olor Atlas ars oh : seta: Sens. Color Atlas of Dental Medicine Editors: Klaus H. Rateitschak and Herbert F. Wolf Orthodontic Diagnosis Thomas Rakosi ~ Itmtrud Jonas Thomas M. Graber a Foreword by Robert E. Moyers 1001 illustrations, most in color 199 © Ge. rg Thieme Verlag, Stuttgart - New York Thieme Medical Publishers Inc., New York ieForeword A short generation ago, the transition from German orthodontic strategies, outlook, and practice to ‘American, and vice versa, was a greater leap than that from the German to the English language. At that time,a German or American orthodontist, when writing about diagnosis or treatment, often began with clinical assumptions strange and disturbing to readers across the Atlantic, In recent years, however, German ortho- dontists have read more extensively of American methods, which are now well known and widely prac- ticed throughout Europe. This has enabled them to merge differing clinical approaches advantageously. Unfortunately, many American orthodontists know litle of German methods of diagnosis and treatment. Functional jaw orthopedic methods, originated by ‘Andreason in Norway and Robin in France, but exploit ed more extensively by German clinicians than most others, have become widely used in North and South ‘America. It should be remembered, however, that some German clinicians have more experience in combining the two approaches — precision bracketed appliances and functional jaw orthopedic devices. This splendid volume is a fine depiction of the authors’ diagnostic methods applied to a variety of clinical cases. The pictorial presentation has seldom been equaled in the orthodontic literature. The writings brief to keep the focus on the differential diagnoses and the results presented, The authors are renowned teach- ers and authors whose differing backgrounds are complementary to the task of bringing this well- received European book to an American audience, Professors Rakosi, Jonas and Graber have done a great favor to their English-speaking colleagues by bringing forth this English-language edition of an estab- lished German contribution to clinical orthodontics. Robert E. Moyers, D.D.S., Ph.D., D.Sc. (hon. Thessaloniki), Dr. Odont. (hon. Lund) Professor Emeritus, School of Dentistry (Orthodontics) and Fellow Emeritus, Center for Human Growth and Development University of Michigan, Ann Arbor, Michigan, USAMI Table of Contents Vv Foreword Vill Preface Fundamental Principles 3. Relevance of Diagnosis 35 Classification of Malposition - Nomenclature 4 Comprehensive Diagnosis 35. Malposition of Individual Teeth 5 Diagnostic Process 37. Malpositions of Groups of Teeth 45. Malocclusion 6 Growth of the Craniofacial Skeleton 47 Ovoriet 8 Inttamembranous'Ossifcation 51. Evaluating the Occlusion 40 Enchondral Ossification 43. Growth Mechanisms 57 Etiology of Malocelusion 44 Endosteal and Periosteal Growth 59 Causes of Malocclusion 15 Cortical Dit 60. Hereditary Abnormalities 417 Relocation and Remodeling 60 Neuromuscular System 49 The “V" Principle 61 Denition 20 Surface Principle 70 Bones 21 Growth Fields 72 Skeletal Malocclusion 22 _ Displacement 74 Soft Tissues 23. Growth Processes 75. Acquired Anomalies 23 Maxillary Growth 78 Developmental Damage 24 — Mandibular Grown 77 Trauma 26 Growth of the Midlace 80 Physical Factors 28 _ Growth Equivalents 82 Premature Loss of Deciduous Teeth 28. Growtn-Controlling Factors 83° Breathing 30. Local Factors Concerning Craniofacial Morphogenesis 85 Bad Habits - Orotacial Dysfunction 31 Factors Influencing Endochondral Ossification 88 Diseases 31 Factors Influencing ntramembranous Osstfcation 32 Degree to Which the Growth Processes Can Be Influenced 33. Mechanism of the Functional Matrices gnostic Procedures 93. Case History 148 Tongue 95 Interpretation ofthe Case History 417 Lip and Cheek Frena 96 Questionnaire - Case History 118 Gingiva 420 _ Palatal Mucosa and Petal Vauit 97. Clinical Examination 421 Clinical Examination ofthe Denton 97 General State 4122. Clinical Examination ~ Record Sheet 98 Denial Age . 102 Biological Age and Hand Radiograph 423 Functional Analysis 423 Examination of the Relationship: Postural Rest Post 108 Special Clinical Examination Habitual Occlusion 408 Cephalic and Facial Examination 423. Determination of the Postural Rest Position 410 Examination of the Soft Tissues 426 Registration ofthe Rest Postion 110 Forehead 428 Evaluation of the Relationship between Rest Posi 111 Nose and Habitual Occlusion 112 Lips 128 Evaluation in the Sagital Plane 114 Chin132 133 Evaluation of the Relationship between Rest Posi- tion and Habitual Occlusion in the Vertical Plane Evaluation of the Relalionship between Rest Pos tion and Habitual Occlusion in the Transverse Plane Examination of the Temporomandibular Joint Clinical Examination (Opening and Closing Movements of the Mandible ‘Temporomandibular Joint - Radiographic Examination Examination of Orofacial Dysfunctions ‘Swallowing Tongue-Thrust Lip Dysfunctions Cheek Dysfunctions Hyperactivity of Mentalis Muscle Functional Analysis - Record Sheet Radiologic Examination Dental Condition Photographic Analysi Profile View Facial Divergence Frontal View Cephalometric Analysis of the Lateral Radiograph Cephalometric Reference Points. Cephalometric Reference Lines Interpretation of Cephalometric Measurements Linear Analysis of Jaw Bases Analysis of the Skeletal Facial Profile Vertical Analysis of the Facial Skeleton Growth Direction - Rotation of the Mandible 194 196 198 200 204 208 207 208 211 213 214 216 218 219 220 221 222 223 224 227 228 231 232 235 Rotation of the Maxillary Base Combinations of Maxillary and Mandibular Rotation Analysis of Incisor Position Radiographic Cephalometric Classification of Malocclusions Cephalometric Radiography ~ Prognostic Assessment Record Sheet - Radiographic Cephalometric Analysis (Lateral Radiograph) ‘Study Cast Analysis * Metric Analysis of Arch Form Dental Arch Wiath “Anterior Dental Arch Length Intramaxillary Symmetry Analysis of Transverse Symmetry ‘Analysis of Anteroposterior Symmetry Palatal Height ‘Analysis of Supporting Zones Prediction from Proportionality Tables Combined Radiologic-Prediction Table Method Space Analysis in the Permanent Dentition ‘Space Analysis, According to NANCE Space Analysis, According to LUNDSTROM Discrepancy Calculation ‘Analysis in the Vertical Plane BOLTON Analysis ‘Analysis of the Apical Base, According to RES Examination of Occlusion Record Sheet - Three-dimensional Analysis of the Dentition ‘Treatment Plan Treatment Planning Case Example 1 Treatment Planning Case Example 2 Treatment Planning Case Example 3 Treatment Planning - Case Examples Record Sheets ‘Acknowledgments References Indexwat Preface This volume is a handy, illustrated manual covering, orthodontic diagnostic techniques. Modern orthodontics includes a series of different types of treatment requiring precise diagnostic techni- ques in order to produce a positive outcome. This atlas includes the examination methods required for everyday treatment. Apart from the conventional examination methods, ie. clinical and radiographic examinations and cast analysis, three aspects which are often neglected are described in detail: ~ Growth of the facial skeleton ‘Types of treatment which promote or guide growth are often employed as a part of orthodontic therapy — assu- ‘ming there is still a potential for growth - with the inten- tion of harmonizing the various components of the facial skeleton. In order to control these natural processes arti- ficially, a precise understanding of them is required. logy of the malocclusion Causative therapy is always desirable and promising, ‘The various types of causative therapy and the elimina tion of the causes depend on the etiologic assessment. — Functional analysis ‘Analysis of function is a part of the clinical examination. If one considers that on the one hand many malocelu- sions are a result of dysfunctions and, on the other hand, a variety of methods are available for treating dysfunc- tions, functional analysis must be taken seriously. This color atlas should enable the operator to assess the malocclusion and simplifies selection of the method of treatment for individual cases. It provides an over- view and serves as a reference book for use in dé practice. Thomas Rakosi Irmtrud Jonas Thomas M. Graber Freiburg/ Evanston August 1992Fundamental Principleslevance of Diagnosis ‘is: The recognition and systematic designation of anomalies; the practical synthesis of the . permitting therapy to be planned and indication to be determined, thereby enabling the tor to act. Recognizing the problem Formulating the problem Carrying out the necessary examinations Interpretation of the results Diagnosis jumerous observations, individual findings and analyses, which allow a broad-based decision to be for the particular patient, are a prerequisite for a correct diagnosis in orthodontics. informations must be objective, relevant, and accurate. The diagnostic criteria should include “the entire orofacial system, yet should also be selective. Certain normsare required for diagnostics, jie. for the assessment of abnormalities of the stomatognathic system. Comparing to an ideal norm (eg. eugnathia) or statistically determined mean values (e.g. Pont index)is unrealistic. Personal, indi- ‘vidual norms do exist for each case which take into account the individual development of the masti- catory system (the “individual optimum” according to Andresen, 1931). Analyzing the individual “data systematically enables diagnosis to be carried out according to type. Grouping the cases together results in larger groups, so-called typical anomalies, which can be divided into further classifications. Atypical anomalies also exist, so-called borderline cases, which depend in their type ‘and number on the respective methods of considering the case and its classification.Comprehensive Diagnosis Nowadays, orthodontic diagnosis should be routinely based on various methods of examination (Fig. 1). The synthesis of these various individual findings deter- ‘mines the orthodontic diagnosis. The individual results must be checked prior to evaluation to ensure that sufficient examinations have been carried out, and that the most relevant examinations were included, and not simply that an immense volume of data has been collect- ed without having included the most relevant details. The comprehensive diagnosis should be a summary ofthe most important facts and should not take insi 1. Essential orthodontic examinations ‘The seven different analytical tech- riques are all ofthe same relev ‘ance for orthadontic diagnosis Prior to cartying out further examinations, the time and effort required should be compared to the possible therapeutic conse- quences, Even in adult cases, where more elaborate diagnostic examinations are necessary the lime and effort required must be relative to the possible results. carried out in exceptional cases for a detailed investiga- tion of specific problems. Computer analysis has also been employed for orthodontic diagnostics over the past few years. The computer enables quick and accurate evaluation of the individual findings. It can correlate the various data and indicate a particular problem. However, the computer cannot make a diagnosis. The practitioner must still cant secondary symptoms into account, as they are ofno relevance to the treatment. The more experienced the orthodontist is, the quicker he or she will recognize the problem, select the appropriate examinations for the case, and make optimum use of it. Certain discussions as to whether the etiological, ical, functional, or radiographical aspects should be considered most important for the diagnosis are unwarranted. However, in some cases further exami tion methods may be required. For example, cinemato- graphic or palatographic registrations should only be interpret and synthesize the data determined by elec- tronic means and plan the therapy. The so-called computer diagnosis often includes a preprogrammed decision which usually leads to standardization of the treatment methods and results in stagnation in one’s speciality. The cause’ of incorrect diagnoses are usually sufficient informations or prejudiced decisions made in order to adapt the case to a particular type of treatment.nostic Process mntic diagnosis can be referred to as a diagnostic ss (Fig. 2). diagnostic procedure commences with the initial ination, during which a large number of individual and analyses of the etiology and particulars of locclusion are clarified by means of synthesis. cbjective is to describe the morphological and func- characteristics of the case, using certain terms, provide a prognosis of the anomaly, ie. forecast the future development of the deformity. le to possible unexpected developments and re- Onthodontc Diagnostic Process actions during the course of treatment, this initial diagnosis must be reviewed regularly. While doing so, the various data obtained during the initial diagnosis, must be checked selectively to ensure that they are still relevant. The objective of regular examinations is to reassess the initially defined therapeutic methods and to establish whether further procedures are necessary or whether the treatment plan should be changed. This is called continuing diagnosis. The main objective of the final check-up is to assess the stability of the treatment results. — 2. Diagnostic process for ‘orthodontics - general course of treatment Once the intial diagnosis and probable prognosis have been established, the necessity for treat ‘ment and the plan of treatment are “Initia! diagnosis: discussed at length with the pat lent. The degree of motivation and future compliance of the patient should be assessed and, when children are being treated, ais. ‘cussed with the parents. {At the beginning of the therapy the entire course of treatment ~ influenced by the growth pro: cesses - usually cannot be predict 6 exactly Aer each phase of treatment, the clinican must check that the therapy is correct, thus, if neces: sary, enabling the course of treat Continuing ciagnosis | Final diagnosis Therapy ‘ment to be adjusted in good time. The diagnostic process is not ‘complete until the treatment has ‘been finalizedGrowth of the Craniofacial Skeleton © Bone formation © Growth mechanisms © Growth-controlling factors © Possil ies of influencing growth mechanisms Various aspects of the growth mechanisms are significant when assessing the etiology of malocclusions and the possible methods of treatment. The development of the craniofacial structures is not merely a symmetrical expansion of the outer bone contours (Fig. 3), but is based or three different growth mechanisms: Increase in size, bone remodeling, and bone displacement. 3. Misconceptions about bone growth Bone growth isnot based on sym ‘metrical enlargement of all struc tures and surfaces, ie. an adult's mandible does not correspond to the photographic enlargement ofa child's mandible, as illustrated Bone is subjected to 2 complex remodeling process which simul- taneously takes place with in crease in size and affects all seo tions ofthe structure (according to Ten Cate, 1980). Unlike soft tissue, bone is a mineralized substance and cannot grow by means of interstitial enlargement but only by apposition of the outer, periosteal, and inner, endosteal surfaces. Deposition and resorption take place simultaneously on the opposing bone surfaces, i.e. the outer and concurrently the inner cortical plates respectively. The deposition on the one side and the resorption of the other side not only causes an increase in proportions but also displaces the bone. New bone formation is closely associated with the bone remodeling process during the entire growth period. The two mechanisms must. be combined in order to ensure a well-balanced increase in dimensions of the bone structures whiles maintaining their shape and proportions. The third principle which applies to facial growth is bone displacement, and is based on the process by which adjacent bones move away from oye another, where they are connected by articular joints (sutures, synchondroses, condyles), due to their increasing size. The various growth mechanisms of the facial skeleton are governed and influenced by endogenous and exogenous factors, respectively, during the entire development period.Mandibular growth 4 Various stages of mandibular growth super- imposed on the condylar smentis directed simu taneously forward and downward, 5 Macerated mandibles of a neonate, a S-year-old and an 6 Various stages of mandibular growth supeIntramembranous Ossification Intramembranous ossification applies to two types of bone: - Bundle bone Lamellar bone Bundle bone develops directly in uncalcified connec- tive tissue. Osteoblasts, differentiating from the mesen- chyme, excrete an intercellular substance containing collagen fibrils. This osteoid matrix calcifies by depos iting apatite crystals. These centers of primary ossifica- Intramembranous ossification 7 1st phase Deposition ofapatte inthe connec tive tissue matrix. This results in a three-dimensional network of loose-packed bundle bone ‘The mineralized tissue particles nse yellow under the 08 (tetracycline staining, fluorescence with blue light excita ® 2nd phat is of lamellar bone (yellow the spicules of bundle bone ne resulting bone is more compact. Either a cortical bone or trabecular bone is formed depending onthe localization (ital taining; fluorescence with blue ight excitation, 9 3rdpt Periosteally derived cortex com posed of bundle bone Tho periosteal, radiating spi: cules of bundle bone can be seen fn the exterior. tis quite apparent that the bone deposited first is, thicker (vital staining; fluorescence with blue light excitation tion exhibit only minimal calcification density. Th apatite deposit is mostly irregular and exhibits a net-typ. structure in both the cortical and medullar areas (Fig. 7) Mineralization takes place very rapidly (several te thousandths of a millimeter per day) and can occu simultaneously over a large area. Apatite depositio increases with time (Fig. 8). The bone tissue is only the considered “mature” when the crystals are arranged i the same direction as the collagen fibrils. The bon tissue separates into outer cortices and a medullar are: which is then dissolved by resorption; this process take place parallel to the advancing bone formation. Th surrounding connective tissue differentiates into periosIts inner layer is rich in cells, has an osteogenic tion and contributes to the formation of the thicker fons of bone (Fig. 9) as well as the endosteum. Bundle bone which, in adults, is usually only formed rapid bone remodeling, is often only a prelimi type of ossification. It is reinforced by lamellar C Unlike bundle bone formation, lamellar bone devel- Gpmens only takes place in a mineralized matrix (e.g. Gaited cartilage or bundle bone spiculae). The mesh Ini bundle bone is filled to reinforce it, until eompsct Done is formed. Iineralized mat , Osteoblast formations appear on the which then form circles and nat ete surround the intercellular substance around a central vessel in several layers (Haversian system or osteon) (rigs. 10, 11), Lamellar bone is formed at a rate of 0.7215 microns per day (Fig. 12). The tissue exhibits a complicated arrangement of fibers, which is respon” sible for its mechanical properties (Pauwels, 1965). The rangement of the apatite in the concentric layers of fibrils meets the functional requirements. Lamellar bones are subject to continual deposition and resorption which can be influenced by environ- jmental factors, for example, orthodontic treatment. Lamellar bone formation 10 Formation of primary osteons The trabeculae of bundle bone that fare deposited periosteally low together to form canals, which are fined with osteoblasts. These are then narrowed down tothe lumen ofthe blood vessels by concentric, ‘Seposiion of lamellar bone. 41. Migration of primary costeons The primary osteons dri d due to further surface deposition of one (calcein staining; fluores: ‘cence with blue light excitation). 412 Conversion to Haversian systems While bone growth is continuing, the primary osteons, which have hited deeper, are being filed Further layers of lamellar bone are deposited on the surface atthe Same time (vital staining; fluores ence with blue light excitation,During enchondral ossification, tissue which is to become bone is first formed in cartilage and, apart from around the joints and epiphyses, is surrounded by peri- chondrium which later forms the periosteum. Osteo- genesis is based on cartilage ossifying to bone. Regard- less of which material existed previously (connective tissue or cartilage), the actual bone formation process always takes place according to the same principle (refer to section “Intramembranous Ossification”). Depending on the locality of the mineralization, it can be differentiated between: ~ Perichondral ossification — Endochondral ossit ‘ion Both types play a role in the ossification of long bones whereas only endochondral ossification takes place in the short and flat bones. 18 Endochondral ossification Remnants of mineralized cartilage (serraied green structures) form the centers of deposition for lamel- lar bone layers (red and yellow) Aight: The results ether spicules of primary spongiosa (as ilustrat ed) oF, when centered inthe cort cal layer, compact bone. Right Section through uncalctied bone (Giferentiat interference contrast, (DIC), according to Nomarski. ‘The osteoid layer is deposited on the remaining calci- fied spicules of the cartilage and then mineralized to form bony spongiosa, with a fine, reticular netlike struc- ture which has cartilage fragments between the osseous spicules (Fig. 13). The bony spongiosa can be converted to compact bone by filling its cavities (Fig. 13). Both endochondral and perichondral bone growth take place toward the epiphyses and joints. The increase in length of the bones during endochondral ossification depends on the growth of the epiphyseal cartilage. Once the epiphyseal line has been closed, the bones no longer increase in length. Unlike bones, cartilage growth is Perichondral ossification commences at the perichot drium, The mesenchymal cells of the tissue becon differentiated to osteoblasts, which surround th diaphyses with a bone sleeve prior to endochondr ossification, thus indirectly influencing its directicin. Endochondral ossification commences with charai teristic changes in the cartilage cells (hypertrophie cartilage) and their surrounding intercellular matr (calcium deposits), i.e. the formation of the so-calle primary spongiosa. Blood vessels and mesenchym: tissue then penetrate these areas from the perichor drium. The transported connective tissue cells becom differentiated to osteoblasts and resorption cells, e. chondroclasts which erode the cartilage in a cavern-lik pattern. based on both appositional and interstitial growth. In those areas where cartilage is being converted to bone various characteristic zones, in accordance with the individual stages, can be differentiated which conti nually blend with one another during the conver- sion process (Fig. 14). The ossification of “primary” cartilage (e.g epiphyseal cartilage) differs from that of cartilage (e.g. condyle cartilage). Environmental influences (for instance, functional orthopedic mechanisms) have a stronger effect on the condylar cartilagedue to its more superficial localization.Ecitysea cartone yale clang ova carne pe cage Pray spon Enchant ossiteaton 44 Growth of the epiphysi cartilage of long bones a Schematicview ofthe epiphyseal plate. The growth is based on the tell division rato of the columnar cartilage zone. 'b During the growth period of the cartilage, the columnar cartilage zone becomes converted to hyper- trophied cartiage zone which, in turn, becomes the primary spon giosa zone. fe With further ossification the cart- Tage zone advances fo the upper edge of the diagram (Eniow, 1968) cartilage, hy ‘The ground substance begins to iy andhypertrophied cartlage calls to dissolve in the underlying ‘mineralization zone (DIC accord ing t Nomarski), The calcified cartilage is parlly resorbed and forms the basis for he spongiosa spicules Right: Fluorography (UV excita tion) shows how the mineralized layers (marked with tetracycline [yellow] and alizarine [pink) at ‘week intervals) retreat from the epiphyseal cartilage zone. 16 Condylar cartilage of the temporomandibular joint The condyiar cartlageisa second ary type of cartlage, which was transtormed phylogenetically from the periosteum, — Histologically, condiylar cartilage is considered 0 have four different zones (longi dinal section): 1) Dense, fibrous connective ts: sue zone sparsely vascula 2) Proliferation zone ol uniter centiated connective tissue cells {mitotic zone), which become di ferentiated to chondroblasts ’3) Hyaline cartilage zone with randomly distbuted chondro blasts and hypertrophied cells The matrix of these cells is more calcified toward the condyle; '4) Endochondral_ ossification zone, in which the cartiage is re sorbed and replaced with tre becular bone. Fight: The cartilage and miner Zao zones (vita staining; luores- sence microscope)The made and direction of the construction bite taken forthe acti- valor appliance (right) are impo tant parameters for stimulating condylar growth. The latter is necessary for skeletal adaption of the new mandibular position which the clinician 18 attempling to achieve with this type of therapy. The altered muscle activity and the stretching of the sot tissues caused by the acrylic blockappear to be imporiant to the condylar ‘growth processes. 18 Histologic changes in the condylar cartilage after ‘anterior translation of the ‘mandible Aller 1 week of treatment with hyperpropuleor, the cell prolifera tion zone in the rat cartlage is thickened without producing no- ticeable changes in the cartilage Not until the appliance has been worn for 4 weeks can the cell pro eration zone and the cartilage zone be seen as signiicantly wider (Petrovic etal, 1975}. 19. Histologic changes in the condylar cartilage after posterior transiation of the mandible After! weekoltreatmentwithachin ‘cap, the cel proliferation zone in the rat carilage is narrowed, Ater wearing the chin cap for 4 weeks the height of the cartlage zone has also decreased. This change therefore, appears to be secondary, as a result of the feduced number of undifferentiat fd cells in the proliferation zone, which later become differentiated to chondroblasts (Petrovic et a 5). r Fbvous connate sue 208 Proteraton 06 — yan carge zone Encacondalesicaton yan catage sre — Endochontalosteaton —Endosteal and periosteal bone growth Cortical drift Relocation and remodeling “V" principle Surface principle Growth fields Displacement Growth equivalents growth takes place according to several basic The following two mechanisms are important for which can also be used to explain the growth bone growth in the facial and cranial regions: ses of the facial skeleton. he theory that bones grow by simple symmetrical — Direct bone growth by means of deposition and ent is wrong Such a simple growth mecha- resorption processes on the bone surfaces, which could not possibly create suchacomplexanddiffe- cause the cortical plate to drift; ted morphology as that of the mandible or maxilla. ch morphology demands differential growth mecha- Displacement of the entire bone due to growth of the ‘and different types of development for the indivi- _bone itself or expansion of adjacent structures. bones. 20. Bone relocation and remodeling “The hard palate of anewbom baby is directly beneath the infraorbital rims. Progressive enlargement of ‘the nasal cavities displaces the palate downward during growth of the facial skeleton. ‘Simultaneously with the down- ‘ward movement, the bones are remodeled by ‘resorption and ‘apposition and increase in size. In ‘adults, the space which formed the hard palate and maxillary arch of the infant is occupied by the expanded nasal chambers (Teo Cate, 1980),Endosteal and Periosteal Growth Approximately half of the cortical plate of the facial and cranial bones is formed by the outer surface, i.e. the periosteum, and the other half by the inner surface, ie. the endosteum. Appositional layers of cortical bone can originate en- tirely from the periosteum or the endosteum (Fig. 21). In other cases, the same cortex is composed of periosteal and endosteal bone layers which are separat- ed by a so-called reversal line Fig. 22). This type of bone 21. Periosteal and endosteal bone formation jone apposition jone resorption Left: Ifthe direction of growth re- mains constant, the right cortical plate isformed periosteally an the left plate endosteally. Both shift in tunison in the direction of growth, ive tothe right, Aight: The direction of growth can ‘change during development ofthe bone. In the area marked with an asterisk, bone formation initially ‘occurs endosteally (above) and, at a later date after reversal of the direction of growth, periosteally (below) (Eniow, 1982) ‘The interface between periosteally ‘and endosteally formed bone is termed the reversal line (-+=rever sal line) Right: Section through an alveolar bone. The yellow staining indicates that endosteal tone formation takes place inthe upper section of the surface facing the tooth and pe riostea formation in the lower sec tion. This leads to rotation of the bone structure fluorescent mi- Croscopic view alter tetracycline staining) Left: Line-drawing ofthe histologic section. growth indicates that there has been a change in th direction of growth at some time. As new cortical bon is always deposited on the surface facing toward th direction of growth, bone formation originating in th endosteum can, at a later date and after reversal of th direction of growth, evert to a type of periosteal bon formation. The reversal line represents the interfac between endosteally and periosteally produced bon layers,tical Drift tone structures have one growth principle in more bone be deposited than resorbed, the thickness of won, which was termed “drift” by Enlow (1963). the. struct ‘increases. During the developmental rhe cortical plate can be relocated by simultaneous period, ‘deposition takes place at a slightly faster rate “am and resorption processes on the opposing than resorption, So that the individual bones slowly teal and endosteal surfaces (cortical drift). The enlarge. cortical plate ‘lepositing and resorb- ‘The teeth follow the drift of their alveolae while bone substance on the outer and inner surfaces, the jaw is growing and thus maintain their position ively, in the direction of growth (Fig. 23). If within the surrounding bony structures despite the bone and deposition take place at the same rate, displacement (Fig. 25). ‘hickness of the bone remains constant. Should —) 23 Cortical drift (@iagrammatc view) ‘a Cortical plate of @ bone. b Increase in thickness due to ‘apposition on one of the surfaces. ‘e When the resorption process on tne side of the bone exceeds the ‘pposition process on the OppOS~ ing side, the thickness ofthe Done will be reduced. ‘d When resorption an one side of the bone corresponds in magni- tude to apposition on the opposing sida, the bone will drift without hanging its size. fe The cortical plate has drifted ‘ommpletly tothe right when com paredtoits orginal postion ina) by the process of surface remodeling (Ten Cate, 1980).24 Cortical drift Formation of lamellar b endosteal surface and resorption ‘onthe periosteal surface cause the fete cortex to dri. Should both surfaces drift at the same rate, the dimensions of the bone will be maintained, ‘The asymmetric coloration around the osteon shown in the canter o picture indicates the direction i (marked at t-week intervals seven different vital dyes; 25. Drift of alveolar sockets growth plion ofthe alveolar bone on the surface facing towardtnedirec- tion of dri and apposition on the ‘opposite alveolar side. By this means, the tooth retains its ana: tomic postion relative tothe alveo: larprocessasthe whole bone dis during growth Fig.24).Theretoreit is necessary that the localization of the alveolar resorption and apposi tion processes are identical yet take place in the reverse direction to the periosteal and endosteal proet The heavy staining in the dentin (layer-by-layer marking with vital are caused by the continual ‘routh o theincisorsinthisradent, W Root of tooth Periodontal space ‘_ Bone deposition Bone resorption ——~cation and Remodeling to new bone deposition on an existing surface, all +r parts of the structure undergo shifts in relative ‘tion; a movement which is termed relocation. "As a result of this process, further adaptive bone Jing is necessary in order to adjust the shape ‘ize of the area to the new relationship. Selective ption and apposition processes functionally il the area to conform to the new physiological ing. Relocation and cyclic, structural remodeling are growth mechanisms which are closely related to one another; Remodeling is based on relocation and is a ‘secondary result of the displacement process. When one level passes into the next due to growth, its position is taken by the following level which undergoes the rele- vant structural changes. The information which initiates the remodeling process is contained within the various soft tissues surrounding the bone. = —) 26 Relocation and remodeling | (iagrammatic view) | ‘The position of the gray zone changes in relation to the original postion (A) duetobone apposition Eejand resorption (-).Asaresultot the level-by-level growth process, the marked area Is translocated from the posterior 10 the anterior order of the ramus, without changing its own positon. Left: Superposition to show the {growth processes of the ramus, Parts ofthe condylar head are con- verted into the nack ofthe condyle ‘uring the process of relocation. The sections through a) and b) show the local remodeling Changes which are necessary 10 ‘dant the form and size of the Structurestotheirnew relative post tions (Enlow, 1982). 27 Relocation and ‘remodeling of the mandible during growth ‘The remodeling process ofthe ra- rmustakes place towarcthe poster jor. The body ofthe mandible be- ‘comes lengthened by remodeling pats of the ramus, which simul faneously sis in backward direc Wan (Eniow, 1968) |28 Primary displacement and bone growth These two basic growlh mech anisms are closely interrelated. Beginning at position (1) the en- tie mandible is displaced down- ward and forward (2), away from its articular joins, by the growth of the surrounding Soft issues, ‘This transitory movernent stimu: lates the enlargement and remo: doling (3) of the condyles and rami which take pace parallel to displacement ‘The bone growth processes are directed upward and backward by an amount that equals the displ: cement ofthe mandible. ‘The changes resulting from these combined processes are shown in (4) {Ton Cate, 980)“y” Principle / tional requirements. Ths informa: tioncausesthehistogeneticactvty ff the osteogenic membranes 10 fespond (Ten Cat, 1980). 34 "Growth centers” ‘This term is atten used to describe ‘ry active growth fields which are ‘significant to the growth processes uch as the cranial and facial Sutures, the mandibular condyies the maxillary tuberosities, the ‘alveolar processes, and the sy” hondroses of the cranial base However, bone grown not only takes place in hese areas. inner land outer growth fields of a given pone also play an active role inthe process (Eniow, 1962)ees —. a Displacement Apart from direct bone growth due to deposition and forces of the soft tissues in the growing face. It ocews } Feorption, the process of displacement, ie. the trans- parallel tobone growth, thus creatinga space around the latory movement of the whole bone caused by the contact surfaces into which the bone can enlarge. The | surrounding physical forces, isthe secondcharacteristic degree of displacement exactly equals the amount of mechanism of skull growth, The entire bone is carried _ new bone deposition, although the direction of displace: way from its articular interfaces (sutures, synchond- ment is always opposite to that ofthe bone deposition. | roses, condyles) with adjacent bones. Bone displacement due to the enlargement of bones Displacement. in conjunction with bone’s own and soft tissue which are nearby or not immediately growth is termed. “primary displacement” by Enlow. adjacent is termed “secondary displacement.” Displacement is initiated by the sum of the expansive the nasomaxillary complex The bone structure grows upward and backward (2) due to deposi tion and resorption processes. Simultaneously, theentecomplex is displaced forward (©). Thus, the necessary space for bone deposi- tion is created around the articular surfaces, Primary displacement ‘always takes place in the oppose tection to the vector of the bone growth Right: Diagrammatic view of the ‘events during primary displace- ment, Tha bone is remodeled and shiled in the opposite direction simultaneously (Eniow, 1982), 36 Secondary displacement fof the nasomaxillary complex This process is nol associated with arouth ofthe Bone itsel. This type of displacement Is initiated by enlargement of adjacent or emote ‘bones and sof tssues. Is effects fransterced from bone to bone and ‘develops in relatively distantareas. Secondary displacement of the rhasomaxillary complex is caused by grow of the middle cranial fossa and the temporal lobe, and is directed forward and downward ©). Fight: Diagrammatic view of ‘secondary displacement. The bone is caried away withoutbeing remodeled (Enlow, 1982).xillary Growth axillary remodeling involves bone deposition on the terior wall of the maxillary tuberosity, resulting in a or lengthening of the bony maxillary arch. Depo on the outer surfaces of the tuberosities and orption on the inner surfaces causes the cortical to drift in a backward direction and the space for pneumatic cavities enlarges (Fig. 37). This posterior elongation of the upper jaw is cou- ed with primary displacement of the maxilla which is ed anteriorly and exactly equals the amount of sterior lengthening (Fig. 38). This increase in overall length of the maxilla creates tensile forces which initiate tensile adaptive sutural growth. Due to growth of the middle cranial fossa, the manilla, the anterior cranial base, the forehead, and the zygoma are shifted in a forward direction. This process leads to secondary displacement of the maxilla, i.e. it is displaced passively due to expansion of the middle cranial fossa without the growth processes of the maxilla itself being directly involved. The extent of secondary displacement corresponds to the degree of anterior extension of the middle cranial fossa (Fig. 38). 37. Remodeling of the upper arch “The upper jaw is extended poster. jorly by means of bone deposition cn the outer cortical surface ofthe maxillary tuberosity and resorption on the inner plate. This causes the pterygopalatine fossa and the plerygomaxilary fissure (PTM) to move posteriorly (the pterygo- maxillary fissure isillustrated as an Inverted teardrop, as on a cepha- logram) Left: The pterygopalatine fossa is positioned between the pterygoid plates and the maxillary tuberosity (Eniow, 1982), 38 Primary and secondary displacement of the maxilla Vertical plane of reference PTM line Horizontal plane of reference = Functional occlusal plane Left; The maxila increases in length and is displaced anteriorly simultaneously (primary time on a particular producing > tissue —————> results 1) Hereditary 1) Continual, 7) Malnutrition 2) Anomalies due to intermittent, tissue 2) Mal- maldevelopment or only once 2) Teeth occlusion 3) Trauma 3) Bone 3) Bone 4) Physical agents 2) Various age levels 4) Cartilage dysplasia 5) Habits (pre- or postnatal) 5) Soff tissue, except 6) Disease muscles 1) Neuromuscular 1) Malfunction Each causal factor primarily affects a particular tissue for a certain period of time, which causes the deformity (Gee above), As far as the time factor is concerned, the specific cause can act continual, intermittent, or operate only once, in any or all developmental stages (pre- or postnatal). The results of these disruptive factors depend on the localization and texture of the tissue most affected by the deformity. The primary tissue site may be: the neuro- ‘muscular tissue, the teeth, the bones, the cartilage tissue, and the other sof issues, except the muscles (see above). The primary deformities caused by these factors are: malfunction, should the neuromuscular tissues be affected primarily; malocclusion, should the teeth be affected primarily; and osseous dysplasia, should the bone tissue be affected primarily (Fig. 135). 135. Causal pathogenesis of anomalies Primary tissue site The etiology ofa dentotacial defor- ity ig datermined by the type ot tissue which is primarily affected : by the causal factor. ‘Anomaly | 7 Neuromuscular tissue In many cases, a combination of allttree anomalies occursas, apart from the primary tissue site the ther tissues, are usually second: arly also involved inthe deformity {> Malfunction > Teeth N Causal factor Bone tissue ——|> pysplasia > Malocclusion60 Hereditary Abnormalities Etiology For a long time, inheritance was considered the most important causal factor in the genesis of dentofacial deformities, although there is nearly no scientific evi- dence to support this thesis. Exact details about the significance of hereditary factors in the etiology of malformations can only be gained by carrying out extensive studies on twins and families. According to current knowledge, the following tissues can be primar- ily affected by genetically transferred dentofacial defor- miities: Neuromuscular System Hereditary deformities of the neuromuscular system consist primarily of anomalies in size, position, tonicity, contractility, and in the neuro- muscular coordination pattern of facial, oral, and tongue musculature. Thus severe deformities of the dentoalveolar region occur with both macroglossia and hypoglossia. The configuration of the lips as well as their compe- tence and function are of great importance if the oro- 136 Genuine Class I malocclusion in three brothers Top row: Profle views Bottom row: Overiet _ Top row: Whereas the oldest bro- ther (left) has normal, competent lips, the younger siblings show a disturbed ip seal (open mouth posture, short, hypotonic upper lip). The youngest child (right) has in addition a hyperfunctioning mentalis muscle. Bottom row: Clinical pictures ofthe corresponding overets The diferent degrees of the ‘malocclusion correlate to the dit- ferent amount of neuromuscular disturbance. ‘The oldest brother (lef), with nor- ‘mal lips, has the smallest overjet and the youngest brother, within ‘competent lips and hyperacivty of the mentalis muscle, has. the largest overet (right. — Neuromuscular system ~ Teeth ~ Bone/cartilage tissue or ~ Soft tissues facial system is to develop optimally. Certain types of lip configuration which occur several times within one family may be hereditary and thus predisposing its ‘members to dysfunction and malocclusion (Fig. 136). It is often difficult to decide whether tongue and lip habits are due to hereditary factors or due to imitation. Rare pathological muscular conditions, such as hyper- trophy and atrophy, can also cause malocclusions. “i a rDentition ‘As has been shown by twin studies, very many features ofthe dentition are hereditary: ~ Size of the teeth ~ Shape of the teeth - Number of teeth ~ Mineralization of teeth ~ Path of eruption and primary position of tooth germ ~ Sequence of eruption Severe deviations in shape and size of the teeth are the most common causes in the genesis of dentofacial malocclusions. From the orthodontic point of view, it is usually not the actual size of the teeth which is relevant (Figs. 137, 138), but rather the size of the teeth in comparison to that of their bony bases (Figs. 139, 140). The prevalence of Aypodontia ~ without taking the third molars into consideration ~ was quoted by Dolder (1934) as being 3.4%; the anomaly being less frequent in the deciduous dentition than in the permanent denti- tion. The third molars are the most often missing tooth, followed in descending order by the lower second premolars, the upper lateral incisors, the upper second Genetic Factors 61 premolars, the lower central incisors, and the upper and lower first premolars. Hypodontia often occurs in combination with other syndromes (e.g. ectodermal dysplasia, cleft of ip, jaw and palate, Down’s syndrome) (Fig. 141). The data on prevalence of hyperodontia show a wider range. Cases of hyperodontia are less common than cases with congenitally missing teeth. All types of tooth can be supernumerary, particularly in the permanent dentition. Hyperactivity of the dental lamina occurs more often in the upper jaw, especially in the anterior and molar regions. The next most affected teeth are the lower premolars and incisors (Fig. 151). The super- nunierary tooth can be formed either normally or atypically. It can also be formed in such a manner that, due to gemination and fusion, the supernumerary struc ture does not develop separately but rather resuits in an oversized tooth (Fig. 156). Supernumerary teeth are common in patients with cleft lip and palate around the cleft area (supernumerary lateral incisors) and in cases of cleidocranial dysostosis (Fig. 154). 137- Microdontia Microdentia ofthe maxillary lateral Ofalithetypes ofteeth, the upper lateral incisors vary most in shape. ‘Anomalies in tooth size can be restricted to individual teeth oF ‘may occur generally. 138 Macrodontia of individual teeth Tooth anomaly in the upper anter- Tor region due to oversized lateral62 Etiology 139. Macrodontia of the upper teeth in relation to the size of ‘basal bone Due tothe disproportion insize be- tween the two structures, the ante. jor teeth are crowded and the pos- terior teeth are severely tipped buccal. 140. Microdontia of the entire ontition in relation to the size of the basal bones ‘The spaces between the teeth are the result ofa size discrepancy be- tween the dental arches and the basal bones. Hypodontia 141 Hypodontia of deciduous teeth CCongenitally missing upper lateral deciduous incisors in a case with familial predispostion to hypo- ontia Right: Corresponding panoramic radiograph, Hypodontia is rare among primary «| teeth i 142. Hypodontia of permanent teeth ‘Occlusion of the patient shown in Fig. 41 att yearsofage. Theupper lateral permanent incisors are missing. “The upper canines have erupted mesial, In Caucasian populations, the ‘most common teeth of the perma- nent dentition 10 be affected by Congenital absence are the lower second premolars and the upper lateral incisors.143 Position of the deciduous tooth in case of congenitally ‘missing permanent tooth Submerging of persistent lower, second deciduous molars - a microsympiom of congenital ab sence of the mandibular second premolars. Hypodontia and occlusal relations 144 Shape of the upper dental arch ‘Theanteriorarch ofthis'2-year-old female patient has been flattened noticeably due to congenitally missing upper lateral incisors. 148. Occlusal findings ‘The discrepancy in anterior tooth ‘size between the upper and lower ‘arch promoted the development of fan anterior cross-bite, 146 Oligodontia Hypodontia of @ large number of teeth in a patient with a bilateral Cleft of lip, jaw, and palate, The pationt shows congenital absence of the upper lateral inc sors, the upper frst and second premolars, the lower left central incisor, and. the lower second premolars. The tooth germs ofthe Upper permanent caninesare dys- topic. Left: The oligodonta in the maxi lary arch futher impedes ts devel opment.eee Inherited oligodontia of varying expression in four siblings 147 Teeth present in the ‘oldest brother Hypodontia of the upper canines, the lower second molar, and the wisdom teeth at the age of 135 1e upper right deciduous 148 Teeth present in the second oldest brother Congenital absence of the upper nines, the upper right lateral the lower second premo: lars at the age of 85 years. The Upper left lateral incisor is hypo- plastic. 149 Teeth present in the youngest brother The third son of the family has vere oligodontia a the age of 10 years ~ congenital absence of the Upper right lateral incisor, the up per righ first premolar, bth upper canines and second. premolars, and lower second premolars. 150 Tooth present in the si The youngest child ofthe family, a 6-year-old gir, has hypodontia o! the upper right lateral incisor, the Upper let second premolar and both lower second premolars. The germotthe upper eft ateral incisor is hypoplastic. The germ of the Upper right permanent canine is in {ectopic postion,151 Hyperodontia Radiograph of 2 22-year-old fe ‘male patient with four upernumer ary teeth Supernumerary teeth are pre- sent in both premolar regions o the lower arch. The germ of acisto molar is apparent in the upper left quadrant iis considered tobe the result of excessive formation of the denial lamina, 152 Mesiodens Supernumerary, rudimentary tooth, which has erupted between the upper central incisors. This type of abnormality is often inherited and is the most common type of iyperodontia.tcan severe Iyimpede the eruption othe anter ior teeth 153. Odontoma ‘Supemumerary mineralized struc ture located near the crown of the Upper right canine which interferes with eruption of the canine and, together withthe pericoronal cyst is retaining i. 184 Hyperodontia in cleidocranial dysostosis Muttiple, ectopic, fuly or partially impacted permanent teeth in a 16 year-old female patient, The supernumerary incisors, ca nines, and premolars aswell asthe persistence of the deciduous den- ition are typical findings in this type of skeletal detectoe nord @ @ 66 00 8 Germination = Incomplete div sion of one single tooth bud. big conan { } Ht 1} «© Fusion = Union ofthe dentin of ‘wo teeth, rom two tooth buds. d Conerescence = Union of the cellular cementum of two teeth, from two tooth buds, Tannenbaum and Alling, 1963). 156 Gomination Incomplete division of the tooth buds ofthe upper central incisors. ™ ‘These oversized, cosmetically un Pp pleasant teeth are typical of this ‘ype of anomaly. Aight: The notch in the incisal ed ge, and the axial groove through the crown, is aresultofincomplete separation of the tooth bud. 187, Twinning Supernumerary tooth inthe lower anterior region, Judging by the shape and size ‘of the teeth, the hyperodontia ‘appears o be a result ofthe bud of the right central incisor dividing {and forming two completely sepa: rate twin teeth, 158 Fusion Fusion between an upper lft con- tral incisor and a supernumerary tooth Aight: Thetooth crowns are partial ly fused. n this case, the union can ‘be separated and the supernumer- ary tooth extracted.Inherited defects of the tooth structure differ from exogenic-induced disturbances in mineralization as follows (Fig. 159) 1) An inherited malformation is present in both the deciduous and permanent dentition. 2) Itis localized in either the enamel or the dentin. 3) Inherited defects of the tooth structure are arranged either irregularly or as vertical ridges and grooves ig. 162). Abnomalities of tooth structures Hereditary Deciduous and permanent dentition Enamel or dentin Irregular or vertical Dysplasias of the enamel can be either hypoplastic or aplastic (Fig. 162). Dentinogenesis imperfecta often occurs together with obliterated pulp chambers, tooth root deformities, and osteogenesis imperfecta (Figs. 160, 161). ‘The fact that retained teeth and ectopic teeth tend to occur frequently in the same families indicates that these abnormalities are determined genetically (Figs. 166- 169). 489. Disturbances in calcifi- cation due to hereditary and ‘environmental factors ‘Comparison of the aitferent patho- logic symptoms of tooth structure, Environmental Deciduous or permanent dentition Enamel and dentin Horizontal ‘ Dentinogenesi imperfecta 160 Clinical findings Hereditary dysplasia of the dentin in a 19-year-old patient. Short, amber-colored upperand lower anterior teeth, with splintered enamel and marked atition ofthe incisal edges are typical clinical findings inthis disturbance intooth formatin. 161 Radiographic findings In cases of dentinogenesis imper fecia, tne radiographs reveal the following findings: Reduced radiographic contrast fof the dentin, obliteration of the pulp chambers and root canals, short, dilated rots ‘Anomalies in the shape of the roots are also present with con: striction in the cervical regions, Radiograph ofthe patient shown in Fig. 160.162 Amelogenesis imperfecta = Hypoplastic type The thin, chalky ~ white and brown enamel is hard and its surface is rough, covered with pits and fis- ‘sures. Atttion occurs at a higher rate than normal and parts ofthe ‘enamel have chipped from the Underying dentin, 163. Amelogenesis imperfecta = Hypomineralized type This 12-year-old girl hasyellowish- brown, very soft enamel, The sur- faces of the teeth are dull and covered with ridges and grooves. Noticeable amounts of enamel have fractured away. The enamel dysplasia is com- bined with an open bite. ‘Amelogenesis impertecta ~ Hypermature type 164 Mixed dentition The permanent teeth have opaque ‘white, dull enamel, and the enamel ‘ofthe incisors shows theft signs (of splintering. The patient is a 9-year-old boy. ‘The disturbance in enamel for ‘mation occurstogether with acom- Plex open bite 165 Early stage of permanent dentition ‘The enamel onthe canines, premo- Jars, and molars has been dis- solved and the dentin has been stained dark brown, The crowns Of the teeth exhibit anomalies in shape and size. Aight: The surtace of the tooth is ‘smooth, Ccclusal findings of the patient shownin Fig. 164,18 years ofage.Impaction of teeth 166 Impacted second deciduous molar Impaction ofthe lower right prim ary second molar in a 9-year-old male patient The space for the unerupted deciduous tooth is resticed due to mesial tipping ofthe adjacenttooth ‘on the distal side, which is typical {or cases of ankylosis. The perma: nent tooth germ has been dis placed distally by the impacted deciduous tooth. In this case the eruption abnor mally is hereditary (reter to Ro. 167), 167. Hereditary impaction of deciduous teeth Radiograph of the 7-year-old bro ther ofthe patient shown in Fig 168, ‘This patient shows ankylosis of the lower left deciduous second molar, The underiying germ ofthe permanent tooth has been dis- placed mesialy The space for the unerupted tooth has been narrowed due to mesial tipping of the fist perma rent molar The eruption of the upper left deciduous second molar is also being disrupted by the same phe nomenon. 168 Transposition of teeth Two adjacent teeth have ex changed positions in the dental arch for genetic reasons. Unilateral transposition ofthe eft upper canine and first premolar, with congenital absence of the Upper lateral incisors Left: Occlusal relation of the left anterior region with the malpost tioned upper teeth Transposition of the upper ca- nine and the premolars is tne most ‘common type observed. 160 ral transposition Both upper canines and frst pre molars are transposed ‘The melalignment i tis female patients due to hereditary factors,Certain genetic factors influence bone development of the mandible, the maxilla, and the other bones in the craniofacial complex, leading to hereditary osseous dysplasia, The following may be affected by these aberrations: ~ Bone size Shape of the bones and the jaw bases = Bone location — Number of bones present 470 Hypoplasia of the ‘mandible, combined with embryopathy Facial profile and anteroposterior jaw relationships in a 3-year-old patient with dysmelia and various ‘rgarie defects. The hypoplasia of the mandibie has resulted in a receding facial profile. The mat formed external ear is also appar entonthe acial view. Dueto severe fetrognathism of the mandible, the lower lip is positioned behind the upper incisors. Fight: This type of soft-tissue morphology causes progressive 2 in overt. 171_ Hypoplasia of the maxilla in Crouzon’s disease (craniofacial dysostosis) The characteristic extraoral symp. toms of Crouzon's disease in this year-old patient are the exo- phihalmos, hypertelorism, the broad root of the nose, and the prottuding lower ip. Right: Due to premature ossi fication ofthe cxanial sutures, this syndrome causes congenital oxy cophaly, with prominent digital crarial markings, malformations of the bony orbits, and hypoplasia of the maxila, ‘The maxillary deficiency causes «a skeletal Class Il relationship. Whereas bone size anomalies account for some of the 1uses of hereditary micrognathism or macrognathism (Figs. 170, 171), variations in bone location represent some of the causes of prognathism or retrognathism, Hereditary variations in jaw shape often cause asym- metres. Unlike agnathism, which is very uncommon, hypo- plasiaand partial aplasia of the jaw bones occur together with craniofacial dysostoses, such as hereditary mal- formations of the area around the first branchial arch (mandibulofacial dysostosis, maxillofacial dysostosis), cleidocranial dysostosis, and Crouzon’s disease (Fig. 171).Deformities of the face and WS caused by embryonic ‘malformation of the second branchial arch 172 Frontal and profile views This 13-year-old patient has hypo: plasia of the right mandibular ramus. The angle othe mouth and the bony chin are distorted toward the site of malformation, Right: The right earisalsoattected by the deformity, The right audit canals blocked and the maldeve. ‘opment othe external ear result in the formation of auricular tags. 173. Radiographic findings in the panoramic view he right ramus is almost com pletely missing. Whereas the right -ondyloid process is vestigial, the coronoid process is well da oped. The rightcorpusofthe manaible, its gonial angle and the right ha of the maxila are underdeveloped Alltooth germs are present in both arches. 174 Radiographic findings in the posteroanterior and lateral cephalogram The vertical development of the right half of the face has been impeded, the occlusal plane ais forted upwards 10 the right, and ‘the mandiole, dueto ts hypoplasia, isshited othe righttoward the site (of malformation, Right: The maldevelopment of the lower jaw is associated with mandi retrognathism.Skeletal Malocclusion Genetics play an important role in the etiology of most skeletal malocclusions. Although previously, mandibular prognathism and Class Il, Division 2 malocclusions were attributed to dominant inheritance, the data derived from family and twin studies have revealed that hereditary malocclusions are nearly always transmitted as polygenic traits (Schulze, 1982), i.e. the individual deformities only develop due to the accumulative effect of several hereditary factors (“additive polygenesis”). The variability in the expres- sion of a malocclusion in one family is due to the Hereditary mar prognathism ( 175. Different degrees of skeletal malocclusion in four siblings Cephalometric lateral radiographs Of the oldest (let) and next oldest ghi) brother. 176. Lateral cephalograms of the two younger siblings Left: Facial skeleton of the youn. ‘gest brother, Right: Craniofacial morph the youngest sister. y of The degree ofthe anteroposterior Imaltelationship increases pro aressively from the oldest to the joungest chil. different numbers of genes involved (intensity) and due to the environmental factors. The exogenic influences, may compensate or enhance the appearance of the malocclusion. The genetically determined traits often only become apparent in the phenotype due to the effect of environmental factors. According to current understanding, the following skeletal malocelusionsare hereditary: Class 11, Division 2, mandibular prognathism, bimaxillary protrusion, skeletal open bites, and skeletal mandibular retrognathism.er eee te a ‘Ocolusion of all four siblings prior to commencing ortho- dontic treatment 177 Oldest brother's occlusion The posterior teeth have only a slight buccolingual overbite and the upper left lateralincisorandtne lower canine are in edge-to-edge relation (see. Fig. 175, let. 178 Next oldest brother's, occlusion ‘The boy shows an unilateral cross- bite on the left side associated with {an anterior cross-bite of the left lateral incisors (see Fig. 175, righ. 178. Youngest brother's ‘celusion ‘The patent is 7 years old and has total cross-bite (see Fig, 176, lf) 180. Youngest sister's occlusion The gitl was born last and has @ right lateral cross-bite in the early stage of the mixed dentition, The Upper leftcentralincisoriserupting into an anterior cross-ite relation (eee Fig. 176, ight,oo eee Soft Tissues As hereditary anomalies of the soft tissues (excluding ——— the neuromusculature) often only have a slight effect ~ Facial clefts on the genesis of orthodontic problems, they are of — Microstomia minor importance. The following hereditary anomalies — Anomalies of the frena of the soft tissues can be observed: ~ Ankyloglossia 181. Labial frenum Clinical picture of a high, wide frenum which is extended into the incisive papilla and occurs to- gether with a central diastema. The anterior tip of the papilla is between the upper centraincisors. The hereditary components ofthe Tabial renum include the height of thepointatattachmentandinetex- I ture of the tissue, 4 Lymphatic tissue 182 Adenoids Endoscopic picture of medium. < sized adenoids. ’As the size and development of lymphatic tsaue may be here: diary, hyperplasia ofthe adenoids tends to un in families. Aight: Postion of the adenoids in felation to the surrounding struc- tures is marked on this cephalo- metric lateral radiograph, 183. Hyperplasia of the tonsils Increases inthe size ofthe tonsils, as wellas ofthe adenoids, often un in families, Hypertrophic lymphatic tissue in the upper respiratory tract n fact as an epigenetic factor and Increase the severity o!amalocclu-Acquired Anomalies Developmental Damage Those malocclusions which, etiologically speaking, were caused by developmental damage during the fetal period, are considered congenital anomalies (Moss, 1962, Enlow, 1982). In many of these cases, the exact causal pathogenesis cannot be determined. The following are included among the causes of these dysplasias proven to date: (embryopathies caused by virus diseases in the mother (eg. measles toxoplasmosis), ionizing radiation, poi- Petar stn Ala siete a sonous effects (e.g. medication) or other teratogenic harmful substances, Fetal damage with this type of genesis and the following craniofacial abnormalities have been proven to be closely connected with one another: Maldevelopment of the first and second branchial arches, micrognathism, oligodontia, and anodontia. ‘The majority of cases with lip-jaw-palate clefts are included in this etiological group. Hereditary embry- onal defects only account for approximately 20% of these patients (Schilli et al., 1970). Fetal alcohol embryopathy 184. Profile and frontal view Physiognomy of a 13-year-old patient with the extraoral. symp: toms characteristic of this syn drome: hypoplasia of the middle section of the face, plosis of the eyelids and a broad nasal root. ‘Apart trom the maldevelopment of ‘other organs, the patient's grown is ‘also stunted, Both are typical of this syndrome, 485. Craniofacial morphology in the cephalometric radio- ‘graph and occlusal relation ‘The hypoplasia ofthe middle sec: tion of the face and the resulting fetruded position of the maxilla ‘caused severe skeletal mandibular prognathism, Left: The patient has @ total cross bite. ‘The skeletal dysplasias of this syndrome are considered to be a result of chondrogenesis being im- ppeded by thefetal alcohol embryo- patty.i Moat mandloua et 186. Profile view and | cephalometric radiograph This 6-year-old boyhashypoplasia and a severely retruded mandible with no chin, resulting from con: ‘genital mandibular dysplasia, ! 187. Radiographic findings in the panoramic view Radiographic survey of the cont rnuous cletts around the mandi ular median line. Apart from the skeletal. deformity, this. patient suffers from agenesia of several lower anterior teeth 188 Clinical picture of the occlusion The sot tssues pullboth segments ol the mandible toward the lingual Right: Placing the tongue between the two segments uprights them toward the vestibule.auma ~ Prenatal trauma ~ Trauma at birth ~ Postnatal trauma enatalintrauterine trauma can cause hypoplasia ofthe indible. Should the fetus be positioned unfavorably ring pregnancy, the facial skeleton very often devel- s asymmetrically, although this is mostly compensat- for during the first few postnatal weeks. ee erate rat zs. Birth injuries are rare nowadays. Previously, forceps delivery very often harmed the areas around the TMJs, which sometimes caused ankyloses of the mandibular joints. Asa result of these ankyloses during early cl hood, mandibular growth was impeded severely, caus- ing the patient to develop a “Vogelgesicht”. Postnatal trauma can occur at any age and in any area of the orofacial system. The consequences are more or less dramatic, depending on the extent and localization of the trauma and at what point in the development phase it occurs. Ankyloses of the ‘temporomandibular joints 189 Occlusion and profile This 19-year-old patient has anky- losis of both TMJs due to traumain early infancy Considerable inhibition of the development of the mandible occured as a result of the early damage to the joins. The patient hasan extreme case of mandibul ‘micrognathism ana the typical pro file of a “Vogelgesicht 190 Frontal and lateral cephe- lometric radiographs Three-dimensional view ofthe fa cial skeleton to cover the vertical and sagittal mandibular dysplasia Despite the ankyloses of the mandibular joints and the distur Dances in mandibular growth, the intercondylar width developed properly.s= See 191 Traumatic deformities of theeth Left: The whitish discolored areas and notches inthe labial surfaces these lower incisors are micro- mptoms of trauma experienced at 2 years of age. The horizontal shape ofthese decalctied zonesis @ typical symptom of acquired damage. Right: The ring-shaped, yellowish wn enamel hypoplasia on this Upper lateral incisor is a result of damage by local deciduous tooth rauma while the permanent teeth were developing 192 Dilaceration Tre crown of the tooth and the hypoplastic root of this upper frst molar are angled acutely. This tocth anomaly isa result ofamaxi lary fracture along the Le Fort plane at 2 years of age. Fight: Radiograph othe dilacerat {6 and displaced tooth ofa female patient at 9 years of age. 193. Deformation and displacement The clinical picture shows anoma: lies of shape and position of the four upper incisors, resuting from trauma tothe deciduous teeth dur ing early childhood, Enamel formation was impeded severely on the upper central inc sore resulting in gangrene. Per ‘apical lesions have caused the formation of fistula. 194 Physical damage to teeth during development ‘The teeth present alter radiothera py at a nasopharyngeal tumor at of age, ‘AS a result of the radiotherapy, wien the patient was 10 years ol, the root formation of the perma: rent teeth is impeded severly. This ‘applies particularly to the upper teath. Further radiographic find- ings are: Hypoplasia of tooth germs 27, 45, 47, and aplasia of the 17, 15, and 25,Accidents involving the dentition are differentiated accor- ding to the various sequelae = Injuries prior to the eruption of the deciduous teeth ~ Injuries to the deciduous dentition = Injuries to the permanent teeth after eruption. Taking the developmental periods of tooth structure into account, the type and localization of tooth mal- development indicate the time at which the accident occurred, Injuries to edentulous infant jaws lead primar- ily to retained teeth, displaced teeth, and malformation of the roots of deciduous teeth. Such injuries do not usually harm the germs of the permanent teeth. Not until the patient is 4 years old do traumatic intrusions of the deciduous anterior teeth usually harm the germs of the permanent teeth. Depending on the stage of the permanent tooth germ’s development when the trauma ‘occurs and on the direction and severity of the intrusion, the crown of the permanent tooth may be damaged to a greater or lesser degree; root formation may be imped- ed, tooth eruption may be disturbed and the teeth may be displaced. Injuries to the permanent maxillary anterior teeth are much more common in patients with an Angle Class II, Division 1 malocclusion. ae 195 Deciduous teeth trauma ‘and damage to the germs of ‘the permanent teeth Sagital section through the maxi lary alveolar process. Left: Topographic relationships of 13-year-old. The germ of the per- nt tooth is only damaged i deciduous tooth intrusion and palatal biting ofthe rt take place simultaneously ‘ight: AS yearsofagethe postion ‘ofthe tooth germ haschanged and is endangered by any intrusion of the deciduous tooth (Eschier, 1974) 196 incisor ectopy Horizontal displacement of the right upper central incisor due to trauma of the deciduous teeth. itis uncertain whether the tooth willecome correctly alignedintne dental arch, Right: Due to the premature loss of the upper right deciduous incisor and the germ of the permanent tooth being displaced, the adjacent teeth have dried toward the gap land. have severely restricted the ‘space for the successional per ‘manent tooth, 197 Deciduous tooth trauma ‘and tooth deformities LoftRadiograph showing trauma ic intrusion of the upper central primary incisors of ay Right: Radiograph of the nent incisors 4 years rauma impeded the development ofthe roots of both teeth, The patient is now & years old land has permanent incisors with Cervical root ractures asa result of another accident at that point in time,— Joost len Physical Factors The following factors, which enhance the development ofan anomaly, or directly cause it, belong to this group: ~ Feeding method ~ Consistency of the diet — Premature loss of deciduous teeth ~ Mouth breathing The feeding methbd during infancy is considered important with regard to the etiology of a retruded mandibular position in the deciduous dentition. The main advantage, from the orthodontic point of view, of breastfeeding compared to bottle feeding is that the baby must activate and protract the jaw musculature much more to press the milk out of the mother’s breast (Fig. 198). This higher functional loading during the first few months ofllife helps to move the mandible anteriorly 198 Feeding intants Due to the advantages it offers regarding, among other things, the development of the dentition, breastfeeding is preferable. Aight: the infant should be bot fad, the NUK nipples are consi dered superior 10 conventional nipples as their physiological shape Is matched to the infants anatomy. > Muscle activity 60x as strong 199. Changing from liquid to solid too (Once the first deciduous molars have erupted, i.e. atthe time the bite is first raised physiologically (at approximately 14 months of ‘age),the child should only begiven ‘solid foots in order to ensure that the deciduous dentition develops normally ‘Above: Deep overbite prior to the ‘eruption ofthe deciduous molars, The posterior alveolar prodesses ‘are in contact with each other. Below: The erupting frst decid ‘uous molars raise the bite and reduce the overbite, The advantages of breastfeeding ‘compared to bottle feeding for the child —> Reduced morbidity —> Satisfied sucking reflex (> fewer sucking habits) and compensates for the physiologic retruded antero- posterior jaw relationship which exists at birth. Even specially shaped nursing nipples cannot fully match the advantages of breastfeeding. The child can already chew once the first deciduous molars have erupted. It is particularly important for the development of normal dentition that the child is given solid food from this point on (Fig. 199). Should the child be given further nonsolid foods, it will become a “temporalis chewer,” i. itwill only carry ‘out chopping movements (Fig. 202), instead of a “masseter chewer” which carries out complete grinding cycles during mastication (Fig. 200). The insufficient functional loading associated with a “temporalis chew- cer” adversely affects the formation of the bone struc- tures, thus the consistency of the foodstuff indirectly influences jaw development.*Masseter chewing” and development of the deciduous dentition 1) High functional load, strong bony framework 2) Food is ground up 8) Deciduous teeth are abraded 4) Lower dental arch is displaced forward 5) First molars are positioned favorably 6) Decreased overbite “Temporalis chewing” and development of the deciduous der 1) Low functional oad, incomplete development ‘of bony framework 2) Food is chewed superficially 3) Minimal abrasion ofthe deciduous teeth 4) Lower dental arch is not displaced anteriorly 5) First molars are in unstable occlusal position 6) Excessive overbite 200 Advantages of “masseter ‘chewing” for the development of the deciduous dentition Left: The masticatory movements {are mainly carried out by the mas- seler, which exerts @ protrusive force on the growing mandible, thus helping to compensate for the child's physiologically retruded mandibular postion. Right: Table showing the charac- teristics of a “masseter chewe 201 Normal, mature deciduous dentition of a “masseter chewer” Ccclusion of a6-year-old git atthe beginning of anterior exiolation The typical characteristics of this ‘masticatory mode are: Physiologic formation of gaps. between the anterior deciduous teeth, anterior displacement ol the mandible and a slight overbite due to abrasion of the deciduous teeth 202 Drawbacks of temporalis chewing” for the development of the deciduous dentition Left: The temporalis caries out most of the work during mastica- {oty excursions. It exerts tension cranially, primarily cranioposte- rioly and tends o promote the for mation of a deep overbite. This muscle does not exert a protrusive force Aight: Table showing the charac- teristics of 203 Abnormal deciduous dentition of a “temporalis ‘chewer” prior to anterior ‘exfoliation ‘The typical symptoms o this mast ccatory mode are: The deep over- bite impedes masticatory tunction- ing, the deciduous teeth are not abraded and the mandible is retrognathic.es Premature Loss of Deciduous Teeth Premature loss of the deciduous teeth also has a physical effect on the etiology of many abnormalities of the jaws and the dentition. The primary effect is the reduction in masticatory potential after premature loss of one or several deciduous teeth. The reduced masticatory potential leads to insufficient functional loading and can impede jaw development along the sagittal, transverse, and vertical planes. The term “premature” applies to any loss of deci- Cariogenie food and premature loss of deciduous teeth 204 Upper deciduous dental ‘arch Premature loss tll upper decidu: us crowns du to the cariogenic ctfec of sugar-saturated infants’ tea 205 Occlusion Occlusal relationship othe patient shown in Fig, 204 ‘Since the masticatory function has been reduced, the jaws cannot be loaded sufficiently 208 Deep overbite in Conjunction with premature loss of deciduous teeth Agingivaly-supporied, deep over- bite ater extensive premature loss Gf upper deciduous teeth over a ong period of time, The lack of tooth support has caused the mandible to rotate for- ward and upward, resulting in @ closed bile or excessive overbite. duous teeth which takes place more than 6 months prior to the expected date of eruption of the underlying permanent tooth germ. A deciduous crown which has been destroyed can neither function asa tooth nor maintain the space for the permanent tooth germ. There is also a risk that per apical infections of carious deciduous teeth will endan- ger the crown formation of the succedaneous tooth germ.gs Breathing In case of an impeded nasal respiration, the paranasal sinuses are not ventilated correctly and the growth- promoting effect of the capsular matrix as described by Moss (p. 33) is reduced. Chronic disturbance in nasal breathing, or habitual mouth breathing are primarily associated with impeded maxillary growth. This maldevelopment of the max- ill results in a narrow jaw with a high palate and dental, crowding as well as retrognathism or prognathism ofthe mandible. The lack of maxillary growth associated with a oronasal respiration is due to the change in tongue position of mouth breathers. As it lies flat in the floor of the mouth it cannot play its normal role in devel- oping the maxilla, As the tongue is displaced downward, the centrifugal and centripetal forces acting on the ‘maxilla are no longer balanced. The functional hyper- activity of the musculature of facial expression, espe- cially of the buccinator, impedes the development of the maxilla. 207 Pressure relationships the head and upper part of the body) In order to be able to breathe nor- rally, the nase must allow sutfic jentairto pass through and the oral airway must be sealed anteriorly Nile inspiring, a low pressure zone develops between the tongue {and the hard palate caused by the slightly stronger traction forces op posing the air pressure. The elastic traction forces of the trach chial system, whichisconnectedto the tongue viathe larynxcana hyo, are of great signiicance. ‘The drawing shows tne down- ward displacement of the larynx {and the diaphragm during inspira n, as a result of the elas traction forces exerted by the tracheobronchial system (alter Ever Mébivs, 1962), 208 Oronasal breathing in conjunction with an anterior cross-bite Let: Occlusal relation. Fight: Habitual mandibular rest position of a 5-year-old patient. To allow oral respiration, the tongue is kept low and the mandible is ‘opened further downward. than ‘normal when al res. Such changes inthe balance ofthe orofacial and masticatory musculature adver- sely tit the normal development of the dentiion the dorsum of the tongue has been marked with a contrast mediumOronasal breathing in Conjunction with a Class Il ‘malocclusion 209 Extraoral findings Proll view of a7-year-old patient showing the retruded postion of the lower jaw. Aight: The patient has a stenosis in the left side of the nose, which impedes normal nasal breathing, E 210 Occlusion us The patiant has anterior crowding in both the upper and lower jaws. 211 Craniofacial morphology and anteroposterior jaw rela- tion Thelateralcophalogram shows the downward and retracted postion {tthe tongue, which is typical for ‘cases with disturbed nasal breath. ing and a Class i malocclusion. Right: Asthe mandibleisinaretru- ded poston, he overet is increa- sed clinicallyBad Habits - Orofacial Dysfunction ~ Pacifier sucking = Thumb sucking ~ Finger sucking ~ Tongue-thrust ~ Lip sucking or biting ~ Cheek sucking = Nail biting or pencil chewing 6 years old SNA 6 SNB 73° ANB 10" ‘SNPog 795° 7 years old ie" 7 55 131 78 60 mn IE Impeded function of the orofacial system is the most common cause of acquired anomalies. The most common bad habits are listed above. Although the different sucking habits may produce vari- ous abnormalities, there is not always a direct causal relation. ‘Apart from the genetic predisposition, the relation- ship between orofacial dysfunction and malocclusion is determined by three essential factors: The intensity, duration, and type of sucking habit ‘Sucking habit and malocclusion 212 Effect of the sucking habit on the dentofacial development Let: Lateral cephalogram of 2 {year-old git prior to acquiring 2 sucking habit The girl has a stele tal Class Il and is inthe early mixed dentition Aight: Configuration of the eran facial morphology t 7 yearsolage. The gitl began her sucking habit when she started school, which influenced the position of both the upper and lower permanent incisors during ther eruption. 213. Roentgenocephalometric sna oie findings SNB 34: Cephalometric tracings of the ANB '7- lateral headplates shown in Fig. SNPog 75° 212, wk 65mm Left Initial situation, fogs 118 ight: Situation 1 year alter ‘commencing the sucking habit When compared to the initial con. dition, the sucking habit caused a labial tipping of the upper and lowerincisorsand an anierioropen bite, Simultaneously, the habit pro 7 moted upward rotation ofthe ante rior maxila during its development {increase inthe angle of inclination ey ‘according to A. M. Schwarz=. ee Mechanics of sucking 214 Apposition of the suc finger on the maxilla Left: Sucking the right thumb, in falving the nok Right: Thumb postion depicted on a radiograph, The patient presses the thumb onto the palate, on both the front section of the maxilla and the upper anterior tooth. The finger also rests onthe lower incisars as a tulerum. 215 Intraoral symptoms Left: Sucking or pressing the thumb against the maxilla pro: ies the development of a Class I malocclusion (same pa: tient asin Fig, 24). Aight: the finger is rested on mandible, the lower teeth are often moved forwards resulting in an edge-to-edge bite or a cross-bite (same patient asin Fig, 216), 216 Apposition of the sucking finger on the mandible Left This9-year-old female patien femonstating a typical finger sucking position: The ring finger and litle finger are pressed onto the lingual side of the mandibular alveolar process and the lower antario teeth; the index and mi: dle fingers rest on the check Right: Radiograph depicting this habit Thistype of sucking habittits the upper and lower teeth toward the labial The change in position of the upper teeth is mostly mechanical ‘and that of the lower teeth @ secondary effact of the forward ward tongue postures - Tongue-thrust can be a primary etiological cause of a malocclusion or it can be a secondary, adaptive factor, as in cases with a skeletal open bite. Inmany cases, the tongue dysfunction persists once the long-term sucking habit or incorrect bottle-feeding during infancy has been discontinued (Fig. 217). Visceral swallowing (infantile swallowing) has a time- linked etiology for tongue-thrust. It is physiologically normal until the child is 4 years old. After this time, the visceral swallowing act is considered an orofacial dys- function. Should this type of deglutition, with tongue- thrust and contraction of the facial musculature, persist in older children and adults, it may be among others a result of a long-term sucking habit associated with an open bite (Figs. 218, 219). 217 Adaptive tongue-thrust Anterior open bite with tongue ‘ystunction, causedbyalong-term sucking habit In many cases, the tongue dyski> nesia persists even after the suck- ing habit has been discontinued ‘0 thatthe malecelusion or dental malaligrment cannol be restored to normal by autonomous adjust- ment Visceral swallowing 218 Tongue posture Tongue posture typical of visceral swallowing, To inate the swallow: ingact,thetipofthetonguerests.on the lower ip. 219 Occlusion Characteristic occlusion in case of persistent visceral swallowing, The tongue is placed continuously between the teeth, resulting in a complex open bite, which is only supported by the molars.Diseases Various general and local diseases may cause malocclu- sions. The most common systemic diseases are endocrine disturbances (impeded increase in jaw length, distur- bances in tooth eruption, reduction in tooth size) and chromosome aberrations which affect the orofacial system (e.g. Franceschetti syndrome, cleidocranial dys- ostosis, trisomy 2/, ectodermal dysplasia, amelogenesis and dentinogenesis imperfecta, as well as certain types of lip- jaw-palate clefts). Cleidocranial dysostosis 220 Craniofacial radiographic ly dominantly inherited skeletal dysplasia results trom disturbances in intramembranous ossification, whereby enchonaral ossticationis usually also involved. Left: Brachycephaly and underde- velopment ofthe middle face with relative hyperplasia of the body of the mandible tending toward a Class Ill malocclusion, which is 'ypicalof his disease, are apparent on this lateral radiograph, Fight: Disturbed —ossfication around he calvarium, which is typi: cal ofthis dysostosis, causes the fontanelles and craniai sutures to remain open fora long time, The persisting deciduous teeth are also visible with hyperodontia and retained permanent teeth 221 Clinical findings Lett: Hypoplasia ol the collarbones and the resulting hypermobility of the shoulder joints are typical of this syndrome, Right: The 16-year-old female patient has retained her entire de. Ciduous denttion except for the lower central incisors. The primary incisors have been subjected to severe attition; the deep overbite is gingivally supported. The following Jocal diseases very often lead to dys- gnathias: — Nasopharyngeal diseases and impeded nasal breathing — Infections of the middle ear in babies and infants with damaged temporomandibular joints ~ Gingival and periodontal diseases which may already occur in the mixed dentition ~ Rare pathologic conditions (tumors and cysts) = Caries and premature tooth extractions- Exogenic Factor 89 Ectodermal dysplasia — hypohidrotic type 222 Extraoral findings of ‘ectodermal disease This disease is a maldevelopment syndrome of derivatives of the This frontal view shows a9 ‘ld female patient with the pathologic symptoms: Light thin halt, underdeveloped eye brows, sparse eyelashes, a broad rose, ridge-tke lip configuration, ‘and pronounced mentolabial sul Loft: Very dry, scaly. skin with Chronic eczema is typical of this disease. 223 Panoramic radiograph Complete anodontia of the man dible. The only permanent tooth which has developed is the upper left molar. The only toeth of the primary dentition, Le. the two upper second deciduous molars, were lost prematurely due to caries. 228 Sk facial profile Lateral cephalogram and facial view ofthe patient show the Underdevelopment of the middle face and lower facial height The hypoplasia of the alveolar processes results from the virtually ‘complete anodontia, and soft-tissue Left: Disturbances in the develop: ment theteeth and skeleton have produced characteristic changes in the sot-tissue profCysts and tooth eruption = Case example ~ 225 Initial situation Panoramic radiograph ola 4-year ‘ld female patient who was sent for treatment of an abscess whi resulted from cariousanterio quadrants 226 Teeth present after formation of the cyst Due to expansion othe proces the getms of the lower canines and premolars were severely ds placed, The lowe incisors erupted pre ure exerted asf 227 Teeth present after ting the cyst the cyethad been ath germs 228 Follow-up nths. after diagnosing teeth axial which re mained between the premolar germs alter treating the cyst have The bone defects in the an mandibular alveolar process nines of this nt to erupt prema: Supernumerary in the maxila inte tion of central incisorDiagnostic Procedures © Case history © Clinical examination Functional analysis © Radiologic examination ‘© Photographic analysis © Cephalometric analysis © Study cast analysiseee ements — Case History The first step in the assessment of orthodontic cases is the critical examination of the case history. The purpose of this is to understand the development of the malocclusion, so that by early elimination of the causative factors, correct therapy can be undertaken. Such an approach increases the likelihood of a more favorable prognosis and greater stability as compared to a purely symp- tomatic approach to orthodontic or dentofacial orthopedic treatment. ‘As a tule, the case history is usually assessed with the help of a special questionnaire. Questions © Family history e Patient history From the family history, one learns about certain malocclussions and other abnormalities (for instance, impaired nasal breathing) present in members of the same family. ‘A relatively large number of dysgnathias are in- herited and transmitted through a dominant gene, whereas in cases of cleft lip and palate, it is mostly through a recessive gene. ‘The patient’s history is divided into three parts. First is the prenatal period, during which the following are of interest: Nutritional disorders, diseases and accidents to the mother during pregnancy. The best-known example of this is the relationship between viral infee- related to the case history are divided into two parts: Hereditary malocclusions 229 Deep bite in the ‘deciduous dentition Most hereditary dysgnathias are already evident in the deciduous enttion. ominantly inherited anomalies include mandibular prognathism, Class i, Division 2, some cases of distoclusion, ske [etal open bite, and bimaxilary protrusion, ‘An excessive vertical develop- ‘ment ofthe anterior maxillary gum paads in the newborn ("Schachtel- biss"; engl. "boxbite? is assessed as the early form of the congeni- tal deep bite tion and cleft formation in the newborn. ‘The questions which relate to the birth include time of birth, the fetal position at birth, and complications. The most detailed part of the patient’s own history is the postnatal development. The manner of feeding, as well as nutritional disturbances are noted (mineralization defects of the teeth). Questions regarding the eruption of, the first deciduous tooth, the child’s general develop- ‘ment (initiation of talking, walking), and information concerning sucking and other “bad habits” are useful. ‘Accidents in childhood, the state of the deciduous dentition, and the early loss of primary teeth should also be noted.Breil a Mt net abi Other more generalized diseases are of interest, in parti- cular conditions which affect the development of the jaws (for instance, rickets, dysostoses). This aspect would also include all diseases which are important in influencing the type of breathing (colds, pneumonias, otitis, allergies). Further evidence of disturbed respira- tion includes the type of breathing during sleep (open mouth, snoring) as well as previous adenoidectomy and/or tonsillectomy. After adenoidectomy, the possi bility of homeostatic adaptation must be considered. 230 Bimaxillary protrusion The hereditary component of this denioalveotar abnormality is usu ally localized in he neuromuscular system, ‘Because of hereditary lip incom- petence, the muscular equilibrium between tongue and tips is dis turbea, Thelabialnctination ofthe anter- ior teeth results from a relative hyperactivity of the tongue muscu lature, Right: Weak tonus ofthe orbicula- tis ors muscle 231 Drug-induced enamel dysplasia Decalcification of six anterior teath ‘and first permanent molars in a 14 year-old patient. Clinical situation following tetracycline treatment for ‘meningitis atthe age of 2 yoars. Teeth which had not yet calaiied at the time of treatment for the ‘meningitisarenotatfected (premo: lars and second molars) 292 Head and neck surgery Dental condition of a 10-year-old patient after surgical closure of a bilateral cleft ip and palate, in the newborn and infant period. ‘Scar tissue can further restrict sagittal and vertical maxillary ‘growth, resuting in mandibular prognathism Specific questions should include medical conditions which may limit orthodontic treatment (for example, diabetes mellitus, epilepsy, blood dyscrasias, rheumatic disease, allergies to nickel and acrylic). Psychologie aspects of orthodontic treatment should be also discussed while taking the history and talking with the patient (motivation of the patient, also of parents in young patients, expectation with regard to treatment result). Such information is helpful to estimate future cooperation during treatment.Interpretation of the Case History In many cases, the findings of the patient's history may give some clues regarding the cause of the malocclusion and help in planning the necessary therapy. Together with the interpretation of the case history, one has to bear in mind that a single etiologic factor does not exist A combination of different endogenous and exogenous factors is responsible for the individual abnormality at a particular time. An inherited tendency may be present as well as the acquired malocclusion. The effect of a sucking habit is significantly less favorable in a vertical as compared with a horizontal growth tendency (see page 192). The course of orthodontic therapy, and the stability of treatment results, may be affected if causative factors of the malocclusion have not been recognized. 233. Interpretation of the patient's history Cause of malocclusions {first impression ofthe cause of a malocclusion can be elicited from the patient's history, which may in fluence the timing of treatment as © In the late mixed dentition © Symptomatic © Causal ‘© In the early mixed dentition (possibly in the deciduous dentition) Endogenous Exogenous wellasthetherapeutic possibilities T ‘Therapy ‘Therapy ‘Acquired malocclusions and predispositions 234. Lip dysfunction in neutroclusion Morphological. relationship in a skeletal Class | case with lip dys function Right: The dyskinesia in this case regultsinonlyaslightchangeofthe overie. 235. Lip dysfunction in distoclusion| Morphological relationship in a Class Il case with concomitant ip ayskinesia Right: Compared with Fig. 294: The functional sofvtssue distur bance leads to a greater overt in the case of distoclusion,96 Case History Questionnaire - Case History 1) Family history Father | Mother | __ Siblings Relatives Rickels (R), colds (C) ‘Adenoids (A), mouth breathing (M) ‘Adenoidectomy (AT), tonsillectomy (1) lett lip (U), jaw (), oF palate (P) ‘Supernumerary teeth (S), missing teeth (MT) Protrusion (P), Class i, Division 2 (0), Class il (M) Open-bite (0), deep bite (0) Dental crowding Orthodontic treatment Miscellaneous: 2) Patient history Prenatal] (course of pregnancy) Diseases: Nutritional disorders: yes/no Psychological problems: yes/no Medication: yes/no ‘Accidents: yes/no When: Type: Birth Premature—normal -late: Position: Course of labor: Normal Forceps Cesarian section Suction cup Weight: Length: Incubator: yes/no - [Postnatal Developmental state at birth: Normal/ underdeveloped / hospitalization Infant feeding: Breastfed up to month bottle-fed up to year spoon-fed atter the ‘month fed solid foods after the month given the following additional foods after the month: Vitamin D: Fluoride preparations up to: First tooth: month Learned to walk during the month Learned to speak during the month Premature loss of deciduous teeth: yes/no Which teeth: ‘Sucking: Which finger right/left, pacifier, corner of the blanket From. to years NUK nipple: yes/no From to years Parafunctions: Nail biting, clenching, bruxism Sleeping habits: Position: Mouth opened closed + Snoring: yes/no Diseases: Rickets - colds pneumonia otitis —asthma allergies ‘Systemic diseases: Allergies: ‘Adenoidectomy /tonsillectomy: Atage of: ‘Accidents: Age: Type: Teeth involved: yes/no Treatment: Operations in the head /neck region:Clinical Examination vet Clinical Examination ‘The clinical findings are the basis of diagnostic procedures. The aim of the investigation is the qesognition ofthe orthodontic problem from the patients point of view as wel! asthe examiner’s,and re amine the need for treatment. Clinical findings are the prerequisite for the correct assessment and interpretation ofthe quantitative analyses, i. the overall generaland the specific clinical findings, Which serve as the foundation of treatment decisions. General State Examination of the constitution and physique of the “Anevaluation of the somatogram provides an indica~ patient, height and weight in relationship o the chrono- tion of the general growth tendency. Further factors logic age and development of the facial skeleton. include the nutritional situation, assessment of mental development, and the dental and skeletal age. 236 Somatogram Left: Registration of chronologic [| | age,neignt incr) weight inka) at tera Faso | the timo of examination 8 544 [+129] Comparison of the dala to aver st S230] age values. The lables arecierent A os], dor boys and ois a oe as q fight Data ae uncerined in thir 8 Tied respective columns. Physical e- ee SSF ie ‘elopmentisiaken as noeralvhon sal Uh a 88 13] | nen soprocatey ovo Hea Yas ‘i el ae 163) ear right: pathologic at | fis, [see BESEIEG cncestem ne nom othe order ot | * | i 2 standard deviations relating 12 i $$) the patient's chronologic age, ye Te height and weight exit as occurs | Uist le in dwarfism, gigantsm, best, O° a anorexia armedical examination ieee required (Kunze and Murken, Uni- 1 ‘ety of Munich, 1974).[pe co. Dental Age Evaluation of the dental status is of great importance for the prognostic assessment of dental development. Chronologic and dental age are synchronous in the normal patient. A child is labeled as an early or late developer if there is a difference of +2 years from the average value. If the chronologic age of the patient is younger than the dental age, one can rely on increased growth to a greater degree than when dental age is retarded in relation to the chronologic age (and possibly biologic age). 287. Timetable of dental ‘development of the primary ‘and permanent dentition 239 Accelerated eruption ‘Accelerated eruption of the lower right premolars attr early extrac: tion of deciduous molars. Right: Insutficient root develop- ment is characteristic of premature eruption During the intraoral eruption stage, the tooth usually has one- thie ofits inal root length Deciduous teeth in the maxila® Dental age can be determined by two different methods: ~ Stage of eruption ~ Stage of tooth mineralization on radiograph. Determination of dental age from observation of erup- tion has been the only method available (Fig. 238) for a long time. In most instances, it is fairly reliable. In certain cases, however, the accuracy of the method is limited (Figs. 239-243). During the quiescent periods in eruption, this approach is inadequate. Permanent teeth in the maxi Scr oh memes tyros oc. [DON Sune Endot Root Tooth Startof__Endof Root | ironed hardssue enamel Erup- formation hardtssue enamel Erup- formation coving 9 Logan and. Kronteld pei 2 Lebel eee onl formation formation tion complete formation formation tion complete 5161 4mo.inutero Tmo. Vy. S-4mo. 4 8y. 7 By 10y Sequenceandtimingoteruntionot S22 4 mo. in utero 9mo. _2¥. 1-12mo. 4 Sy. 8 By Ty. the permanent denition re gene- 5545” S mo. in utero 1eme. aky 4 5mo. 6 7y. 11-12. 13-18% tically determined and ethnically S444 Smo. inutero 14mo. 2y. ay. B= By. O11 y 12-139 diferent, but are. scarcely_in 22ky 6 Ty. tO-tey. 12-14 fuenced_by endocrine cit ‘tinh 73. d10y. bance. Gils are sightly more 3y 12135, 14-169 acvanced 7 8y. 1218y. 17-21. 18-25. Mandibular teeth usually develop before “Mandibular testh develop a tow months maxilary tath to St year botore the maxilary Estimation of dental age trom dental eruption emergence ofthe teth of single dental groups 238 Correlation table ot Boys oir dental age and number of te e833 as 1 2 9 4 erupted teeth Esimation of dental age for DOYS ing. cont. §=—=i'*):~=«=‘“)?:~C«i OCHS. =) and gis separate (Matiegka and In. 6:11 7:03 7:11 8:08 Ine. lat 6:07 7:00 7:05 8:00 Luxasova. Canine 10:00 10:07 11:02 11:10 Canine 9:02 9:10 10:05 11:02 Premoler! 9:01 9:01 10:04 14:01 Premolar! B11 9:08 "8:11 10:08. Tne dental age is determined irom remelarl 10:01 10:07 11:02 11:10 Premolarl 9:10 10:02 10:09 11:09 {ables by comparison of the numn- Molar! yy Molar ik ee ber of eruped ttn win average Molaril «10:09 11:02" 11109 12:08 Molar «10:05. 10:10 11:04 12:00 Dates given in years: months *) Eruption occurs earlier than could be determined in this study.‘Acceleration in dental development and eruption timing Tae False '¢ Endocrine disturbance 1 Diabetes metitus ‘¢ Early loss of deciduous teeth « Inflammatory processes of alveolar bone: Tre False Retardation in dental development and eruption timing '¢ Severe organic disease '¢ Prolonged periods of deficiency '¢ Endocrine disturbances ‘2 Bone disease ¢¢ Environmental influence ‘¢ Post-traumatic situation ‘Alveolar tone hyperplasia (Leontiasis ossea) ‘Fibrous gingival hyperplasia, (€lephantiasis gingivae) ee — 240 True delay of eruption Retarded change to permanent dentition as a late sequela of rickets Intraoral dental status of a 10. year-old with mineralization de fects of the upper central incisors and the four lower front teen as a symptom of vitamin D deficiency at the age of 2 years, Right: Panoramic radiograph. Dis ‘crepancy between chronological {10 years) and dental age (7 years ‘and 11 manths) 241 Retarded eruption The cause of delayed eruption of the upper incisors is deficient ‘space in the upper anterior region in this B-year-old patient Right: The radiograph shows the postion of the tooth germs in the Upper anterior region. Undermin. ing resorption of the deciduous lateral incisors by the central per ‘manent incisors as characteristic feature ofa primary dental crowd: ing. 242 False retarded eruption ‘Atypical eruption; in. comparison with the opposite side, delayed ‘eruption of the upper let perma: nent incisors and the lft canine in a 13-year-old patient Fight: Displacement of tooth germs following trauma 10 the primary teeth, causing intrusion of the upper left deciduous incisors, at 5 years of age, 243 Factors determining ‘tooth eruption and dental age Table showing the different local land. systemic factors influencing denial development. Let: Accelerating factors. Right: Reterding factors.