Melvin L. Moss

The primary role of functional matrices in facial growth

Abstract 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 functional matrix hypothesis revisited. 1. The role of mechanotransduction

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.

The capsular matrix

Abstract 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.

The functional matrix hypothesis revisited. 4. The epigenetic antithesis and the resolving synthesis

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.

Implantation of porous polymethylmethacrylate resin for tooth and bone replacement

This study suggests that: 1. The porous plastic material tested is compatible with and showed no undesirable reactions in subcutaneous, intracerebral, intramuscular, and especially, intraosseous sites. 2. By standardizing porosity (e.g., a desired hole, any dimension, uniformly distributed) with the implant material (P.P.M.M.), one can predict with a degree of certainty that connective-tissue (collagen fibers) or hard-tissue (osteogenesis and reparative bone) ingrowth into these micropores will definitely occur. 3. The various shapes employed for implantation of the plastic material were not carcinogenic and did not cause a malignant reaction in any implanted region. 4. A close amalgamation with adjacent tissues was a result regardless of the implant site (e.g., intramuscular, intracerebral, or subcutaneous). Intraosseously, there was a variation. Depending upon the pore size, one observes either connective tissue or osseous ingrowth into the micropores. At a 100 micron pore size (B material), connective tissue ingrowth into the P.P.M.M. was seen. At the 450 micron size (E material), osseous tissue ingrowth into the P.P.M.M. was clearly observed. 5. The P.P.M.M. implant material can be used as a tooth replacement (e.g., for a root) at a small pore size (100 micron) and as a bone replacement (e.g., for bony defects) at a larger pore size (450 micron). 6. To secure vascularization of the implant material, porosity throughout is indicated at a large pore size. Surface porosity regardless of size will encourage only soft-tissue ingrowth into the implant material. 7. Any hard-tissue size or shape can be duplicated with the material, at any pore size, with compatibility to the adjacent tissue, regardless of the region of placement in the body. 8. There is a possibility of bone induction or stimulation of bone growth in predetermined directions with all its implications (e.g., periodontal disease). The replacement and repair of any hard tissue in the body (e.g., bone and teeth) are possibilities.

Fluorocarbon Enhancement of Skin Flap Survival in Rats.

Fluorocarbons exhibit two unique properties: oxygen saturation in direct proportion to the percent administered and low viscosity which improves microcirculation. These properties were investigated in improving survival in random skin flaps in rats. Modified McFarlane flaps were raised in 30 Sprague-Dawley rats and divided into three equal groups. Group 1 rats served as controls, group 2 rats were hemodiluted with Ringers lactate, and group 3 rats were hemodiluted with Fluosol-DA (20%). All groups were kept in a high (80%) oxygen environment for 48 hours. Areas of necrosis were measured using a computer system. Necrosis in control flaps averaged 14.96 percent; in flaps hemodiluted with Ringers lactate, 10.12 percent; in flaps hemodiluted with Fluosol, 4.76 percent. These differences were statistically significant. We conclude that fluorocarbons significantly enhance flap survival in rats.

EFFECT OF RADIATION ON THE DEVELOPMENT OF FACIAL STRUCTURES IN RETINOBLASTOMA CASES

Abstract 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.

When does a random flap die

A random flap can be constructed, its circulation determined, and the ischemic portion identified. Left untreated for a period, the critical ischemia time, the ischemic portion will die and is clinically recognized several days later. What is not known is when this tissue, destined to die, actually dies. To ascertain this time, we compared the percent necrosis of a distal 3 X 3 cm segment of a 10 X 3 cm reverse McFarlane random flap with a known distribution of necrosis to the percent necrosis of the distal 3 X 3 cm of full-thickness skin grafts taken from a similar reverse McFarlane flap at 0, 4, 8, 12, and 16 hours after pedicle construction. Implicit in this experiment is the assumption that necrosis of the full-thickness skin grafts in excess of that of control animals represented skin no longer viable. Sometime between 8 and 12 hours, the percent necrosis of the full-thickness skin grafts surpassed that of the control, and it was concluded that this graft was dead prior to grafting. Thus it is suggested that critical ischemia time and death of the flap tissue are nearly identical, and the latter occurs at between 8 and 12 hours.

Studies on orthocephalization

In the period from 14 to 150 days, the zygomatic arch of the rat skull possesses a marked positional stability in relation to the parietal bone, the basisphenoid bone and the length axis of the skull.

Epigenetic regulation of the shape and position of the auricle in the rat.

We hypothesized that epigenetic (non-genomic) factors, related to muscular function, significantly regulate the shape and position of the auricular cartilage. We tested this experimentally by doing unilateral partial and total facial neurectomies, auricular myectomies, and ear rotations with skin excisions in rats. The neurectomies produced muscle atrophy, abolished the horizontal scaphoid ridging, and produced characteristic changes in the auricular shape. The myectomies of extrinsic auricular musculature alone were followed routinely by complete muscle regeneration and no changes in shape. The auricular rotations, with skin excision, produced an antihelix-like complex analogous to the human ear--a configuration that was permanent and was accompanied by muscle relocation. The findings are believed to support our hypothesis.