Genetic Preprogrammed Theory (Growth Sites)

Early theorists believed that the sizes and shapes of bones were genetically determined within their cells and that sutural patterns were therefore predetermined. Because bone size and shape are defined by sutures in the head, these pioneers theorized that the position of sutures limits and controls the expansion of bones. Baume² described “growth centres” as places of endochondral ossification with tissue-separating force, resulting in an increase in skeletal mass, and “growth sites” as regions of periosteal or sutural bone formation and modeling resorption that are adaptive to environmental influences.³ The cells of the sutures grew into the void left as the bone segments pulled apart from the tissue-separating force. In other words, growth sites are where growth literally takes place, and growth centers are areas in which genetically predetermined growth takes place. This theory was tested by experiments involving suture removal and transplantation, and the conclusion was that sutures are not primarily responsible for growth.⁴ This theory is no longer accepted as correct.

Cartilage-Mediated Growth (Scott)

In 1953, Scott theorized that the cartilage of the nasal septum “is an extension of the cartilage of the cranial base.”⁵ In its growth, the cartilage of the nasal septum separates the facial bones from one another and from the cranial portion of the skull and allows growth to take place at the sutures by the ordinary mechanism of surface deposition. He held that the nasal septum and also the mandibular condyles and synchondroses (otherwise known as cephalic cartilages) are growth centers. As the nasal septum grows, it puts tension on the sutures of the nasomaxillary complex, thereby displacing it forward and downward, with resultant growth occurring at pressure-related growth sites. Tension occurring in the maxillary sutures causes new bone growth when the sutures are pulled apart. Therefore, suture growth is passive and secondary.

Latham⁶ theorized that a septomaxillary ligament (connection between the septum and maxilla) in the fetus causes the maxilla to be pulled forward by the septum as the maxilla grows. It is unknown whether this ligament plays a role in postnatal growth, and experimentation related to the role of the nasal cartilage in this concept is unknown. Animal experimentation involving removal of septal cartilage shortly after birth⁷ or secondary to trauma seems to result in midface hypoplasia, but such experiments cannot clearly prove that the cartilage removal causes the growth deficiency. Cartilage seems to play some role that has not yet been precisely determined.

The Functional Matrix Hypothesis (Moss)

The most fundamental dictum of the functional matrix hypothesis was stated by Moss,^8,9 as follows:

The basic premise of this theory is that bone and cartilage do not regulate their own growth. This theory proposes that craniofacial bony growth occurs as a reaction to—or in response to—the functional matrix surrounding it. A functional matrix consists of the cells that comprise muscle, soft tissue, teeth, glands, and nerves, as well as the functioning volumes of various cavities associated with the head and neck region (e.g., nasal, orbital, oral, pharyngeal, and neurocranial). A feedback system exists between the functional matrix and the bone and cartilage involved. Growth of cranial size occurs in response to growth of the brain, growth of the bony orbits occurs in response to the size of the orbit, and growth of the facial bones occurs in response to growth of the surrounding soft tissues. The resultant enlargement of the associated cavities of the head and neck occurs because of the functional demands of the airway, breathing, and eating “spaces.” The craniofacial bones are in a dependent relationship with the surrounding soft tissues. Critics state that Moss’s theory explains what happens during growth but does not explain how it happens. Moss’s theory is quite useful in clinical practice because it allows separate assessment of each functional unit in the craniofacial skeleton (i.e., brain = cranium, eye = orbit, jaws (mandible) = mastication, nasomaxillary complex and associated airways = respiration, and the ear = temporal bone). The functional matrix operates within the genetic constraints of the cells and tissues involved.

Facial growth involves intimate morphogenic and biomechanical relationships among all of its component tissue parts, each influenced by and in turn influencing the other. A fundamental principle is that no part is developmentally independent or self-contained.¹¹

At this time, all theories of growth control mechanisms are speculative, with strengths and faults in each. Further research is required before any definite conclusion can be made.

Osteogenesis

A review of bone formation is required for a discussion of craniofacial growth. The initial step in osteogenesis is the laying down of primary or woven bone. Primary bone is immature bone defined by random orientation of collagen fibers and is temporary, except in a few locations such as the tooth sockets and sutures of the cranial bones. Primary bone generally either becomes secondary (lamellar) bone or is removed to leave bone marrow cavities. Secondary bone differs from primary bone in that its collagen has an orderly pattern and it has an increased number of osteoblasts. Osteogenesis occurs through intramembranous ossification in mesenchyme and endochondral ossification in preexisting cartilage.

Endochondral Bone Formation

In endochondral bone formation, simultaneous removal of cartilage and subsequent formation of bone occur. Endochondral bone formation is more complex than intramembranous bone formation. Various zones exist in active endochondral bone formation, including the zones of reserve cartilage, proliferating cartilage, hypertrophic cartilage, calcified matrix, and resorption. The hypertrophic cartilage cells enlarge, and the surrounding matrix becomes calcified. A separate collar of bone forms around the circumference of the center of this cartilage bar. This is periosteal or, more precisely, perichondral bone. A vascular bud migrates into the cartilage and a primary marrow cavity forms. Meanwhile, activity at the various zones continues. Erosion of the cartilage takes place at the two ends of the expanding primitive marrow cavity, and bone forms on the spicules of the cartilage at the erosion front. The epiphyseal plate of long bones allows simpler visualization of this process (Fig. 184-1).

Figure 184-1. Endochondral bone formation at an epiphyseal plate.

This descriptive review of bone formation can be supplemented by a molecular view of bone formation.¹²

General

The faces of infants and children clearly differ from those of adults. Matching an infant’s photograph with that of the corresponding adult photograph is challenging because of the changes that occur with growth and development of the craniofacial region. A baby’s face is pudgy and round, relatively wide, and vertically short; the nose is small; the eyes appear relatively far apart; and there is a prominent forehead.

Infants have a large head relative to their body size. Their facial complex, which includes the nasomaxillary complex and mandible, is much smaller than the calvaria and basicranium (Figs. 184-2 through 184-4). With growth and development of the facial complex come changes in the size ratio of the cranium to the face. In infants the cranium-to-face ratio is approximately 3 : 1; whereas in adults it is approximately 2 : 1 (see Fig. 184-4).

Figure 184-2. The skulls of an infant (approximately 8 months of age), a 5- to 6-year-old, a 10- to 12-year-old, and an adult. Note the bony craniofacial changes with increasing age.

Figure 184-3. Photographs of two siblings from birth to adulthood, demonstrating changes in the craniofacial complex with growth and development. The girl is shown at birth, 10 months, 2.5 years, 6 years, 10 years, 14 years, and 18 years of age, with the last photo in adulthood at 25 years of age. Her brother male is shown at birth, 7 months, 2 years, 5 years, 9 years, 15 years, 19 years, and 25 years of age.

Figure 184-4. The size ratio of the cranium to the face changes considerably during growth and development. In the newborn, the cranium/face ratio is approximately 3 : 1, whereas in adults, this ratio is approximately 2 : 1.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

With growth, increasing demands are made on the respiratory and masticatory systems. As part of the growth of the facial complex, the nose, mandible, and maxilla increase in size—resulting in the larger, coarser features of the adult face in comparison with the child’s (see Fig. 184-3). The facial complex increases in size relative to the cranium. Similarly, body size increases relative to head size, to result in normal adult body and head proportions (Fig. 184-5).

Figure 184-5. Schematic drawing showing the changes in body proportions during normal growth and development.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

Craniofacial Regions of Growth

The craniofacial complex can be divided into three regions: (1) the neurocranium, which is further divided into the calvaria and basicranium; (2) the nasomaxillary complex; and (3) the mandible. Figures 184-2 and 184-3 show the changes that occur in the craniofacial complex from birth to adulthood. The embryonic human skull has 110 ossification centers, many of which fuse, to result in 45 bones in the neonatal skull and ultimately 22 bones in the young adult skull.¹ Table 184-1 summarizes the changes in size of various anatomic sites that take place during growth and development from infancy to adulthood.^1,14–25

Table 184-1 Normal Craniofacial Growth and Development

Data from references 1, 14–25.

Neurocranium (Calvaria = Roof and Basicranium = Floor)

Calvaria

The calvaria comprises the frontal, parietal, and parts of the temporal, occipital, and sphenoid bones. These bones are formed by intramembranous ossification, with the exception of noncalvarial parts of the occipital, temporal, and sphenoid bones, which are formed through endochondral ossification. These bones initially are separated by fontanelles, which develop into sutures early and then finally fuse in adult life (Fig. 184-6).

Figure 184-6. Newborn skull fontanelles.

As the child’s brain grows, the calvarial bones are displaced. This displacement theoretically results in the deposition of new bone on the sutural edges. Growth of bone is seen on both the internal and external tables of the calvaria. This also results in an expanded medullary space. Significant thickening occurs from infancy to adulthood. The ascendancy (dominance) of the neurocranium over the facial complex during the early stages of life is clearly related to the inordinately early development of the brain.²¹ The major portion of calvarial growth is completed by the age of 4 years (Fig. 184-7).

Figure 184-7. Top view of skulls showing the shape change that occurs from infancy to adulthood. Shown are infant (approximately 8 months of age), 5- to 6-year-old, 10- to 12-year-old, and adult skulls.

Basicranium

Growth of the cranial base creates space for the enlarging brain and oronasal structures with their associated airway. The basicranium grows more slowly than the neurocranium. At birth and at 10 years of age, the cranial base exhibits 63% and 95%, respectively, of its ultimate size.²¹ The basicranium comprises parts of the occipital, temporal, sphenoid, and ethmoid bones. The occipital, temporal, and sphenoid portions form through endochondral ossification. The ethmoid and inferior nasal concha form solely by intramembranous bone formation.

In the midline, synchondroses are present (Fig. 184-8). These synchondroses remain after the chondrocranium (cartilage precursor of the basicranium) has ossified. During childhood, the spheno-occipital synchondrosis is the principal growth cartilage of the basicranium, and its growth persists into early adolescence.^3,11 Other synchondroses of the basicranium are the sphenoethmoidal, intersphenoidal, sphenofrontal, and frontoethmoidal synchondroses, all of which play a minimal role in postnatal growth. The synchondroses have zones similar to those in the epiphyseal cartilage of long bones. However, growth occurs in two directions, resulting in elongation of the basicranium until its ultimate ossification is completed (Fig. 184-9).

Figure 184-8. Diagrammatic representation of the synchondroses of the cranial base, showing the location of these important growth sites.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

Figure 184-9. Diagrammatic representation of growth at the intersphenoid synchondrosis. A bank of immature proliferating cartilage cells is located at the center of the synchondrosis, whereas a band of maturing cartilage cells extends in both directions away from the center. Endochondral ossification occurs at both margins. Growth at the synchondrosis lengthens this area of the cranial base. S, sphenoid sinus.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

The development of ossification center sutures and synchondroses in the chondrocranium throughout childhood hase been chronicled by means of computed tomography (CT). These data can provide standards for skull base maturity. In addition, postnatal normal CT variants and magnetic resonance imaging (MRI) assessment of the cranial base have been characterized.^26,27

In newborns and infants, the cranial base is quite flat. With growth into childhood, a more convex superior or flexed appearance emerges, with further enlargement during adolescence and adulthood. The spheno-occipital synchondrosis becomes more flexed as the maxillary portion of the nasomaxillary complex moves toward the foramen magnum and moves under the anterior cranial fossa (Fig. 184-10). Components of the cranial base can be seen more clearly in older pediatric skulls than in infant skulls. The foramen magnum approaches adult size and the primary dentition has erupted by 3 years of age. By 8 years of age, the occipital bone has fused around the foramen magnum, and the secondary dentition is erupting. The major difference between the adolescent and adult skull is fusion of the spheno-occipital synchondrosis. Fusion of this synchondrosis begins at approximately 15 years of age for boys and at 12 or 13 years of age for girls on the cerebral surface. Ossification on the external aspect is complete by age 20¹ (Fig. 184-11). The chondrocranium-basicranium is a junction between both the neurocranial and facial complex bones. Its alteration affects not only neurocranial and skull growth but also facial morphology.³

Figure 184-10. Flexion of the cranial base. With growth, a more convex superior or flexed appearance develops from infancy to adulthood. A, Infant. B, Adult.

Figure 184-11. Basal extracranial views of the skulls of an infant (at 8 months of age), a 5- to 6-year-old, a 10- to 12-year-old, and an adult. Components of the cranial base are more clearly seen in the older skulls. Note the open spheno-occipital synchondrosis in the 5- to 6-year-old skull and that the most posterior molar on the right side of the photograph is not the patient’s—it was inserted.

Nasomaxillary Complex

The nasomaxillary complex develops through intramembranous ossification. It includes the nasal, lacrimal, maxillary, zygomatic, pterygoid, and vomer bones.

The nasomaxillary complex is displaced forward and downward from the cranial floor (basicranium) as a result of growth of the associated soft tissues. New bone growth occurs at sutural contact surfaces on both sides of the suture, with a resultant increase in the size of both bones involved (Fig. 184-12). Bone is added at the frontal maxillary, zygomaticotemporal, zygomaticosphenoidal, zygomaticomaxillary, ethmoidomaxillary, frontoethmoidal, nasomaxillary, nasofrontal, frontolacrimal, palatine, and vomerine sutures. Interaction between the basicranium and the nasomaxillary complex constantly occurs. Rotatory displacement is caused by the downward and forward growth of the middle cranial fossa, resulting in greater or lesser amounts of displacement and remodeling growth in the posterior and anterior parts of the maxilla, depending on the biomechanical forces involved.¹¹

Figure 184-12. As growth of the surrounding soft tissues translates the maxilla downward and forward, opening space at its superior and posterior sutural attachments, new bone is added on both sides of the sutures.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

The anterior surface of the maxilla is an area of significant resorption (Fig. 184-13). Even though bone is being resorbed here, the maxilla is still growing forward. This is a good example of remodeling and displacement (Fig. 184-14). Growth and development of the nasomaxillary complex are shown in Figure 184-15. Vertical nasomaxillary growth occurs at the frontomaxillary, frontozygomatic, frontonasal, ethmoidomaxillary, and frontoethmoidal sutures as a result of orbital and nasal growth.

Figure 184-13. As the maxilla is carried downward and forward, its anterior surface tends to resorb. Resorption surfaces are shown in gold. Only a small area around the anterior nasal spine is not affected.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

Figure 184-14. Surface remodeling of a bone—in the direction opposite that in which the bone is being translated by growth of adjacent structures—creates a situation analogous to that depicted in this cartoon. The wall is being rebuilt to move it backward at the same time the platform on which it is mounted is being moved forward.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

Figure 184-15. Anterior view of the skulls of an infant (8 months of age), a 5- to 6-year-old, a 10- to 12-year-old, and an adult. Note the overall change of skull shape and the facial complex/cranium ratio, the relationship of the orbits to the floor of the nose, nasomaxillary and mandibular growth, and dental changes.

The orbits, which are linked to cranial growth, are quite large at birth because of their relationship with the globe. Orbital remodeling is quite complex—50% of postnatal orbital growth is achieved by the age of 2 years, and it is almost complete by age 7 years.²¹ The superior aspect of the orbit in toddlers is similar to that in adults, although the inferior aspect differs. The floor of the nose is almost at the level of the inferior orbital rim in infants; then the distance progressively increases so that the floor is significantly lower in adults. The eyes in the adult face are not much farther apart than those in a child’s. According to Enlow and Hans,¹¹ however, “because of the larger nose, higher nasal bridge, increase in the vertical facial dimension and the widening of the cheekbones, the eyes of the adult appear much closer together.” The main contribution to the widening face is from the lateral expansion of the zygomaticomaxillary sutures and the intermaxillary suture growth. Eruption of the primary and secondary teeth results in an increase in the size of the maxilla. As the maxilla moves downward and forward and secondary teeth erupt, the maxillary sinuses increase in size as well.

Sinuses

At birth, the maxillary sinus is large enough to be seen radiologically. Relatively rapid growth occurs between ages of 1 and 4 years; by age 5, the sinus has started to expand laterally beyond the infraorbital foramen, although its floor does not extend below the nasal cavity. As the permanent dentition erupts, there is growth inferiorly of the floor of the sinus. By the age of 16 years, the maxillary sinus reaches full size (Fig. 184-16). The ethmoid sinuses are present at birth and have attained adult size by the early teens. The frontal sinus distinguishes itself from the ethmoids around age 5 and demonstrates a variable growth rate until reaching adult size in late puberty. The sphenoid sinus is the last to develop and is present radiologically at approximately age 6. Growth of the sphenoid sinus continues well past puberty into the early adult years.²⁸

Figure 184-16. Maxillary sinus growth in an infant (8 months of age), a 5- to 6-year-old, a 10- to 12-year-old, and an adult. Drawings from x-ray images of skulls.

Shah and coworkers reviewed 91 CT scans in 66 patients (16 obtained serially over time) between the ages of 0 and 12 and demonstrated periods of significant growth in the paranasal sinuses in children. The ethmoid sinuses were the first to fully develop, followed by the maxillary, sphenoid and frontal sinuses.²⁹

Mandible

The mandible forms in relation to the first branchial cartilage, otherwise known as Meckel’s cartilage. Meckel’s cartilage is interesting in that it is not replaced by bone. Instead, membranous bone forms lateral to Meckel’s cartilage, and Meckel’s cartilage then disappears³⁰ (Fig. 184-17). At birth, the mandible comprises two bones with the symphysis menti between them. This suture closes by the age of 1 year, after which the major portion of mandibular growth occurs posteriorly.

Figure 184-17. Diagrammatic representation of the relation of the site of initial bone formation in the mandible to Meckel’s cartilage and the inferior alveolar nerve. Bone formation begins just lateral to Meckel’s cartilage and spreads posteriorly along it without any direct replacement of the cartilage by the newly forming bone of the mandible.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

Resorption occurring anteriorly and deposition occurring posteriorly result in the overall growth of the mandible (Fig. 184-18). Although the condyles are a major site of growth, they are not a master growth center, as was previously thought.

Figure 184-18. As the mandible lengthens, the ramus is extensively remodeled—so much so that the bone at the tip of the condylar process at an early age can be found at the anterior surface of the ramus some years later. Given the extent of surface remodeling changes that occur, it is an obvious area to emphasize endochondral bone formation at the condyle as the major mechanism for growth of the mandible.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

Variation of endochondral bone growth occurs at the articular contact portion of the condyle. The main contribution of condylar cartilage is to provide regional adaptive growth by maintaining the condylar area in a proper anatomic relationship with the temporal bone as the whole mandible is simultaneously being carried downward and forward.¹¹ The mandible grows by enlarging and widening in response to the increase in size of the muscles of mastication and an enlarging oropharynx, which accommodates the concomitant growth of the nasomaxillary complex. The ramus grows posteriorly and at the same time increases the inter-ramal dimension along with the laterally expanding cranial floor. The coronoid processes grow superiorly and buccally, with the anterior edges of the rami being continually resorbed in the process. The condyles grow posteriorly, superiorly, and laterally (Fig. 184-19). Even though it is a single bone, Sperber¹ described the mandible functionally as six skeletal subunits. These subunits are the alveolar, coronoid, and angular bones, the condylar process, and the chin, all of which are attached to the “body” of the mandible. Moss’s concept of functional matrices then influences the growth of each subunit (teeth: alveolar unit; action of the temporalis muscle: coronoid process; masseter and medial pterygoids: angle and ramus; lateral pterygoid–condylar process, perioral muscles, tongue, and expanding oropharyngeal cavity: entire mandible).

Figure 184-19. Mandibular growth as viewed from the perspective of vital staining dyes. Note the minimal changes in the body and chin area, whereas exceptional growth and remodeling occur in the ramus, moving it posteriorly. The correct concept of mandibular growth is that the mandible is translated downward and forward and grows upward and backward in response to this translation, maintaining its contact with the skull.

(From Proffit WR. Contemporary Orthodontics. 2nd ed. St Louis: Mosby; 1993.)

The infant mandibular arch is U-shaped; whereas the adult arch is more V-shaped (Fig. 184-20). The gonial angle (the angle between the ramus and the body) is more obtuse in infants than in adults (Fig. 184-21). Mandibular growth takes place in two specific growth spurts, the first between the ages of 5 and 10 years and the second between ages 10 and 15 years.³¹ Growth in mandibular width is completed during early adolescence. Growth in mandibular length is complete 2 to 3 years after menstruation in females and approximately 4 years after attainment of sexual maturity in males. Growth in mandibular height is complete in the late teens in females and early twenties in males (see Fig. 184-21).

Figure 184-20. With mandibular growth, the U shape of the infant mandible (top) changes to more of a V shape, as seen in the adult (bottom).

Figure 184-21. Lateral view of the skulls of an infant (at 8 months of age), a 5- to 6-year-old, a 10- to 12-year-old, and an adult. Note that the gonial angle of the mandible is more obtuse in the infant. The overall change in size of the mandible through time is dramatic.

Internal and external rotational changes of the mandible occur during growth and, of course, in conjunction with rotational changes in the maxilla (Fig. 184-22). Bjork and Skieller³² described this in detail using metallic implants. Miller and Kerr³¹ supported their findings but used a digitizer program for longitudinal follow-up with cephalograms in a number of patients. Overall mandibular growth is not uniform and steady, because corpus length and ramus height grow in an irregular pattern.^25,34 Jaw rotation influences the degree of tooth eruption.

Figure 184-22. Superimposition on implants for a patient with a normal growth pattern showing surface changes in the mandible from ages 4 to 20 years. For this patient, there was a −19 degree internal rotation but only a −3 degree change in the mandibular plane angle. Note dramatic remodeling in the area of the gonial angle, with a net resorption during this period. This surface remodeling or external rotation compensates for, and conceals the extent of, the internal rotation.

(From Bjork A, Skiller V. Normal and abnormal growth of the mandible: a synthesis of longitudinal cephalometric implant studies over a period of 25 years. Eur J Orthod. 1983;5:1.)

Craniofacial cephalometric and anthropometric studies are abundant in the literature, and normative data are available. A review of these topics is beyond the scope of this chapter; however, these measurements may be used to assist in the interpretation of optimal growth and development in the clinical situation.^35–42

Radiotherapy

Ionizing radiation is widely recognized as detrimental to the growth of developing tissue. In a majority of cases, this consequence is a result of the application of full doses to radiosensitive tumors.⁴⁶ Rhabdomyosarcoma and undifferentiated sarcomas constitute the most common type of malignant tumor of soft tissue of childhood. Of these sarcomas, 35% are found in the head and neck region. Retinoblastoma is the most frequent malignant ocular tumor in childhood and is a frequent indication for radiotherapy in the pediatric population.^47,48 Multimodal therapy (radiotherapy and chemotherapy) has been effective in the treatment of these tumors with a 3-year relapse-free survival rate of between 70% and 100%.^49–52 The value of radiotherapy has not been questioned given its success rate,⁵³ but as more children have been cured of cancer and the survival rates have increased, concerns about the long-term side effects of these therapeutic regimens (alone or in combination) have arisen.^50,51

The effects of radiation therapy on facial growth, as well as radiation’s collateral effects, are detailed in Table 184-2. Virtually 100% of children who have received radiotherapy suffer from alterations in the development of facial soft tissues, and in more than 60% of these children, the facial bones are affected.^47,54 The younger the patient at the time of irradiation, the greater the effects on craniofacial development.^51,55,56 These side effects are more frequent and more severe within the first 10 years after irradiation.⁵⁴

Table 184-2 Side Effects of Radiotherapy

Data from references 46–48, 50, 51, 53; and from Berkowitz RJ, Neuman P, Spalding P, Novak L, Strandjord S, Coccia PF. Developmental orofacial deficits associated with multimodal cancer therapy: case report. Pediatr Dent. 1989;11:227; Larson D, Kroll S, Jaffe N, Serure A, Goepfert H. Long-term effects of radiotherapy in childhood and adolescence. Am J Surg. 1990;160:349; Sklar CA. Overview of the effects of cancer therapies: the nature, scale and breadth of the problem. Acta Paediatr Suppl. 1999;88:1; and Sonis AL, Tarbell N, Valachovic RW, Gelber R, Schwenn M, Sallan S. Dentofacial development in long-term survivors of acute lymphoblastic leukemia. A comparison of three treatment modalities. Cancer. 1990;66:2645, 1990.

It has been difficult to determine the safest dose of irradiation that keeps side effects on growing tissue to a minimum but at the same time is effective in eradicating the cancer.^46,53,54 Techniques for radiotherapy administration have changed during the past 20 years. The principal aim is to achieve a balance between cure and late toxicity of the treatment.⁵⁴ Changes to minimize undesirable effects include radiotherapy with megavoltage, hyperfractionation, three-dimensional therapy, intensity-modulation, and conformal radiation with multiple fields.^47,55 In all children undergoing radiotherapy of the head and neck, it is mandatory that multidisciplinary follow-up be part of the ongoing management.

Functional Endoscopic Sinus Surgery

FESS has become the standard of care in the surgical management of chronic sinusitis and other sinus disorders in the pediatric population. Its effectiveness has been accepted when clear indications for surgery are established.^57,58 However, concerns have arisen regarding potential negative effects on the growth and development of paranasal sinuses and the nasomaxillary complex in the pediatric patient.⁵⁹

A knowledge of sinus anatomy during different stages of development, as well as of pathologic circumstances such as chronic sinusitis, is imperative in decisions regarding FESS in the pediatric population.^28,60–62

The absolute and relative indications for FESS in the pediatric population varied during the 1990s and into the millennium. These changes were related to the evolving definitions of sinus disorders and short- and long-term outcome measures.^60,63–68 This topic is covered in Chapter 195.

Although the relationship between nasal breathing and sinus development remains unclear, it is generally accepted that the development of the paranasal sinuses is linked to the growth of the nasomaxillary complex. A reasonable assumption, therefore, is that any intervention at this level, either an endoscopic technique or a Caldwell-Luc procedure, on a growing patient will have negative effects on the normal process of remodeling, expansion, and pneumatization.

Results of animal studies have varied depending on the species and the intervention. Kraut and Kronman examined 36-day-old New Zealand White rabbits and unilaterally filled their maxillary sinuses with polyhydroxyethylmethacrylate without adverse effect on craniofacial growth.⁶⁹ Mair and coworkers studied eight newly weaned piglets subjected to unilateral FESS. The researchers examined the piglets 6 months after surgery, noting significant reduction of the facial growth and maxillary-ethmoidal sinus development on the operated side.⁷⁰ Carpenter and associates found significant restrictive effects on piglet facial skeletal development after FESS.⁷¹ Verwoerd-Verhoef and Verwoerd demonstrated that controlled resection of the bony sinonasal wall and partial resection of anterior ethmoid did not affect later development of nasal bones and maxilla on 20 young New Zealand White rabbits.⁷²

Several studies in children have been undertaken. Mair and coworkers analyzed the uncinate processes and ethmoids of 84 children (mean age of 6 years; age range, 1 to 18 years) who previously had undergone FESS. In children younger than 9 years of age, woven and lamellar bone were present, in contrast with the presence of exclusively lamellar-mature bone in the children older than 9 years of age. These results suggest that the safest age at which a pediatric patient should be operated on is 9 or older.⁷⁰ Kosko and colleagues in 1996 presented five cases of children (mean age of 30 months) who had undergone bilateral FESS for refractory chronic sinusitis. At mean postoperative month 42, four children showed unilateral maxillary hypoplasia and one child showed bilateral hypoplasia without apparent changes in facial symmetry.⁵⁹ Sinus hypoplasia can be from primary causes related to individual development or secondary causes associated with a response to facial trauma, chronic sinusitis, or FESS, which has affected the activation of bone formation factors or the removal of growth centers.^59,61,73

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