Within dentistry, the terms function, dysfunction and parafunction have slowly begun to lose their critical individual meaning, thereby potentially sacrificing the significance of their considerable and diagnostically relevant differences.
Oftentimes, a presentation of data regarding the patient’s dysfunction (electronic measurements, varying types of imaging, and complex descriptions of signs and symptoms), collected while the patient is sitting in the practitioner’s office, is mistakenly presented as the etiological diagnosis, when it is parafunction that is the perpetuating or causative source of the patient’s condition. The resulting treatment plan then revolves around management, rather than prevention. Recognizing and acknowledging the differences between function, dysfunction and parafunction can make for a more accurate assessment of the etiology of a patient’s condition. The resulting diagnostically driven treatment plan then addresses the causative or perpetuating source of the patient’s condition, parafunction. Treatment can then become an active prevention, rather than ongoing management1.
NORMAL MANDIBULAR FUNCTION In order to fully appreciate parafunction (and then provide a treatment to prevent it), a clear understanding of the normal, functional role of the masticatory musculature is essential. Normal mandibular function is best understood by observing it in its dynamic components: rest position, opening, and closing.
When not chewing, swallowing or talking, the mandible resides at its “rest position”. This position occurs in the absence of voluntary trigeminally innervated elevator musculature activity2. Without active elevation, the opposing maxillary and mandibular teeth are not occluding. As the pulling force of gravity attempts to depress (open) the mandible, the stretching of the sympathetically innervated spindle fibers3 (which reside within the elevator musculature, primarily the temporalis) elicits a reflexive tension to the intrafusal fibers of the spindles, providing a degree of elevation, thereby maintaining a constant “freeway space” (of approximately 2mm) between the opposing molar teeth. As the involuntary sympathetic tone varies (due to a stressful physical or emotional situation, for example), so does the tension within the spindle fibers, thereby altering their length4. This results in dynamic alterations of the freeway space5. Sudden bursts of sympathetic activity recruit trigeminal activity, producing varying durations and intensities of teeth clenching.
Functional depression (opening) and elevation (closing)
Starting from the rest position, functional mandibular depression (opening) results from the simultaneous contraction of two muscle groups that insert on opposite ends of the mandible: the lateral pterygoids and the digastrics. As the digastrics pull the chin “down and backward”, the lateral pterygoids (at the opposite end of the mandible) pull the condyles “forward”, with the overall effect being the rotational opening (depression) of the mandible.
Functional elevation (closing) ensues as the temporalis, masseters and medial pteryoids contract while the digastrics and inferior bellies of the lateral pterygoids relax. During functional mastication, the resistance of the bolus of food elicits a proportional intensity of contraction of the elevators during elevation. Depending on the purpose of the elevation, the lateral pterygoids may maintain a degree of tension, thereby influencing the mandible’s path of closure and initial tooth contacts.
For example, if the purpose of closure is incising with the anterior teeth, the lateral pterygoids maintain a degree of tension during the elevation, depending on the required degree of protrusion. Incising food with the anterior teeth obligates the lateral pterygoid to remain actively tensed during the closing stroke, maintaining the condyle in an advanced and anteriorly braced posture against the eminence of the temporal bone. The reduced efficiency of the resulting level arm, combined with reflexive suppression of elevator intensity by anterior tooth contacts, provides a governing limit of the intensity of the elevation during incising. If mastication with the molars is intended, then the lateral pterygoids will relax during the elevation.
Adaptive capacity of the lateral pterygoid
Occasionally, there exists a premature contact during mastication (teeth typically don’t physically occlude with each other during mastication, as the bolus of food is residing within the freeway space). In the event this tooth contact interferes with the efficiency of the chewing strokes (a sudden and forceful tooth contact during mastication will instantly cease the elevation and trigger a reflexive opening), a lateral pterygoid will maintain a degree of functional tension during the closing (elevation) of the mandible (Fig. 1). This natural and protective “programming” capacity of the lateral pterygoid serves to alter the condyle’s position during mastication, thereby allowing the avoidance of the interference6.
The functional elevation stroke of mastication (or swallowing) is complete upon the occluding (or near approximation) of the teeth, which normally remain “in occlusion” for only .2 seconds7. The occluding of the teeth triggers the functional reflexive contraction activity of the depressors (re-opening) and the relaxation of the elevators.
Parafunction of the masticatory system occurs following normal mandibular elevation, with the elevators maintaining tension, continuing with the purposeless occluding of the teeth. The intensity of the continued occluding elevation dictates the degree of resistance encountered by the reflexive discluding attempts of the lateral pteryoids. This muscular conflict allows for potentially destructive acts that vary in frequency (the number of times the act occurs), duration (how long each act lasts), intensity (the degree of contraction of the conflicting musculature), and the position of the mandible during the act. Of these four variables (frequency, duration, intensity and position), the intensity of the act is the most influential of the potential resulting signs and symptoms. Significant parafunction occurs almost exclusively during sleep, where intensity of elevation can exceed voluntary maximum8, thereby disguising its activity from the patient. While potentially able to adversely affect the patient’s quality of life, the intensity and nature of the parafunction is reflected in the clinical dysfunctional presentation, making its diagnosis illusive to the practitioner1.
Parafunctional excursive clenching
One example of a parafunctional act is excursive clenching (Fig. 2). Following the occluding of the posterior teeth, the elevator muscular continues to maintain mandibular elevation, but in a asymmetrical manner, allowing one lateral pterygoid to advance its condyle with less resistance than the other.
Unlike protrusive clenching, where both condyles are braced and loaded in their naturally intended anterior/superior orientation, in excursive clenching, one condyle advances translates more than the other, as the opposite (contralateral) side’s restrictive elevation is more stabilizing. As the ipsilateral condyle translates, medial strain increases on the condyle, as it is pulled toward the pterygoid plate by its respective lateral pterygoid. Whereas the articular disc that resides between the condyle and the temporal eminence is designed to be “loaded” in an anterior/superior direction (as in normal anterior incising), the medial pull of the lateral pterygoid during excursive clenching can exert an excessive strain and pathologic load to the condyle and disc. Excursive (or unilateral) clenching can cause and/or perpetuate internal derangements and is commonly recognized as a “temporomandibular (joint) disorder”.
Chief complaints including combinations of headache, migraine, face pain, jaw pain and/or restriction, neck pain and/or restriction, and sinus pain and/or pressure may present a seemingly complex and multifactorial diagnosis, when in reality they may all be a direct result of varying degrees and orientations of nocturnal masticatory parafunction. The cornerstone of successful patient care is a diagnostically driven therapeutic protocol. Often times, the dysfunctional presenting signs and symptoms are mistaken for the etiologic source of the patient’s complaints1.
The therapeutic goal then becomes directed at addressing the parafunction by altering one or more of its four components: intensity, duration, frequency, and position. Medications that alter sleep patterns (rarely will any of the medications used in pain management not alter sleep patterns) can significantly and unpredictably influence the duration and frequency of parafunctional activity (although unfortunately with the occasional undesired effect of increasing the activity).
Traditional dental therapy has been directed at addressing the interferences within the scheme of the occluding teeth, and/or the position of the mandibular condyle during the parafunctional event, oftentimes with the assumption that these are the causative or perpetuating etiological factors of the parafunction.
Identification and removal of the occluding interferences that influence parafunctional activity can decrease the resistance to the lateral pterygoids’ attempts at translating the condyle(s). The resulting reduction or elimination of the parafunctional strain and load to the TM joint may reduce or eliminate the associated dysfunctional signs and symptoms. If these clinical signs and symptoms had been the patient’s chief complaint, the practitioner concludes the occluding scheme had been the etiologic source of the parafunction, rather than irritating and influential resistance to parafunction.
The mandibular condyles’ position is constantly changing, corresponding to the nature of the activity. For example, the clinical incisal height of the initial occluding teeth upon mandibular elevation dictates the anterior/posterior and inferior/superior condylar orientation, and creates the vertical dimension of occlusion (VDO). The mandible’s natural vertical dimension of rest (VDR) occurs with the mandible slightly depressed from the VDO, providing for approximately 2mm of freeway space. Therapeutically increasing the freeway space (the VDR) through TENSing (transcutaneous electrical nervous stimulation) of the spindle fibers within the elevating musculature, allows the dental practitioner to proportionately increase of the corresponding VDO (by various means of providing removable or permanent dental prosthetics), while still allowing for a natural degree of freeway space. This mandibular advancement or “anterior repositioning” of the VDO can be beneficial, for example, for those patients whose articular disc is permanently displaced anterior to the condyle in their presenting VDO and may also beneficially alter the nature of the parafunctional activity, thereby reducing or eliminating the associated dysfunctional signs and symptoms.
A therapy used to reduce the intensity of the elevation during the parafunctional act utilizes an anterior removable prosthetic during sleep, which replicates the effect of incisor-only contacts. Providing contacts exclusively to the incisors minimizes the intensity of the elevator musculature, while maintaining the condyles in their naturally braced positions against the temporal eminence9. The available resistance encountered by the lateral pterygoids during parafunction is significantly reduced, while the device is customized to create a minimal inter-occlusal distance, thereby minimizing the extent of condylar translation and resultant strain during excursive and protrusive parafunction. The suppression of the intensity of the parafunctional clenching and resultant minimization of joint strain and load reduces or eliminates the associated dysfunctional signs and symptoms, thereby allowing the practitioner to proceed with restorative dentistry. Although a pre-fabricated modified-anterior-midline-point-stop device that the practitioner retrofits and customizes has been approved for marketing by the United States Food and Drug Administration for the prevention of medically diagnosed migraine pain and for the prevention of temporomandibular disorders10, a practitioner can easily fabricate such a device in his own lab.
Parafunction of the masticatory system occurs following closure and during intense occluding of the teeth (of which considerable significance occurs during sleep), while dysfunction is a clinical observation of the results of parafunction. Dysfunctional signs and symptoms are often misdiagnosed as the causative and/or perpetuating components of the patient’s presenting condition. The nocturnal suppression of the intensity of the parafunctional clenching and minimization of joint strain and load reduces or eliminates the associated dysfunctional signs and symptoms, thereby allowing the practitioner to proceed with restorative dentistry.
Prior to developing the therapeutic protocol for the NTI, a modified-anterior-midline-point-stop device, James P. Boyd, DDS had suffered from daily all-day headaches, frequent migraine attacks and chronic TMJ pain with dysfunction for 12 years. Dr. Boyd practices in Solana Beach, California, lectures frequently throughout the country, and provides educational content on the NTI website for dentists: www.HeadacheHope.com. Dr. Boyd can be contacted on the Dentaltown.com message boards or at Jim@DrJimBoyd.com.
Barry Glassman, DMD maintains a private practice in Allentown, PA, with a concentration on chronic pain management and temporomandibular joint dysfunction. He is a Diplomate of the American Academy of Craniofacial Pain, a Diplomate of the International College of Craniomandibular Orthopedics, and a Diplomate of the American Academy of Pain Management. He is on staff at the Lehigh Valley Hospital where he serves as a resident instructor of Craniofacial Pain and Dysfunction. Dr. Glassman serves as a guest lecturer throughout the year and hosts in-house courses on both Pain Management and Sleep Disorders. He teaches a three-day course on TMD and Parafunctional Control with the co-author, Dr. Jim Boyd, as well as a three-day intensive TMD Seminars with Dr. Jack Haden. Dr. Glassman can be reached at DrBGlass@aol.com.
1. Okeson, J Management of TM Disorders and Occlusion 2nd ed., Mosby, p. 157-160
2. ORGANIZATION AND FUNCTION OF JAW MUSCLES, UCLA School of Dentisty www.dent.ucla.edu/sod/courses/OB422c/LECT10.doc
3. Muscle Spindle and Stretch Reflexes, Kings College of London http://www.kcl.ac.uk/teares/gktvc/vc/lt/mspindle/
4. Needle electromyographic evaluation of trigger point response to a psychological stressor” McNulty, Hubbard, Gervitz, Berkoff. Psychophysiology 31, 1994
5. Dawson, Evaluation, Diagnosis, and Treatment of Occlusal Problems. 2nd ed. Mosby, p.59
6. Dawson, Evaluation, Diagnosis, and Treatment of Occlusal Problems. 2nd ed. Mosby, p.25
7. Gibbs CG, et al: Occlusal forces during chewing and swallowing as measured by sound transmission. J Pros Dent 46:443, 1981
8. Bruxing patterns in man during sleep, J Oral Rehabil, 11(2):123-7 1984 Mar
9. Dawson Evaluation, Diagnosis, and Treatment of Occlusal Problems. 2nd ed. Mosby, p280
10. NTI Tension Suppression System, www.nti-tss.com