Facial growth (N. E. Carter)

15 May

Orthodontic treatment is usually carried out on children at a time when the face is growing. The clinician must be aware of the impact of growth upon the progress and outcome of treatment, and of how growth may hinder or help treatment. Orthodontic treatment itself may have some effect upon the growth of the face, and a basic knowledge of the processes of facial growth is essential for the practising clinical orthodontist.

Facial growth

Fig. 4.1. Synchondrosis: ossification is taking place on both sides of the primary growth cartilage (Photo: D. J. Reid).

The face is a very complex structure, and its growth and development are the result of many interacting processes. The purpose of this brief account is to highlight just a few aspects of facial growth which are relevant to clinical orthodontic practice, particularly the later stages of growth which very often coincide with orthodontic treatment. Of course, facial appearance is the result of growth of both hard and soft tissues, but the teeth are hard tissue structures and the main focus of study has been on growth of the bony facial skeleton.
Bone is laid down in two ways: by replacing cartilage and by membrane activity. Bone does not grow interstitially, i.e. it does not expand by cell division within its mass; rather, it grows by activity at the margins of the bone tissue.
4.2.1. Endochondral ossification
At cartilaginous growth centres, chondroblasts lay down a matrix of cartilage within which ossification occurs. At primary growth centres, these cells are aligned in columns along the direction of growth, in which there are recognizable zones of cell division, cell hypertrophy, and calcification (Fig. 4.1). This process is seen in both the epiphyseal plates of long bones and the synchondroses of the cranial base. Growth at these primary centres causes expansion despite any opposing compressive forces such as the weight of the body on the long bones, and thus the bones on either side of the spheno-occipital synchondrosis are moved apart as it grows. Condylar cartilage also lays down bone, and for a long time this was thought to be a similar mechanism to epiphyseal growth, but developmentally it is a secondary cartilage and its structure is different Proliferating condylar cartilage cells do not show the ordered columnar arrangement seen in epiphyseal cartilage, and the articular surface is covered by a layer of dense fibrous connective tissue (Fig. 4.2). The role of the condylar cartilage during growth is not yet fully understood, but it is clear that it is different from that of the primary cartilages and its growth seems to be a reactive process in response to the growth of other structures in the face.
4.2.2. Intramembranous ossification
Bone is both laid down and resorbed by the investing periosteum and by the endosteum within the bone. These processes of deposition and resorption together constitute remodelling (Fig. 4.3). Growth does not consist simply of enlargement of a bone by deposition on its surface: periosteal (surface) remodelling is also needed to maintain the overall shape of the bone as it grows. Thus, as well as having areas where new bone is being laid down, a growing bone always undergoes resorption of some parts of its surface. At the same time, endosteal remodelling maintains the internal architecture of cortical plates and trabeculae, but of course it cannot cause the bone to enlarge. Remodelling is a very important mechanism of facial growth, and the complex patterns of surface remodelling brought about by the periosteum which invests the facial skeleton have been studied extensively.
Fig. 4.3. Periosteal remodelling, showing reversal lines where bone resorption has been followed by deposition (Photo: D. J. Reid).
The bones of the face and skull articulate together mostly at sutures, and growth at sutures can be regarded as a special kind of periosteal remodelling — an infilling of bone in response to tensional growth forces separating the bones on either side (Fig. 4.4).
Growth which causes the mass of a bone to be moved relative to its neighbours is known as displacement of the bone; an example is forward and downward translation of the maxillary complex (Fig. 4.5). The change in position of a bony structure owing to remodelling of that structure is called drift, and Fig. 4.6 shows an example of this where the palate moves downwards during growth as a result of bone being laid down on its inferior surface and resorbed on its superior surface.
Fig. 4.5. Forward and downward displacement of the maxillary complex associated with deposition of bone at sutures. (After Enlow, D. H.: Facial Growth, W. B. Saunders Co., Philadelphia, 1990.)

It is not intended to describe in any detail here the processes by which the face grows, rather to give a picture of the patterns of facial growth. Early cephalometric growth studies gave the impression that, overall, as the face enlarges it grows downwards and forwards away from the cranial base (Fig. 4.7). However, it is now known that growth of the face is much more complex than this, involving many growth processes in the mandible, mid-face, cranial base, and so on. All of these are going on at the same time, and the overall pattern of growth results from the interplay between them. They must all harmonize with each other if a normal facial pattern is to result, and small deviations from a harmonious facial growth pattern will cause discrepancies of major significance to the orthodontist.
Different systems have different growth patterns in terms of rate and timing, and four main types are recognized: neural, somatic, genital, and lymphoid (Fig. 4.8). The first two are most relevant here.
Neural growth is essentially that which is determined by growth of the brain, and the calvarium follows this pattern of growth — in other words the bones grow in response to the growth of another structure. There is rapid growth in the early years of life, but this slows until by about the age of 8 years growth is almost complete. The orbits also follow a neural growth pattern.
Somatic growth is that followed by most structures. It is seen in the long bones, amongst others, and is the pattern followed by increase in body height. Unlike neural growth, somatic bone growth seems to be more an intrinsic property of the bones and under fairly tight genetic control. Growth is fairly rapid in
the early years, but slows in the prepubertal period. The pubertal growth spurt is a time of very rapid growth, which is followed by further slower growth. The pubertal growth spurt occurs on average at 12 years in girls, but in boys it is later at about 14 years. Although the timing of facial growth has been studied less extensively than the timing of growth in stature, growth of the facial skeleton follows approximately a somatic growth pattern.
Fig. 4.6. Downwards migration of the hard palate due to drift. (From Enlow, D. H.: Facial Growth, W. B. Saunders Co., Philadelphia, 1990.)
Fig. 4.7. Superimpositions on the cranial base showing overall downwards and forwards direction of facial growth. Solid line 8 years, broken line 18 years of age.
Postnatal growth patterns
Fig. 4.8. Postnatal growth patterns shown as percentages of total increase (From Scammon, R. E.: The Measurement of Man, University of Minnesota Press, 1930.)
Thus different parts of the skull follow different growth patterns, with much of the growth of the face occurring later than the growth of the cranial vault. As a result the proportions of the face to the cranium change during growth, and the face of the child represents a much smaller proportion of the skull than the face of the adult (Fig. 4.9).
Fig. 4.9. The face in the neonate represents a much smaller proportion of the skull than the face of the adolescent (Photo: B. Hill).
The calvarium is that part of the skull which develops from the membrane bones surrounding the brain and therefore it follows the neural growth pattern. It comprises the frontal bones, the parietal bones, and the squamous parts of the temporal and occipital bones. These bones articulate with each other at sutures, which at birth are not yet united. Six fontanelles are also present at birth which close by 18 months. By the age of 6 years the calvarium has developed inner and outer cortical tables which enclose the diploë. Its growth consists of a combination of drift and displacement. Drift occurs because the intracranial aspects of the bones are resorbed while bone is laid down on the external surfaces. There is displacement as the bones are separated by the growing brain, with fill-in bone growth occurring at the sutures to maintain continuity of the cranial vault.

Growth of the cranial base is influenced by both neural and somatic growth patterns. As in the calvarium, there is both remodelling and sutural infilling as the brain enlarges, but there are also primary cartilaginous growth sites in this region — the synchondroses. Of these, the spheno-occipital synchondrosis is of special interest as it makes an important contribution to growth of the cranial base during childhood, continuing to grow until about 15 years of age, and fusing at approximately 20 years. Thus the middle cranial fossa enlarges both by anteroposterior growth at the spheno-occipital synchondrosis and by remodelling. The anterior cranial fossa enlarges and increases in anteroposterior length by remodelling, with resorption intracranially and corresponding extracranial deposition.
Fig. 4.10. Antero-posterior growth at the spheno-occipital synchondrosis affects the anteroposterior relationship of the jaws.
The spheno-occipital synchondrosis is anterior to the temporomandibular joints but posterior to the anterior cranial fossa, and therefore its growth is significant clinically as it influences the overall facial skeletal pattern (Fig. 4.10). Growth at the spheno-occipital synchondrosis increases the length of the cranial base, and since the maxillary complex lies beneath the anterior cranial fossa while the mandible articulates with the skull at the temporomandibular joints which lie beneath the middle cranial fossa, the cranial base plays an important part in determining how the mandible and maxilla relate to each other. For example, a Class II skeletal facial pattern is often associated with the presence of a long cranial base which causes the mandible to be set back relative to the maxilla.
In the same way, the overall shape of the cranial base affects the jaw relationship, with a smaller cranial base angle tending to cause a Class III skeletal pattern, and a larger cranial base angle being more likely to be associated with a Class II skeletal pattern (Fig. 4.11).
The anterior part of the cranial base is used in cephalometric analysis as a reference structure from which measurements can be taken, remote from the face itself and thus unaffected by orthodontic treatment. It is often represented by the Sella–Nasion line (see Chapter 6).
Fig. 4.11. View (i) Low cranial base angle associated with Class III skeletal pattern. View (ii) Large cranial base angle associated with a Class II skeletal pattern.
The maxilla derives from the maxillary processes of the first pharyngeal arch and from the frontal process. Ossification is intramembranous, beginning laterally to the cartilaginous nasal capsule.
Clinical orthodontic practice is primarily concerned with the dentition and its supporting alveolar bone which is part of the maxilla and premaxilla. However, the middle third of the facial skeleton is a complex structure and also includes, among others, the palatal, zygomatic, ethmoid, vomer, and nasal bones. These articulate with each other and with the anterior cranial base at sutures. Growth of the maxillary complex occurs in part by displacement with fill-in growth at sutures and in part by drift and periosteal remodelling.
The maxilla enlarges anteroposteriorly by deposition of bone posteriorly at the tuberosities, which of course also lengthens the dental arch. Forward growth of the maxilla is thus anterior displacement as bone is laid down on its posterior aspect (see Fig. 4.5). The zygomatic bones are also carried forwards, necessitating infilling at sutures, and at the same time they enlarge and remodel. In the upper part of the face, the ethmoids and nasal bones grow forwards by deposition on their anterior surfaces, with corresponding remodelling further back, including in the air sinuses, to maintain their anatomical form.
Downward growth occurs by vertical development of the alveolar process and eruption of the teeth, and also by inferior drift of the hard palate, i.e. the palate remodels downwards by deposition of bone on its inferior surface (the palatal vault) and resorption on its superior surface (the floor of the nose and maxillary sinuses) (see Fig. 4.6). These changes are also associated with some downward displacement of the bones as they enlarge, again necessitating infilling at sutures. Lateral growth in the mid-face occurs by displacement apart of the two halves of the maxilla, with deposition of bone at the midline suture. Internal remodelling leads to enlargement of the air sinuses and nasal cavity as the bones of the mid-face increase in size.
Thus there are complex patterns of surface remodelling on the anterior and lateral surfaces of the maxilla which maintain the overall shape of the bone as it enlarges. Despite being translated anteriorly, much of the anterior surface of the maxilla is in fact resorptive in order to maintain the concave contours beneath the pyriform fossa and zygomatic buttresses.
Maxillary growth ceases on average at about 15 years in girls and rather later, at about 17 years, in boys.
Growth at the condylar
Fig. 4.12. Growth at the condylar cartilage elongates the mandible, causing anterior displacement, while its shape is maintained by remodelling, including posterior drift of the ramus. (After Enlow, D. H. 1990 Facial growth, Saunders, Philadelphia, 1990.).
The mandible derives from the first pharyngeal arch and is a membrane bone, ossifying laterally to Meckel’s cartilage. Secondary cartilages appear, including the condylar cartilage, but the role of the condylar cartilage in the growth of the mandible is not yet entirely clear. It seems probable that, since it is a secondary cartilage, it is not a primary growth centre in its own right, but rather it grows in response to some other controlling factors. However, what is clear is that normal growth at the condylar cartilage is required for normal mandibular growth to take place.
However, most mandibular growth occurs as a result of periosteal activity. Muscular processes develop at the angles of the mandible and the coronoids, and the alveolar processes develop vertically to keep pace with the eruption of the teeth. As the mandible elongates with growth at the condylar cartilage, so its anterior part is displaced forwards, while at the same time periosteal remodelling
maintains its shape (Fig. 4.12). Bone is laid down on the posterior margin of the vertical ramus and resorbed on the anterior margin, and this posterior drift of the ramus allows lengthening of the dental arch posteriorly. At the same time the vertical ramus becomes taller to accommodate the increase in height of the alveolar processes. Remodelling also brings about an increase in the width of the mandible, particularly posteriorly. Lengthening of the mandible and anterior remodelling together cause the chin to become more prominent, an obvious feature of facial maturation especially in males. Indeed, just as in the maxilla, the whole surface of the mandible undergoes many complex patterns of remodelling as it grows in order to maintain its proper anatomical form.
Direction of condylar growth
Fig. 4.13. Direction of condylar growth and mandibular growth rotations:
View (i) Forward rotation
View (ii) Backward rotation
Mandibular growth ceases rather later than maxillary growth, on average at about 17 years in girls and 19 years in boys, although it may continue for longer.
Early studies of facial growth indicated that during childhood the face enlarges progressively and consistently, growing downwards and forwards away from the cranial base (see Fig. 4.7). These studies looked only at average trends and failed to demonstrate the huge variation which exists between the growth patterns of individual children. Later work by Björk has shown that the direction of facial growth is curved, giving a rotational effect (Fig. 4.13). The growth rotations

were demonstrated by placing small titanium implants into the surface of the facial bones, and subsequently taking cephalometric radiographs at intervals during growth. Since bone does not grow interstitially, the implants could be used as fixed reference points on the serial radiographs from which to measure the growth changes.
Mandibular growth rotations
Fig. 4.14. Mandibular growth rotations reflect the ratio between the anterior and posterior face heights, here shown relative to the Frankfort horizontal plane: (i) forward rotation, (ii) backward rotation.
broken line
Fig. 4.15. Forward growth rotation. Solid line 11 years, broken line 18 years of age.
Growth rotations are most obvious and have their greatest impact on the mandible; their effects on the maxilla are small and are almost completely masked by surface remodelling. In the mandible, however, their effect is significant, particularly in the vertical dimension. Mandibular growth rotations result from the interplay of the growth of a number of structures which together determine the ratio of posterior to anterior facial heights (Fig. 4.14). The posterior face height is determined by factors including the direction of the growth at the condyles and vertical growth at the spheno-occipital synchondrosis. The anterior facial height is affected by the eruption of teeth and vertical growth of the soft tissues, including the masticatory musculature and the suprahyoid musculature and fasciae, which are in turn influenced by growth of the spinal column. The overall direction of growth rotation is thus the result of the growth of many structures.
Forward growth rotations are more common than backward rotations, with the average being a mild forward rotation which produces a well-balanced facial appearance. A marked forward growth rotation tends to result in reduced anterior vertical facial proportions and an increased overbite (Fig. 4.15), and the more severe the forward rotation the more difficult it will be to reduce the overbite. Similarly, a more backward rotation will tend to produce increased anterior vertical facial proportions and a reduced overbite or anterior open bite (Fig. 4.16).
Not only is the vertical dimension affected, but there are also important antero-posterior effects. For example, correction of a Class II malocclusion will be helped by a forward growth rotation but made more difficult by a backward rotation. Growth rotations may also have an effect on the position of the lower labial segment. A forward growth rotation tends to cause retroclination of the lower labial segment which is often associated with shortening of the dental arch anteriorly and crowding of the lower incisors. A possible explanation for this is that, as the lower arch is


carried forwards with mandibular growth, forward movement of the lower incisor crowns is limited by contact with the upper incisors, causing them to crowd. This is common in the very late stages of growth when mandibular growth continues after maxillary growth has finished, although facial growth is only one of a number of possible aetiological factors in late lower incisor crowding.

Thus growth rotations play an important part in the aetiology of certain malocclusions and must be taken into account in planning orthodontic treatment. It is necessary to try to assess the direction of mandibular growth rotation clinically. This is not entirely straightforward since the effect of growth rotation upon the mandible is masked to some extent by surface remodelling, particularly along the lower border of the mandible and at the angle. However, it is possible to make a useful assessment of a patient’s facial growth pattern by examining the anterior facial proportions and mandibular plane angle as described in Chapter 5. Increased facial proportions and a steep mandibular plane indicate that the direction of mandibular growth has a substantial downward component, while reduced facial proportions and a horizontal mandibular plane suggest that the direction of growth is more forwards. It is also helpful to examine the shape of the lower border of the mandible. A concave lower border with a marked antegonial notch is associated with a backward rotation, while a convex lower border is associated with a forward growth rotation (see Figs 4.15 and 4.16).
The importance of the oral musculature in orthodontic practice is that it influences significantly the form of the dental arches, since the teeth lie in a position of equilibrium between the lingual and bucco-labial musculature. Therefore they are important factors in the aetiology of malocclusion, and greatly affect the stability of the result after orthodontic treatment.
The facial musculature is well developed at birth, considerably in advance of the limbs, because of the need for the baby to suckle and maintain the airway. Other functions soon develop: mastication as teeth erupt, facial expressions, a mature swallowing pattern (as opposed to suckling), and speech.
The lips, tongue, and cheeks guide the erupting teeth towards each other to achieve a functional occlusion. This serves as a compensatory mechanism for a discrepancy in the skeletal pattern; for example, in a Class III subject the lower incisors may become retroclined and the upper incisors proclined to obtain incisor contact. Sometimes this compensatory mechanism fails, either because the skeletal problem is too severe or the soft tissue behaviour is abnormal. An example of this is where lower lip function worsens a Class II division 1 malocclusion by acting behind the upper incisors rather than anteriorly to them. In the late stages of growth the lips lengthen as they mature, tending to become more competent.
Muscle growth must be coordinated with the growth of the associated bones, with the muscles lengthening as their bony attachments separate. Neuromuscular activity regulates the positions of the jaws, and it has been suggested that the whole process of facial skeletal growth is determined by the soft tissues which surround the bones.
The mechanisms that control facial growth are poorly understood but are the subject of considerable interest and research. As with all growth and development,


there is an interaction between genetic and environmental factors, but if environmental factors can make a significant impact on facial growth then the possibility exists for clinicians to alter facial growth with appliances.

It is often difficult to distinguish the effects of heredity and environment, but it is helpful to consider how tightly the growth and development of a structure or tissue are under genetic control. Two simple examples illustrate this: gender is genetically determined and does not change no matter how extreme the environmental conditions, while obesity is very strongly affected by the nature and amount of food consumed. Most structures, including the facial skeleton and soft tissues, are influenced by both genetic and environmental factors, and the effect that the latter can have depends upon how tightly growth is under genetic control.
Genetic control is undoubtedly significant in facial growth, as is clearly shown by facial similarities in members of a family. The extent to which the facial skeleton itself is under genetic control has been debated at length in recent decades, with the development of two opposing schools of thought. Growth at the primary cartilages is regarded as being under tight genetic control, with the cartilage itself containing the necessary genetic programming. Therefore those who view growth of the whole facial skeleton as being directly and tightly genetically controlled have looked for primary cartilaginous growth centres in the facial bones. The condylar cartilages seemed to fulfil this role in the mandible, while the nasal septal cartilage was thought to serve a similar function in the maxilla. However, the structure and behaviour of these cartilages is different from primary growth cartilages, and at present it is thought that, while their presence is necessary for normal growth to take place, they are probably not primary growth centres in their own right.
The other school of thought proposed that bone growth itself is only under loose genetic control and takes place in response to growth of the surrounding soft tissues — the functional matrix which invests the bone. This idea looks to the example of the neural growth pattern of the calvarium and orbits, which develop intramembranously and enlarge in response to growth of the brain and eyes. However, the functional matrix theory ran into difficulty with regard to facial growth as there are no similarly expanding structures within the middle and lower face. It has attracted a lot of attention as, if taken to its logical conclusion, it implies that orthodontic appliances can be used to alter facial growth.
There is much yet to be understood about how growth of the face is controlled. As to whether appliances influence facial growth, the truth appears to lie some-where between the two extremes of opinion, but research in this field faces considerable problems, some of which are discussed in Chapter 18 in relation to functional appliances. At present, the evidence is that the impact of current orthodontic treatment methods on facial growth is on average quite small, but there is considerable variation in the response of individual patients.
It would be extremely useful if we could predict the future growth of a child’s face, particularly in cases which are at the limits of what orthodontic treatment can achieve. For growth prediction to be useful clinically it would need to be able to predict the amount, direction, and timing of growth of the various parts of the facial skeleton to a high level of accuracy.
At present there are no known predictors which can be measured, either clinically on the patient or from radiographs, which will enable future growth to be predicted with the necessary precision. Much work has been done to try to find


measurements which can be taken from cephalometric radiographs which will predict future facial growth to a useful level of precision, but so far with limited success. Assessment of stature (height) and secondary sex characteristics help to indicate whether the patient has entered the pubertal growth spurt, an important observation when functional appliances are being considered. Since growth of the jaws follows a somatic growth pattern, the possibility has been investigated that observation of the developmental stage of other parts of the skeleton would give an indication of the stage of facial development. The stage of maturation of the metacarpal bones and the phalanges as seen on a hand–wrist radiograph is used as a measure of skeletal development, but the correlation of this with jaw growth has been found to be too poor to give clinically useful information.

The best which can be done is to add average growth increments to the patient’s existing facial pattern, but this has only limited value. This can be done manually using a grid superimposed on the patient’s lateral cephalometric tracing, and average annual growth increments are read off to predict the change in position of the various cephalometric landmarks. Computer programs can be used for the same purpose, after the points and outlines from the lateral skull radiograph have been digitized. These programs can refine the prediction process further but they still have to make some assumptions about the rate and direction of facial growth. Unfortunately, the assumption that a patient’s future growth pattern will be average is least appropriate in those individuals whose facial growth differs significantly from the average, and who are the very subjects where accurate prediction would be most useful. As growth proceeds, the rate and direction of growth in an individual vary enough that study of the past pattern of a patient’s facial growth does not allow prediction of future growth to the level of precision required for it to be clinically useful. However, many clinicians find it helpful to assess the direction of mandibular growth rotation (see Section 4.8) on the assumption that this pattern is likely to continue.
Clinical experience has shown that for most patients, whose growth patterns are close to the average, it can be assumed for treatment-planning purposes that their growth will continue to be average.
Björk, A. and Skieller, V. (1983). Normal and abnormal growth of the mandible. A synthesis of longitudinal cephalometric implant studies over a period of 25 years. European Journal of Orthodontics, 5, 1–46.
A summary of the implant work on mandibular growth rotations.
Enlow, D. H. and Hans M. G. (1996). Essentials of facial growth. Saunders, Philadelphia.
The Bible of facial growth.
Houston, W. J. B. (1979). The current status of facial growth prediction: a review. British Journal of Orthodontics, 6, 11–17.
An authoritative assessment of the value of growth prediction.
Houston, W. J. B. (1988). Mandibular growth rotations — their mechanism and importance. European Journal of Orthodontics, 10, 369–73.
A concise review of the aetiology and clinical importance of growth rotations.
Mills, J. R. E. (1983). A clinician looks at facial growth. British Journal of Orthodontics, 10, 57–72.
A clear description of the facial growth processes from a clinical orthodontic viewpoint.
Low cranial base angle

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