Copyright @ 2010 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited. Nasal Reconstruction for Maxillonasal Dysplasia Anthony D. Holmes, FRACS,*Þ Shu Jin Lee, MRCS, MD,*Þ Andrew Greensmith, FRACS,*Þ Andrew Heggie, FRACDS (OMS),*Þ and John G. Meara, MBA, FRACS*Þ Background: Maxillonasal dysplasia, Binder type (Binder syn- drome and nasomaxillary hypoplasia), is a spectrum of deficient nasomaxillary osteocartilaginous framework, deficient nasal soft tissues, and a short columella. The correction of these deformities is challenging, and results are often disappointing. Tissue expansion with multiple bone grafts for nasal augmentation from childhood has been advocated as a means to address the constricted soft tissues. However, bone grafts in children have been associated with unpre- dictable growth and resorption. Agreeing with the principle of serial nasal augmentation that commences in childhood, we used allo- plastic material for tissue expansion followed by definitive recon- structive rhinoplasty at the completion of growth and orthognathic surgery as required. Definitive rhinoplasty mainly used a 1-piece costochondral graft cantilevered to the frontal bone. Materials and Methods: Thirty-one patients over a period of 27 years were reviewed. The patients were divided into 2 groups based on the age of presentation, namely, prepubertal and post- pubertal. The prepubertal group underwent serial tissue expansion of the constricted nasal envelope with customized silicone implants and final reconstruction by costochondral rhinoplasty at the end of puberty. The postpubertal group underwent 1-stage costochon- dral rhinoplasty. The definitive rhinoplasty used a cantilevered 1- piece costochondral graft retaining the dorsal periosteum that was dowelled into the frontal sinus wall. Results: In the prepubertal group (n = 20), 41 silicone implants were placed in the childhood years for tissue expansion of the nasal enve- lope. One patient developed implant infection, and another required replacement after extrusion. Long-term follow-up showed minimal resorption of the costochondral graft in the pre-expanded prepubertal group and minimal to moderate graft resorption in the postpubertal group. Conclusions: Successful treatment of maxillonasal dysplasia is de- pendent on the following: an understanding of the underlying patho- logic anatomy, namely, that of the constricted nasal tissues, serial tissue expansion of the nasal envelope in childhood, and definitive cos- tochondral rhinoplasty at the end of growth. Early tissue expansion with the placement of alloplastic silicone implants effectively stretches the constricted nasal soft tissues in Binder syndrome to limit graft resorption after definitive nasal reconstruction with costochondral rib grafts. There is a possible role for similar tissue expansion in the postpubertal patient with alloplastic material before costochondral grafting if the soft tissues are inadequate. Long-term resorption of cantilevered, 1-piece, periosteum-covered costochondral grafts was minimal. Key Words: Maxillonasal dysplasia, maxillonasal dysostosis, nasomaxillary hypoplasia, Binder syndrome, Binder association (J Craniofac Surg 2010;21: 543Y551) M axillonasal dysplasia results from hypoplasia of the osteo- cartilaginous framework of the nasomaxillary region 1Y11 and deficiency in anteroposterior growth of the nasomaxillary com- plex. 12,13 This results in significant shortage of both the bony framework and the soft tissues of the nose. The osseous deficiency is evident in the deficient length and projection of the caudal por- tion of the nose with the pathognomonic feature being absence of the anterior nasal spine. 2,4,5,7,10,11 There is deficiency of the nasal soft tissue envelope and the nasal lining and, in partic- ular, a distinctive short columella (Fig. 1). The nasomaxillary hypo- plasia may be associated with a normal or class 3 dental occlusal relationship. 3,7,11,14 Correction of the nasal deformity in maxillonasal dysplasia is challenging, and results are often disappointing. 3,15,16 Many sur- geons approach the correction of the nasal bony and soft tissue deficiencies separately. Attempts to correct the foreshortened nose have been unsatisfactory with obvious scarring resulting from V-Y or similar procedures to lengthen the nose, 17Y19 forehead flaps to provide additional skin covering, 17 and skin grafts for nasal dor- sal inlays. 20 Composite conchal grafts for nasal lengthening re- quire multiple operations and provide only small amounts of nasal lengthening. 3,21 The problem of deficient nasal lining has been previously addressed with local turnover hinge flaps, nasolabial flaps, 17 and intranasal epithelial inlays that require permanent sup- porting prostheses 3,22,23 to overcome scar contraction. Correction of the bony deformity was first attempted using the LeFort II osteotomy that was championed to provide simulta- neous correction of both the nasomaxillary hypoplasia and the fore- shortened nose. 3,4,24Y27 The LeFort II osteotomy does not adequately address the retruded midface, and the nose was insufficiently lengthened. 12,27 Others used additional bone and cartilage grafts in- serted via visible external incisions for paranasal augmentation and nasal lengthening, and local flaps are used for columella elongation. 27 These procedures are often associated with visible scarring 16 and un- predictable growth 28 and resorption of bone grafts. 16 Obvious scarring also followed the use of the trapdoor incision over the nasal dorsum for nasal lengthening 29 and the paranasal incision for LeFort II os- teotomies. 27 The LeFort II advancement can lead to the conversion of normal or mild class 3 occlusion to severe class 2 occlusion. 4,27 The LeFort I osteotomy alone was unsatisfactory because it accentuates the nasal retrusion. 30 TECHNICAL STRATEGY The Journal of Craniofacial Surgery & Volume 21, Number 2, March 2010 543 From the *Department of Plastic and Maxillofacial Surgery, Royal Children’s Hospital, Melbourne, Victoria, Australia; and †Department of Plastic Sur- gery, Children’s Hospital Boston, Boston, Massachusetts. Received October 23, 2009. Accepted for publication November 15, 2009. Address correspondence and reprint requests to John G. Meara, MBA, FRACS, Children’s Hospital Boston, Boston, MA 02115; E-mail: john.meara@childrens.harvard.edu Copyright * 2010 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0b013e3181d024b0