.001); the correlation between the T2-T1 changes was low (r=-0.322, p=0.008). Table 3.7. Crowding in treated groups T1 T2 Change (T2-T1) (n=67) (n=75) (n=67) Variable Median IQR Median IQR Median IQR II 0.90 2.00 1.50-2.50 3.10 2.40-3.80 0.20-2.10 TSALD -0.70 -0.20 -0.70-0.20 -1.00 -1.40-0.60 -1.40-0.30 †Bold data is significant at p<0.001; Data was pooled since no sex differences were found for II or TSALD In terms of the post-treatment skeletal measures, all linear measures were significantly larger in males than females (Table 3.8). Significant increases in both anterior and posterior face heights occurred over time in both sexes (Table 3.9). Males showed greater increases in 109 posterior face height (2.5 mm) and ramus height (2.1 mm) than females. 110 111 Comparison of post-treatment (T1) dental measures in males and females in treated groups Male (n=26) Female (n=41) Diff Variable Median IQR Median IQR p OB* 1.50 1.20-2.10 1.85 1.10-2.38 0.734 OJ* 2.60 1.90-2.80 2.20 1.80-2.58 0.100 L1-APg 1.50 0.30-2.40 1.45 0.45-2.58 0.609 IMPA 90.60 87.90-95.40 90.50 86.05-95.45 0.423 0.002 ICW 26.95 26.30-27.60 25.90 25.00-26.70 0.018 IMW 36.80 35.78-37.98 35.60 34.40-37.05 Arch depth* -17.75 -18.88--16.70 -17.10 -17.90--15.85 0.053 II 2.00 1.475-2.525 2.00 1.60-2.60 0.584 TSALD -0.30 -0.53-0.23 -0.20 -0.70-0.20 0.918 †Bold data is significant at p<0.05, *indicates skewed/kurtotic data Table 3.9. Comparison of post-treatment (T1) skeletal measures in males and females in treated groups Male (n=31) Female (n=44) Diff Variable Median IQR Median IQR p AFH 127.90 122.90-132.30 121.75 117.73-124.10 <0.001 <0.001 UFH 57.80 55.50-59.10 53.60 52.25-55.60 0.026 LFH 71.80 69.10-75.60 69.30 66.08-72.88 <0.001 PFH 83.30 78.90-87.80 75.30 73.00-77.45 <0.001 RH* 49.30 45.70-53.80 44.80 43.13-47.30 0.002 L1-MP 42.20 41.10-44.20 40.15 38.68-41.85 0.005 L1-Me 43.00 41.80-45.50 41.10 39.50-43.00 LFH:AFH 0.57 0.55-0.58 0.57 0.56-0.59 0.078 0.001 PFH:AFH 0.66 0.63-0.68 0.63 0.61-0.65 <0.001 MPA 33.80 30.90-36.30 37.20 34.83-40.85 0.001 PMA 24.20 21.50-27.40 28.70 26.20-32.45 †Bold data is significant at p<0.05, *indicates skewed/kurtotic data Table 3.8. Arch forms also showed significant sex differences (Table 3.10). Males had significantly larger intercanine (1.05 mm) and intermolar widths (1.20 mm) than females. Although the arches were 0.65 mm deeper in males, this difference was not significant. Both sexes showed greater variation in intermolar than intercanine width. There were no significant sex differences in the dental changes that occurred, except for intermolar width, which increased slightly (0.20 mm) in males and decreased slightly (-0.40 mm) in females. Generally, there were increases in overbite, increases in overjet, proclination or retroclination of the lower incisors, distal movement of lower incisor relative to the face, decreases in ICW, minor changes in IMW, decreases in arch depth, and increases in crowding (Table 3.11). Females were generally more hyperdivergent than males. Females had significantly larger mandibular plane (3.4 degrees) and palatomandibular plane (4.5 degrees) angles than males. Males showed reductions in most of the divergence measures over time, whereas females demonstrated little or no change. Males showed 2.15 and 1.60 degrees more closure of the MPA and PMA, respectively. Lower to anterior face heights (LFH:AFH) were maintained over time and showed no significant sex differences. 112 Comparison of dental changes (T2-T1) of males and females in treated groups Male (n=26) Female (n=41) Diff Variable Median IQR Median IQR p Δ OB 0.75 -0.13-2.15 1.65 0.80-2.20 0.108 Δ OJ 0.15 -0.43-0.95 0.50 0.10-1.08 0.086 Δ L1-APg -0.50 -1.33-0.90 -0.50 -1.10-0.40 0.893 Δ IMPA -0.85 -2.70-3.15 0.25 -3.40-3.13 0.692 Δ ICW -1.45 -1.78--0.75 -1.70 -2.30--0.75 0.325 0.008 Δ IMW 0.20 -0.43-1.03 -0.40 -0.90-0.30 Δ Arch depth -1.20 -1.83--0.70 -1.90 -2.30--0.95 0.113 Δ II* 0.75 -0.03-1.98 1.10 0.40-2.15 0.367 Δ TSALD* -0.65 -1.15--0.28 -0.70 -1.65--0.25 0.685 †Bold data is significant at p<0.05, *indicates skewed/kurtotic data Table 3.11. 113 Comparison of skeletal changes (T2-T1) in males and females in treated groups Male (n=30) Female (n=44) Diff Variable Median IQR Median IQR p Δ AFH 3.10 0.90-5.53 4.45 1.65-5.48 0.516 Δ UFH 1.25 -0.13-2.95 1.65 0.70-2.80 0.484 Δ LFH 1.85 0.45-3.03 2.15 0.20-3.28 0.656 <0.001 Δ PFH 5.40 3.50-8.20 2.95 1.68-4.58 <0.001 Δ RH 4.60 3.20-6.30 2.50 1.03-3.10 Δ L1-MP 2.05 0.60-2.75 1.70 1.33-2.50 0.671 Δ L1-Me 2.30 0.35-3.10 1.85 1.25-2.48 0.589 Δ LFH:AFH* -0.002 -0.008-0.006 -0.001 -0.009-0.004 0.800 <0.001 Δ PFH:AFH* 0.026 0.015-0.040 0.009 -0.003-0.015 <0.001 Δ MPA* -2.80 -3.93--0.93 -0.65 -1.60-0.55 0.005 Δ PMA* -2.00 -4.20--0.73 -0.40 -1.85-0.40 †Bold data is significant at p<0.05, *indicates skewed/kurtotic data Table 3.10. All measures of posttreatment divergence were significantly interrelated, with correlations ranging from 0.255 to 0.914. The lowest correlation was between LFH:AFH and PFH:AFH (r=-0.255; p=0.027); the strongest association was between PFH:AFH and MPA (r=-0.914, p=<0.001). Changes in divergence also showed moderate to moderately high correlations (r=0.550-0.937, p<0.001), with the exception of LFH:AFH with PFH:AFH (p=0.186) and LFH:AFH with MPA (p=0.112), which were not significantly related. Based on the entire sample, correlations between posttreatment skeletal dimensions and post-retention crowding were generally not statistically significant (Table 3.12). There was a weak correlation (r=0.235, p=0.043) between the mandibular plane angle and irregularity. correlations showed Sex specific no associations for males, and a significant association between PMA and II (r=0.320) for females. The pooled samples showed statistically significant, but weak (Table 3.13), correlations between changes in II and post-treatment ramus height (r=-0.258), posterior to anterior face height (PFH:AFH) (r=0.261), the mandibular plane angle (r=0.287), and the palatomandibular angle (r=0.282). A weak correlation was also found between the 114 posterior to anterior face height ratio (PFH:AFH) and TSALD (r=-0.262). When the sexes were evaluated separately, males again showed no significant correlations. Females showed moderate correlations between irregularity changes and AFH, LFH, LFH:AFH, PFH:AFH, mandibular plane angle, and palatomandibular angle, ranging from 0.327-0.447. Correlations between TSALD changes with PFH:AFH and MPA also attained significance (r=0.414 and 0.361, respectively). When changes were related to changes, significant moderate correlations were found between changes in TSALD and changes in dentoalveolar heights (Table 3.14). The pooled sample showed correlations between changes in TSALD and changes in L1-MP (r=-0.353), as well as changes in L1Me (r=-0.468). These correlations can again be attributed to females, who showed that changes in TSALD were related to changes in L1-MP (r=-0.445) and changes in L1-Me (0.643). Changes in crowding were unrelated to the skeletal changes in males. 115 Variable AFH UFH LFH PFH RH L1-MP L1-Me LFH:AFH PFH:AFH MPA PMA r 0.040 0.276 -0.006 -0.057 -0.089 -0.015 -0.043 -0.149 -0.051 0.075 -0.082 116 MALE (n=31) T3 TSALD p p r 0.830 -0.053 0.777 0.133 0.104 0.579 0.973 -0.156 0.402 0.760 0.158 0.395 0.635 0.181 0.330 0.935 -0.008 0.966 0.818 0.008 0.967 0.424 -0.320 0.079 0.786 0.138 0.459 0.688 -0.129 0.491 0.662 -0.162 0.384 T3 II Table 3.12 (continued) FEMALE (n=44) T3 II T3 TSALD p p r r 0.177 0.251 -0.076 0.622 -0.166 0.281 -0.038 0.805 0.231 0.132 -0.061 0.694 -0.091 0.558 0.096 0.534 -0.120 0.437 0.058 0.708 -0.018 0.908 0.012 0.940 0.011 0.944 0.022 0.885 0.285 0.061 -0.059 0.703 -0.185 0.230 0.128 0.407 0.296 0.051 -0.259 0.089 0.320 0.034 -0.056 0.716 Table 3.12. Correlations between post-retention (T2) crowding and post-treatment skeletal measures (T1) in treated subjects POOLED (n=75) T3 II T3 TSALD Variable p p r r AFH -0.045 0.704 0.112 0.340 UFH -0.131 0.262 0.167 0.152 LFH 0.063 0.589 -0.022 0.849 PFH -0.183 0.116 0.200 0.086 RH -0.204 0.079 0.143 0.219 L1-MP -0.104 0.375 0.088 0.453 L1-Me -0.084 0.475 0.084 0.474 LFH:AFH 0.156 0.182 -0.161 0.168 PFH:AFH 0.164 0.159 -0.125 0.286 0.235 0.043 MPA -0.198 0.088 PMA 0.221 0.057 -0.103 0.381 †Bold data is significant at p<0.05 Variable AFH UFH LFH PFH RH L1-MP L1-Me LFH:AFH PFH:AFH MPA PMA r -0.111 0.170 -0.102 -0.267 -0.257 -0.099 -0.113 -0.187 -0.116 0.104 0.002 117 MALE (n=26) Δ TSALD p p r 0.591 -0.085 0.681 0.405 -0.056 0.786 0.621 -0.156 0.447 0.188 0.026 0.901 0.205 -0.019 0.925 0.631 -0.147 0.473 0.583 -0.126 0.541 0.361 -0.160 0.435 0.571 0.064 0.756 0.615 -0.028 0.893 0.992 0.048 0.815 Δ II Table 3.13 (continued) FEMALE Δ II p r 0.342 0.029 0.031 0.845 0.370 0.017 -0.078 0.630 -0.149 0.352 0.063 0.697 0.119 0.460 0.298 0.059 -0.327 0.037 0.398 0.010 0.447 0.003 (n=41) Δ TSALD p r -0.265 0.094 -0.277 0.079 -0.204 0.200 0.229 0.150 0.250 0.114 -0.124 0.439 -0.121 0.450 -0.059 0.716 0.414 0.007 -0.361 0.021 -0.194 0.224 Table 3.13. Correlations between change in crowding (T2-T1) and post-treatment skeletal measures (T1) in treated subjects POOLED (n= 67) Δ II Δ TSALD Variable p p r r AFH 0.020 0.871 -0.065 0.603 UFH -0.040 0.746 -0.052 0.678 LFH 0.121 0.328 -0.140 0.260 PFH -0.209 0.089 0.202 0.101 -0.258 0.035 RH 0.154 0.212 L1-MP -0.070 0.575 -0.071 0.568 L1-Me -0.023 0.854 -0.082 0.507 LFH:AFH 0.136 0.274 -0.086 0.491 0.261 0.033 -0.262 0.032 PFH:AFH 0.287 0.019 MPA -0.238 0.053 0.282 0.021 PMA -0.095 0.445 †Bold data is significant at p<0.05 Variable Δ AFH Δ UFH Δ LFH Δ PFH Δ RH Δ L1-MP Δ L1-Me Δ LFH:AFH Δ PFH:AFH Δ MPA Δ PMA r -0.106 -0.096 -0.179 -0.022 0.062 0.227 0.350 -0.050 0.193 -0.091 -0.209 118 MALE (n=26) Δ TSALD p p r 0.615 0.122 0.562 0.646 0.091 0.665 0.392 0.300 0.145 0.917 0.110 0.601 0.770 0.017 0.937 0.276 -0.227 0.275 0.086 -0.260 0.210 0.807 0.022 0.917 0.345 -0.249 0.219 0.667 0.224 0.281 0.317 0.208 0.318 Δ II Table 3.14 (continued) r 0.246 0.169 0.132 -0.259 -0.232 -0.003 0.092 -0.014 -0.327 0.289 0.086 FEMALE (n=41) Δ TSALD p p r -0.343 0.028 0.122 0.291 -0.210 0.188 0.412 -0.230 0.148 0.103 -0.249 0.116 0.144 -0.042 0.796 -0.445 0.004 0.986 -0.643 <0.001 0.567 0.620 0.080 0.620 0.538 -0.099 0.538 0.640 0.075 0.640 0.766 0.048 0.766 Δ II Table 3.14. Correlations between change in crowding (T2-T1) and change in skeletal measures (T2-T1) in treated subjects POOLED (n=67) Δ II Δ TSALD Variable p p r r Δ AFH 0.119 0.343 -0.160 0.201 Δ UFH 0.077 0.541 -0.066 0.599 Δ LFH 0.016 0.896 -0.049 0.695 Δ PFH -0.191 0.124 -0.083 0.508 Δ RH -0.155 0.214 0.016 0.900 -0.353 0.004 Δ L1-MP 0.098 0.434 -0.468 <0.001 Δ L1-Me 0.184 0.140 Δ LFH:AFH -0.101 0.420 0.073 0.558 Δ PFH:AFH 0.143 0.252 0.098 0.434 Δ MPA 0.171 0.170 0.129 0.302 Δ PMA 0.014 0.911 0.072 0.586 †Bold data is significant at p<0.05 Discussion Both incisor irregularity and TSALD must be measured in studies evaluating crowding. Correlations between II and TSALD ranged from moderate to moderately high (r=0.61 and 0.78). Similar correlations have been reported for pretreatment crowding (r=0.5338; r=-0.6839), and postretention crowding (r=-0.6040). These two indices measure different aspects of crowding, which could affect the results.26,44,18 Irregularity is “sensitive” to axial displacements and rotational changes of teeth, whereas TSALD reflects the difference between space required and space available. At best, one measure explains less than half of the variation in the other. Most measures of facial divergence showed significant associations with one another. However, LFH:AFH repeatedly showed low to moderately low correlations with the other variables, except with PMA (r=0.58-0.66). Our associations are comparable to those previously reported,45,46 indicating that, with the exception of anterior facial height proportions, most of the indices could be substituted for one another. The fact that vertical ramus growth is an important determinant of facial divergence may explain why the proportions of the anterior face are less related to the other measures. 119 Untreated Cross-Sectional Sample The untreated subjects showed relatively large amounts of incisor irregularity prior to treatment, but only mild crowding. Median irregularity was severe (8.5 mm), but TSALD was relatively small (-3.4 mm). This suggests only minor decreases in arch length despite significant changes in axial and rotational positions of the incisors. The amount of II observed in the present study compares favorably with amounts of II previously reported.14,17,47 Others have reported much lower pretreatment II.22,48-55,16 These differences might be related to sampling variations. Divergence showed relatively few associations in untreated individuals. Although the palatomandibular angle showed a moderate correlation with irregularity in females, no other divergence measure was found to relate to crowding in either sex. Because of the cross-sectional nature of this study and younger age of males, variability in growth status may have obscured the results. In addition, the relatively small sample size for males and restricted range of crowding would tend to provide lower correlation coefficients. Importantly, posterior facial height growth is partially responsible for mandibular crowding. There were significant moderate correlations between crowding and 120 increased vertical dimensions of the posterior face in untreated males; males with the largest posterior heights exhibited the greatest crowding. This supports the findings of McReynolds and Little,31 who found that patients with greater posterior face height exhibited greater postDriscoll-Gilliland et al.26 also showed retention crowding. a positive moderate correlation between the growth of posterior face height (Ar-Go) and space irregularity in a sample of 44 untreated individuals studied between 14 to 23 years. In contrast, Bishara et al.56 found little or no relationship between posterior face height and TSALD. It should be noted however, that because their cephalograms came from machines with varying magnifications, the linear results should be approached with caution. Treated Longitudinal Sample Increases in mandibular crowding commonly occur after retention has been discontinued. Generally, the treated sample maintained satisfactory stability over the 15.9 year posttreatment period. They showed only small, but significant, post-treatment increases in irregularity (0.9 mm) and TSALD (-0.7 mm). After approximately 12 years without retainers, 93% of the subjects exhibited only minor TSALD (<4 mm) and 68% has satisfactory II (<3.5 mm). 121 The crowding that occurred in the present study was similar to amounts previously reported for patients treated with extractions in private practices, for which increases in II range from 0.34-1.3 mm.26,22,48,57 It is difficult to know whether sample characteristics, retention protocol, band spaces remaining after treatment, or band space after removal of fixed retainers, contributed to the lower levels of crowding observed. Interestingly, the changes in crowding that occurred post-treatment, in this and other studies from private practitioners, were similar to, or on the low end of, values reported for untreated samples (II ranges from 0.472.58 mm; TSALD ranges from 0.1-2.78 mm).26-28,56,58-62 This suggests that crowding is probably not related to treatment itself, but to other factors such as age, sex, ethnicity, number of teeth present, among others.29 Males and females exhibited similar amounts of posttreatment crowding. A lack of sex differences in crowding has been previously reported for other treated26,58,63 and untreated26,28,60 patients. Based on a large cross-sectional sample of 9044 individuals, Buschang and Shulman29 found significantly larger II (0.48 mm) among males than females. If a difference exists, it is likely small and can only be appreciated using an extremely large sample. 122 Generally, females were more divergent than males and remained more divergent over time. Females had significantly larger mandibular plane angles, palatomandibular angles, and posterior to anterior facial height ratios than males. The sex difference could have been due to the fact that males had greater increases in posterior face height and ramus height than females. In other words, the sex difference pertains mainly to growth in the posterior aspects of the face; LFH:AFH showed relatively minor changes in both sexes, indicating that the anterior portions of the face remain proportional over time. The fact that males are less divergent than females has been previously reported.45,64-66 Individuals with increased facial divergence appear to be more prone to post-treatment crowding than individuals with average divergence. The associations between crowding and divergence were greater in females than in males, probably because they exhibited greater mandibular divergence than males. Interestingly, the changes in divergence were not predictive of crowding, likely because these dimensions showed relatively small changes over time. Although some studies have not found a relation,38,39 others have found differences in crowding related to facial divergence.35,36,24,23 Importantly, the association between 123 crowding and divergence is not strong, indicating that it is one of many factors that must be considered. Divergence might be at least partially related to crowding due to changes in the transverse dimension. It is well established that hyperdivergent individuals have narrower arch forms.35,67,68 Since narrow arches limit the space available for the teeth, this could result in crowding.69,70 Postretention, low to moderate correlations were shown between arch width and crowding (r=0.282-0.443); arch width was also related to facial divergence (r=0.2580.322). Other studies have found relations between facial divergence and transverse dentoskeletal67,71 measures in untreated subjects. For example, Forster et al.71 found decreases in arch width with increasing MP-SN angles, but only in males, and did not find any relation to crowding. Other studies have not found relations between arch form and divergence72 or arch width and crowding.73 Vertical eruption of the lower incisors also appears to be associated with post-treatment crowding. Patients with greater amounts of lower incisor eruption had greater increases in TSALD (Table 3.14). This was especially true for females, although males showed some tendency for increased irregularity with eruption. In females, L1-MP explained 20% and L1-Me explained 41% of the variation in 124 crowding. Relationships between increased eruption and crowding have been previously demonstrated.26,17,32 There also was a significant relationship between TSALD and increases in the anterior face height, which is reasonable because increases in facial height might be expected to result in greater incisor eruption. Men also showed large increments of anterior face growth, but these changes were not linked to changes in crowding because males also underwent even larger increases in posterior face height. This suggests that males had greater forward mandibular rotation, resulting in less lower incisor eruption and greater proclination of the incisors, both of which could decrease or limit crowding. The results of this study have important clinical implications. Individuals, particularly females, with hyperdivergent growth patterns may be predisposed to crowding. Therefore, vertical control of growth (i.e., high-pull headgear or vertical-pull chin cup) during treatment could help in preventing future crowding. Although the associations found between crowding and divergence were low, they are comparable to correlations found for other factors relating to crowding, supporting the belief that there are many small, yet important, contributors to crowding (Figure 2.14). 125 Patients should be advised that minor posttreatment alignment changes are a normal consequence of aging. Because vertical growth continues far into adulthood, retention must be a life-long commitment. Figure 2.14. Revised progression of malalignment. 126 Summary and Conclusions Based on a treated sample of 76 Caucasian adolescents aged 14-18 posttreatment followed for at least 5 years posttreatment, and an untreated sample of 75 Caucasian adults aged 15-30 pretreatment, the following conclusions can be drawn: 1) Posttreatment crowding was generally acceptable and showed only small increases in patients who had been out of retention for approximately 12 years. 2) Craniofacial and dental arch measures are larger in males than females. 3) Females exhibit greater facial divergence than males. 4) Females with greater lower incisor eruption and reduced posterior facial growth, and males with greater posterior facial dimensions, show greater amounts of crowding. 5) Facial divergence is related to crowding, more so in females, but it is only one of many factors involved in crowding. 127 References 1. Proffit W, Fields, Jr. H, Sarver D. Contemporary Orthodontics. 4th ed. St. Louis: Mosby; 2007. 2. 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Am J Orthod Dentofacial Orthop. 1995;107:613-617. 134 APPENDIX A Customized Cephalometric and Model Analyses 135 Customized cephalometric digitization regimen Figure A.1 depicts a customized cephalometric digitization regimen based upon landmarks from Riolo et al., 1974. The corresponding cephalometric analysis is found in Table A.1. Figure A.1. Customized cephalometric digitization regimen. Adapted from Riolo et al., 1974 136 Customized model digitization regimen Figures A.2-4 depict a customized model digitization regimen based upon landmarks from Moyers et al., 1976. The corresponding model analysis is found in Table A.2. Figure A.2. Calculation of Arch perimeter. Adapted from Kuroda et al., 2010. Figure A.3. Figure A.4. Calculation of intecanine width, intermolar width, and arch depth. Adapted from Kuroda et al., 2010. Calculation of Irregularity Index. 137 Adapted from Little, 1975. Table A.1. Customized cephalometric analysis. Measures Angular/Proportional Linear SN-GoMe (MPA) N-Me (AFH) PP-GoMe (PMA) N-ANS (UFH) LFH:AFH ANS-Me (LFH) PFH:AFH S-Go (PFH) Ar-Go (RH) L1-GoMe (L1-MP) L1-Me L1-APg IMPA Overjet Overbite Table A.2. Customized model analysis. Measures Linear ICW IMW AD TSALD II 138 APPENDIX B Error Study 139 Error Study Appendix B contains the method error for the cephalometric and model measurements. Method error was calculated according to Dahlberg’s statistic, 1980 (√(∑d2/2n)) using 24 replicas. Table B.1. Method error study (n=24) Measurement Interpretation Units Method Error N-Me Anterior face height mm 0.65 N-ANS Upper face height (UFH) “ 0.56 ANS-Me Lower face height (LFH) “ 0.55 S-Go Posterior face height “ 0.51 Ar-Go Ramus height “ 0.60 L1-GoMe L1 dentoalveolar height “ 0.79 L1-Me L1 dentoalveolar height “ 0.79 SN-GoMe Mandibular plane angle Deg 0.62 PP-GoMe Palatal plane to mandibular plane angle “ 0.78 (AFH) (PFH) (RH) (L1-MP) (MPA) (PMA) L1-APg Lower incisor protrusion “ 0.82 IMPA Lower incisor inclination “ 1.38 Overbite Vertical distance between U1 and L1 tips mm 0.76 Overjet Horizontal distance between U1 and L1 “ 0.53 tips ICW Intercanine width 0.19 IMW Intermolar width “ 0.10 Arch Depth Arch depth “ 0.09 II Incisor irregularity “ 0.26 TSALD Tooth-size-arch-length-discrepancy “ 0.46 140 VITA AUCTORIS Avrum I. Goldberg was born on October 17, 1980 to Mrs. Debbie and Dr. Sheldon Goldberg in Vancouver, British Columbia; he is the oldest of two children. After graduating from West Vancouver Secondary School he went on to receive his undergraduate education locally at Capilano College and the University of British Columbia. He moved across the country to pursue his dental education in Halifax, Nova Scotia, completing a degree of Doctor of Dental Surgery with distinction in 2006. Following graduation he worked for three years in general practice with his father before returning to school to begin his graduate orthodontic training at Saint Louis University. He married Amy Mihaljevich on July 26, 2009 in Tower Grove Park. After graduation, Dr. Goldberg plans to return to Canada to practice orthodontics. He is currently a candidate for the degree of Master of Science in Dentistry (Research). 141