9 Pediatric Head and Neck Reconstruction Eric M. Genden and Marita Teng
The majority of diseases affecting the upper and lower jaws of children are benign.1 Consequently, the surgical resection of such diseases requires only narrow margins and, in turn, commonly necessitates minimal reconstruction. In some cases, however, larger resections resulting in a significant deformity may be necessary to obtain appropriate diseasefree tissue margins. In cases that result in a significant bony defect, the options for reconstructing the jaw include nonvascularized bone grafts and vascularized composite flaps. For select defects, nonvascularized bone grafts may provide a simple method of bony reconstruction, assuming the surrounding tissue bed is well vascularized and the patient has a good nutritional status. Occasionally, however, the patient has been previously exposed to chemotherapy or radiation, or has sustained a significant bony defect, requiring a vascularized bone flap. A variety of childhood diseases may affect the mandible or maxilla; however, sarcomas are the most common form of malignancy.2 Although surgical resection plays an important role in the treatment of this disease, most often these patients have been previously treated with chemotherapy, radiation, or combination therapy. As a result, the recipient bed is often compromised with regard to healing,3,4 thus limiting the application of adjacent tissue transfer or nonvascularized bone grafts. Although strategies to minimize the effect of chemotherapy and radiation on the healing of soft tissue and growth of the craniofacial skeleton have been investigated,3 under these circumstances free vascularized tissue remains the most reliable source of bone and soft tissue. When a surgical resection of the pediatric patient is indicated, prompt reconstruction is essential to both long-term psychological well-being5,6 and normal craniofacial development.3,4 Over the last decade, there has been a trend to embark on early surgical reconstruction of children with craniofacial disorders, which has resulted in a series of reports investigating the role of surgical reconstruction on psychological development.5,7 Many of these studies were prompted by a common anecdotal experience among reconstructive surgeons that children who underwent early
reconstruction of craniofacial deformities seemed to socialize postoperatively with their peers and their parents in a more positive way than did their unreconstructed counterparts. Early studies by Pertschuk and Whitaker8 supported these experiences, demonstrating an increase in self-esteem and peer acceptance following surgery. Examination of the long-term effects of facial disfigurement on social development has demonstrated convincing evidence that attractiveness plays a definitive role in normal socialization patterns, and that children with unreconstructed craniofacial deformities are more prone to an inhibited personality style, low self-esteem, and impaired peer relationships.9 It has been postulated that these children harbor a poor self-image at an early age, resulting in the development of antisocial behavior in adolescence.9 Similarly, it has been suggested that adults have lower expectations of disfigured school-age children, leading to underachievement, social withdrawal, and occasionally depression.10 When early surgical intervention occurs, however, these children tend to psychosocially adjust in a rather short period of time. Commonly, both peer and family interactions occur more naturally as these children resolve their avoidance disorders.5,6,8 In addition to a healthy psychological development, a normal physical development is important in the lives of these patients. Although mandibular and maxillary reconstruction in children is uncommon, when faced with this challenge it is essential that special consideration be given to issues related to the growing child, so that the goal is to achieve optimal restoration of mastication, deglutition, and cosmesis. Similar to reconstruction of the adult mandible, bone stock, soft tissue, and skin paddle design are important factors in addressing the specific reconstructive requirements of the patient. In contrast to the adult patient, however, the pediatric patient is growing. Because of this characteristic unique to this population, surgical reconstruction of the upper and lower jaws requires an understanding of the changes in bone and soft tissue architecture at both the donor site and the mandibulofacial complex as a result of growth and development. The commonly used donor sites,
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Reconstruction of the Head and Neck including fibula, iliac, and scapula, all possess growth centers, areas of the bone that monitor and regulate growth and development. Disruption of the growth center as a result of bone flap harvest can lead to abnormal development and long-term functional consequences. Understanding the anatomic location of these growth centers and their role in normal development is essential to preventing long-term functional deficits. Similarly, the process of craniofacial development is a dynamic one in which mandibular, maxillary, and basicranial growth are intimately interrelated. The disruption of these relationships, as occurs with a mandibular or maxillary ablation, can result in abnormal development of the midface, mandible, and skull base, leading to profound orodental consequences. Restoration of these relationships with free flap reconstruction, however, can reestablish mandibulomaxillary occlusion and condylar-basicranial articulation, leading to normal craniofacial development and oromandibular function. In the adult patient, the selection of a donor site is based on factors such as the requirements of the defect and the patient’s comorbidities.11 The pediatric patient, however, is usually healthy and in good nutritional status. Although issues related to tissue requirements for restoration of the defect are important in choosing a donor site, there is an additional parameter that is of critical importance: the longterm development at the reconstructed site as well as the donor site.
◆ NORMAL DEVELOPMENT OF THE UPPER AND LOWER JAWS
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Normal craniofacial development, including growth of the mandible and maxilla, results from a series of complex mechanisms that have been the focus of intense debate among investigators and clinicians. Facial growth is a dynamic process that Enlow12 refers to as the “ongoing equilibrium” that exists among the skull base, muscle stress, and occlusal relationships. After birth, the pediatric craniofacial skeleton grows through two distinct mechanisms: epiphyseal proliferation and bone remodeling. Epiphyseal proliferation is largely responsible for increases in bone length and projection (Fig. 9.1), a process that is dominant during the first 18 years of life. After age 18 the epiphyseal plate of the mandible, which is located in the proximal zone of the conical subcondylar ridge, fuses. Consequently, the majority of the longitudinal growth in this region is complete. Prior to fusion, however, the epiphysis exists as a three-dimensional structure responding to the influence of the surrounding soft tissues, traction forces of the muscles of mastication, and the condylar relationship with the cranial base. During the course of facial skeletal development, the mandibular epiphysis adapts the intercondylar distance to the widening cartilaginous synchondrosis of the cranial base, highlighting the ever-important relationship between normal mandibular growth and normal basicranial development. A disruption of the epiphysis, the muscles of mastication, or the temporomandibular joint prior to the fusion of the epiphyseal plate, can result in abnormal mandibular
Fig. 9.1 The projection and growth of the mandible is a result of epiphyseal growth demonstrated by the growth and extension of the condylar neck.
projection and malocclusion.13 The role of epiphyseal growth, particularly in the prepubescent pediatric patient, cannot be overemphasized; however, a second mechanism of bone growth called remodeling, plays an equally important part in mandibular contour and symmetry. In contrast to epiphyseal growth, remodeling is a process that occurs both during the prepubescent period and throughout adulthood. Adjustments in the downward and forward projection of the mandible occur through deposition of bone at the posterior margin of the ramus along with corresponding resorption at the anterior margin.12 Likewise, mandibular contour and increased width occur as a function of buccal bone deposition and concomitant lingual resorption. The two simultaneous processes of epiphyseal growth and bone remodeling occur in different areas within the same bone simultaneously, and there is no histologic difference in new bone created by either process. Although epiphyseal fusion occurs in early adolescence as part of a genetically preprogrammed process, remodeling continues throughout adult life largely in response to the mechanical stress applied by the muscles of mastication (Fig. 9.2).14–16
Fig. 9.2 Mandibular and maxillary growth occur throughout development. The growth is stimulated by muscular and mastication stress. If there is a breakdown in this stimulation, growth will be disrupted.
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9 Pediatric Head and Neck Reconstruction Understanding these principles is important in surgical reconstruction because disruption of the mandible prior to epiphyseal fusion may result in a different long-term developmental abnormality from a similar surgical disruption after epiphyseal fusion. Furthermore, it is important to recognize that girls reach mature mandibular height and depth at a mean age of 13, on average, which is 2 to 5 years earlier than do boys. The maxilla serves as the infrastructure of the midface; however, it also plays an important role during facial development by providing an occlusal surface for the mandible. This occlusal relationship functions as a feedback loop that helps to guide both midface and mandibular development. The ultimate form of the midface is a result of two separate but related processes. The first is referred to as primary displacement, or growth of the maxilla bone itself, and the second is secondary displacement, or movement of the maxilla as a result of growth of the surrounding articulating skeleton.12 Primary displacement results from the genetic propensity for the maxillary bone to enlarge as a child ages, therefore contributing to vertical maxillary growth. During this process, periosteal resorption occurs on the nasal side of the palate, whereas periosteal deposition occurs on the oral side of the palate. This leads to a downward projection of the maxilla and an enlargement of the nasal chambers. Normal maxillary width occurs as a result of bony accretion at the suture lines and resorption at the lateral nasal wall. Secondary displacement is characterized by growth of the surrounding craniofacial skeleton, namely the skull base and the mandible, which serve to further displace the maxillary complex downward and forward. Normal dental occlusion acts to guide maxillary projection and preserve both the cosmetic and functional harmony of the midface. Although primary and secondary displacement are essential to normal maxillary growth, a third mechanism is equally important in the development process. The traction forces associated with the muscles of mastication and the axial loading forces associated with mastication also contribute to the development process. A disruption in any or all of these growth mechanisms prior to skeletal maturation inevitably leads to a morphologic change in maxilla. Vertical maxillary growth is normally complete by age 14 in girls and age 16 in boys, and fusion between the palatine processes and the maturation of maxillary width occurs at 18 years of age. Much of what is known about facial development after ablative surgery is derived from experimental animal models.17 It is clear, however, that disruption of the developing maxilla or the maxillary suture lines prior to fusion will significantly affect midface development. When disruption of the pediatric midface hinders normal occlusal contacts, there may be a profound effect on both mandibular and maxillary development. Occlusal contact provides bone stress, a key component to the induction of bone growth; therefore, the occlusal interaction between the maxilla and the mandible is paramount to ensure normal craniofacial development. It is for this reason that unreconstructed defects of the pediatric maxilla can lead to significant disturbances in facial growth and aesthetic form.
DONOR-SITE SELECTION The Fibular Donor Site Although the developmental implications of performing a surgical ablation on a pediatric patient may be profound, if careful consideration is not given to the reconstruction, the morbidity associated with a donor-site harvest may be equally disturbing. Three donor sites have been applied to pediatric mandibular and maxillary reconstruction: the fibula, the scapula, and the iliac crest.18,19 Fibular growth, which has been studied quite extensively, occurs in a classic endochondral pattern as the three ossification centers (one in the shaft, and one in each of the distal and proximal epiphyses) are responsible for proportionate growth (Fig. 9.3). The growth plates lie within 1 to 2 cm of each end of the bone, proximal and distal to where a harvesting osteotomy is commonly made. The majority of growth occurs in the
Fig. 9.3  The fibular growth plates lie within 1 to 2 cm of each end of the bone, proximal and distal to where a harvesting osteotomy should be made.
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Reconstruction of the Head and Neck proximal epiphyseal plate that fuses by age 15 in girls and age 17 in boys.20 Similar to that in the adult, the fibula offers the longest segment of bone of the three donor sites; however, the stock of bone, particularly in patients under the age of 13, may lack the height appropriate to stabilize osseointegrated implants. In such cases, the fibula can be “double barreled”21 by creating a midpoint osteotomy and
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folding the bone upon itself. This results in an increase in the bone height and a more stable foundation for osseointegrated implants (Fig. 9.4). The double-barreled fibula can be secured upon itself by placing a vertical lag screw or circumosseous wires at each end of the complex. Essential to achieving a successful long-term reconstruction, transferred bone must grow at a rate similar to that of
Fig. 9.4 The stock of bone of the fibula, particularly in patients under the age of 13, may lack the height appropriate to stabilize osseointegrated implants. The bone graft can be “double barreled” to increase bone stock height. This is helpful for the eventual placement of osseointegrated implants.
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9 Pediatric Head and Neck Reconstruction the native mandible or maxilla. Concern regarding growth of the transferred bone, particularly in a developing child, has led investigators to find the ideal transplantable epiphysis. Epiphyseal transfer in the iliac and fibula has proven successful in the treatment of epiphysiodesis and acetabular defects in children; however, the necessity to transfer an epiphyseal growth plate in jaw reconstruction has not been clearly demonstrated.22–24 Epiphyseal plates are not routinely transferred during the harvest of the fibula; however, the fibula will continue to grow at a rate comparable with that of the adjacent native mandible (Fig. 9.5).25–28 It is likely that this occurs because a growth center remains within the shaft of the transferred bone. It has been shown experimentally, however, that when an epiphyseal plate is transferred in a vascularized bone segment, it retains the potential for growth.26,29 Although it has not been reported clinically, this may serve as a potential source for condylar reconstruction in the prepubescent pediatric patient. Harvesting the fibula from a growing limb has raised concerns among reconstructive surgeons; however, there is little clinical evidence that suggests long-term limb growth is adversely affected.18,30 Although experimental evidence in rats suggests that the fibula exerts a restrictive effect on tibial growth such that removal of the fibula leads to longitudinal tibial overgrowth,28 we have not observed this clinical phenomenon in our series.18 The most significant delayed complication associated with fibular harvest, particularly in children under the age of 8, is the development of a valgus deformity.30,31 An ankle valgus may result from a variety of etiologies including multiple hereditary exostoses, poliomyelitis, congenital pseudarthrosis of the fibula, and fibular harvest. When it does occur, it can lead to chronic pain syndromes and a profound gait disturbance. Several strategies
Fig. 9.6 Ossification of the scapula proceeds in a superior to inferior pattern until approximately age 10, when the scapula is roughly 12 cm long and the distal epiphysis has decreased to only 4 cm. A smaller but equally important growth plate exists superiorly, adjacent to the glenoid fossa.
have been proposed for both the prevention and the management of this deformity, including partial epiphysiodesis with staples, tibiofibular (TF) synostosis, and transphyseal fibula-tibial screw.31 Omokawa et al30 reviewed 13 cases of pediatric fibular harvest in which patients were divided into two groups: one received a TF synostosis and the other did not undergo a synostosis. The postoperative observation period ranged from 5.8 years to 16.5 years. In the former group, a valgus deformity was observed in only one patient, whereas in the latter group all of the children under the age of 8 years developed a valgus deformity. Irrespective of the method of tibiofibular stabilization, it is clear that in children under 8 years of age who did not undergo a synostosis, the prevention of a valgus deformity is essential following fibular harvest.
The Scapular Donor Site
Fig. 9.5 Clinical case. Two years following a fibular reconstruction of the hemi-mandible, growth and symmetry are stable.
Unlike the fibula, the scapula is a flat membranous bone; however, the lateral scapular border is analogous to a long bone whose distal end is formed by a large osteocartilage epiphyseal plate. At birth, the distal 7 to 8 cm of the scapula are composed entirely of hyaline cartilage, and it is this osteocartilage apophysis that is responsible for the development of four fifths of the scapula.32 Ossification proceeds in a superior to inferior pattern until approximately age 10, when the scapula is roughly 12 cm long and the distal epiphysis has decreased to only 4 cm (Fig. 9.6). A smaller, but equally important growth plate exists superiorly, adjacent to the glenoid fossa.32 Mainly responsible for vertical scapular growth, the superior growth plate lies outside the range of harvested bone, and therefore should not be directly affected. Both superior and inferior growth plates fuse at
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Reconstruction of the Head and Neck approximately age 20, so that normal scapular development is disrupted after harvesting bone from the distal scapula in the pediatric patient. Similarly, the lateral border of the scapula serves as a traction epiphysis, growing in response to traction by the teres and triceps muscle groups.29 A disruption in the muscular attachments or a disruption in the lateral scapular border, may lead to an arrest in scapular development. Concerns regarding the long-term consequences of a bone harvest in this region have been addressed by Teot et al,32 who examined a series of three patients who had undergone scapular free flap reconstruction of congenital limb amputation. They found that harvesting bone from the lateral border and distal scapula resulted in a moderate scapular size discrepancy. They compared plain radiographs of the operated scapula with the nonoperated scapula 5 years postoperatively, and found that although there was a 3-cm discrepancy in scapular length as a result of arrested growth, there was no appreciable limitation to range of motion or strength when compared with the contralateral scapula. They concluded that the upper growth plate must compensate for disruption of the scapular epiphysis, although there is no objective data to support this claim. Similarly, in our series we have found that pediatric patients recover completely following harvest from the scapular donor site. With the aid of physical therapy, full range of motion and strength are recovered within 6 weeks.18 The scapular donor site has been used quite extensively for pediatric limb reconstruction; however, it has not been commonly used for pediatric jaw reconstruction. Although the presence of an active epiphysis as part of the bone graft has a theoretic advantage for reconstructing a growing patient, this issue has not been carefully studied. Because it has been shown that transferred epiphyseal bone will continue to grow at a rate that is linearly related to the amount of stress applied to that bone,16 it is important to achieve orodental rehabilitation as soon as possible. Although the lateral border and distal tip of scapula provide bone adequate for the retention of osseointegrated implants in adults,33 the pediatric scapula may be quite thin and limit implant stability. In this situation, nonvascularized onlay bone grafts placed either primarily or secondarily may be used to augment the scapular bone to facilitate implant stability. The placement of implants followed by implant-borne dentures will in turn provide the bone stress necessary to stimulate continued bone growth.
The Iliac Donor Site
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The entire length of the iliac crest, from the anterior-superior to the posterior-superior iliac spines, is composed of cartilage at birth. Growth occurs in an epiphyseal fashion in several areas of the pelvic girdle, including the acetabulum and the iliac crest, which grow until the second decade of life (Fig. 9.7). The mechanical demands applied to the pelvis by both its upper and lower muscular attachments play an integral role in pelvic remodeling, which occurs into young adulthood. A disruption in the epiphysis prior to its fusion may have a profound effect on the development of the pelvic girdle. Rossillon et al34 reviewed 21 children over an average
Fig. 9.7  Growth of the iliac occurs in an epiphyseal fashion in several areas of the pelvic girdle including the acetabulum and the iliac crest, which grow until the second decade of life.
of 3 years and 10 months who had undergone a surgical disturbance of the iliac epiphysis. They demonstrated that 16 of these children developed iliac hypoplasia as a result of premature arrest in growth; however, no functional evaluation was performed on the children in this series. Like the lateral scapular border, the iliac crest serves as a traction epiphysis where the dynamic interaction between the iliac crest and its muscle attachments play a crucial role in acetabular development and hence gait stability. Lee et al35 examined the effect of an injury of the iliac apophysis on the subsequent growth of the pelvis. They examined immature New Zealand rabbits and found that excision of any more than one third of the iliac apophysis resulted in retarded growth of the iliac bone. A similar study by Olney et al36 found that a lesser injury, such as a splitting of the iliac apophysis, was enough to adversely affect normal iliac development. In the adult population, disturbance of gait after iliac crest free flap harvest has been documented in up to 11% of patients37,38; however, there is little published on the long-term effects of iliac crest harvest in the pediatric population. Boyd19 reviewed five patients between the ages of 16 and 27 years who had undergone mandibular reconstruction using a free vascularized iliac crest free flap. He found minimal donor-site morbidity in his series of young adults; however, the youngest patient in his series was 16 years old. Although this donor site has been suggested as ideal for pediatric mandibular reconstruction,39 the probability of postoperative gait disturbance in a younger age group has discouraged most surgeons from utilizing this donor site. As a result, there are no reported series of iliac crest free flap reconstructions in the prepubescent pediatric population.
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9 Pediatric Head and Neck Reconstruction
◆ GROWTH OF VASCULARIZED BONE GRAFTS Although fibular and scapular flaps have been used quite extensively by plastic surgeons for the reconstruction of acquired and congenital limb abnormalities, there is little reported on the long-term growth of the transferred bone after mandibular and maxillary reconstruction. Although one may consider that the information gleaned from pediatric extremity reconstruction can be applied to bone growth in the reconstructed jaw, it is not clear that these principles can be universally applied. There is good evidence that osteocyte viability is preserved after the transfer of non– epiphyseal-containing vascularized bone grafts25–28; however, the bone growth may be unpredictable. Experimental evidence suggests that vascularized membranous bone grafts utilized in the reconstruction of mandibular and zygomaticomaxillary defects in immature animals contribute to normal craniofacial development in a more predictable fashion than nonvascularized bone grafts,40 but there is little evidence to support this clinically. It has been speculated that the growth of transferred bone grafts is influenced by the adjacent craniofacial skeleton. We have seen symmetrical maxillary and mandibular growth in pediatric patients reconstructed with both scapular and fibular free flaps; however, the influence of the native craniofacial bone on bone graft growth is a difficult relationship to establish. Clearly, the proven linear relationship between bone stress and bone growth16 may be responsible for symmetrical growth of the transplanted bone, making this issue particularly complicated.
◆ CONCLUSION Pediatric reconstruction is relatively rare. Although most of the concepts for adult reconstruction hold true for the pediatric patient, the potential for donor-site morbidity is unique in the pediatric population. The knowledge of growth plate and ossification centers is important in limiting donor-site morbidity.
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6. Padwa BL, Evans CA, Pillemer FC. Psychosocial adjustment in children with hemifacial microsomia and other craniofacial deformities. Cleft Palate Craniofac J 1991;28:354–359 PubMed 7. Pertschuk MJ, Whitaker LA. Social and psychological effects of craniofacial deformity and surgical reconstruction. Clin Plast Surg 1982;9: 297–306 PubMed 8. Pertschuk MJ, Whitaker LA. Psychosocial adjustment and craniofacial malformations in childhood. Plast Reconstr Surg 1985;75:177–184 PubMed 9. Pillemer FG, Cook KV. The psychosocial adjustment of pediatric craniofacial patients after surgery. Cleft Palate J 1989;26:201–207, discussion 207–208 PubMed 10. Richman LC, Eliason M. Psychological characteristics of children with cleft lip and palate: intellectual, achievement, behavioral and personality variables. Cleft Palate J 1982;19:249–257 PubMed 11. Urken ML, Buchbinder D, Costantino PD, et al. Oromandibular reconstruction using microvascular composite flaps: report of 210 cases. Arch Otolaryngol Head Neck Surg 1998;124:46–55 PubMed 12. Enlow DH. Facial Growth, 3rd ed. Philadelphia: WB Saunders, 1990 13. Enlow DH. Facial growth and development. Int J Oral Myol 1979;5:7–10 PubMed 14. Thilander B. Basic mechanisms in craniofacial growth. Acta Odontol Scand 1995;53:144–151 PubMed 15. Moss ML. The function matrix concept. In: Grabb WC, Rosenstein SW, Bzoch KR, eds. Cleft Lip and Palate: Surgical, Dental, and Speech Aspects. Boston: Little, Brown; 1971 16. Kiliaridis S, Bresin A, Holm J, et al. Effects of masticatory muscle function on bone mass in the mandible of the growing rat. Acta Anat (Basel) 1996;155:200–205 17. Enlow DH, Harvold EP, Latham RA, Moffett BC, Christiansen RL, Hausch HG. Research on control of craniofacial morphogenesis: an NIDR Stateof-the-Art Workshop. Am J Orthod 1977;71:509–530 PubMed 18. Genden EM, Buchbinder D, Chaplin JM, Lueg E, Funk GF, Urken ML. Reconstruction of the pediatric maxilla and mandible. Arch Otolaryngol Head Neck Surg 2000;126:293–300 PubMed 19. Boyd JB. Mandibular reconstruction in the young adult using free vascularized iliac crest. Microsurgery 1988;9:141–149 PubMed 20. Pritchett JW. Growth and growth prediction of the fibula. Clin Orthop Relat Res 1997;334:251–256 PubMed 21. Horiuchi K, Hattori A, Inada I, et al. Mandibular reconstruction using the double barrel fibular graft. Microsurgery 1995;16:450–454 PubMed 22. Brown K, Marie P, Lyszakowski T, Daniel R, Cruess R. Epiphysial growth after free fibular transfer with and without microvascular anastomosis. Experimental study in the dog. J Bone Joint Surg Br 1983;65:493–501 PubMed 23. Sawaizumi M, Maruyama Y, Okajima K, Motegi M. Free vascularised epiphyseal transfer designed on the reverse anterior tibial artery. Br J Plast Surg 1991;44:57–59 PubMed 24. Taylor GI, Wilson KR, Rees MD, Corlett RJ, Cole WG. The anterior tibial vessels and their role in epiphyseal and diaphyseal transfer of the fibula: experimental study and clinical applications. Br J Plast Surg 1988;41:451–469 PubMed 25. Weiland AJ, Phillips TW, Randolph MA. Bone grafts: a radiologic, histologic, and biomechanical model comparing autografts, allografts, and free vascularized bone grafts. Plast Reconstr Surg 1984;74:368–379 PubMed 26. Donski PK, Carwell GR, Sharzer LA. Growth in revascularized bone grafts in young puppies. Plast Reconstr Surg 1979;64:239–243 PubMed 27. Mizumoto S, Tamai S, Goshima J, et al. Experimental study of vascularized tibiofibula graft in inbred rats: a preliminary report. J Reconstr Microsurg 1986;3:1–11 PubMed 28. Tamai S. Experimental vascularized bone transplantations. Microsurgery 1995;16:179–185 PubMed 29. Téôt L, Bossé JP, Gilbert A, Tremblay GR. Pedicle graft epiphysis transplantation. Clin Orthop Relat Res 1983;180:206–218 PubMed 30. Omokawa S, Tamai S, Takakura Y, Yajima H, Kawanishi K. A long-term study of the donor-site ankle after vascularized fibula grafts in children. Microsurgery 1996;17:162–166 PubMed 31. Davids JR, Valadie AL, Ferguson RL, Bray EW III, Allen BL Jr. Surgical management of ankle valgus in children: use of a transphyseal medial malleolar screw. J Pediatr Orthop 1997;17:3–8 PubMed 32. Teot L, Souyris F, Bosse JP. Pedicle scapular apophysis transplantation in congenital limb malformations. Ann Plast Surg 1992;29:332–340 PubMed
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Reconstruction of the Head and Neck 33. Moscoso JF, Keller J, Genden E, et al. Vascularized bone flaps in oromandibular reconstruction. A comparative anatomic study of bone stock from various donor sites to assess suitability for enosseous dental implants. Arch Otolaryngol Head Neck Surg 1994;120:36–43 PubMed 34. Rossillon R, Desmette D, Rombouts JJ. Growth disturbance of the ilium after splitting the iliac apophysis and iliac crest bone harvesting in children: a retrospective study at the end of growth following unilateral Salter innominate osteotomy in 21 children. Acta Orthop Belg 1999;65:295–301 PubMed 35. Lee EH, Chen F, Chan JW. The effect of surgery on the iliac apophysis: an experimental study. J Pediatr Orthop 1998;18:406–409 PubMed 36. Olney BW, Schlehr FJ, Asher MA. Effects of splitting the iliac apophysis on subsequent growth of the ilium: a rabbit study. J Pediatr Orthop 1993;13:365–367 PubMed
37. Forrest C, Boyd B, Manktelow R, Zuker R, Bowen V. The free vascularised iliac crest tissue transfer: donor site complications associated with eighty-two cases. Br J Plast Surg 1992;45:89–93 PubMed 38. Beirne JC, Barry HJ, Brady FA, Morris VB. Donor site morbidity of the anterior iliac crest following cancellous bone harvest. Int J Oral Maxillofac Surg 1996;25:268–271 PubMed 39. Hildago DA, Shenaq SM, Larson DL. Mandibular reconstruction in the pediatric patient. Head Neck 1996;18:359–365 PubMed 40. Antonyshyn O, Colcleugh RG, Anderson C. Growth potential in suture bone inlay grafts: a comparison of vascularized and free calvarial bone grafts. Plast Reconstr Surg 1987;79:1–11 PubMed
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