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A Question of the Role of the in the Growth of the Premaxillary Segment R. A. LATHAM, B.D.S., Ph.D. T. G. DEATON, A.B. C. T. CALABRESE, M.D. Chapel Hill, North Carolina 27514

Research on the problem of antero-posterior growth retardation of the maxillae following cleft and palate surgery has been relatively neglected compared to that on growth retardation in width (3, 5). Most of the work on normal forward growth of the middle third of the has centered on the role of the cartilaginous component of the (4, 6, 9, 10, 11). However, with reference to treatment of cleft lip and palate, it is important that information be obtained about the role of the vomer. An observation is reported on growth retardation in the upper in dogs with artificial cleft palate and extirpation of the vomer which suggests that the dog might serve as a useful model for studying this problem in the human. Material and methods Observations were made on five dogs with surgically placed clefts of the , (Figure 1) and five which had congenital complete clefts of the secondary palate (Figure 2). The artificial clefts were made in the palate of five puppies under anesthesia by removing a median strip of palatal mucosa and an 8 mm wide portion of palatal from the incisive canal to the posterior border of the hard palate. The greater part of the vomer was removed using a round dental bur, leaving the cartilaginous nasal septum intact. The nasal mucosa was incised and the edges sutured to the oral mucosa to cover the exposed bone (7). The periods of survival following cleft formation were from nine weeks to two years and four months (Table 1). Of the congenitally cleft animals (Table 2), the Shetland Sheepdog received no surgery and the clefts of four Golden Retrievers were surgically closed at the age of about 10 weeks. I Findings Anterior of the incisor teeth became conspicuous 8 weeks following surgery in all 5 dogs with artificial clefts (Figure 3). The third lateral incisor Dr. Latham and Mr. Deaton are affiliated with the Dental Research Center and Department of Orthodontics, School of Dentistry, University of North Carolina at Chapel Hill; Dr. Calabrese is affiliated with the Division of Plastic and Reconstructive Surgery and Surgery of the , and held the position of Research Associate in the Dental Research Center during this work. This investigation was supported by N.LH. research grant number DF 02668 from the National Institute of Dental Research and by N.LH. grant number RR 05333 from the Division of Research Facilities and Resources. 351 352 Latham and others

FIGURE 1. Photograph of dog 1 palate FIGURE 2. Photograph of dog 6 palate showing surgically placed cleft. showing congenital cleft. Shetland Sheepdog, 22 weeks. TABLE 1. Dogs With Artificial Cleft Palate

age when post- no. breed tiff/562555 operative TABLE 2. Dogs With Congenital Cleft Palate

no. breed survival 1 Mongrel 7 weeks 21 weeks 2 Mongrel 7 weeks 9 weeks 6 Shetland Sheepdog 22 weeks 3 German 8 weeks 10 weeks 7 Golden Retriever surviving Shepherd 8 Golden Retriever surviving 4 Mongrel 8 weeks 106 weeks 9 Golden Retriever surviving 5 Mongrel 8 weeks 18 weeks 10 Golden Retriever surviving

articulated with the mesial surface of the lower canine which prevented further deterioration of the antero-posterior incisor relationship (Figure 4). This _ ___ resulted in a deep wear groove on the mesial surface of the lower canines. In _ three dogs the arch alignment of the incisor teeth was collapsed lingually. _- The 5 dogs with congenital clefts maintained a normal jaw relationship __ throughout the period of observation (Figure 5). __ Discussion Atherton (7) observed that the position of the premaxillae in the human with bilateral cleft was similar to that of the normal premaxillae in animals. He found that cleft of the canine primary palate did not affect the position of the ROLE OF VOMER 353 premaxillae and that the protruded premaxillae of the human bilateral cleft merely conformed to the characteristic mammalian growth pattern. What the premaxillo-maxillary sutures allow in the dog in terms of forward premaxillary growth, the bilateral clefts allow in the case of the human premaxillae. Therefore, for experimental purposes, it is possible to regard the premaxillary condition in the newborn dog as a model of the bilateral cleft condition in the human. In view of the bony continuity between the premaxillary and maxillary parts of the upper jaw in the normal human facial , it appears that the vomer functions only in a minor supporting role. In the long snouted animals, the supporting stresses of the premaxillary segment are shared amongst the premaxillary sutural articulations, namely the bilateral premaxillo-maxillary sutures and the premaxillo-vomeral suture. The premaxillo-vomeral suture, and hence the vomer itself, provides support of a similar order as that provided by the premaxillo-maxillary sutures. Thus, in the dog, it may be presumed that the vomer makes a more important contribution to the growth and support of the upper jaw than in the normal human. In bilateral cleft lip and palate in man, in

FIGURE 3. Profile view of dog 5, 18 weeks old, show- ing anterior crossbite indica- tive of retarded upper jaw growth.

FIGURE 4. Profile view of dog 4, aged 2 years 6 months, showing anterior crossbite indicative of re- tarded upper jaw growth and locking of upper lateral in- cisor.

354 Latham and others

FIGURE 5. Profile of dog 7, 31 weeks old, with repaired congenital cleft of secondary palate showing normal oc- clusal relationship of the teeth.

which the connections between the premaxillary segment and maxillae are absent, the vomer becomes the only bony support of the premaxillary segment and carries an abnormally heavy functional load. The question arises, "How much will the vomer tolerate surgical interference with its structural integrity, mucoperiosteal investment and blood supply without losing its growth potential and capacity for maintaining the premaxillary segment in a normal position?" In the artifically cleft dogs there was disturbance of growth in the premaxillary region similar to that in the repaired human bilateral cleft patient. Factors capable of influencing upper jaw growth and resulting in premaxillary retrusion in patients with repaired cleft lip and palate include: tightness of the upper lip, the presence of scar tissue (3, 5), vomerine resection for setting back the protruded premaxillary segment, and vomerine destruction subsequent to its denudation in raising extensive vomero-septal flaps (2). In analyzing the nature of the antero-posterior growth retardation in these dogs, the effect of a tight lip does not appear applicable. The growth retardation may then be attributed to either the tethering effect of scar tissue at the anterior edge of the artificial cleft or to disruption of the vomer. With regard to the former, there was minimal exposure of raw surface with the technique utilized, and the cleft was not near to the incisors (i.e. 26-30 mm) and the premaxillo- maxillary sutures were not involved. Lynch and Piel (8), using a technique similar to ours, formed clefts in dogs, removing not only part of the vomer, but also part of the nasal septum. They reported that surgical closure of these clefts caused retardation of subsequent growth in jaw width and attributed this to scar tissue tethering. They did not comment on upper jaw growth retardation in the antero-posterior dimension. With regard to antero-posterior growth retardation, there is a case for presuming that the difference between our dogs with artificial clefts and those with congenital cleft palate may be the presence of a normal vomer in the latter. However, the determination of whether vomeral disruption or mucosal scar tissue is the actual causative factor may be determined by further research. It is likely that this may result in greater emphasis on the role of the vomer in overall facial growth following cleft palate repair.

ROLE OF VOMER 355

Summary

Antero-posterior retardation of upper jaw growth became evident in all five dogs with surgically placed clefts and extirpation of the vomer within 8 weeks following surgery. Five control dogs with congenital cleft palate maintained a normal jaw relationship. The evidence indicated that the difference in growth between the two groups may be explained in terms of the role played by the vomer in the growth and support of the upper jaw in the dog. This observation suggests that the dog may be used as a model for the study of retardation of growth in the antero-posterior dimension and indicates a need for research concerned with the role of the vomer in the human bilateral cleft condition. Acknowledgements: Thanks are due to Mrs. Theis, Mebane, North Carolina for the gift of the Shetland Sheepdog, and to Dr. A. Aylesworth for permission to study his Golden Retrievers with congenital cleft palate. Thanks are also due to Mr. T. Edwards, Learning Resources Center, School of Dentistry, for photography and to Miss Martha Thompson for help with the manuscript. Reprints: Dr. R. A. Latham Department of Paediatric Dentistry Faculty of Dentistry University of Western Ontario London, Ontario N6A 5B7 CANADA

References 1. ATHERTON, J. D. The natural history of the bilateral cleft. Angle Orthod., 44, 269-278, 1974. 2. Cronin, T. D. Personal Communication (1974). 3. HERFERT, O. Fundamental investigations into problems related to cleft palate surgery. Brit. J. Plast. Surg., 11, 97-105, 1958. 4. KreEmEnak, C. R., D. F. and S. E. Demjen. The role of the cartilaginous nasal septum in maxillofacial growth: Experimental septum removal in Beagle pups. L. A.D.R. 47th General Meeting, Abstract no. 32, p. 48, 1969. 5. KrEmEnNax, C. R., W. C. Hurrmaxn, and W. H. Oum. Growth of maxillae in dogs after palatal surgery: I., Cleft Palate J., 4, 6-17, 1967. 6. LatHaAM, R. A. The septopremaxillary ligament and maxillary development. J. Anat. London, 104, 584, 1969. 7. LatHam, R. A., R. B. Winstow, and A. G. Bevin. Induction of new palatal growth as an aid to cleft closure in dogs: Neopalate formation. Brit. J. Plast. Surg., 27, 264-273, 1974. 8. J. B., and R. Prit. Retarded maxillary growth in experimental cleft palates. Amer. Surgeon, 32, 507-511, 1966. 9. Sarnat, B. G. The face and after surgical experimentation with the septovomeral region in growing and adult rabbits. Acta Oto-Laryngologica, suppl. 268, 1-30, 1970. 10. Sarnat, B. G., and M. R. WexuLer. Longitudinal development of snout deformity after septal resection in growing rabbits. Brit. J. Plast. Surg., 22, 313-323, 1969. 11. Scott, J. H. The of the nasal septum. Brit. Dent. J., 95, 37-43, 1953.