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4 Facial and Palatal Growth

Samuel Berkowitz

4.1 Maxillary and Mandibular Growth osteogenic process is particularly sensitive to bio-
Concepts mechanical stresses and strains, and it responds to
tensions and pressure by either bone deposition or
It is not the author’s intent to write a definitive treatise resorption.
on facial growth and its control processes because Tension, as traditionally believed, specifically in-
there are better sources for such information. How- duces bone formation. According to the traditional
ever, because the history of cleft palate treatment has wisdom, when tension is placed on a bone, the bone
been influenced by what clinicians think is the correct grows locally in response. Pressure, on the other hand,
facial growth process, it behooves the author to sup- if it exceeds a relatively sensitive threshold limit,
port or refute the various facial-palatal growth con- specifically triggers resorption. According to this
cepts based on his own clinical findings. theory when muscle and overall body growth are
complete, the bone attains biomechanical equilibri-
um, that is, the forces of the muscles are then in
4.1.1 Newborn Palate with a Cleft balance with the physical properties of the bone. This
of the Lip or Palate turns off osteoblastic activity, and skeletal growth
Is bone missing, adequate, or in excess? What is the Unfortunately for traditional schools of thought,
geometric palatal relation of the palatal segments at growth control in the human body is more complex
birth? With complete clefts of the lip and palate, are than this. Moreover, it is now known that there is not
the palatal segments collapsed or expanded? Can the a direct, one-to-one correlation between tension-dep-
palatal segments be stimulated to develop to a larger osition and pressure-resorption.
size by neonatal orthopedic appliances? A number of
studies have attempted to determine whether the cleft
palate was deficient or adequate in osteogenic tissue; 4.1.3 Functional Matrix Theory [2, 3]
unfortunately, the investigators were limited by pauci- (Figs. 4.1, 4.2)
ty of data, lack of homogeneity in their samples, and
the hazards of estimating growth from cross-section- Enlow [1] goes on to explain that, with the develop-
al data. ment of the Functional Matrix Principle, a number of
important hypotheses began to receive attention. One
of these is that the “bone” does not regulate its own
4.1.2 Genetic Control Theory: growth. The genetic and epigenetic determinants of
Craniofacial Growth skeletal developments are in the functional tissue ma-
is Entirely Predetermined trix, that is, muscle, nerve, glands, teeth, neurocranial
fossa, and nasal, orbital, oral, and pharyngeal cavities.
Enlow [1] writes that, in the past, it was thought that This is primary while the growth of the skeletal unit is
all bones having cartilage growth plates were regulat- secondary. However, although the Functional Matrix
ed entirely and directly by the intrinsic genetic pro- Principle describes what happens during growth, it
gramming within the cartilage cells. Intramembra- does not account for how it happens. Experiments
nous bone (maxillary) growth, however, was believed have shown that mechanical forces are not the princi-
to have a different source of control. This type of pal factor controlling bone growth.

Fig. The nasomaxillary complex. is displaced downward and forward away from the of the composite of soft tissues in the growing face. As this takes place. 4. The process of new bone deposition does not cause displacement by pushing against the articular contact surface of another bone. curs. the condyle and ramus grow upward and backward into facial region (center). Similarly. for example. ing of the nasomaxillary part of the growing face. in toto. the whole mandible is displaced “away” from tact with floor of the cranium (top).1. Displacement thus comes longer and wider to accommodate (1) the increasing proceeds downward and forward as growth by bone deposition mass of masticatory muscles inserted onto it. The whole maxillary re. This then triggers new bone growth at the the “space” created by the displacement process. is in con. toward its contact with the cranial floor). Rather. (Reprinted (From [1]) with permission from [1]) . its articulation in each glenoid fossa by the growth enlargement gion. 4. and the two separate bones thereby remain in constant articu- lar junction..e. (2) the enlarged simultaneously takes place in an opposite upward and back. Berkowitz Fig. As this oc- cranium by the expansive growth of the soft tissues in the mid. Note that the various sutural contact surfaces between the nasomaxillary ramus “remodels” as it relocates posterosuperiorly. new bone is added immediately onto the contact surface.24 S. the bone is carried away by the expansive force of all the growing soft tissues surrounding it.2. It also be- composite and the cranial floor (bottom). and (3) the vertical lengthen- ward direction (i. breadth of the pharyngeal space.

provide for the growth of the whole maxilla. developed from criticisms of the “sutural theory. type of displacement. sets up fields of tension in all the Growth control is determined by genetic influences maxillary sutures. capacity for growth as a result of compression.” cutaneous and submucosal connective tissues. at their sutures in response to the tension created by ance between them is still. Synchondrosis. are also involved in the operation of the functional This theory has also been rejected because bone tissue matrix. The whole maxilla is displaced in an Principle introduced by Moss [2. the Scott [4. the sub. the facial bones grow in 4. but the nature of the bal. 3]. It does not. at best. the deposition of new bone is a response to tissues and not in the hard part of the bone itself.. The idea that additions of new bone on the poste- the sum of all the soft tissues operating in association rior surface of the elongating maxillary tuberosity with that bone. all combine to move the facial bones is a special tissue uniquely structured to provide the passively along with them as they grow. and mandibular condyles are actual growth bones by Sharpey’s fibers. the nature of the force that produces concept states.” Clinicians in- Enlow [1] identifies the maxillary tuberosity as volved in cleft palate treatment. Bones do not by themselves have the physiological ing determinant of the skeletal growth process. displacement rather than the force that causes it. The Functional Matrix Concept is fundamental to Although the “sutural push theory” is not tenable. The ously places each bone and all of its parts in correct basis for this theory is that the pressure-accommodat- anatomic positions to carry out its functions. Moreover. nasal along (displaced) with the soft tissues attached to the septum. Thus. plates has been abandoned. Of course. the expansion of the facial muscle.1. with a resulting tissues. [20–34] accepted Scott’s thesis that cartilage and . depending on the status of the not adapted to a pressure-related growth process. the bone and any cartilage present thrust of the whole maxilla downward and forward. bone growth at the various maxillary sutures pro- arily dependent on the growth of pace-making soft duces a pushing apart of the bones. The nasal septum hypothesis was soon adopted by tors. This causes the soft tissues to amount of compression needed to produce a pushing inhibit or accelerate the rate and amount of subse.4 Cartilage-Directed Growth: a subordinate relationship with all the surrounding Nasal Septum Theory [4–12] soft tissues. not of their own doing) carried Cartilages are the leading factor. of growth. ing expansion of the cartilage in the nasal septum is the functional factors are the very agents that cause the source of the physical force that displaces the max- the bone to develop into its definite shape and size illa anteriorly and inferiorly. tion. play as a source for the mechanical force that carries out the process of displacement. No sin. Chapter 4 Familial Exudative Vitreoretinopathy 25 Most researchers agree that a notable advance was but rather is responsible for the lengthening of the made with the development of the Functional Matrix maxillary arches. The bones then. This means that the bone itself does “push” the maxilla against the adjacent pterygoid not regulate the rate and direction of its own growth. The concept also comes into nizing sutures. [13–15] and Burston [16–19] and their followers however. It is functional and mechanical equilibrium between the believed that the stimulus for sutural bone growth is bone and its soft tissue matrix. Scott’s hypothesis.Another theory held that The course and extent of bone growth are second. the tension produced by the displacement of the bone. many investigators in cleft palate centers around the not all of the individual links are involved in all types world and became more or less the standard explana- of growth changes. the displacement process. but not in the old conceptual way. The genetic determi. that any given bone grows in this forward movement is a subject of great controver- response to functional relationships established by sy. Sutural growth is compensatory. accordingly to and to occupy the location it does. This. because they give essential feedback informa. capacity to push away bones. uncertain. move in relation to each gle agent is directly responsible for the master control other. The sutural connective tissue is quent bone growth. As the tissues continue to grow. because it and the nerves. However. This continu.According to this now widely accepted explanation. the vessels. for the nasomaxillary centers. an understanding of the overall process of bone Enlow reports that some students of the facial growth growth control. the bones are passively (i. This theory complex. Indeed.e. It involves a chain of regulatory links. while they enlarge and biomechanical forces. nants of the growth process reside wholly in the soft Thus. the control process encompasses many fac. such as McNeil being a major site of maxillary growth. The orly. ed to certain pressure-related growth sites. is not capable of growth in a field that requires the tion to the soft tissues. in brief. 5] believes that cartilage is specifically adapt- oral and nasal epithelia lining the spaces. This concept has had a great impact in control processes are looking anew at growth mecha- the field of facial biology. replacing the “sutural theory. the functional soft tissue matrix is the actual govern. It deals with what anterior direction as it grows and lengthens posteri- determines bone and cartilage growth in general.

brought on by such stimulating appliances. are not only retruded within the development of the maxilla appears to be normal the cranium but are also deficient in osteogenic tissue. Addition. have been totally different. the associ. As McNeil saw it. both palatal segments in bilateral clefts of the lip McNeil was correct in stressing that surgery should be and palate (BCLP). McNeil’s interpretation of the ef- fects of clefting on the various vegetative functions. which can vary among patients. His conclusions cur after palatal surgery (with minimum scarring) is were based on conjecture. pressure forces created by “function. and not move medially into a collapsed relation- particular regions and in particular directions so that ship. shape. studying palatal size in a cleft the growing nasal septum.4. the embryopathogenesis of complete clefts of the lip also causing abnormal growth and development of and palate and their treatment at the neonatal period. being detached from Mestre et al. such as the chondrocranium. The results of Berkowitz’s 3D palatal growth stud- ies [37] show marked acceleration in palatal growth during the first 2 years without orthopedic treatment. The inability of of tolerance. can be stimulated to Berkowitz concluded that “catch-up growth” can oc. of McNeil’s other stated benefits such as reduction of ing of the cleft is due to growth of the underlying bone middle ear infections.1. tion of the larger segment moves medially and lates palatal growth. neously. will lead to and forward vector of facial growth. The resulting narrow. wrote that the palatal processes. This is an expression of the palate’s inherent 2. following Scott’s thesis. not on objective data. has not been support- al” orthopedic appliances. opposite to be true. thereby increasing the chance of having a long. grow forward is totally erroneous.2 The Need to Prevent Collapse guides their growth. McNeil’s claim that the lesser segments in UCLP. do not receive their growth population that had not been operated on. genic deficiency does exist to varying degrees. the palatal structures. to make contact with the alone is unsatisfactory because it will reduce “valu. has led many clinicians to question the accuracy it can intensify normal forces. and both segments in BCLP. and the nasal septum. using a sample of cases that have not had neonatal If McNeil had had the benefit of serial casts. Even as reduced to a minimum compatible with sound clinical early as the 1960s. growth potential. McNeil [13–15] made other faulty observations. 5] further suggests that the nasal septum far medially and becoming collapsed with the buccal plays more than a secondary role in the downward segments in crossbite. ance will stimulate the underdeveloped cleft seg- sure. 16). and osteogenic deficiency. report that impetus and. This force needs to be applied to gery. he suspects. This. 14]. and in reducing palatal growth. quality. al growth leads to a reduction in the soft palate cleft as Among them: well.1. I am confi- of noncleft cases – show that growth occurs sponta. with most of the growth changes occur- ring at the area of the maxillary tuberosity and not . 1. and extent of the surgery that deter- palatal processes can be stimulated to increased size mines the effect on maxillary growth and that osteo- through the use of functional orthopedics. They believed that the cartilagi- nous centers. [36]. prior to lip surgery to prevent them from moving too Scott [4. They do conclude that it is the He goes still further and believes that the deficient type. describing faulty respiratory. Our re- search on serial palatal growth changes supports this conclusion that palates with clefts are highly variable 4. performed (see Chap. Is it Possible? Unfortunately.26 S. well-functioning soft palate after surgical clo. premaxillary portion of the greater segment and able” tongue space and lead to harmful speech habits. McNeil [13–15] further believes that the palatal seg- ated synchondroses. In UCLP. the premaxillary por- Whereas McNeil states that his procedure stimu. sucking. thereby narrowing the cleft backward to make contact with the lesser segment space. which are within the limits ed by controlled objective research. ment in unilateral clefts of the lip and palate McNeil [14] goes on to suggest that an obturator (UCLP) to move forward. abnormal movements of the tongue and give rise to McNeil [13. and swallowing patterns. therefore. Berkowitz’s [35] 3D palatal growth studies – due to the action of compressive lip muscle forces. He mistakenly believed that the orthopedic appli- flexible. after the lip is united. should be ments should be manipulated to an ideal relationship viewed as the true centers of skull and facial growth. in unoperated cases. will act to stimulate bone growth in an the manipulated arch to remain intact after lip sur- anterior direction.1 Stimulation of Bone Growth – in size. many orthodontists found the reasoning and accepted surgical principles. dent. his in- maxillary orthopedic treatment and a control sample terpretation of clinical events would. Berkowitz periosteum carry an intrinsic genetic message that 4.4.

The splanchnocranial skeleton cleft of the lip and palate needs to be refuted. and mechan- blow. apart? The increments of growth observed at the sutural Enlow’s [1] report on current thinking on palatal edges of these bones. The periosteal membranes are growth. by virtue of the undoubted ability of all carti. responding to the role of nasal sep. high-level pressure induces resorption. Postnatal cavity growth exclusively by removing bone. In human. Moss fur.) lages. functional matrix theory than the nasal septum theo- nous interstitial growth is the major source of the ex. (The use of presurgical orthopedic cial skeletal growth is not dependent on any prior. (2) that all cranial cartilaginous tissues (septal. serves to protect and amount causes vascular occlusion and interference support the functional spaces for respiration and with osteoblastic formation of new bone. both osseous and cartilagi- condylar. not the cause of it). 18–22. splanchnocranial bones are within this capsule. states that Scott’s hypothesis is based on the left over after the upper facial structures complete following assumptions: (1) that in the fetal skull. there seems to be more support for the In Scott’s hypothesis. as well as the changes in spatial position. the nasal septal cartilage plays a secondary compen- eral endochondral ossification centers of the ethmoid satory role. On the contrary.e. All cranial bones and cartilages originate and grow with- One last but significant characterization of a newborn in soft tissue capsules. Covering membranes are quite sen. 12]. nasal capsular growth. constructed to function in a field of tension (as by the The nasal skeleton is characterized by a relatively pull of a muscle). of these two areas is independent of the other and that ance of the intramembranous vomer (and of the sev. growth “impetus” of the nasal septal carti. great normal variation in form. olfaction. The nasal capsule sitive to direct compression because any undue (and septum). although it is universally realized that much secondary. causing both vertical and an- olar growth associated with canine development teroposterior growth. [38]. complex. and (3) that following the prenatal appear. sinuses and the turbinates) the remaining unossified At present. shape in bones and cartilages are responses to matrix adapted kind of tissue. unit growth comes about in the following manner. in espousing Scott’s theory pansive force that “pushes” on the subjacent mid-fa. Unfortunately. The nasal cavity is not a space haphazardly [4. functional cranial analysis to nasal and mid-facial laginous tissues to undergo interstitial expansive skeletal growth demonstrates that the growth of each growth. it is assumed that cartilagi. and nous. the nasal septum theory is somewhat portions of the cartilaginous nasal capsule continue accepted as a reasonable explanation by a number of to be capable of such interstitial expansion. The growth of the upper face is. clinicians who favor presurgical orthopedic treat- ther suggests that the nasal septal cartilage grows as a ment. Movement of the cleft palatal segment demonstrated repeatedly that growth in size and anteriorly is only possible as a result of reactive shape. Because the explain the dynamics that can make this possible. is secondary. the alterations of size and Bone is necessarily both a traction. processes [39]. or in synchondroses) are primary growth nous. McNeil. he does not oro-facial capsule to expand responsively. Enlow[1] writes that recent research has shown ically obligatory responses of the skeletal units to such that pressure is detrimental to bone growth. from its inception. of all mechanical forces being applied through the use of skeletal units is always secondary to primary changes pinned maxillary orthopedic appliances or from a in their functional matrices. rather than a primary morphogenetic one. are passively translated in space within their expand- wardly directed forces from the cleft lip-cheek muscle ing capsule. compensatory response to the primary more needs to be understood about facial growth growth of related oro-facial matrices and that mid-fa. Moss believes that it has been (Fig. As a result of such spatial displacement. and at the mandibular condylar growth processes delivers McNeil’s thesis a mortal cartilages. to explain the “retropositioned maxillary complex rel- . are secondary. compensatory. separative movements (i. Bone is pressure sensitive and increases the respiratory functioning space.. to the functional demands for increased respiratory tal cartilage in mid-facial growth as put forth by Scott volume. the expansion of the original nasal capsule and its derivatives are cartilagi. the olfactory spaces are fully conversely.2). nasal cavity is the primary morphogenetic event. growth of the enclosed oro-facial matrices causes the ward the midline before birth. especially when the tongue fits within the the individual bones will be distracted (or separated) cleft space and acts to move the palatal segments passively from one another. Chapter 4 Familial Exudative Vitreoretinopathy 27 at the anterior portion of the palate except for alve. 4. cial skeletal structures.” However. they How can segments be collapsed if there are no in. Osteoclasts. This secondary skeletal protraction facial mask. the their growth. The application of the theory of centers. in part. McNeil exists within an oro-facial capsule. primary. The primary states that “in BCLP lateral segments are collapsed to. ry. a response Moss et al. function to “relieve” the degree of pressure formed at birth. Clinically.and pressure. or treatment is covered in greater detail in Chaps.

NS. . pm. 4. dinal cephalometric findings of a continuous increase ture system and the nasal septum increases the depth in the Sella–Frontale dimension with little increase in and height of the upper face.3–4. reflection of condylar mandibular of the direction of facial growth. did not have access to serial palatal and facial growth records to support such a view. At this ward and forward translation of the upper face by age. Spheno-ethmoidal circumaxillary a concept based on a plane at the level of the anterior suture system: se. fe. it can more accurately be explained in relationship to the embryopathogenesis of facial development: the failure of migrating undifferentiated mesenchymal cells from the neural crest to reach the facial process- es [41. synchronization of the amount. zygomati- analysis of craniofacial growth. Basion Horizontal is growth. Berkowitz ative to the mandible and osteogenically deficient palatal processes” in complete clefts of the lip and palate. Coben states that the comaxillary. C. carrying the magnum as the reflection of mandibular growth car- mandibular dentition downward and forward.5 Basion Horizontal Concept: The Direction of Facial Growth (Figs. Growth of the tains a constant sagittal spatial relation to the foramen mandible is reflected away from Basion. Longitu- growth of the spheno-ethmoidal/circumaxillary su. frontomaxillary. fm. em. (Reprinted from [43]) foramen magnum (Basion) and the vertebral column. Postnatal craniofacial growth systems to the age of without including Coben’s Basion Horizontal Concept 7 years (first decade). border of foramen magnum parallel to Frankfort hor. the eyeballs. and the spheno-eth- mandible. resorption are minor factors in these early years.3. the growth in this suture system produces space growth of the spheno-occipital synchondrosis. while for the eruption of the maxillary first molars. which is the most reliable means of judging the geometric relationship of the maxillary to the mandibular arches within the face. and direction Before age 7. the teeth in the lateral palatal seg- ments were in either a Class I or Class II relationship but were never in a Class III relationship. the thickness of the frontal bone before age 7 support The Basion–Articulare dimension is essentially the concept that bone apposition and remodeling stable postnatally. Spheno-occip- ital synchondrosis.1. nasal septum. zygomaticotemporal (not shown). growth of the upper face is dominated by of growth of the cranio-maxillary complex and of the the nasal septum. vertical facial growth and the eruption of the denti.5) [43] No discussion on craniofacial growth is complete Fig. 4.4). ries the lower teeth downward and forward. 1). moidal/circumaxillary suture system (Fig. zt. showed that at 3–6 years of age. ethmoidal-maxil- izontal where Basion is the point of reference for the lary. If palatal osteogenic deficiency does exist. lm. There are two distinct phases of craniofacial tion. However. indicating that the mandible main. The cranio-maxillary complex housing the maxillary dentition is translated upward and forward from Ba- sion by growth of the cranial base. ptp.28 S. palatomaxillary. 42] (see Chap. timing. The di. Berkowitz’s [40] serial casts study of CUCLP and CB- CLP cases using the Angle occlusal classification sys- tem. On this basis. 4. growth because of a change in the system of upper fa- Normal maxillo-mandibular development requires cial development after the approximate age of 7 years. lacrimal-maxillary. Spheno-ethmoidal. away vergence of the two general vectors develops space for from the cranial base. one can conclude that it is not the lack of a growth impetus from the nasal septum that explains the presence of a small cleft palatal segment at birth. 4. Cartilaginous growth: SO. Surface ap- growth concept which Basion Horizontal represents is position-modeling resorption development (stippled area): that craniofacial growth is reflected away from the minor contribution. zm. The cranial base vector represents the up. pterygopalatine. fronto-ethmoidal.

space for the erupting upper first molars results from growth of the spheno. Spheno-ethmoidal circumaxillary suture system: Sutural growth no longer primary system of upper fa- cial development. Growth of the mandible translates the lower duced by maxillary alveolar apposition as the maxil. 4. reflection of condy- lar mandibular growth – active to facial maturity. The Sella–Frontale dimension stabilizes. Postnatal craniofacial growth systems from age 7 years (second decade). This create space for vertical facial development and tooth eruption. 4. who reasoned [43] b Basion Horizontal. the maxillary dentition upward and forward away from the foramen magnum. C. Chapter 4 Familial Exudative Vitreoretinopathy 29 a Fig. General vectors of craniofacial ethmoidal/circumaxillary suture system. and the thickness of the frontal bone begins to increase by surface apposition and remodeling until maturity.4). Spheno-occipital synchondrosis-active through puberty. Surface apposition-modeling resorption de- velopment (stippled area): Now major method of upper facial development and alveolar growth [43] At about age 7. before age 7.5a . the initial pri- mary system of spheno-ethmoidal/circumaxillary su- tural growth of the upper face is replaced by surface apposition and remodeling resorption (Fig. growth. the growth system of the upper face changes with the closure of the spheno-ethmoidal su- ture. It is b significant that. Cartilaginous growth: SO. 4. The two diverging vectors lary dentition erupts downward and forward. 4. Basion Horizontal Coordinate com- that the spheno-ethmoidal suture must be viewed as puter Craniofacial serial schematic line graph of Fig. dentition downward and forward.4. a Basion Horizontal. Fig.5. The interpretation is that after age 7. concept was supported by Scott [12]. nasal septum – growth completed. After age 7. Growth of the cranial base translates the upper face and space for the upper second and third molars is pro.

6. differences in the morphology of the mandible in per- sons with cleft lip and/or palate.6. and 4. Longitudinal cephalo- metric growth studies confirm this interpretation Recent studies have revealed a series of often subtle (Fig. there is no further in Cleft Palate (Figs.5). 4. Dahl [44] and Chieri- ci and associates [45] found that. the condylar head determine the direction and extend of mandibular growth part of the major circumaxillary suture system.2 Mandibular Development that once part of the suture closes. 4. Various growth changes that occur.30 S.7) growth in that suture system. 4. 4. Berkowitz Fig. in persons with .

found no nial angle in patients with unilateral CLP was more significant differences between normal and cleft chil- obtuse.7 a–c.Comment: This clefts of the hard palate only. Chapter 4 Familial Exudative Vitreoretinopathy 31 a c b Fig. c Hypodivergent cial Analysis system for this (Fig. Mazaheri and coauthors [46] other than a more obtuse gonial angle. a normal population. b Neutral growth pattern. so that its effective length was less than in those with cleft lip and palate (CLP) and normal in the normal population. Bishara [49] studied Danish children with repaired 4. Aduss [47] observed that the mandibular go. and that the anterior cranial base appeared to dren either at birth or at 3 years of age. In the to the cranial base and that its mandibular plane was Pierre Robin sequence. three general patterns of mandible was significantly more posterior in relation postnatal growth have been demonstrated. a Hyperdivergent pattern with posterior of the face. the mandibular plane Krogman and colleagues [51] found no difference was steeper and the gonial angle more obtuse than in in mandibular dimensions in the BCLP population. and again in a later study of patients with CUCLP [50]. See Coben’s Basion Horizontal.3 Patterns of Postnatal Growth cleft palates only. Rosenstein [48] also found the mandibles to be smaller.5) growth pattern with anterior growth rotation. he noted that the Based on the serial studies. Facial growth rotations resulting form differential series is not a true reflection of the growth of various components vertical growth. of the lip and palate. 4. and in complete bilateral clefts steeper than normal. comparing mandibular arch dimensions. groups. Coordinate Craniofa- growth rotation. most cases demonstrate substan- . They also noted that the length and width of the mandible were found the temporomandibular joint to be positioned significantly less in persons with cleft palate only than farther back. Robertson and Fish [52]. In that study. 4. with steeper mandibular plane angles. be elevated.

moves progres- mandibular ramus (e. for example. quential remodeling changes in the shape and size of served in some instances of unilateral agenesis of the each region. This progressive. growth process. The reason why a bone must remodel mity of the mandible neither improves nor worsens in during growth is because its regional parts become the course of time. sequential move- ment of component parts as a bone enlarges is termed relocation. e Long shallow face with severe tongue problem.. mouth breather.1 Bone Remodeling During Growth the mandible. hemifacial microsomia) and sively posteriorly by a combination of deposition and in the growth of the maxilla and neurocranium in resorption. (Courtesy of R. b Prognathic mandible with recessive maxilla. d Slightly retro. 4. and an inability to close the lips. Not all faces are the same. Chronic closed bite with short denture height. mandibulofacial (Fig. the anterior part of the ra- some forms of premature craniofacial synostosis. Severe overbite and overjet. “drift” moves each part from one location to the growth process is so deranged that the severity of another as the whole bone enlarges. The ramus. This produces a growth elonga- tion of the corpus.g. In the second pattern. extreme- of facial patterns. The Biology of Occlusion and the Temporomandibular Joint in c Brachyfacial type with dental protrusion. The whole ramus is thus relocated posteriorly. This calls for se- the deformity increases with age. 1972) tial improvement through “catch-up” in the growth of 4. f Extremely mandibular plane angle. This has been ob. the pattern of growth is such that the de- formity observed in infancy or early childhood is Enlow [1] states that remodeling is a basic part of the maintained throughout the growth period. Modern Man.3. Berkowitz a b c d e f Fig. Various types bite.8 a–f.8) dysostosis. and the posterior part of the lengthening corpus becomes re- located into the area previously occupied by the ra- . The third pattern is one in which moved.32 S. 4. Ricketts. The defor. As it does so. a Retrognathic mandible with steep ly wide openbite. mus becomes remodeled into a new addition for the mandibular corpus. Relocation is the basis for remodeling. therefore treatment gnathic type with protrusive maxillary denture and severe deep most vary according to the facial growth pattern.

). 123–127. Mestre J. Moss M. The analysis of facial growth.) Proc Roy Soc Med 1959.2 Maxillary Growth 18. 52:52–60. Penoff JH. Cronin TD. Cleft Palate J 1979. Intraoral traction for position- References ing the premaxilla in the bilateral cleft lip. Rosenstein SW (eds. p. 30:78–85. A new concept of the early maxillary growth 9. London: E&S Livingston Ltd. McNeil CK. Berkowitz S (eds. Philadelphia. Further studies on the growth of the human face.. Introductory concepts of the growth process. Plast and Re- and palate clefts. rotational manner relative to the cranial base. 1. Latham RA. 35. Burston WR. Pitman and Sons. Philadelphia: W. Primary orthodontic treatment for the cleft the small variation. Furthermore. In: Grabb WC. Amer J Orthod 1956. In: Wallace: AB (ed. Scott JH. Dejesus J. Therefore. 36. 23. Passive role of 1964. Early treatment of cleft lip constr Surg 1983. 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