Treatment of Disturbance of Functional Occlusion Syndrome (DOFOS™) Introduction
There is increasing recognition in the medical and dental arenas, that temporomandibular related head and neck pain can occur without outward signs of a problematic joint (Brossman, 1995). It is often instigated by occlussal alteration from tooth loss, fillings, crowns (Brossman, 1995), orthodontic work or wisdom tooth eruption or extraction. The temporomandibular joint (TMJ) consists of three bones: the mandible and the left and right temporal bones of the skull (Brossman, 1995). The mandible is the only major bone with the same functional anatomic joint at both ends (Brossman, 1995b), with both joints functioning as a single bilateral anatomic unit. This is referred to as the craniomandibular articulation (Brossman, 1995b). Although still synovial joints, specific features distinguish the temporomandibular joints from joints of other bones. While other synovial joints are covered by hyaline cartilage, the articular surfaces of the TMJ are covered with fibro- cartilage (Brossman, 1995b). Within the bilateral articular capsules, a fibro-cartilage articular disk separates the joint into two separate compartments with differing functions. The TMJ is classified as a ginglymoarthrodial joint, both hinge and sliding, since the superior joint compartment performs the sliding type arthrodial translating motion, while the inferior joint compartment functions in the hinge like ginglymus motion (Brossman, 1995b). The TMJ capsule does not entirely encase the joint. It is incomplete in the anterior aspect, allowing for condylar motion in an anterior direction during wider opening movement and excursive motion (Brossman, 1995b). The mandible, as mesodermal bone structure, is unique in having teeth, ectodermal derivatives, incorporated into its structure (Brossman, 1995b). During normal functional movements, the mandibular portion of the craniomandibular articulation comes to an unyielding end point of closure, the dentition of the maxillary arch (Brossman, 1995b). Although the fibro-cartilage disk between the condyle and the fossa is not meant to dislodge during movement, including forwards, backwards, and laterally, an estimated 50% of the population have one or both articular disks displaced anteriorly in the joint, resulting from a malocclusion (Brossman, 1995). When the condyles slide down the articular eminence, and forwards in their sockets, this motion of translation allows the lateral movement of mastication (Brossman, 1995). Functional mastication involves not only the masseter but the temporalis. It moves the mandible laterally, grinding food between molars (Newbury, 1994b). Humans shear their omnivorous diet, using cuspids and incisors, and grind with molars, requiring a joint that can move laterally as well as in an opening and closing (Brossman, 1995) motion. Humans' pattern of chewing, mostly a grinding action, relies on molar teeth. In the ideal occlusion, food is ground without direct molar to molar contact, except in a straight line closure (Brossman, 1995). The grinding action, without actual physical contact of the molars, results from the interaction of the cuspid teeth during the chewing cycle (Brossman, 1995). Ideal functional occlusions disconnect the molar areas almost immediately after the mandible begins to reverse its lateral excursion (Brossman, 1995). Functional mandibular movements should be painless, allowing adequate mastication (Kreutziger, 1994), and ensure that the molar teeth withstand a great deal of pressure, by directing it straight down to the roots. With a malocclusion, upper and lower teeth lock when clenched and will not allow lateral excursion. The mandible is then forced to perform excessive up and down movements (Newbury, 1994b). Since the muscles of mastication exert as much as 300 pounds of pressure per square inch (Myo-Tronics, undated), damage (Newbury, 1994b) occurs rapidly. Over time, force applied from the side have a damaging effect on the molar teeth. The neurologic feedback mechanism, attached to the chewing apparatus is designed to prevent unwanted molar contacts (Brossman, 1995). This is achieved by the pterygoid group muscles instigating automatic small adjustments in mandible position during chewing. Malocclusions require this protective mechanism to be in use constantly during mastication, overworking the positional adjusters. They become hypertonic and cause discomfort (Brossman, 1995). These muscles, which also attach to the condyle and fibro-cartilage disk are a prime cause of dislocation of the disc (Brossman, 1995). If these muscles are never able to recuperate, they gradually draw the disc forward in the fossa (Brossman, 1995), stretching the ligamentous connection of the discs in the posterior section of the articulation. The disc then easily assumes an anterior dislocation (Brossman, 1995) (see appendix A). Once the pterygoid group are entrapped in this self perpetuating cycle of muscle spasm, the larger muscles of mastication become affected, and muscle bracing, an exaggerated form of a protective mechanism, ensues (Brossman, 1995). This in turn activates the Dural Defense System (Ferreri, undated), a survival reflex found in the muscles of the TMJ to protect the Central Nervous System and its skeletal protectors, the skull and spinal cord. When the jaw is braced, the muscles of mastication, lock the sutures of the skull together and increase tension in the cranial dura by flexing the sphenoid (Ferreri, undated). Through reactivity with the pelvic structure (Ferreri, undated), the coccyx and sacrum are pulled forward, increasing tension in the spinal dura and stabilizing the spinal cord. Although this ensures resilience in times of danger, when sustained indefinitely, it results in systemic dysfunction and pain. This cycle is initiated every time the maloccluded teeth are in contact, which apart from eating, includes the two thousand times a day that the average person swallows (Myo-Tronics, undated and Atkinson, 1995). Every function of the TMJ has a dramatic reaction in some bodily location (Ferreri, undated), with the feeding function of this structure specifically relating to the neurological control of the digestive mechanism (Ferreri, undated). Other patho-physiologic factors associated with TMJ dysfunction are metabolic, neurologic, vascular, hormonal, and nutritional. It can be a predisposing, initiating or perpetuating (Brossman, 1995b) factor in many disorders. To date, no single treatment or combination of procedures has been effective in randomised controlled trials (Albino, J. et al. 1996). Well documented disastrous consequences of TMJ surgery (Albino, J. et al. 1996) led to conclusions that non surgical intervention is preferable (Carr, 1995). The present study will focus on an innovative approach to TMJ dysfunction, proven to be successful in clinical practise (Newbury, 1994). Disturbance of functional occlusion syndrome (DOFOS), is an acronym coined to describe a systemic condition caused by prolonged muscle damage and cramp, originating at the jaw and progressing to involve the rest of the body, causing damage, pain and instability (Newbury, undated). DOFOS begins with teeth that grow, or are orthodontically arranged, so that during mastication, when upper and lower teeth contact, they interlock excessively, preventing normal mandibular movement, and imposing dysfunctional patterns of use (see appendices B and C). This causes the muscles of mastication, including the temporalis, to spasm and cramp (see appendix D). Headaches are the primary symptom of temporalis spasm and associated tissue damage that initiates all the systemic effects (Newbury, 1991). If the cramp is so severe that it occludes blood vessels, it results in the throbbing pain characteristic of migraine (Newbury, 1994b). Headaches are usually used as an indicator of the severity of the condition and as reflection of treatment progress (Newbury, 1994b). The strong upward pull of the temporalis damages soft and hard tissue, including the condyles, fibro-cartilage disk and lateral pterygoids muscles (Newbury, 1991). Cramped head muscles initiate a wave of muscle damage and cramp to the neck and shoulders (Newbury, undated) and initiate the cascade of muscular compensation and dysfunction (Newbury, undated) throughout the body (see appendices E and F). The skeletal framework is compromised by hyper tonicity of muscles at rest (Atkinson, 1995), resulting in poor posture. The stiffness in muscles and joints locks in the dysfunctional position (Newbury, undated). This scenario can occur whenever the arrangement of teeth alters (Newbury, 1994b). If this occurs during growth, the cramped muscles pull the mandible upwards, closing the gap, and not allowing the teeth to grow to their full height. This results in an over-bite which entrenches the locked position as muscle fibres remain shortened (Newbury, 1994). The aim of treatment is to allow the muscles of mastication to function without impediment, by correcting the malocclusion. To accomplish this, the mandible must be lowered to allow the temporalis to work at its correct length. The mandible then functions correctly, and the muscle damage resolves (Newbury, undated). This is achieved by attaching a thin sheet of plastic, to a custom made dental appliance. This unlocks the teeth, allowing lateral movement during mastication (see appendix G). The thickness of the plastic is increased as the temporalis' cramp resolves, and the shortened vertical fibres increase. The plastic thickness is cautiously increased in response to symptoms (Newbury, 1994b). If increased too rapidly, the excessive stretch will cause pain (Newbury, 1994) and damage. Once an improvement is noted, pain may recur if the muscles movement is obstructed. This may be caused by the biting surface becoming rough due to dents. Lower teeth will fall an lock into these crevices, preventing the sliding movement (Newbury, 1994). Dents are filled in at regular intervals. A decrease in dents indicates improvement in muscular condition. The appliance allows short lower back to erupt to full height, eliminating the over-bite and gradient in tooth height (Newbury, 1994). It allows lower back teeth to grow, because its biting surface holds the mandible down and keeps back teeth apart, allowing lower molars to grow to normal height (Newbury, 1994). When they contact upper back teeth, they lock and the muscles cramp again so the back teeth are conservatively trimmed and shaped to prevent locking (Newbury, 1994). The purpose of the present study was to monitor the first phase of DOFOS treatment. It was predicted that although the frequency and intensity of symptoms, particularly headaches, would increase prior to each adjustment, as treatment progressed, they would diminish. Method
An upper Bio DOFOS appliance was worn by the subject for the study's duration (see appendix H). Although various types of DOFOS appliances are available, the present study will only monitor the effects of an upper Bio DOFOS appliance (BDA), which the subject required. During BDA adjustment sessions, dental drills, equipment and occlussal equilibration carbon paper were used. The subject completed one page from a bound journal of questionnaires for each day of the treatment phase (see supplementary volume for raw data). The questionnaire, based on Newbury's diagnostic check list (1991) (see appendix I), devised for this study (see appendix J) , used a linear pain scale (Brossman, 1995) to assess levels of comfort in each symptom. The symptoms monitored were based on the subject's pathologies. SPSS for Windows and DeltaGraph for Windows were used to analyze the data and present the results graphically. ProcedureImpressions were taken by the dentist and an upper BDA appliance was constructed by a technician. It was fitted to the subject. The subject recorded her symptom severity daily. Variables that may affect each symptom were also recorded but not analysed in this study. The appliance was adjusted at intervals determined by treatment protocol and adapted to the subject's responses. Results The actual data is presented as a stacked bar graph in figure 1. The eight adjustments are marked with an asterisk. The same data, with each group's degree of comfort adjusted to the same scale, is presented in figure 2 as a line graph. It clearly displays that the standard deviation of comfort levels decreased during the study, while the mean remained fairly constant. The mean degree of comfort per symptom group is displayed in figure 3, as a bar graph. It shows that somatic comfort levels were higher than comfort levels for other group, and that somatic comfort levels soared as soon as treatment commenced. Figure 1 ![]() Figure 2 ![]() Figure 3 ![]() The correlation coefficients displayed in table 1, suggest that the somatic comfort level largely determined the overall degree of comfort. Table 1 Correlation between Degree of Total Comfort and Symptom Group Degree of Comfort
Figure 4 is a bar graph of somatic comfort levels throughout the study. It shows that each symptom in this group improved dramatically initially and continued to improve, except for symptoms involving areas from the neck down. Comfort levels for these areas declined as treatment progressed. Figure 4 ![]() The correlation coefficients displayed in table 2 revealed that headache comfort level scores largely determined the overall somatic comfort level. Table 2 Correlation between Degree of Total Somatic Comfort and Individual Somatic Symptom Degree of Comfort
Figure 5 displays comfort levels regarding headaches during the study. It reveals that adjustments, (indicated by an asterisk), that were done when comfort levels were low resulted in an immediate, dramatic improvement. This improvement did not occur when adjustments were made when comfort levels were already moderate or high. This graph also indicates that headache comfort levels consistently remained at a higher level towards the study's conclusion. Figure 5 ![]() Discussion As predicted, there was a response of general increased comfort levels. The sharp decline in intensity and frequency of headaches during DOFOS treatment supports previous research (Newbury, 1994). As expected there was a decline in comfort, especially regarding headaches, before each adjustment was due. The low comfort levels experienced after some adjustments is explained by the comparatively large changes in the plastic layer of the BDA following the adjustment which would understandably tax the somatosensory nerves (Lewis, 1997) in this region, resulting in discomfort. The following improvement was attributed to the gradual lengthening of the vertical muscle fibres as intended. An unexpected occurrence towards the end of the study was the eruption of molar teeth, usually expected only in advanced stages of treatment. In this instance, the subject became aware of teeth clashing as the jaw moved (Newbury, 1994). This required shaping of the biting surface of the teeth and an increase in the plastic sheet of the UBDA. Comfort levels plummeted during this time of major adjustment. Although extraneous variables were recorded, it was beyond the scope of this study to incorporate them into analysis. Consideration of other factors which may impinge or enhance treatment need to be evaluated. Self report measures provide useful insight over an extended period, however reliance on them has been regarded as a weakness by previous researchers. Incorporating measures of physiological changes such as electromyogram (EMG), hormone levels and blood glucose levels would be a useful adjunct. Replication of the present study, monitoring more subjects, throughout the phases of DOFOS treatment would allow a more thorough analysis of results. Extending the period of observation to completion of treatment, and beyond, with follow ups at certain intervals, would allow an analysis of the long term effects of DOFOS intervention. Monitoring many patients would contribute knowledge about the effects of treatment on diverse symptoms. In cross sectional epidemiological studies, no gender differences in TMJ susceptibility were found, but in clinical practise the greater number of patients are women (Albino, J. et al. 1996). It has been suggested that females are more vulnerable (Brossman, 1995), due to oestrogen's role in muscle function (Newbury, 1994). Lack of oestrogen in women with advanced DOFOS is a suspected potentiator of muscle cramp (Newbury, 1994b).Clinical research has revealed that menstrual and fertility disorders show a dramatic improvement following correction of DOFOS. This would be a prime area for controlled investigation. Little research has been conducted into ethnic or racial variation in susceptibility to TMJ dysfunction (Albino, J. et al. 1996). It has been suggested that the prevalence of TMJ disorders in western cultures is due to incomplete development of the mandibular structure, due to lack of use in childhood. Researchers studying traditional diets of indigenous cultures, find comparatively large mandibles. The very action of joint movement, necessary with a fibrous diet, appears to be critical for normal joint physiology. Motion, the purpose of any joint, is necessary for its nutrition and lubrication (Brossman, 1995b). Genetic, biochemic and nutritional factors that predispose certain individuals to malocclussal pathologies would provide useful preventative information. Application of the results of the present study are limited by its design, however these findings indicate that the DOFOS protocol has merit in solving the complex riddle of TMJ dysfunction. Acknowledgement Thank you to Dr Renton Newbury and staff for their support. References Albino, J.E.N., et al. (1996). Management of temporomandibular
disorders. National Institute of Health. [Web Site].
Atkinson, M. (1995). TMJ dysfunction, assessment and treatment. Unpublished lecture, Heartwood Institute, Garberville, California, U.S.A. Brody, L.R. (1985). Gender differences in emotional development: A review of theories and research. Journal of Personality, 53:2, 102-141. Brossman, R.E. (1995). Headache Pain, Trigger Point Pain, and
Temporomandibular Joint Dysfunction.
Brossman, R.E. (1995b). Some of The Finer Points About Temporomandibular Joint Anatomy and Physiology.
Carr, S. (1995). Conquering the Pain of TMJ. Business West, 11:1, 24. Ferreri, C. (undated). The Temporomandibular Joint. Unpublished. Neural Organisation Technique. Kreutziger, K. (1994). Surgical management of the temporomandibulalar joint in resection of regional tumors. Southern Medical Journal, 87:1, 215. Lewis, D. (1997). The Tao of Natural Breathing. San Francisco: Mountain Wind Publishing. New Information about Headaches. (undated). Myo-Tronics Research, Inc. Seattle, Washington, U.S.A. Newbury, R.D. (undated). Do you have DOFOS. Dandenong: DOFOS Australia. Newbury, R.D. (1991). DOFOS Check List. Dandenong: DOFOS International. Newbury, R.D. (1994). The Upper BDA. Dandenong: DOFOS Pty Ltd. Newbury, R.D. (1994b). Understanding Your Treatment. Dandenong: DOFOS Pty Ltd. Newbury, R.D. (undated). What you should know about DOFOS. Dandenong: DOFOS Australia. Appendix A: Ideal occlusion and malocclusion ![]() Ideal occlusion Teeth fit together in a comfortable relation ship. There is no need for the jaw to adjust to avoid pain and muscular discomfort. ![]() Malocclusion In order to achieve closure and avoid pain, the jaw shifts to accommodate the teeth, causing stress in and around the temporomandibular joints and muscles. From Denar Corporation. (1982). Appendix B: Normal anti-DOFOS teeth relationships ![]() From DOFOS Australia. (undated). Do you have DOFOS? Appendix C: Incorrect bite ![]() From DOFOS Australia. (undated). Do you have DOFOS? Appendix D: Temporalis muscle attached to mandible ![]() From Newbury, R.D. (undated). What you should know about DOFOS. Appendix E: Tooth-muscle chart no picture available From Eversaul, G. (undated). Dental Kinesiology. Appendix F: Organs and acupuncture meridians reflexively associated with tooth position ![]() From Callinan, P. (1994) Osteitis: A hidden dental health hazard. Australian WellBeing Magazine, 54, 46-48. Appendix G: Chewing action ![]() From DOFOS Pty. Ltd. (1994). Understanding your treatment. Appendix H: Upper BioDOFOS appliance ![]() From DOFOS Pty. Ltd. (1994). The Upper BDA. Appendix I: DOFOS check list, used for clinical diagnostic purposes no picture available From Newbury, R. (1991). DOFOS Check list user's guide. Appendix J: Questionnaire developed for the present study ![]() please click to return to the table of contents Copyright © 1997 DOFOS™ is a trademark of DOFOS Pty. Ltd. |