Chapter 5

CHAPTER 5) EFFECTS OF STRAINED CRANIOFACIAL GROWTH

REDUCED MAXILLARY EXPANSION

The reduced expansion of the upper jawbone produces a reduction in the cross-sectional area of the nasal airway, which triggers compensations that affect mandibular posture and thereby also facial growth by the light steady forces of postural tonus.  Blocking the nasal airway in monkeys produces lowered jaw posture and reshaping of the tongue to form an oral airway passage.  Similar airway protective reflexes shape craniofacial growth in humans. One researcher concluded, "When we examine cephalometric landmarks in individuals affected by mongolism and achondroplasia, we see that respiratory function has been protected by different kinds of facial adaptation in each group.  The adaptive changes in mongoloids have been described earlier as very localized effects on parts of the skull that spare the respiratory passages but reduce the size of the olfactory and masticatory components.  In achondroplastics nasal airway volume is protected in spite of the mid-face deficiency and the increased cranial base flexure by an adaptive counter-clockwise rotation of the palatal plane.  The biologic problem of respiratory survival is solved by a shortened palate in one group and by downward or counter-clockwise palatal tipping in the other."  Blocking the nasal airway in a child causes a change in the direction of facial growth downward and backward, as can be seen in the serial cephalograms below.

 

POSTERIOR POSITION OF THE MANDIBULAR CORPUS

The redirection of the growth of the mandibular corpus more downward and backward has shifted it into the space needed for the pharyngeal airway, which evokes a reflex reaction in the postural muscles, which also affects craniofacial growth, because light steady forces, like the steady forces of postural tonus, shape bones.  The pharyngeal airway is bounded in front and on both sides by the mandible and in back by the cervical spine.  To maintain adequate airway passage through it, neuromuscular reflexes control the resting tensions of all the muscle of the area in the service of airway preservation.  These airway protective reflexes controlling the jaw muscles (especially the superior lateral pterygoids, the genioglossus, and the geniohyoids) keep the mandible protruded as far as needed to permit breathing.   After orthognathic surgery to retrude the front of the mandible for esthetic reasons, muscle resting postures still maintain a constant minimal distance between the back of the hyoid bone and the posterior pharyngeal wall.  In some instances, the base of the tongue actually moves forward as the front of the mandible is moved backward.  Muscular adaptations occur all the way down to the level of the clavicle.

ADAPTIVE TONGUE POSTURES

The tongue will acquire whatever shape and posture it needs to maintain a patent airway.  In monkeys with blocked airways, it responds by resting very low in the mouth to maintain an oral airway passage.  In modern humans with narrow palates or strained bites, it often acquires a resting posture interposed between the teeth in order to provide a cushioned platform against which the mandible can rest while maintaining a patent airway.  

CHANGE IN ORBITAL SHAPE

The longer and narrower orbits make the eyeballs also longer and narrower.  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 longer narrower eyeballs could be responsible for the epidemic of myopia in modern societies.  In almost all animals which use vision, a process called emmetropization shapes the eyeball 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.  However in humans this emmetropization process slows at about age 6.  After that age, emmetropization may not be able to keep compensating for the rapid facial growth of 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 increasing in severity at the end of the second decade when the period of rapid facial growth stops. Similarly to the increase in facial length causing myopia, the increase in asymmetry and irregularity in facial growth could be responsible for the rise of astigmatism and other irregularities of the shape of the eyeball which also develop in concert with myopia during the period of rapid facial growth.

FORWARD HEAD POSTURE

As the average posture of the mandibular corpus progressively shifts down and back, the average posture of the head progressively shifts forward. Forward posture of the head and backward posture of the mandible are highly correlated in population studies.  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 prevent the mandible from shifting as far forward as the head.¹³⁴   Backward mandibular posture can cause forward head posture by evoking adaptations to protect the airway.  The mandible surrounds the pharynx on three sides, and the cervical spine borders its fourth.  Shifting the mandible 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 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 responsive 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 seen in the increased variability of head posture in the blind, and its power to alter muscle resting postures can be seen in its ability to bend the whole cranium in bipedal mice and also to produce extreme head extension in people with palpebral ptosis (eyelid droop).  As a result of these righting reflexes, the head can only extend by simultaneously translating forward, as illustrated below.  

TMJ DISORDER SYMPTOMS

The misfit between the upper and lower jawbones can produce a variety of symptoms in the teeth that most directly accomodate the strain, especially in steeply interdigitated teeth that cannot easily undergo even tiny shifting in their occlusal relationships.

However, strained jawbone growth does 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.  As a result of the important role of adaptation in TMJ disorders, anything that diminishes adaptive capacity (such as stress) can increase symptoms, and anything that enhances adaptive capacity (including nutritional support, relaxation, aerobic exercise, etc,) can eliminate symptoms. Better enabling the patient to adapt to a strained jaw system can relieve the effects of the strain without ever eliminating the strain. 

LOSS OF ADAPTIVE CAPACITY

Unfortunately, the same loss of jaw muscle strength and narrowing of the mandibular range of motion that have caused dysfunctional facial growth in the last couple of centuries have also caused a coincident loss of adaptive capacity. In the articular areas, loss of weeping circulation leads to a thinning of the condylar cartilage ⁴²  and atrophic degenerative changes characterized by reduced proteoglycan content and alteration of proteoglycan structure^43-44.  A loss of the rhythmic compressive loading across the facial 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 

In the mandibular joints, diminished strength, range and variability of the functional movements of the mandible has caused a decrease in weeping circulation that may limit the potential for remodeling activity.  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 have enough variability and range of motion to provide accessory circulation throughout the periodontal ligament spaces during chewing.   

 THE ROLE OF STRESS

Stress diminishes adaptive capacity, because it increases background tonus in all of the body's muscles.  If one group of muscles is already operating at bordeline resting circulatory capacity, even a slight elevation of its resting tension can cause it to become symptomatic by lowering resting circulation below a threshold level.  Because the jaw closing muscles dwarf the jaw opening muscles, increased stress alters mandibular posture by holding it further closed at rest.    

CHANGES WITH AGE

As a product of the interaction between two variables that change with age, (adaptation and continuous facial growth); the natural course of a TMJ disorder shows age related trends.   Facial growth continually produces mechanical stresses and strains which must be accomodated by adaptation mechanisms, and adaptation is continually trying to catch up with the effects of the dysfunctional facial growth.  The rate at which adaptation wins that race determines the subsequent symptomatology.

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 in the teenage years, especially in post-pubescent females.  After puberty, female growth patterns and male growth patterns diverge, with females developing more of the tendency toward backward facial rotation, narrow midfaces, and retrusive mandibles.

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 distinct facial growth patterns that are more likely than others to lead to TMJ disorders, the occurrence of various symptoms fluctuates a lot in this rapidly growing population.  In any group of teenagers, there will be a significant percentage who will report that they are currently suffering from TMJ disorder symptoms, but it may be different ones who are suffering in different years.

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 growth and other adaptive capabilities may slow even more.  The adaptive systems are constantly trying to adapt to stresses and strains which are constantly being created by the slow dysfunctional 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. Eventually the soft tissues of the articular eminence thicken to provide cushioning and adaptation of the retrodiskal tissues creates a pseudo-disk that can restore functional capacity and reduce or eliminate symptoms, but the internally deranged TMJ remains more vulnerable to injury than a normal TMJ.

The jaw muscles become involved, because muscles are responding organs.  In response to an inflamed joint, they automatically acquire a state best described as protective bracing. Reflex protective bracing 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.  

This protective bracing state was designed by evolution to help us cope with acute conditions.   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.

MIDLIFE

At midlife and beyond, the symptoms dissipate due to a decrease in muscle reactivity. Arthrokinetic reflexes play key roles in maintaining the cycles of pain and dysfunction (tissue damage and muscles tensions) that often perpetuate TMJ disorders.  With age these reflexes become less easily triggered and their muscle tightening becomes less intense.  As a result, while signs of TMJ disorders such as joints noises and degenerative changes on imaging usually increase in severity, symptoms of TMJ disorders usually disappear during the same time period.  The body may have been designed to accept some arthritic degeneration in old age. The TMJ disorder symptoms that occasionally arise in midlife are usually brief and less myogenous than the symptoms found in younger people.  

ELDERLY

In the elderly, although the TMJs keep undergoing more arthritic damage every year as seen on imaging like X-rays or MRI, TMJ disorder symptoms disappear. They may have difficulty with chewing due to a bite that is less than ideal or does not even fit the mandibular movements determined by the TMJs.  They may report neurologic symptoms such as tics, neuralgias, and orofacial dyskinesia and also otic symptoms such as tinnitus and hearing loss that remain following earlier injury.  However, most of the symptoms just involve a misfit between the stable central bracing positions of the bite and the TMJs, the dental joints and the temporomandibular joints, and they are easily resolved by bite adjustment.  

 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.