Occlusion in OBE

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The Relationship Between Occlusionand TMD: An Evidence-Based DiscussionHenry A. Gremillion, DDS, MAGD

From the Department of Orthodontics and the Parker E. Mahan Facial Pain Center, University of FloridaCollege of Dentistry, Gainesville, FL

The form, function, and pathofunction of the dynamicmasticatory system comprises one of the most fascinating,

basic, and important areas of study in dentistry. Todayshealth care professional is faced with the stark reality that themost common reason patients seek medical or dental care inthe United States is due to pain or dysfunction. Pain in theorofacial region is a frequent occurrence in the generalpopulation. Lipton et als1 study of 45,711 householdsrevealed that 22% of the US population experienced orofacialpain on more than one occasion in a 6-month period.Certainly it comes as no surprise that the most commonlyexperienced orofacial pain is odontogenic in nature. Howev-er, non-odontogenic orofacial pain such as temporomandib-ular disorder (TMD) is also common. TMD has been definedas BA collective term referring to a number of clinicalproblems involving the masticatory musculature, the tempo-romandibular joint(s), and associated structures or both[(p. 116).2 Recent studies indicate the prevalence of TMD-re-lated pain to be 12%.3 It has been reported that 10 millionAmericans suffer from TMD-related complaints each year.4,5

Cardinal signs and symptoms of TMD are pain in the

temporomandibular region, limitation or disturbance in man-dibular movement and/or masticatory functional ability, andtemporomandibular joint sounds.6 Our current understandingof the complexity of innervation in the head and neck regionreveals the dynamic interaction between a number of cranialand cervical nerves to include the trigeminal system, which maycomplicate the evaluation of the orofacial pain patient. Thisshared neurologic circuitry may make the etiology of paindifficult to diagnose.7 Confusion with regard to diagnostic andclinical decision making is compounded by the fact that signsassociated with TMD occur quite commonly in the generalpopulation.Seventy-five percentof those evaluated in onestudy

exhibited at least 1 sign such as joint noise or palpationtenderness and33% of this nonpatient population exhibited atleast 1 symptom8 that would potentially prompt that individualto seek evaluation and care. Signs and symptoms in the generalpopulation have been found to occur in females only slightlymore frequently than males, at a ratio of approximately 2:1 ascontrasted to patient populationsthat are significantly biasedtoward the female population.9-13

Personal communication with the administrative staff of theNational Institute of Dental Research (NIDR) revealed that in1993 approximately one-third of its total funding for the studyof pain was allocated to TMD research. Since that timesubstantial monetary resources have been expended in aneffort to better understand TMD. Yet little consensus existswith regard to a universally accepted diagnostic classificationschema because most formats are based on signs andsymptoms rather than cause (etiology) and epidemiologicinformation.4,5 A suggested classification of myogenous andarthrogenous TMD may be found inFigure 1.

Few areas in dentistry exist in which there have beengreater debate and controversy than that related to TMDetiology. Heretofore, the diversity of opinion could be ex-plained by the fact that the following exists: (1) a lack ofscientifically derived evidence with regard to many areas inthis complex field; (2) significant clinical/research bias; (3)great dependence on anecdotal reports; and (4) lack of scien-tifically validated definitive cause-and-effect relationships.

There exists a functional homeostatic balance between thevarious components of the masticatory system including the

teeth, periodontium (hard and soft tissue supportingstructures), masticatory and cervical musculature, temporo-mandibular joint structures, and the psyche of eachindividual. This balance may be disrupted by a number offactors acting either alone or in combination resulting in theexpression of signs and symptoms associated with TMD.Basic science research has provided an enhanced under-standing of pathogenesis, those cellular events and reactionsand other pathologic mechanisms occurring in the develop-ment and maintenance or recurrence of TMD. Slavkin5

stated that, BUnderstanding these interrelationships shouldimprove how we promote health, reduce disease and enhance

diagnosis and treatment[ (p. 109). A model representingfactors that may compromise the adaptability of themasticatory system is represented inFigure 2.

One of the areas of greatest debate relates to the associationbetween occlusal factors as a causal role and TMD. Althoughocclusion has been recognized as an important etiologic orperpetuating cofactor, the degree to which it plays a role hasnot been definitively delineated. Few terms in dentistry areused in the broad context as is malocclusion. Malocclusion isdefined as Bany deviation from acceptable contact of opposingdentitions or any deviation from normal occlusion[(p. 82).14

This definition begs the question, BWhat is normal

occlusion?[An average of the results of 14 studies regarding

J Evid Base Dent Pract 2006;6:43-471532-3382/$35.002006 Elsevier Inc. All rights reserved.

doi:10.1016/j.jebdp.2005.12.014

ARE WE PRACTICINGACCORDING TO THEEVIDENCE?
http://dx.doi.org/10.1016/j.jebdp.2005.12.014http://dx.doi.org/10.1016/j.jebdp.2005.12.014


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the prevalence of malocclusion reveals that 42% of thepopulation represent a Class I malocclusion, 23% exhibit aClass II malocclusion, and 4% have a Class III malocclusion.15

Therefore, only 31% have what would be termed normalocclusion. One may ask whether or not these occlusal relation-ships are truly aberrant or are we simply looking as staticrelationships in a dynamic orthopedic system?

The clinician is faced with the daunting task of determin-ing on a case-specific basis whether occlusal factors are

related to each patients TMD symptoms. If a causal or

cofactor role is determined, the clinician must then decidewhat the optimum occlusal contact relationship should be forthe patient. The answers to these key questions are extremelyimportant in the development of a case-specific, evidence--

based treatment plan. Many different approaches, somereversible and some irreversible, have been advocated in thetreatment of TMD. Yet few validated outcomes have beenpresented in the scientific literature. Upon review of theavailable literature it is clear that there exists a dichotomy of

opinion related to occlusion as a causal factor of TMD. A

Myogenous TMD Arthrogenous TMD

Localized myalgia

Myositis

Myospasm

Myofascial pain

Contracture

myotatic

myofibrotic

Hypermobility

Developmental disorders

Autoimmune conditions

Inflammatory conditions (with or without

articular disc derangement)

capsulitis

synovitis

retrodiscitis

Articular disc derangement

Degenerative joint disease

Ankylosis

fibrous

boney

Fracture

Figure 1. Basic subclassification of myogenous and arthrogenous TMD.

JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE

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number of studies have suggested a positive association;

however, an equal number have found no or minimalassociation. For example, an association between open bite,posterior crossbite, and deep bite and the occurrence ofTMD has been reported.16 Additionally, a multiple logisticregression analysis to compute the odds ratio for 11 commonocclusal features for asymptomatic controls as related to 5TMD subgroups found several occlusal factors to demon-strate odds risk ratio of at least 2.17,18 Yet the authorssuggested that occlusal factors were related to TMD in only15% of cases. These occlusal features that were identified to

be potentially related include anterior open bite, overjetgreater than 6 mm, centric relation/intercuspal position

(CR/IP) slide greater than 4 mm, unilateral lingual crossbite,and 5 or more missing posterior teeth. Other occlusalschemes were not found to be statistically significant.

Leonardo da Vinci extolled the virtues of scientific studywhen he wrote, BAnyone who falls in love with practicewithout science is like a sailor on a ship without a compass ora sail; neither knows where he is heading[ (p. 69).Evidence-based dentistry is the rational integration ofsystematic assessments of clinically relevant scientific evi-dence relating to the patients oral and medical history andcondition with the dentists clinicalexpertise and the patientstreatment needs and preferences.19 In evidence-based practice

it is essential that the clinician/scientist identify the best

scientific evidence, develop clinical expertise, and considerthe patients circumstances. Turpin20 recently stated, BThepurpose of using the evidence-based approach is to close thegap between what is known and what is practiced and toimprove patient care based upon informed decision making(p. 1).[ It is well accepted that the hierarchy of what is

considered to be B

best evidence[

in descending order is thefollowing: (1) randomized controlled clinical trials; (2)nonrandomized controlled clinical trials; (3) cohort studies;(4) case-control studies; (5) crossover studies; (6) casestudies; (7) consensus of opinion of experts in the appropriatefields of research or clinical practice. Koh and Robinson21

completed a review of 660 randomized/quasi-randomizedstudies published between 1966 and 2002 that addressedocclusal therapy as a means of treating TMD. They foundonly 6 studies that met criteria for inclusion. The dataobtained from 392 patients in these trials indicated anabsence of evidence to definitively indicate that occlusaladjustment treats or prevents TMD. They emphasized thatfuture studies must use standardized diagnostic criteria andoutcome measures when evaluating TMD.

The conflicting information gleaned from the multitude ofstudies related to occlusion as a causal factor or use ofocclusal therapy as a means of treating TMD may not revealthe total story. It is mandatory that the clinician/scientistconsider the dynamic nature of the masticatory system. It has

been stated that proper occlusion of the dentition occurs in adynamic relationship with the oral and facial musculature,periodontium, supporting osseous framework, temporoman-dibular joints, and the enveloping neuromuscular system.22

While it may be said that the manner in which teeth fit is

important, what the individual does with his or her teeth maybe more important when discussed in the context ofrelationship with TMD.

The temporomandibular synovial system obeys the lawsof orthopedics as do other synovial systems. However, thisdynamic orthopedic masticatory system demonstrates anumber of unique features, including the following:

1. the right and left temporomandibular joints function asone unit held together by the dense cortical bone of themandible

2. the articulating surfaces of each TM joint are fibrocarti-laginous

3. the articular disc separates the temporomandibular jointinto 2 compartments allowing for complex movement

4. the temporomandibular joint is a ginglymoarthrodial(hinge-gliding) joint

5. this unique articulation has a rigid end point, contact ofthe teeth, where the greatest forces are generated

Dynamic occlusal function affects multiple interfaces, such as(1) tooth-to-tooth interface, (2) tooth/supporting structureinterface, (3) the TM joint interface, and (4) muscle activity(functional and parafunctional). Mechanical stresses at eachof these interfaces have been shown to be associated with a

potential compromise in the integrity of tissues. Additionally,

Anatomy Stress Nutrition

Trauma Gender

Pain Depression

Parafunction

Occlusion

Sleep disorders Posture

Homeostasis Pathology

Adaptive Capacity

Figure 2. Endogenous and exogenous factors that maydisrupt the dynamic equilibrium (adaptive capacity) ofthe masticatory system leading to the developmentand/or maintenance of temporomandibular disordersigns and symptoms.


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we must consider the various case-specific factors that mayaffect each persons adaptability, such as

variable directions of muscular loading forces selective action of multiple dental and articular constraints

influenced by:9

duration of load9 degree of load9 host resistance

Review of the literature regarding oral parafunction andTMD provides insight as to a potential relationship betweenwhat goes on at the tops of the teeth and the various interfacesof occlusion. Carlsson andcolleagues23 reported datacollectedin a 20-year longitudinal study. At baseline, 402 randomlyselected 7-, 11-, and 15-year-old subjects were evaluated forocclusal factors, oral parafunction, tooth wear, and TMD.Twenty years later, 320 subjects were assessed for the samevariables. Logistic regression indicated that childhood paraf-

unction (bruxism, tooth clenching, nocturnal grinding, andnail biting) were predictors of the same oral parafunction 20years later. They also reported that childhood parafunctionand an Angle Class II malocclusion were predictors of toothwear in adulthood. Magnusson et al24 reported that evaluationof this same study population at the 4-, 5-, 10-, and 20-yearmarks revealed significant correlation between bruxism andTMD symptoms. Another recent publication reported on theassociation between morphologic occlusion and functionalocclusal factors and TMD symptoms.25 In this study, 4310subjects were evaluated. No specific occlusal factor was foundto be significantly associated with TMD symptoms. However,

parafunction demonstrated a positive relationship to TMDsymptoms (odds ratio 3.4). A number of studies havesuggested that distalizing forces resulting from occlusalcontacts have the potential to cause TM joint internalderangement.26-29 Additionally, it is clear that degenerativetemporomandibular joint disease is the result of maladaptationto increased joint loading.30-33 An oxidative-stress mechanisminvolving free radicals and other chondrodestructive factorshas been recently been posited.32,33

Changes may also take place at the neuromuscularinterface. Isometric contraction such as that associated withclenching the teeth has specific local effects to includeincreased pressure within the muscle, obstruction of bloodflow, decreased oxygen saturation, decreased glycogensaturation, and impaired removal of catabolic by-products.Free radicals have been implicated in exercise-induced muscledamage.34 Muscle overuse and eccentric contractions have

been demonstrated to cause muscle fiber damage withassociated edema/effusion, which may last for up to 80days. However, pain does not parallel the effusion, generallyreaching peak levels 3 to 4 days posttrauma. A local release ofmediators substance P and calcitonin gene-related peptideinto the extracellular space may signal other cells (mast cells)to initiate humoral or cellular-based inflammation and set thestage for peripheral sensitization of nociceptors.

In conclusion, it is evident that the scientific literature hasnot convincingly demonstrated a definitive relationship

between static occlusal factors and TMD. TMD representsa multifaceted/multifactorial group of conditions that sharecommon signs and symptoms. Although a multitude offactors have been theorized to initiate TMD, there exist

individual variables that are unlikely to play a causal role.There are many theorized etiologic factors yet to bescientifically validated. The true determining factor(s) may

be related to the individuals host resistance/adaptivecapacity. If we are to take an evidence-based view ofocclusion and TMD we must be able to differentiate betweenan occlusal contact and an occlusal interference. It ismandatory that we recognize the potential destructive effectsof parafunction. We must also consider the cyclic nature ofTMD. Therefore, it may be more appropriate to view TMDcases in which occlusal function serves as a significant factorin TMD as a maladaptive occlusion. This term takes intoconsideration peripheral and central sensory and motorfactors involved in masticatory system pathofunction on acase-specific basis and is supported by the recognized effectsof mechanical stress on the stomatognathic system.

REFERENCES

1. Lipton JA, Ship JA, Larach-Robinson D. Estimated prevalence anddistribution of reported orofacial pain in the United States. J Am DentAssoc 1993;124:115-21.

2. Okeson JP, ed. Differential diagnosis and management considerations oftemporomandibular disorders. In: Orofacial pain: guidelines forassessment, diagnosis and management. Chicago: Quintessence Pub-lishing Co, Inc; 1996. p. 113-84.

3. Dworkin SF, Huggins KH, LeResche L, et al. Epidemiology of signs andsymptoms of temporomandibular disorders: clinical signs in cases andcontrols. J Am Dent Assoc 1990;120:273-81.

4. National Institute of Health Technology and Assessment Conference.Management of Temporomandibular Disorders. NIH Technol AssessStatement 1996 Apr 29- May-1;1-31. Bethesda, MD: NIH.

5. Slavkin HC. Lifetime of motion: temporomandibular joints. J Am DentAssoc 1996;127:1093-8.

6. McNeill C, ed. Introduction. In: Temporomandibular disorders:guidelines for classification, assessment, and management. 2nd ed.Chicago: Quintessence Publishing Co, Inc; 1993:11-18.

7. Sessle BJ, Hu JW, Amano N, et al. Convergence of cutaneous, toothpulp, visceral, neck and muscle afferents onto nociceptive andnonnocieptive neurons in trigeminal subnucleus caudalis (medullarydorsal horn) and its implications for referred pain. Pain 1986;27:219-35.

8. Rugh JD, Solberg WK. Oral health status in the United States. J DentEduc 1985;49:398-404.9. Schiffman E, Fricton JR. Epidemiology of TMJ and craniofacial pain.

Fricton JR, Kroening RJ, Hathaway KM, eds. TMJ and craniofacialpain: diagnosis and management. St. Louis: Ishiaku Euro AmericanPubl; 1988. p 110.

10. Agerberg G, Carlsson GE. Functional disorders of the masticatory system.I. Distribution of symptoms according to age and sex as judged frominvestigation by questionnaire. Acta Odontol Scand 1972;30:597-613.

11. Helkimo M. Studies on function and dysfunction of the masticatorysystem. I. An epidemiological investigation of symptoms of dysfunctionin Lapps in the North of Finland. Proc Finn Dent Soc 1974;70:37-49.

12. Glass EG, McGlynn FD, Glaros AG, et al. Prevalence of temporoman-dibular disorder symptoms in a major metropolitan area. J CraniomandPract 1993;11:217-20.


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