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The purpose of this study was to clarify the differences in the nature of craniofacial growth between subjects with normal occlusion and patients with unilateral cleft lip and palate (CLP) in terms of the size, shape and principal growth direction of craniofacial skeleton using finite element method (FEM). Lateral cephalograms were taken of 40 subjects as normal group and 178 patients as CLP group. These subjects were divided into seven developmental ages of 4-, 6-, 8-, 10-, 12-, 14- and 18-year-old. For the finite element analysis, the craniofacial complex was discretized into seven structures or elements with three nodal points in each after tracing each lateral cephalogram on acetate paper. For each stage, the growth parameters in CLP group were compared to those in normal group. The growth of upper facial skeleton and maxillary complex was more remarkably inhibited in CLP than in normal group. Especially, the growth inhibition of posterior maxillary complex in a vertical direction was remarkable in CLP group at any ages. Difference in the size and shape of entire mandibular skeleton between CLP and normal groups was not apparent. It is suggested that grow timing and peak velocity, an essential and key determinant to the success in orthodontic treatment, have been clarified in this study more clearly than in previous studies. It is hopefully anticipated to explore some key determinants to predict individual growth of the craniofacial skeleton near future.

In two interrelated articles, the current revision of the functional matrix hypothesis extends to a reconsideration of the relative roles of genomic and of epigenetic processes and mechanisms in the regulation (control, causation) of craniofacial growth and development. The dialectical method was chosen to analyze this matter, because it explicitly provides for the fuller presentation of a genomic thesis, an epigenetic antithesis, and a resolving synthesis. The later two are presented here, where the synthesis suggests that both genomic and epigenetic factors are necessary causes, that neither alone is also a sufficient cause, and that only the two, interacting together, furnish both the necessary and sufficient cause(s) of ontogenesis. This article also provides a comprehensive bibliography that introduces the several new, and still evolving, disciplines that may provide alternative viewpoints capable of resolving this continuing controversy; repetition of the present theoretical bases for the arguments on both sides of these questions seems nonproductive. In their place, it is suggested that the group of disciplines, broadly termed Complexity, would most likely amply repay deeper consideration and application in the study of ontogenesis.

Although the initial versions of the functional matrix hypothesis (FMH) theoretically posited the ontogenetic primacy of "function," it is only in recent years that advances in the morphogenetic, engineering, and computer sciences provided an integrated experimental and numerical data base that permitted recent significant revisions of the FMH--revisions that strongly support the primary role of function in craniofacial growth and development. Acknowledging that the currently dominant scientific paradigm suggests that genomic, instead of epigenetic (functional) factors, regulate (cause, control) such growth, an analysis of this continuing controversy was deemed useful. Accordingly the method of dialectical analysis, is employed, stating a thesis, an antithesis, and a resolving synthesis based primarily on an extensive review of the pertinent current literature. This article extensively reviews the genomic hypothesis and offers a critique intended to remove some of the unintentional conceptual obscurantism that has recently come to surround it.

The following case report describes the expanding role of pediatric dentists in treating children with craniofacial pathology. Retinoblastoma is the most common intraocular malignancy in childhood and is approximately the tenth most common pediatric cancer in the United States. Treatment consists of enucleation, or removal of the entire globe followed by placement of orbital implants. Un-restored anopthalmic sockets exhibit growth retardation and can lead to facial disfigurement. Maxillofacial prosthetic (MFP) rehabilitation can be especially challenging in younger, pre-cooperative or behaviorally compromised children and requires the skills and participation of a pediatric dental specialist as part of the MFP team. The following case report involving a 3 yr-old girl with retinoblastoma describes such challenges. The objective of the maxillofacial prosthetic team was to provide custom-built, acrylic, bilateral ocular prostheses in as comfortable and atraumatic manner as possible. The case was a success and underscores the value of a multidisciplinary dental approach for the treatment of children with very special needs.

Intercellular gap junctions permit bone cells to intercellularly transmit, and subsequently process, periosteal functional matrix information, after its initial intracellular mechanotransduction. In addition, gap junctions, as electrical synapses, underlie the organization of bone tissue as a connected cellular network, and the fact that all bone adaptation processes are multicellular. The structural and operational characteristics of such biologic networks are outlined and their specific bone cell attributes described. Specifically, bone is "tuned" to the precise frequencies of skeletal muscle activity. The inclusion of the concepts and databases that are related to the intracellular and intercellular bone cell mechanisms and processes of mechanotransduction and the organization of bone as a biologic connected cellular network permit revision of the functional matrix hypothesis, which offers an explanatory chain, extending from the epigenetic event of muscle contraction hierarchically downward to the regulation of the bone cell genome.

The periodic incorporation of advances in the biomedical, bioengineering, and computer sciences allow the creation of increasingly more comprehensive revisions of the functional matrix hypothesis. Inclusion of two topics, (1) the mechanisms of cellular mechanotransduction, and (2) biologic network theory, permit this latest revision; presented here in two interrelated articles. In this first article, the several possible types of intracellular processes of mechanotransduction are described. These translate the informational content of a periosteal functional matrix stimulus into a skeletal unit (bone) cell signal. The correlation between the strengths of the endogenous electrical fields produced by muscle skeletal muscle activity, and those to which bone cells maximally respond are stressed. Further, a physical chain of macromolecular levers, connecting the extracellular matrix to the bone cell genome is described, suggesting another means of epigenetic regulation of the bone cell genome, including its phenotypic expression.

Conventional methods of roentgenographic cephalometry will yield differences in interpretation of growth or treatment changes depending on which methods of superimposition are used. The finite element method of analysis has been reported to have significant advantages since it does not require a reference frame to describe the changes that have taken place. This article describes the growth of a patient with a Class II, Division 1 malocclusion during approximately 2 years of orthodontic treatment with the use of conventional cephalometric growth and static analyses, as well as the finite element method. Thirty cephalometric points were digitized on the pretreatment and the posttreatment lateral cephalograms of a patient undergoing orthodontic treatment between the ages of 10 and 12 years. The finite element method provided a reference frame invariant description of the size, shape, change, and rotation of each of the 12 finite elements representing different anatomic structures.

An allometric centered model of craniofacial growth was tested by several computer-assisted statistical methods on the pure longitudinal growth data of twenty-four close-bred female rats and on cross-sectional human cranial growth data. The study demonstrated that such a model was heuristic and, being incapable of exact definition, was deemed inappropriate for further use in modeling of craniofacial skeletal growth. The necessity for vigorous testing of any hypothesis concerning the modeling of craniofacial growth is stressed.

Much of the continuing controversy concerning the roles of genomic and nongenomic (epigenetic) processes in the regulation (causation) of growth is resolved by an analysis of the several types of causation. It can be shown that the combination of genomic and epigenetic factors is a necessary cause of craniofacial growth. A review of some recent literature serves to clarify this conclusion which is of potential clinical use since therapeutic intervention is always an epigenetic event.

A brief review of the fundamental postulates of the method of functional cranial analysis is given, with particular emphasis on the definition of the functional matrix. Two basic types of such matrices—periosteal and capsular—are described. Periosteal matrices include muscles and teeth, while the capsular matrices are conceived of as volumes enclosed and protected by both the neurocranial and the orofacial capsules. In the neural skull the capsular matrix is the neural mass. In the facial skull this matrix is the functioning space of the oronasopharyngeal cavity. We note the following differences between the activity of periosteal and capsular functional matrices. Periosteal matrices act upon skeletal units in a direct fashion by the processes of osseous deposition and resorption (or of cartilaginous or fibrous tissue multiplication. Their net effect is to alter the form (size and shape) of their respective skeletal units. Capsular matrices act upon functional cranial components as a whole in a secondary and indirect manner. They do so by altering the volume of the capsules within which the functional cranial components are embedded. The effect of such growth changes is to cause a passive translation of these cranial components in space. Cranial growth is a combination of the morphogenetically primary activity of both types of matrix. Growth is accomplished by both spatial translation and charges in form.

The dense connective tissues of the mouse and cat are selectively stained following the vital introduction of chlorazol fast pink. In addition, the newly formed areas of bone and of cartilage are intensely stained, while other areas of these two tissues are unstained. The staining reactions of this dye parallel that of trypan blue, vitally as well as in vitro.

Analysis of published odontometric data on human dental sexual dimorphism indicates that this characteristic is most clearly expressed by the canine teeth. Review of the several processes involved in coronal odontogenesis suggests that such dimorphism is related to an absolutely longer period of amelogenesis for both deciduous and permanent dentitions.

This study of cranial skeletal growth kinematics details the conceptual principles underlying the development of an allometric network model of such growth. This model is tested by the analysis of longitudinal rat and cross-sectional human growth data and by comparison of this model with a previously described allometric centered model. It is shown that the network model is superior to the centered model in three ways: (1) The allometric network model permits growth prediction when allometric constants are known; (2) the network model has significantly smaller errors than the centered model; and (3) the network model is capable of displaying growth kinematics of both the neural and facial skulls while in time there are marked transformations, such as relative rotations of two sets of cranial anatomic points.

The angular process of the human mandible alters its inclination with age, changing from a medial to a lateral flare during the transition from the neonatal to the adult stages. The morphological change in this mandibular skeletal unit is shown to be associated with a change in orientation of a portion of the related functional matrix, the masseter muscle. This change to an oblique line of action from an originally vertical one is associated with an increase in the functional movement of protraction at the temporo-mandibular joint. No other physiological parameters of muscle function seemingly are associated with this skeletal alteration. The processes of interaction between the functional matrix and its related skeletal are as yet unknown.

Eleven cases of retinoblastoma treated by enucleation and radiotherapy at infancy were followed up and studied to the time of puberty. Radiation dermatitis and stunting effect of the growth of the face were noted in this group of patients. Method and result of plastic surgical repair were presented.

The position of the three neural foramina describing the course of the inferior alveolar nerves was studied, with the aid of a previously determined logarithmic spiral, in cases of anterior open-bite and deep overbite. In anterior open-bite, the position of the foramen ovale was shown to be characteristically lower on this spiral than it is in any other condition studied; indeed, it is a diagnostic characteristic. The significance of this finding in the discussion of the problems of mandibular size and shape in these conditions was discussed. The etiologic role of periosteal and capsular functional matrices in the development of anterior open-bite was analyzed, and capsular matrices, with their related processes of passive translative growth, were held to be developmentally primary. Finally, an associated difference in the spatial location of the oral space in anterior open-bite was discussed. In essence, anterior open-bite was found to be a condition associated with specific spatial and developmental abnormalities of the oral functioning space, acting as a capsular matrix. All observed skeletal tissue changes are but secondary, compensatory, and mechanically obligatory responses to the morphogenetically and temporally prior alterations of this capsular matrix. Clinicians should carefully differentiate between the causes of an observed deformation of the orofacial skeleton and its etiologic factors. In anterior open-bite, they are completely different.

Amino acid analysis of protein from the enamel of shark teeth and from teleost scales shows the presence of collagens which can be classified chemically as ectodermal. This finding, together with results from a histological examination of the development of these tissues, constitutes strong evidence that both proteins are derived from the ectoderm, like the enamel of higher vertebrates. Since both are calcified, calcification cannot be a specific property of collagens of mesodermal origin alone.

Summary Two cases are described which present craniofacial dysostosis, patent ductus arteriosus, hypoplasia of the labia majora, and dental anomalies. The relationship of the new syndrome to that of other well-recognized symptom complexes and the dubious value of grouping a large number of etiologically different conditions under the “first arch syndrome” are discussed.

The morphogenetic role of two types of functional matrix-periosteal and capsular—in craniofacial growth is examined. The term growth is defined inclusively to include the changes in size and shape as well as changes in spatial position in time. The periosteal matrices are responsible for transformative growth, the changes in size and shape. The capsular matrices are responsible for translative growth, the changes in position. The role of oronasopharyngeal functioning spaces as competent, primary, morphogenetic agencies is detailed. The volumetric expansion of these capsular functional matrices is capable of accurate quantitative description.

An odontometric study of the deciduous teeth of 21 Liberian Negro children is reported. These data were obtained from dental casts alone. Statistical comparisons were made of the mesiodistal diameter alone with two American White populations and the three Japanese populations. Maxillary teeth, with the exception of the cuspids were larger in the Negro sample, while only the Negro mandibular molars were significantly wider. This situation resulted in an alteration of Negro maxillary tooth size order. Comparisons were made with other populations reported in the literature which led us to stress the fact that, as yet, no satisfactory sample of deciduous tooth measurements are available for any population. A discussion of tooth form differences stresses the point that teeth differ in both attributes of form, i.e., in shape as well as in size between the several major racial groups. The processes by which these shape differences are brought about were discussed and it was suggested that differing relative growth rates may well be one cause. An allometric analysis of fetal molar tooth growth showed, again, that a sharp interphase occurs in all teeth, with a subsequent decrease in specific growth rate. This interphase corresponds to the initiation of cuspal calcification.

Liberian Negro deciduous dentitions have arch dimensions which significantly exceed those of a variety of White populations. Winged incisors were present in 14.3% of the Negro population, again exceeding White values. No differences were noted in incisal overbite or overjet. Diastemal spaces were greater in the Negro dentitions than in the White, but the significance of this is as yet unknown. An exceptional finding was the absolute lack of Class II (distocclusion) in the Negro series. A discussion of functional occlusion stressed the necessity for the inclusion of such dynamic factors as dental abrasion, mesial migration and physiological rest position in future studies of comparative dental anthropology.

A RECENT report (Cooper,101953) has indicated that ligation of the anterior choroidal artery in patients with paralysis agitans may ameliorate the tremor and rigidity associated with this syndrome and permit greater range of voluntary movement. Precisely why ligation of this vessel has been associated with these beneficial effects has not been answered, but it has been postulated that they probably are the result of localized ischemia and/or necrosis of portions of the globus pallidus. It has previously been determined (Carpenter, Whittier, and Mettler,91950) that localized stereotaxic lesions of the globus pallidus can ameliorate or abolish choreoid hyperkinesia in the Rhesus monkey resulting from localized lesions of the subthalamic nucleus of Luys. However, bilateral simultaneous lesions in the monkey which destroyed approximately 10% of the pallidum on each side have not been compatible with survival. It is claimed by Spiegel and Wycis* that patients with paralysis agitans