THE CAUSE OF TMJ DISORDERS

The search for the cause of TMJ disorders has been a wild ride, leaving a wake of confusion that still plagues the field, because dental researchers have never understood the central role of the bite in the pathological process. The bite affects jaw muscle function and facial growth, which shapes the TMJs, and an unstable or displaced bite can prevent healthy harmonious facial growth, but dentists do not intervene. As a result, many people suffer from ongoing jaw system strains that continue during the slow facial growth of adulthood.

TMJ disorders were first discovered almost a century ago in denture patients who had lost vertical dimension (the height of the bite platform), and they are still blamed on loss of vertical dimension by some dentists. Later, when people with good natural teeth and tall bite platforms came to dominate the TMJ disorder population, the search shifted to other bite related features such as condyle position and jaw muscle imbalances. Then, after dentists were unable to connect the cause to bite features, the search for the cause broadened to include ligament laxity (Ehlers-Danlos),  whiplash, cervical spine injuries, accumulated microtraumatic TMJ injuries from bruxism, central nervous system stress, personal habits such as fingernail biting, and various systemic conditions. Many still blame nocturnal bruxism, although studies show it is not more frequent in TMJ disorder patients. Others blame old injuries, such as forceps delivery or childhood trauma, although the TMJs have not even formed in young children and have remarkable healing abilities.  The latest fad is to blame a tight lingual frenum, although there is no scientific or even common sense support for that explanation in the vast majority of cases (# 6 in the MISCONCEPTIONS file under the tab TMJ DISORDERS). 

THE MULTI-FACTORIAL THEORY - Looking at the varied types of events that precede the onset of symptoms led some researchers in the 1980's to conclude that the cause must involve some combination of predisposing, initiating, and perpetuating factors. They focused on psychosocial conditions such as stress and coping strategies, and they changed the name of the condition to temporomandibular disorder (TMD) in order to move the focus away from the TMJ itself and onto contributing factors. They advise patients to not expect to be cured by treatment, but to know that their symptoms can be effectively managed by addressing their multiple causal factors, which unfortunately also creates multiple expenses.

However, other researchers pointed out that the stress and anxiety associated with TMJ disorders are just as likely to be a result of the disorder as a cause of it. In fact, all pain conditions involving skeletal muscles have a biopsychosocial component, because the state of the brain affects muscle tonus. Also, symptoms caused by an ongoing mechanical strain depend on the ability of the patient to adapt to the strain, which depends on emotional factors; but that does not make the emotional factors causes of the condition.

TMJ disorders do not have some unique relationship with psychosocial factors, and effectively treating them does not require eliminating all the multiple potential contributing causal factors; it requires relieving the mechanical strain at the root of the problem, which requires understanding the role of the bite. When dentists are polled about the cause of TMJ problems, about half of them still point to the bite, even though authorities tell them that there is no evidence for their belief and it is simply the result of confirmation bias. The problem is that dentists can't show evidence that bites play an important role, because they can't collect evidence about something they can't measure, and they have never had a way to measure the functional characteristics of bites. One of the goals of this website is to explain the central role of the bite, in three long files under the FOR DOCTORS tab.  

THE STRAINED FACIAL GROWTH PATTERN - The many causes cited to support the multi-factorial theory are actually just triggering events, like the straw that broke the camel's back or the weakest link, because the jaw system was functioning under progressive mechanical strain due to a strained growth pattern, until something pushed the system beyond the point where its adaptive mechanisms could prevent tissue damage. The cause of the strain was not that tough bagel you tried to chew or the time you twisted your neck putting on a tight sweater, it was a dysharmony among the components of the jaw system due to a facial growth pattern that continually produces mechanical strains between jawbones that can never achieve a perfect fit, because they lack the regulation that is normally provided by healthy strong jaw muscles.

ADULT FACIAL GROWTH - The strained jawbone growth pattern at the root of the problem slows down about ninety percent after the second decade, but then continues slowly throughout adulthood. Such slow growth is difficult to prove; and it represents an incovenient truth for orthodontists, so many of them attribute it to remodeling. However, remodeling is adaptive. It occurs constantly in all bones and joints as they fine tune their shapes to fit small changes in weight bearing and functional forces. In contrast, adult jawbone growth is progressive, - it follows the same general pattern of previous facial growth, with additional increases in vertical height at about the same rate our teeth used to wear down.

Adult facial growth was programmed into our genetics to reduce airway flow resistance with age to compensate for the loss of muscle strength that occurs during adulthood at about 5% per decade so the respiratory muscles don't have to keep increasing their effort when people get old. Adult facial growth was also needed to maintain the stability of bite table so that facial height remained stable in proportion to postural height no matter how fast the teeth wore down. Our ancestors who used strong bite forces and wore their teeth down quickly stimulated more rapid jawbone growth to compensate for it.

Today the growth patterns that cause most TMJ disorders are the long narrow midface and the backwardly displaced mandible. These growth patterns were never seen in human skeletal remains before the last couple of centuries, and they have arisen at the same time as TMJ disorders, because they are caused by weak jaw muscles that fail to stimulate horizontal jawbone growth and by restrictive bites that inhibit horizontal jawbone growth and redirect that growth vertically. Usually the mandible rotates down and back, crowding the tongue against the pharyngeal wall and restricting the space available for airway passage in the oropharynx. Very similar growth patterns have been induced experimentally in animals simply by softening their diets or damaging their jaw muscles, and they are seen in humans with muscle disease or jaw muscle damage. 

THE FEMALE FACIAL GROWTH PATTERN - The link between jaw muscle weakness and restricted horizontal jawbone growth explains why females after puberty are the primary victims of TMJ disorders; because their jaw muscles do not develop as rapidly as male jaw muscles during and after the post-pubertal growth spurt, causing their mandibles to rotate more down and back (clockwise), while male mandibles rotate more counter-clockwise. This difference in the growth pattern of the male and female mandibles can be seen in Behrents' comparison of the average male and female adult growth patterns, seen below. Solid line is earlier, dotted line is later. The mandible rotates counterclockwise in adult males and clockwise in adult females. The Y-axis (N-S-Gn) decreases in males and does not change in females. The mandibular plane angle (S-N/Go-Gn) decreases in males and increases in females. Males also had greater posterior vertical development of the mandible than females. 

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THE TROUBLE WITH OVERBITE - is that it can restrict the horizontal facial growth that is needed to accomodate adequate airway passage, but dentists do not recognize that restriction, because dental schools teach that overbite is simply a feature of a normal bite. Dentists even learn that the front teeth should contact when the back teeth contact in CR, which is not a feature of natural bites and simply reflects the fact that dentistry has never understood the bite. In natural human dentitions that have achieved functional capacity, the front teeth do not contact in overbite until the mandible shifts anteriorly, like a ball in a socket. The role of the anterior overbite is to keep the dental arches in close proximity during childhood to prevent the early fast forward growth of the mandible from pushing the lower teeth past the upper teeth. Then, in natural denitions, the overbite gradually disappears as mandibular advancement drives the mandibular anterior teeth gradually up the palatal surfaces of the maxillary anterior teeth like a ball riding up one side of a socket and onto their incisal edges, where they form a stable anterior bracing platform for the mandible that is generally continuous with the stable posterior bracing platform (rather than a dual bite). Today, our overbites persist throughout adulthood despite the continual slow growth of the basal bones. The pressure on the overbite from mandibular advancement can splay the upper front teeth or crowd the lower front teeth. In the presence of weak jaw muscles, it is more likely to redirect mandibular growth down and back, carrying the mandibular corpus into the space needed for the pharyngeal airway and reflexively producing forward head posture to compensate for the mandibular intrusion by using the posterior neck muscles to tip the head back, which pulls the mandible forward relative to the pharynx and thereby preserves the airway space. Strong jaw closing muscles can prevent the downward component of rotation, but the mandible usually stays locked back posteriorly behind a steep anterior overbite, restricting the space available for airway passage in the nasopharynx.

1. Behrents RG. Growth in the aging craniofacial skeleton. Ann Arbor: University of Michigan center for Human Growth and Development, 1985.

2. Al-Taai N, Persson M, Ransjo M, et al. Craniofacial changes from 13 to 62 years of age. Eur J Orthod March 2022