Chapter 5


The change to a more vertical, backwardly rotating, retrusive, narrow, and asymmetrical facial growth pattern and the diminution of some regulatory facial growth mechanisms do not necessarily cause symptoms.  Human facial growth is designed to maintain functional capacity in spite of a wide variety of genetically varied facial components and many different types of tooth and jaw injuries.  Symptoms only occur when adaptation to the dysfunctional facial growth pattern is unable to establish and maintain adequate functional harmony in the masticatory system. 


The disorder that comprises the symptoms that result from dysfunction of the masticatory system is best described as a functional disorder.   A functional disorder is a medical condition that impairs the normal function of a bodily process, but where the body looks normal under examination.  Unlike in a structural disorder or a psychosomatic disorder, a single physical cause of the symptoms often cannot be identified.  The mechanical stimuli produced by normal function evoke responses that are not conducive to health.  A variety of tissues may be affected.  Whatmore and Kohli describe how signaling errors can work to the detriment of the system.  Germs and injuries can have additional detrimental effects, and they often act as the straw that broke the camel's back.  

Unfortunately, in trying to establish a diagnosis, we too often blame the straw.  Dental researchers trying to determine the cause of symptoms in TMJ disorders compare subtle changes in anatomy between those who report symptoms and those who don't report symptoms.  In many of these cases, the differences between these two groups is not the particular type of facial growth strain but the diminished adaptive capacity in the symptomatic group.


Symptoms occur when adaptation fails to prevent damage to tissues.  Almost any tissues can be affected.  Usually the damage occurs in tissues that can be seen as a weak link, - an area that is particularly vulnerable to the effects of the dysfunction.  In the masticatory system, this most commonly includes the muscles, joints, or dentition.

Because 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.


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.  Many of the adaptive properties of the masticatory system rely at least partially the presence of strong rhythmic chewing forces to provide accessory circulation to the tissues undergoing adaptation.  The long lever arm formed by the mandible functioned much like a pump handle driven up against the skull thousands of times each day. In the vascular and metabolically active retrodiskal plexus, condylar movements acted like a piston to pump waste products from the synovial tissues into venous circulation while allowing ingress of fresh oxygen and nutrients between each pumping action. 41 In the midfacial buttresses supporting the articular areas, functional forces bent membrane bones rhythmically back and forth. In tendons and ligaments, functional forces provided rhythmic tugs that stimulated the periosteum.  

In the articular areas, long smooth chewing strokes with sufficient variability to provide alternate compression and release in all portions of the articular zone kept the avascular tissues supplied with oxygen and nutrients while helping them eliminate waste products by weeping circulation. Studies have shown that loss of weeping circulation due to insufficient jaw function leads to a thinning of the condylar cartilage 42, immobilizing a synovial joint produces atrophic degenerative changes in that joint characterized by reduced proteoglycan content and alteration of proteoglycan structure 43 44, and remobilizing an injured joint with continuous passive motion dramatically reduces the time needed for healing. 45  The loss of chewing forces in modern humans has very likely diminished some of that accessory circulation.

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 Sutures are important sources of adaptive growth, and functional forces maintain the adaptability of sutures by keeping them open and metabolically active. Ossification and closure of sutures deprives these areas of their adaptive potential. 

In the temporomandibular 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, diminished functional forces and occlusal wear have both limited the ability of opposing teeth to shift relative positions and thereby accommodate the diverse growth patterns in the upper and  jaws.  Opposing teeth with deeply interdigitating occlusal surfaces cannot shift relative to each other as easily as opposing teeth with rounded or flattened occlusal surfaces.  In addition, periodontium that receive inadequate functional forces may experience diminished accessory circulation by depriving them 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.  In healthy masticatory function, the teeth are loaded primarily in an axial direction, with a small and variable range of movement horizontally. During each loading event, some fluids in the direction of compression were forced through the bony socket out of the surrounding periodontal ligament space and into venous circulation, followed by a subsequent rebound of the tooth which brought in new fluids from arterial circulation. Diminished function is likely to diminish such accessory circulation, and diminished accessory circulation in turn is likely to limit the ability of the teeth to adaptively shift positions.   



Stress is an important source of diminished adaptive capacity.  For that reason, a stressful episode is a common trigger for TMJ disorder symptoms, and relaxation is frequently successful at eliminating the symptoms, at least temporarily.  Diminishing overall stress has been shown so effective at reducing symptoms that a few decades ago Laskin and other researchers concluded that stress was the primary cause of TMJ disorders.

 Stress also can trigger TMJ disorder symptoms by increasing the resting background tonus in the jaw muscles from a level at which they receive just enough resting circulation to a level at which they receive insufficient circulation to prevent cell damage.  Stress 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 in its resting tension can cause it to become symptomatic by lowering resting circulation in at least some areas below a threshold level.

Because of the mass of jaw closing muscles dwarfs the mass of jaw opening muscles, stress can alter mandibular posture by holding the mandible further closed at rest - sometimes so far that the teeth maintain contact.  In other parts of the body, stress does not alter the positions of bones, - it just holds them more tightly between equally strong muscles pulling in opposite directions.  However, the jaw muscles are not similarly balanced between openers and closers. Because the powerful jaw closing muscles are all vertically arranged and dwarf the jaw opening muscles, an increase in stress holds the mandible further closed.  


During the industrialization of our diet in the last couple of centuries, chronic stress has increased.  Evolution equipped our bodies with reflex responses to deal with acute stress.  When these reflex responses are triggered chronically, they are ineffective and often cause other health problems.    


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.


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.


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. In one study, Behrents found that, in post-pubescent facial growth, the mandible grows more retrognathically in females.   Relative to the rest of the cranium, the mandible grows straight downward in females, while it grows downward and forward in males, as shown in his illustration below.

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Another study found that 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

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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.

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A similar growth trend characterizes modern european faces (dashed lines) when compared to aborigine faces (solid lines) as shown in the figure on the right below; and also modern myotonic dystrophy patients (dashed lines) when compared to normals (solid lines) as shown on the left and in the center below.

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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.


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.


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.  


Finally, although their TMJs keep undergoing more arthritic damage every year as seen on imaging like X-rays or MRI, the TMJ disorder symptoms almost completely disappear in the elderly. They may have difficulty with mechanical operation of the joints, shifting of the bite, occasional pain, and some ear problems like dizziness or difficulty hearing, but those symptoms almost always just need minimal treatment to resolve.  There are also occasionally neurologic symptoms such as tics, neuralgias, and orofacial dyskinesia and also otic symptoms such as tinnitus and hearing loss.  In most cases, if dysfunction of the masticatory system is producing symptoms, the dysfunction involves unusual stressors such as extreme loss of vertical dimension in dentures or tooth loss that has completely eliminated the stability of the dental occlusion.  

The symptoms that are localized to the TMJs usually just involve a misfit between the stable central bracing positions of the dental occlusion and those of the TMJs.  The misfit can arise due to changes in the dental occlusion or by rapid degenerative remodeling in one or both joints.   The symptoms usually just involve inability to masticate effectively. 


Recent research has shown that, in some TMJ disorder patients, the state of neurotransmitters in the brain causes a hypersensitivity that can make even normal functional stimuli painful.  This condition of centrally caused hypersensitivity is usually associated with sleep disorders and depression as well.  Treatment that is solely directed at the peripheral condition (the TMJs or the jaw muscles) cannot relieve the symptoms unless that treatment is combined with more centrally directed treatment modalities such as antidepressants, cognitive behavioral therapy, or meditation.


When adaptation fails to protect all the tissues adequately, symptoms occur. The tissue damage  may occur in any component of the masticatory system, and careful analysis usually reveals some degree of response in the muscles, bones, joints, and dentition.  Clinicians describe a constellation of symptoms including dental problems, facial pain, headaches, dizziness, eustachian tube blockage, subjective hearing loss, postural strains, visual problems, and pain from muscles extending all over the body.  However, usually the one component which forms the weakest link in the chain undergoes most of the damage and produces the clinical symptoms.  The particular process which produces the damage in any one individual is variable and depends on many factors.  


Symptoms produced directly by the degenerative process in one or both TMJs go through stages of inflammation and adaptation.  The inflammation may be brief and clinically insignificant or may become chronic and persist for years.  Even if the inflammation persists for decades, eventually adaptation occurs. 


Many of the symptoms are produced by the tightening of the jaw muscles in response to inflammation in a TMJ.  Inflammation in any joint triggers reflex protective bracing in the muscles which cross that joint. Protective bracing involves decreased functional forces and increased resting tensions.  Reflex protective bracing was designed to protect acutely injured joints in evolution.  When increased resting tensions are maintained chronically, they cause an anatomical shortening of the muscle fibers known as contracture.  Contracture inhibits resting circulation and may cause build-up of waste products in little pockets known as trigger points.  Trigger points can cause pain in areas far from their location (referred pain).

Muscle reactivity seems to play a role in producing symptoms and maintaining the disorder associated with the jaw system.  The big jaw closing muscles are all oriented vertically, so increased resting tensions in the jaw closing muscles produced increased compressive force in the TMJs.  This increased compressive force can exacerbate the degenerative process in the TMJs, and the increased degeneration produces increased inflammation which then triggers more tightening of the jaw closing muscles, causing a vicious cycle of pain and dysfunction.




The narrowing of the sides of the midface and the increased protrusion of the center of the midface has affected the shapes acquired by the bony orbits and thereby also very likely the shapes of the eyeballs themselves.  The orbits are comprised on their lower and inner (medial) aspects by membrane bones of the midface and on their roofs by a plate of membrane bones that gets pushed forward by growth of the anterior part of the cranial base.  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 orbits which have been produced by the average change in facial shape 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.  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.  In myopic eyes, the growth in length of the eyeball far exceeds the growth in height and width of the eyeball.  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) At the end of the second decade, the development of myopia commonly stops when facial growth slows enough to allow emmetropization to compensate for any small subsequent changes in orbit shape. 

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 and rapid facial growth.



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.