Connecticut Symposium, a synopsis

Connecticut Symposium, a synopsis

EDITORIAL Connecticut Symposium, a synopsis Part I T he Connecticut Symposium was designed to cover clinical and bioengineering aspects of dento...

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EDITORIAL

Connecticut

Symposium,

a synopsis

Part I

T

he Connecticut Symposium was designed to cover clinical and bioengineering aspects of dentofacial orthopedics by facilitating a dialogue between professionals engaged in different areas of treatment and research. The discussion focused on methods for the measurement of orthopedic changes and the effect of appliances on various tissues as related to facial morphology and function. The fourteen presentations will be summarized in three editorials. Dr. Charles J. Burstone opened the program with a presentation entitled “Evaluating Craniofacial Alterations-New Methodologies. ” There is evidence at this time that we can produce craniofacial alterations in the facial skeleton in human beings, but there is a great deal of debate about the magnitude of these changes. On an animal level, it has been demonstrated that you can change the maxilla’s position in space and produce remodeling. Evidence in lower animals indicates that you can alter mandibular growth. Some of the basic mechanisms can also be working in the human being as well. Since it is possible to retard the downward and forward growth of the maxilla, it is important clinically to show the amount and stability since it may not have significance if small or unpredictable. We see in the literature a number of fallacies in using conventional cephalometrics to study the effects of what our orthodontic appliances can do to the face. Variations in growth direction and in our ability to identify points can produce a pseudo-orthopedic effect by improper superimposition. Simple rotation on the cranial base will give the illusion of orthopedic change. It is also fallacious to assume that if our patient does not grow exactly like the mean, it is the result of an orthopedic effect. There is a great deal of variation in the way individuals grow. For example, if we measure the distance from articulare to pogonion for mandibular growth, we typically get 4.75 2 1 mm. standard deviation of growth in a 14%-year-old boy or girl. It can normally vary within 3 standard deviations from 1 to 8 mm. There is a 7 mm. range in the amount of growth that one might expect at this age. There would still be 000%9416/82/040333+03$00.30/O

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1982 The C. V. Mosby

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one individual out of 100 who would vary more than this in a normal population. Similarly, for evaluation of the maxilla at any age, people superimpose on sellanasion. The stability of SNA has been reported many times in the literature. The normal variation of 3 standard deviations would allow the maxilla actually to move back 2.8 mm. and forward as much as 3.47 mm. Inappropriate conclusions are often drawn from assumptions concerning the mean value applied to an individual’s growth. Use of the mean is fine in an epidemiologic study of two groups, but not on an individual basis. Also, rotational changes in mandibular position, as from Class III elastics or from occipital headgear, should be differentiated from growth alterations. There is also the fallacy of using increments that are derived from chronologic age rather than developmental age on the basis of data around peak velocity. Use of chronologic age in females might indicate that there is no growth spurt in the growth of the mandible. Bjork introduced the use of implants into orthodontics. They can move, however, and you do have a problem with orientation of the head (head holder for later superimposition). A new approach using stereometrics involves implants and a system of cross marks with orientation points. The patient can be randomly placed and the head holder is not necessary. If you take two views, you have all the information you need for the computer to reconstruct in three-dimensional space. The mean difference of all measurements is very close to 0, with a standard deviation of 0.19 and a percent error on the average of 1.5 percent. The Connecticut system uses rods that project from a box, in which the patient is placed, for the reference system or x , y , z coordinates on the x-ray. Another method of measurement is laser holography, where monochromatic coherent light from a laser is used. With a beam splitter, the light is split into the reference beam that is reflected directly on a photographic plate. The other beam is split off through mirrors that will then bounce on the bone (maxilla) and back. If you look at the photographic plate in the same setup and illuminate it with just a reference beam, you 333

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will see the maxilla in three dimensions. When we double-expose we will get fringes on the skull. As we increase the magnitude of force on a portion of the skull, the fringes will come closer together. The fringes will then cross a point, and if you count the number of fringes that cross a point you can determine the displacement. A TV camera is used to scan the holograms and to make the actual determination. You can see on the monitor what happens in the mouth. lnstead of individually digitizing photographs, it is all done by computer without the need of direct photography. The advantage of the holographic technique is that it allows us to make noninvasive and very accurate measurements in three-dimensional space. Professor Melvin L. Moss discussed “The Kinematics and Dynamics of Craniofacial Growth. ” Kinematics is simply the study of growth behavior alone. It involves what, when, and how much movement whereas dynamics relates to the biologic processes underlying those kinematics. The study of the dynamics can be and must be held independent of the study of kinematics. In craniofacial growth, however, we have frequently been confusing kinematics and dynamics. All customary methods of roentgenographic cephalometrics, whether in two or three dimensions, use one point held fixed in position and one line segment held fixed in orientation. The growth behavior of all other points studied then is dependent upon the method of registration and fixation. When you have a plethora of methods, so that the kinematics of growth behavior of all other points studied is directly related to your method of superimpositioning, there is no valid method by which you can decide which method displays the growth behavior more correctly than another. The simplest starting position about any growing system in biology is to say that is grows exponentially; it multiplies. If two biologic parts in the same object are each growing exponentially, the simplest mathematical assumption to make is that the growth of both objects will be related by a center of allometry. Growth radially away from one common center or node would be allometric. There will be some constant ratio between their growth rates. Biologic structures that permit allometric growth are structurally stable. If you use three only points, you will always get a center. Four points are therefore the minimum. You can, manually or by computer, use coordinate locations to two decimal points from head films to search, either rotate or translate, transform the coordinates freely, and look for the best fit. If you do not look closely at the deviation, you can convince yourself that there really is a center of allometry.

Am. J. Orrhud. Arm/ 1982

Search of cross-sectional data demonstrated an area about one quarter the internal diameter of the skull in which an allometric center producing equally small variations could be placed. No known method of mathematical analysis will permit you to demonstrate beyond statistical doubt that there is an allometric center. Other mathematical models being investigated are the growth network model and the finite element analysis model for which Moss has hope. This has been an object lesson in not fooling yourself, in not taking what appears to be visually a very interesting technique or concept and trying to establish it. Understanding concepts and techniques of mathematical formulations and the testing of these results for limitations must become a portion of the armamentarium of the future clinician. Robert M. Ricketts distinguished three different types of orthopedics by presenting the topic, “Orthopedics in the Eyes of the Clinician. ” First, natural orthopedics or a change in the relationships of skeletal parts occurs with natural growth or under the influence of genetic or environmental causes without therapy. Second, therapeutic orthopedics and induced growth or morphologic change in skeletal relations results from mechanical or therapeutic means that we have at our disposal. The third is surgical orthopedics, a change brought about by surgery on bone, joint, muscle, or any involved tissue. Ricketts took forty patients whose frontal and lateral head films were traced and set up an investigative program. He surveyed 362 measurements to determine the best set of measurements that could be used in a descriptive manner and points of superimpositioning with the least change that could be used on a longitudinal basis with the idea of evaluating growth and treatment changes altogether. In the frontal view two poles were found. The face did not grow from one center point. It was as if the face were growing together in a midline, and this begins to explain why we see so much diversity in our patients with asymmetries. Ricketts believes that any time you have a change in the angle basion-nasion-point A or the facial axis, it is something you are causing by therapeutic measures in a particular patient. In the Michigan sample and the Ricketts sample, the standard deviation of change of the facial axis was only 2 and 1.5 degrees, respectively, in that IO-year experience. The chin is coming down its original facial axis approximately 2.5 mm. a year. Thus, we have a way of making an appraisal with this as a frame of reference. Comparing groups that had been treated by mandibular posturing devices with a computer-predicted

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pattern of growth (VTO) revealed, after 4 years, that mostly a change in the teeth was accomplished. In the Bimler sample, there was little difference between mandibular posturing and predicted growth of the face. Twenty-three g-year-old patients treated for 18 months with activators of the Harvold type demonstrated 25 percent improvement in growth. The corpus-to-condylar axis angle was not closing and thus appeared to grow as a Class III malocclusion. In another sample of 33 bionator cases (15 males, 18 females) the facial axis had not changed. The angle basion-nasion-point A was reduced a little with 1 to 2 mm. of additional growth in the mandible. Thirty-seven cases treated with the Frankel appliance in the United States indicated less growth in the mandible than would have been predicted for the normal when placed in the RMDS computer. The basion-nasion-point A angle did not change, and the lower incisors moved forward slightly. There were width increases in patients under 12 years of age, but no more than shown by Ricketts with quad-helix or headgear treatment and not full banding. Other cases treated by Frankel and evaluated by Ricketts indicated that there may have been a temporary alteration in mandibular growth. Cephalometrically, they did take advantage of growth in this way. W e can alter skeletal parts. Alteration appears permanent in the maxilla. W e seem to make a temporary alteration in the mandible through coupling of the teeth, creating function. Over a period of time, genetics, the natural forces of gravity, and the pattern of the entire structure of the head and neck apparatus seem to reestablish and take over. Mandibular growth seemsto be averaged out until any previous apparent stimulation is not significant, according to our analysis. A paper on “Muscular Involvement in Facial Deformities” was developed by W illiam J. Gonyea. Muscle is intimately involved in the growth process of bone. Very little, however, is known about how muscle influences abnormal bone growth. Vertical maxillary dysplasia or long-face syndrome is characterized by a considerably longer lower face than midface. Gonyea investigated the potential role of musculature in the development of this variation. A biopsy specimen was taken from the masseter muscle on its deep anterior surface and treated histochemically. Two types of motor units are found which include the alpha motor neuron, its axons, and all the fibers that axon innervates. Motor units have different functions. They go from low-velocity motor units to fast-twitch motor units. Slow motor units do

not produce as much tension as the fast motor units and are reasonably fatigue resistant (high in mitochondrial activity and oxidative enzyme activity). The fast motor unit is very powerful but low in oxidative capability and is fatigued within 2 minutes in its ability to produce tension or movement. Intermediate fast-twitch fibers are more fatigue resistant, although they contract reasonably rapidly. The deep masseter normally shows two fiber types dominated by the fast glycolytic or 2B fibers; 50 to 60% are fast twitch. Type 1, or slow twitch, fibers constitute 32 to 40%. There is a small representation of intermediate fibers (4 to 5%). This is reasonably consistent. Functional characteristics of these motor units are that Type 1 is fatigue-resistant with very little tension and is probably used in postural or tonic activity. The muscle is producing less tension and less EMG activity in the long-face patient compared to the control. Histologically, we see that the slow fibers are considerably larger than the fast fibers. There is considerable reduction of fast-twitch fibers compared to control tissue and a considerable increase in the number of intermediate fibers. This indicates that there are structural differences in the protein of ATPase in sensitivity rather than to different pH ranges. Looking at the oxidative enzyme, we see that the 2B or fast fibers are lighter than the slow fibers, as we would expect. When an otherwise healthy muscle shows some pathosis, we see a dramatic shift from Type 2B fibers being dominant toward the slow-twitch and/or intermediate fiber, Type 2A, dominating. In our healthy muscle of the long face, we always see a shift to the slow-contracting fibers. What does this mean? Is there a possibility, then, that during growth the low tension produced by this muscle with an excess of Type 1 fibers is not stabilizing the growth process? The maxilla then continues to grow downward. The reverse of that would be a muscle that has too many fast-twitch fibers and produces too much tension or the short-face syndrome. Or, are all these simply manifestations of a bone-growth problem? W e do not know. The evidence so far indicates that the proportion of Type 1 and Type 2 fibers is genetically determined. However, this may simply be induced by the stretching. The muscle may, in fact, be outside its physiologic limits and may have an inability to adapt. W e cannot ignore the muscle. The muscle here may be involved in the abnormal growth process. Wayne G. Watson (This synopsis will be continued in the May issue)