Chapter 5
CHAPTER 5) EFFECTS OF ALTERED GROWTH
The altered modern craniofacial growth patterns have had surprisingly profound effects on a number of our modern health problems.
REDUCED NASAL AIRWAY PASSAGE
The reduced expansion of the upper jawbone reduces the cross-sectional area of the nasal airway, because the roof of the palate is the floor of the nose. Also, most modern palates are V-shaped instead of U-shaped, making the common location of the narrowing in the premolar area, just below the anterior portion of the nasal cavity, where nasal airway flow is most commonly restricted. The non-laminar nasal airway flow can cause downstream effects in the pharynx.
The restricted nasal airway flow triggers compensations to provide an oral airway passage. Experimentally blocked nasal airways in monkeys produce lowered jaw posture to allow an oral airway passage, making them grow long narrow faces. Naturally blocked nasal airways in humans evoke a similar reaction, but it also includes a backward component, because lowering the human mandible rotates it down and back around a center in the ramus, rather than at the condyles in monkeys, making humans with restricted nasal airways grow long narrow and retrusive faces. The effects of nasal blockage can be seen in the serial cephalograms below of a child with a permanently blocked nasal airway.
REDUCED PHARYNGEAL AIRWAY PASSAGE
The redirection of the mandibular corpus downward and backward, - whether from nasal airway obstruction, weak jaw closing muscles, or maxillo-mandibular synostosis - carries it into the area needed for airway passage through the lower oropharynx and hypopharyx. In people with stronger jaw muscles, the jaw closing muscle are able to prevent the backward component of the rotation, so the mandibular corpus is simply locked back posteriorly, shifting it into the upper oropharynx and nasopharynx. In both types of responses, the failure of the mandible to advance with age increases airway flow resistance with age, instead of reducing it to compensate for the weakening of the respiratory muscles, which also occurs with age.
FORWARD HEAD POSTURE
A common response to a growth pattern in which the mandible impinges on the pharyngeal airway is to extend the head to reopen the airway. Forward posture of the head and backward posture of the mandible are highly correlated in population studies.
The causal relationship can go both ways. Forward head posture can cause backward mandibular posture by stretching the muscles and fascia that attach the mandible to the clavicles and sternum and thereby preventing the mandible from shifting as far forward as the head.134 However, much more commonly, backward mandibular posture causes forward head posture by evoking airway protective adaptations to maintain an adequate gap between the hyoid bone and the cervical spine. The mandible and hyoid bone surround the pharynx on three sides, and the cervical spine borders its fourth. Shifting the mandible and the hyoid bone suspended from it backward toward the cervical spine diminishes the cross-sectional area of the pharyngeal airway, which reflexively causes the muscles of the area to tip the head back (extension) in order to rotate the mandibular corpus and hyoid bone upward and forward away from the cervical spine in order to restore the lost pharyngeal airway space. The increase in pharyngeal airway space produced by such head extension has been demonstrated with imaging. The ability of pharyngeal airway blockage to trigger head extension can be inferred from findings that most children with swollen tonsils have extended head posture which normalizes quickly after tonsillectomy.
However, the head cannot just tip back, because visual and vestibular reflexes (the so-called righting reflexes), keep it level with the horizon. The regulatory effect of the visual orientation reflex can be inferred from the significantly increased variability of head posture in the blind, and its power to alter muscle resting postures can be seen in its ability to produce extreme head extension in people with palpebral ptosis (eyelid droop) and dramatically in its ability to bend the whole cranium in bipedal mice. As a result of these righting reflexes, the head can only extend by simultaneously translating forward, as illustrated below.
ADAPTIVE TONGUE POSTURES
The tongue is the guardian of the airway, and it is composed of intertwined muscles from almost every direction that enable it to bend and twist in almost any direction. It will acquire whatever shape and posture it needs to maintain a patent pharyngeal airway. When the maxilla has not expanded enough for the upper teeth to fit around the tongue, the tongue cannot fit up in the palate, so it must find another place to rest while maintaining an open airway. Sometimes it acquires a resting posture interposed between the teeth. It can rest between the buccal segments, producing a scalloping of the sides of the tongue, or it can rest between the front teeth, causing an anterior open bite. In extreme conditions, like the facial growth in myotonic dystrophy illustrated in chapter 4, the adaptive tongue posture maintains the framework of the entire midface despite the inferior drag of a mandibular corpus pulling it very far down and back.
INCREASED MYOPIA
The longer and narrower facial growth makes our orbits grow longer and narrower, which could be responsible for the epidemic of myopia in modern societies. The intimate relationship between orbit shape and eyeball shape is suggested by the correlation between their relative volumes. One researcher commented, “Analysis of the orbit, eye, and spherical equivalent refractive error (SER) reveals a strong relationship between relative size of the eye within the orbit and the severity of myoptic refractive error. An orbit/eye ratio of 3 for females and 3.5 for males (or an eye that occupies approximately 34% and 29% of the orbit, respectively), designates a clear threshold at which myopia develops, and becomes progressively worse as the eye continues to occupy a greater proportion of the orbital cavity. These results indicate that relative size of the eye within the orbit is an important factor in the development of myopia, and suggests that individuals with large eyes in small orbits lack space for adequate development of ocular tissues, leading to compression and distortion of the lithesome globe within the confines of the orbital walls.”97
The timing of the development of myopia supports this explanation. In animals which use vision, a process called emmetropization shapes the orbit to fit the focal length of the lens by controlling growth of the dense connective tissue of the sclera enveloping the eyeball. Emmetropization matches the eye's optical power to its axial length so that the unaccommodated eye is focused at distance. Animal studies have shows that poor image quality on the retina can cause the scleral tissues to strengthen or weaken in an attempt to move the retina to the best location for a clear image. In humans, this emmetropization process slows at about age 6, after which it may not be able to keep compensating for the rapid facial growth and elongation of the orbits during adolescent and teenage years. Myopia develops due to the increase in prolate to oblate proportions of the eyeball that occur during the period from 7 to 19 years of age.98 It typically stops progressing at the end of the second decade when the period of rapid facial growth stops.
Even astigmatism could be a product of the altered facial growth patterns, because astigmatism is due to eyeballs that are not quite round, and the verticalization of the orbits occurs more laterally than medially, making our orbits look lower laterally and less rectangular compared with pre-industrial orbits when viewed from the front. The increase in asymmetry could also increase astigmatism.
LOSS OF FUNCTIONAL HARMONY
Without sufficient biting forces to coordinate the diverse growth processes of the craniofacial components, those components do not achieve the goodness of fit that keeps them healthy. The misfit can produce strains in the TMJs and between the teeth, especially steeply interdigitated teeth that cannot easily shift positions to accommodate the slightly divergent growth patterns in their basal bones. During the normal functional range of motion, the muscles are not firing in smooth patterns, but in engrams that protect the dentition; and support does not flow smoothly back and forth between the dentition and the TMJs, but jumps back and forth between the TMJs and the dentition in different mandibular positions, with the articular disks of the TMJs often shifting in irregular patterns to maintain supporting contact at the TMJs. Chewing forces are not distributed and absorbed evenly across the craniofacial framework. Some may even occur on the balancing side. The loss of functional harmony produces stresses and strains throughout the jaw system.
LOSS OF ADAPTIVE CAPACITY
The stresses and strains do not necessarily cause symptoms. Human facial growth is designed to maintain functional capacity in spite of a wide variety of facial growth patterns and even many different types of injuries. Symptoms only occur when adaptation fails, usually allowing damage to occur in whatever tissues form the weak link in the system. However, the same loss of jaw muscle strength that has altered and dysregulated facial growth in the last couple of centuries has also caused a loss of adaptive capacity. The system is no longer pumped regularly by strong smooth functional forces that drive out waste products.
In the TMJs, diminished strength and range of functional mandibular movements has diminished weeping circulation, which limits the potential for remodeling activity, causes thinning of the condylar cartilage,42 and leads to atrophic degenerative changes characterized by reduced proteoglycan content and alteration of proteoglycan structure.43-44 Monkeys raised on soft diets have less dense fibrous tissue in the articular zone of the temporomandibular joints. One researcher points out, "Experimental studies in mice, rats, rabbits, and non-human primates have shown that mechanical loads are vital for maintaining normal growth, morphology, and function of the secondary cartilage of the temporomandibular joint... In vitro studies confirm that normal mechanical loading stimulates cell division, matrix synthesis, and enzyme activity in the tissues of the TMJ."
In the dentition, the diminished pumping of the teeth limits their ability to shift relative positions and thereby accommodate the diverse growth patterns in the upper and jaws. The periodontal tissues that receive inadequate functional forces get deprived of the rhythmically alternating compressions and releases that provide accessory circulation throughout the periodontal ligament spaces during chewing.
Surrounding the upper jawbone, loss of the rhythmic compressive loading across the circum-maxillary sutures has decreased suture widths and increased suture ossification. Similar effects have been demonstrated experimentally by gluing sutures together, pinning them together with metal plates, or softening the diet.146
TMJ DISORDERS
When symptoms result from the stresses and strains due to the loss of functional harmony, those symptoms comprise what has come to be know as a TMJ disorder. As a product of the interaction between two variables that change with age, (adaptation and strains produced by dysharmonious growth); the natural course of a TMJ disorder shows age related trends.
CHILDREN
There are few signs or symptoms of TMJ disorders during childhood, when tremendous adaptive capacity prevents damage to tissues. Even in the presence of injuries or genetic defects that cause extreme structural abnormalities, the tissues grow in a manner that prevents localized damage. The signs and symptoms that occasionally appear are usually fleeting and seem to affect boys and girls about equally.
TEENS
Symptoms generally begin to appear after puberty, especially in females, when female growth patterns and male growth patterns diverge, with females developing more of the tendency toward backward facial rotation, as seen below.
The same growth trend towards mandibular retrognathia, on average, characterizes teens who develop TMJ disorder signs and symptoms (dotted line) compared with normals (solid line) on the left below, teens who show evidence of degenerative osseous remodeling of one or both TMJs (dotted line) compared with normals (solid line) in the middle illustration below, and also the one of two identical twins who developed TMJ disorder symptoms (dotted line) compared to her sister (solid line) on the right below.147
The same retrognathic growth tendency can be seen in profile photographs of the two identical twins whose X-ray tracings are seen in the right side illustration above.
While there are some facial growth patterns that are more likely than others to lead to TMJ disorders, the occurrence of symptoms fluctuates a lot in this rapidly growing population. In any group of teenagers, some will report symptoms one year, and a partly different group will report symptoms the next year.
EARLY ADULTHOOD
Distinct groups of chronic TMJ disorder patients appear after the second decade, primarily in women. Facial growth slows at this age to adult levels, but adaptive capacities may slow even more. The adaptive systems are constantly trying to adapt to stresses and strains which are constantly being created by the slow strained facial growth pattern that continues through most of adulthood. Women continue to grow more retrognathically than men, and women continue to represent the vast majority of TMD disorder patients.
Most TMJ disorder patients initially develop symptoms as a result of the dislocation of the articular disk from its normal intra-articular position in at least one TMJ and the subsequent bruising of the vascular retrodiskal tissues which got pulled into the joint space following the disk. The loss of the disk from the articular zone deprives the involved TMJ of cushioning and lubrication, making it susceptible to damage by triggering events such as minor trauma, a period of increased central nervous system stress, a long dental appointment, or destabilization of the bite. Even normal jaw function can damage the vulnerable retrodiskal tissues.
The jaw muscles become involved, because muscles are responding organs. In response to an inflamed joint, they acquire a state of reflex protective bracing, which changes jaw muscle behavior in three ways. 1) It causes increased resting tension, because the muscles hold themselves tightly at rest as if they are constantly on guard. 2) It causes decreased functional tensions, because the muscles fire weakly during function as if they are afraid of damaging the articular structures. 3) It causes overlap of firing activity (co-contraction) of jaw opening and closing muscles because the muscles work against each other in order to more tightly control mandibular movements.
Protective bracing was designed by evolution to help protect acutely injured joints. When maintained chronically, it can contribute to self-sustaining cycles of tissue damage and muscle tension. Over time, muscles that are held tight often undergo contracture and develop trigger points. Thus, many of the symptoms found in TMJ disorders at this stage are most directly produced by the muscles reacting to the joint conditions.
Over time, these TMJs heal naturally. Eventually the soft tissues of the articular eminence thicken to provide cushioning and adaptation of the retrodiskal tissues creates a pseudo-disk that restores functional capacity and eliminate symptoms. The healing process may take hours or years. It almost always occurs by middle age.
MIDLIFE
At midlife and beyond, the symptoms dissipate due to a decrease in muscle reactivity. Arthrokinetic reflexes play a key role in maintaining the cycles of pain and dysfunction (tissue damage and muscles tensions) that perpetuate TMJ disorders. The joint damage triggers muscle tightening, which causes more joint damage. With advancing age, and these reflexes become less easily triggered and their muscle tightening becomes less intense; because the TMJs were designed to accept some arthritic degeneration in old age. As a result, while TMJ joint noises and degenerative changes on imaging increase in severity, the symptoms "burn out". Older people may have difficulty chewing due to articular components that don't fit together well or jaw muscle tension due to an unstable bite, but they rarely have inflamed TMJs or acute symptoms.
PREVENTION
Preventing these problems requires overseeing and controlling the craniofacial growth process to ensure sufficient horizontal growth to maintain adequate tongue and airway space. In people with relatively weak jaw muscles, it does not require developing strong jaw muscles like our ancestors, but it requires preventing the mandible from rotating too far down and back. In people with relatively strong jaw muscles, it may require altering the contours of the bite table to distribute the forces from bruxism evenly around the dentition.
FOOTNOTES:
146 Katsaros C, Diliaridis S, Berg R. Functional influence on sutural growth. A morphometric study of the anterior facial skeleton of the growing rat. Eur J Orthod 1994;16:353-360.
147 Dibbets J M H, Van Der Weele L, Uildriks AK. Symptoms of TMJ dysfunction: Indicators of growth patterns? J Pedodontics 1985;9:265-284.