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Conference Report: Symposium on "The Facial Skeleton in Clefts", sponsored by the American Cleft Palate-Craniofacial Association, May 13-14, 1990, St. Louis, Missouri

The genetic, developmental, anatomical, diagnostic, nosological, surgical, and psychosocial aspects of clefts of the face were the concerns of an interdisciplinary symposium chaired by K. Dryland Vig (University of Michigan). The etiopathogenesis of facial clefting was elaborated upon by G.H. Sperber (University of Alberta), who indicated that clefting represented either failure of completion of normal embryogenesis (because of primary malformation or secondary mechanical deformation) or disruption of previously intact structures. The locations of clefts are at precise and predictable embryological junctions in malformations, but are diverse and unique in disruptions. The etiology of clefting may be genetic, teratogenic, mechanically disruptive, or multifactorial. These causes predicate the location, recurrence risk, treatment, and preventive strategies of clefting. The clinical application of recurrence risk to genetic counseling was addressed by A. Aylsworth (University of North Carolina). All birth-defect families are candidates for counseling. Risk assessment depends on correct diagnosis of the above-stated etiopathogeneses. Syndromic and nonsyndromic patterns require different approaches to evaluation, risk assessment, and counseling. Nonsyndromic anomalies are inhomogenous. Counseling is based upon both theoretical risk and empirical data, carrying limitations. The anatomical aspects of facial clefting were dealt with by S. Schendel (Stanford University), who indicated the various degrees of involvement of hard and soft tissues. Clefts include both hypoplasia and tissue displacement, and their classification by Tessier facilitates comparisons of remote and local tissue dysplasias in holoprosencephaly, cephaloceles, and lip and palate clefts. Growth considerations in untreated clefts allowed M. Mars (Hospital for Sick Children, London) to examine intrinsic vs. iatrogenic dysmorphology in unoperated cleft-lip and -palate subjects. He reported on cephalometric and dental analyses of adult male Sri Lankan untreated, unilateral cleft-lip and -palate subjects, revealing unilateral tooth size reduction in cleft-palate subjects, narrowed dental arch widths, and increased overjets in CLP subjects. The consequences of surgery on facial growth, already distorted and attenuated in facially dysmorphic infants, were determined by B.R. Ross (University of Toronto). The effects of iatrogenic forces vary, depending on cleft type, underlying facial pattern, and the nature and timing of surgical and orthodontic treatment. Surgery interferes with growth, indicating earlier (<12 months) rather than later (21-33 months) intervention, to be balanced against functional demands. Awareness of normal post-natal development and growth of the midface was emphasized by D. Carlson (University of Michigan) in understanding abnormal midface form. He superbly detailed the roles of bone remodeling, sutural and nasal septal growth, and "functional matrices" in midface morphogenesis, indicating growth and resorption sites requiring clinical consideration. The long-term results of secondary bone grafting and its effect on facial growth were described by G. Semb (Universities of Oslo and Manchester), who demonstrated that such grafting into 653 clefts during the mixed dentition stage did not impair facial growth and facilitated normal tooth eruption into the previously cleft region. The technical aspects of midfacial reconstruction in cleft patients were addressed by B. Epker (John Peter Smith Hospital, Fort Worth, Texas). A multivariable approach to cleft assessment provided rational treatment for attainment of optimal reconstruction. Psychophysical evaluation of facial cleft patients was undertaken by J. Tobiasen (University of Kansas), who has designed a scale of facial impairment in cleft lip patients to facilitate assessment of social adjustment and the costs and benefits of surgical intervention. The impairment of speech in cleft patients concerned L. D'Antonio (Loma Linda University), who analyzed the components of voice production (respiratory, laryngeal, orofacial, nasal) and their dysfunctions. They may be syndromically linked in compensatory processes to produce characteristically disordered speech. The feeding and swallowing patterns of normal and cleft palate infant pigs and macaques were studied by R. German (Washington University, St. Louis), who determined by cineradiography that although initial milk acquisition (a pump suction mechanism) is impaired by clefts, the subsequent transportation through the oral cavity and oropharynx resembles that in normal animals. Recent advances in imaging of facial clefts were illustrated by J. Marsh (Washington University, St. Louis) with computer re-formating of CT scans to create shaded surfaces and volumetric images, facilitating precise diagnosis of the extent of clefting and allowing surgical planning and treatment assessment to occur. The outcome of maxillary surgery in facial clefts was presented by A. Hegtvedt and T. Turvey (University of North Carolina) in achieving improved esthetics, occlusion, speech, and respiration. The clinical epidemiology of facial clefts was assessed by W. Shaw (University of Manchester), who indicated the strengths and weaknesses of CLP study designs from anecdotal case reports, through case series, retrospective and non-experimental comparative studies, and randomized trials, with planning of statistical design and analysis being the key to success. R. Marks (University of Florida) reinforced this theme of a methodological basis for clinical studies to avoid "fatal flaws" in epidemiology. The results of a randomized clinical trial of ear disease in cleft patients-conducted by J.L. Paradise (University of Pittsburgh), who advocated myringotomy and tympanostomy to avoid hearing and speech impairment-closed the symposium.