ARE WE PRACTICING ACCORDING
The Relationship Between Occlusion
and TMD: An Evidence-Based Discussion
Henry A. Gremillion, DDS, MAGD
From the Department of Orthodontics and the Parker E. Mahan Facial Pain Center, University of Florida
College of Dentistry, Gainesville, FL
The form, function, and pathofunction of the dynamic
masticatory system comprises one of the most fascinating,
basic, and important areas of study in dentistry. Today’s
health care professional is faced with the stark reality that the
most common reason patients seek medical or dental care in
the United States is due to pain or dysfunction. Pain in the
orofacial region is a frequent occurrence in the general
population. Lipton et al’s1 study of 45,711 households
revealed that 22% of the US population experienced orofacial
pain on more than one occasion in a 6-month period.
Certainly it comes as no surprise that the most commonly
experienced orofacial pain is odontogenic in nature. Howev-
er, non-odontogenic orofacial pain such as temporomandib-
ular disorder (TMD) is also common. TMD has been defined
as BA collective term referring to a number of clinical
problems 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 million
Americans 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, and
temporomandibular joint sounds.6 Our current understanding
of the complexity of innervation in the head and neck region
reveals the dynamic interaction between a number of cranial
and cervical nerves to include the trigeminal system, which may
complicate the evaluation of the orofacial pain patient. This
shared neurologic circuitry may make the etiology of pain
difficult to diagnose.7 Confusion with regard to diagnostic and
clinical decision making is compounded by the fact that signs
associated with TMD occur quite commonly in the general
population. Seventy-five percent of those evaluated in one study
exhibited at least 1 sign such as joint noise or palpation
tenderness and 33% of this nonpatient population exhibited at
least 1 symptom8 that would potentially prompt that individual
to seek evaluation and care. Signs and symptoms in the general
population have been found to occur in females only slightly
more frequently than males, at a ratio of approximately 2:1 as
contrasted to patient populations that are significantly biased
toward the female population.9-13
J Evid Base Dent Pract 2006;6:43-47
1532-3382/$35.00
 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.jebdp.2005.12.014
TO THE EVIDENCE?
Personal communication with the administrative staff of the
National Institute of Dental Research (NIDR) revealed that in
1993 approximately one-third of its total funding for the study
of pain was allocated to TMD research. Since that time
substantial monetary resources have been expended in an
effort to better understand TMD. Yet little consensus exists
with regard to a universally accepted diagnostic classification
schema because most formats are based on signs and
symptoms rather than cause (etiology) and epidemiologic
information.4,5 A suggested classification of myogenous and
arthrogenous TMD may be found in Figure 1.
Few areas in dentistry exist in which there have been
greater debate and controversy than that related to TMD
etiology. Heretofore, the diversity of opinion could be ex-
plained by the fact that the following exists: (1) a lack of
scientifically derived evidence with regard to many areas in
this 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 the
various components of the masticatory system including the
teeth, periodontium (hard and soft tissue supporting
structures), masticatory and cervical musculature, temporo-
mandibular joint structures, and the psyche of each
individual. This balance may be disrupted by a number of
factors acting either alone or in combination resulting in the
expression of signs and symptoms associated with TMD.
Basic science research has provided an enhanced under-
standing of pathogenesis, those cellular events and reactions
and other pathologic mechanisms occurring in the develop-
ment and maintenance or recurrence of TMD. Slavkin5
stated that, BUnderstanding these interrelationships should
improve how we promote health, reduce disease and enhance
diagnosis and treatment[ (p. 109). A model representing
factors that may compromise the adaptability of the
masticatory system is represented in Figure 2.
One of the areas of greatest debate relates to the association
between occlusal factors as a causal role and TMD. Although
occlusion has been recognized as an important etiologic or
perpetuating cofactor, the degree to which it plays a role has
not been definitively delineated. Few terms in dentistry are
used in the broad context as is malocclusion. Malocclusion is
defined as Bany deviation from acceptable contact of opposing
dentitions 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
 JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE

Myogenous TMD Arthrogenous TMD

Localized myalgia Hypermobility

Myositis Developmental disorders

Myospasm Autoimmune conditions

Myofascial pain Inflammatory conditions (with or without

Contracture articular disc derangement)

myotatic capsulitis

myofibrotic synovitis

retrodiscitis

Articular disc derangement

Degenerative joint disease

Ankylosis

fibrous

boney

Fracture

Figure 1. Basic subclassification of myogenous and arthrogenous TMD.

the prevalence of malocclusion reveals that 42% of the
population represent a Class I malocclusion, 23% exhibit a
Class II malocclusion, and 4% have a Class III malocclusion.15
Therefore, only 31% have what would be termed normal
occlusion. One may ask whether or not these occlusal relation-
ships are truly aberrant or are we simply looking as static
relationships 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 patient’s TMD symptoms. If a causal or
44 Gremillion
cofactor role is determined, the clinician must then decide
what the optimum occlusal contact relationship should be for
the patient. The answers to these key questions are extremely
important in the development of a case-specific, evidence--
based treatment plan. Many different approaches, some
reversible and some irreversible, have been advocated in the
treatment of TMD. Yet few validated outcomes have been
presented in the scientific literature. Upon review of the
available literature it is clear that there exists a dichotomy of
opinion related to occlusion as a causal factor of TMD. A
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JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
Anatomy Stress Nutrition
Parafunction Trauma Gender
Occlusion Pain Depression
Sleep disorders Posture
Homeostasis Pathology
Adaptive Capacity
Figure 2. Endogenous and exogenous factors that may
disrupt the dynamic equilibrium (adaptive capacity) of
the masticatory system leading to the development
and/or maintenance of temporomandibular disorder
signs and symptoms.
number of studies have suggested a positive association;
however, an equal number have found no or minimal
association. For example, an association between open bite,
posterior crossbite, and deep bite and the occurrence of
TMD has been reported.16 Additionally, a multiple logistic
regression analysis to compute the odds ratio for 11 common
occlusal features for asymptomatic controls as related to 5
TMD subgroups found several occlusal factors to demon-
strate odds risk ratio of at least 2.17,18 Yet the authors
suggested that occlusal factors were related to TMD in only
15% of cases. These occlusal features that were identified to
be potentially related include anterior open bite, overjet
greater 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 occlusal
schemes were not found to be statistically significant.
Leonardo da Vinci extolled the virtues of scientific study
when he wrote, BAnyone who falls in love with practice
without science is like a sailor on a ship without a compass or
a sail; neither knows where he is heading[ (p. 69).
Evidence-based dentistry is the rational integration of
systematic assessments of clinically relevant scientific evi-
dence relating to the patient’s oral and medical history and
condition with the dentist’s clinical expertise and the patient’s
treatment needs and preferences.19 In evidence-based practice
it is essential that the clinician/scientist identify the best
Volume 6, Number 1
scientific evidence, develop clinical expertise, and consider
the patient’s circumstances. Turpin20 recently stated, BThe
purpose of using the evidence-based approach is to close the
gap between what is known and what is practiced and to
improve patient care based upon informed decision making
(p. 1).[ It is well accepted that the hierarchy of what is
considered to be Bbest evidence[ in descending order is the
following: (1) randomized controlled clinical trials; (2)
nonrandomized controlled clinical trials; (3) cohort studies;
(4) case-control studies; (5) crossover studies; (6) case
studies; (7) consensus of opinion of experts in the appropriate
fields of research or clinical practice. Koh and Robinson21
completed a review of 660 randomized/quasi-randomized
studies published between 1966 and 2002 that addressed
occlusal therapy as a means of treating TMD. They found
only 6 studies that met criteria for inclusion. The data
obtained from 392 patients in these trials indicated an
absence of evidence to definitively indicate that occlusal
adjustment treats or prevents TMD. They emphasized that
future studies must use standardized diagnostic criteria and
outcome measures when evaluating TMD.
The conflicting information gleaned from the multitude of
studies related to occlusion as a causal factor or use of
occlusal therapy as a means of treating TMD may not reveal
the total story. It is mandatory that the clinician/scientist
consider the dynamic nature of the masticatory system. It has
been stated that proper occlusion of the dentition occurs in a
dynamic 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 may
be more important when discussed in the context of
relationship with TMD.
The temporomandibular synovial system obeys the laws
of orthopedics as do other synovial systems. However, this
dynamic orthopedic masticatory system demonstrates a
number of unique features, including the following:
1. the right and left temporomandibular joints function as
one unit held together by the dense cortical bone of the
mandible
2. the articulating surfaces of each TM joint are fibrocarti-
laginous
3. the articular disc separates the temporomandibular joint
into 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 of
the teeth, where the greatest forces are generated
Dynamic occlusal function affects multiple interfaces, such as
(1) tooth-to-tooth interface, (2) tooth/supporting structure
interface, (3) the TM joint interface, and (4) muscle activity
(functional and parafunctional). Mechanical stresses at each
of these interfaces have been shown to be associated with a
potential compromise in the integrity of tissues. Additionally,
Gremillion 45

we must consider the various case-specific factors that may
affect each person’s adaptability, such as
• variable directions of muscular loading forces
• selective action of multiple dental and articular constraints
influenced by:
9 duration of load
9 degree of load
9 host resistance
Review of the literature regarding oral parafunction and
TMD provides insight as to a potential relationship between
what goes on at the tops of the teeth and the various interfaces
of occlusion. Carlsson and colleagues23 reported data collected
in a 20-year longitudinal study. At baseline, 402 randomly
selected 7-, 11-, and 15-year-old subjects were evaluated for
occlusal factors, oral parafunction, tooth wear, and TMD.
Twenty years later, 320 subjects were assessed for the same
variables. Logistic regression indicated that childhood paraf-
unction (bruxism, tooth clenching, nocturnal grinding, and
nail biting) were predictors of the same oral parafunction 20
years later. They also reported that childhood parafunction
and an Angle Class II malocclusion were predictors of tooth
wear in adulthood. Magnusson et al24 reported that evaluation
of this same study population at the 4-, 5-, 10-, and 20-year
marks revealed significant correlation between bruxism and
TMD symptoms. Another recent publication reported on the
association between morphologic occlusion and functional
occlusal factors and TMD symptoms.25 In this study, 4310
subjects were evaluated. No specific occlusal factor was found
to be significantly associated with TMD symptoms. However,
parafunction demonstrated a positive relationship to TMD
symptoms (odds ratio 3.4). A number of studies have
suggested that distalizing forces resulting from occlusal
contacts have the potential to cause TM joint internal
derangement.26-29 Additionally, it is clear that degenerative
temporomandibular joint disease is the result of maladaptation
to increased joint loading.30-33 An oxidative-stress mechanism
involving free radicals and other chondrodestructive factors
has been recently been posited.32,33
Changes may also take place at the neuromuscular
interface. Isometric contraction such as that associated with
clenching the teeth has specific local effects to include
increased pressure within the muscle, obstruction of blood
flow, decreased oxygen saturation, decreased glycogen
saturation, and impaired removal of catabolic by-products.
Free radicals have been implicated in exercise-induced muscle
damage.34 Muscle overuse and eccentric contractions have
been demonstrated to cause muscle fiber damage with
associated edema/effusion, which may last for up to 80
days. However, pain does not parallel the effusion, generally
reaching peak levels 3 to 4 days posttrauma. A local release of
mediators substance P and calcitonin gene-related peptide
into the extracellular space may signal other cells (mast cells)
to initiate humoral or cellular-based inflammation and set the
stage for peripheral sensitization of nociceptors.
46 Gremillion
JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
In conclusion, it is evident that the scientific literature has
not convincingly demonstrated a definitive relationship
between static occlusal factors and TMD. TMD represents
a multifaceted/multifactorial group of conditions that share
common signs and symptoms. Although a multitude of
factors 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 be
scientifically validated. The true determining factor(s) may
be related to the individual’s host resistance/adaptive
capacity. If we are to take an evidence-based view of
occlusion and TMD we must be able to differentiate between
an occlusal contact and an occlusal interference. It is
mandatory that we recognize the potential destructive effects
of parafunction. We must also consider the cyclic nature of
TMD. Therefore, it may be more appropriate to view TMD
cases in which occlusal function serves as a significant factor
in TMD as a maladaptive occlusion. This term takes into
consideration peripheral and central sensory and motor
factors involved in masticatory system pathofunction on a
case-specific basis and is supported by the recognized effects
of mechanical stress on the stomatognathic system.
REFERENCES
1. Lipton JA, Ship JA, Larach-Robinson D. Estimated prevalence and
distribution of reported orofacial pain in the United States. J Am Dent
Assoc 1993;124:115-21.
2. Okeson JP, ed. Differential diagnosis and management considerations of
temporomandibular disorders. In: Orofacial pain: guidelines for
assessment, 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 and
symptoms of temporomandibular disorders: clinical signs in cases and
controls. J Am Dent Assoc 1990;120:273-81.
4. National Institute of Health Technology and Assessment Conference.
Management of Temporomandibular Disorders. NIH Technol Assess
Statement 1996 Apr 29- May-1;1-31. Bethesda, MD: NIH.
5. Slavkin HC. Lifetime of motion: temporomandibular joints. J Am Dent
Assoc 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, tooth
pulp, visceral, neck and muscle afferents onto nociceptive and
nonnocieptive neurons in trigeminal subnucleus caudalis (medullary
dorsal 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 Dent
Educ 1985;49:398-404.
9. Schiffman E, Fricton JR. Epidemiology of TMJ and craniofacial pain.
Fricton JR, Kroening RJ, Hathaway KM, eds. TMJ and craniofacial
pain: diagnosis and management. St. Louis: Ishiaku Euro American
Publ; 1988. p 1–10.
10. Agerberg G, Carlsson GE. Functional disorders of the masticatory system.
I. Distribution of symptoms according to age and sex as judged from
investigation by questionnaire. Acta Odontol Scand 1972;30:597-613.
11. Helkimo M. Studies on function and dysfunction of the masticatory
system. I. An epidemiological investigation of symptoms of dysfunction
in 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 Craniomand
Pract 1993;11:217-20.
March 2006
JOURNAL OF EVIDENCE-BASED DENTAL PRACTICE
13. Heft MW. Prevalence of TMJ signs and symptoms in the elderly.
Gerontology 1984;3:125-30.
14. McGivney GP. Glossary of prosthodontic terms. J Prosth Dent 1994;
71(1):50-112.
15. Gremillion HA. TMD and maladaptive occlusion: does a link exist? J
Craniomandib Pract 1995;13(4):205-6.
16. Tanne K, Tanaka E, Sakuda M. Association between malocclusion and
temporomandibular disorders in orthodontic patients before treatment. J
Orofac Pain 1993;7(2):156-62.
17. Pullinger AG, Seligman DA, Gornbein JA. A multiple logistic regression
analysis of the risk and relative odds of temporomandibular disorders as
a function of common occlusal features. J Dent Res 1993;72(6):968-79.
18. McNamara Jr JA, Seligman DA, Okeson JP. The relationship of occlusal
factors and orthodontic treatment to temporomandibular disorders.
Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular disorders
and related pain conditions. Seattle: IASP Press; 1995.399-427.
19. Lund AE. How do you define and see evidence-based dentistry? J Am
Dent Assoc 2003;134(6):690.
20. Turpin DL. Consensus builds for evidence-based methods. Am J
Orthod Dentofacial Orthop 2004;125:1-2.
21. Koh H, Robinson KH. Occlusal Adjustment for treating and preventing
temporomandibular joint disorders. Cochrane Database of Systematic
Reviews 2003;1.CD003812.
22. MacDonald JW, Hannam AG. Relationship between occlusal contacts
and jaw-closing muscle activity during tooth clenching: part I. J Prosthet
Dent 1984;52(5):718-28.
23. Carlsson GE, Egermark I, Magnusson T. Predictors of bruxism, other
oral parafunctions, and tooth wear over a 20-year follow-up period. J
Orofac Pain 2003;17(1):50-7.
24. Magnusson T, Egermark I, Carlsson GE. A prospective investigation
over two decades on signs and symptoms of temporomandibular
disorders and associated variables. A final summary. Acta Odontol
Scand 2005;63(2):99-109.
Volume 6, Number 1
25. Gesch D, Bernhardt O, Mack F, John U, Kocher T, Alte D. Association
of malocclusion and functional occlusion with subjective symptoms of
TMD in adults: results of the Study of Health in Pomeraina (SHIP).
Angle Orthod 2005;75(2):183-90.
26. Isberg A, Isacsson G, Johansson AS, Larson O. Hyperplastic soft-tissue
formation in the temporomandibular joint associated with internal
derangement. A radiographic and histologic study. Oral Surg Oral Med
Oral Pathol 1986;61(1):32-8.
27. Isberg AM, Isacsson G. Tissue reactions of the temporomandibular
joint following retrusive guidance of the mandible. Cranio 1986;4(2):
143-8.
28. Yang Y, Yatabe M, Ai M, Soneda K. The relation of mandibular
laterotrusion with ipsilateral TMJ clicking. J Oral Rehabil 2001;28(1):
64-7.
29. al-Ani MZ, Gray RJ, Davies SJ, Sloan P. A study of the relationship
between lateral guidance and temporomandibular joint internal
derangement. Eur J Prothondont Restor Dent 2003;11(2):65-70.
30. Westesson PL, Rohlin M. Internal derangement related to osteoar-
throsis in temporomandibular joint autopsy specimens. Oral Surg Oral
Med Oral Pathol 1984;57(1):17-22.
31. de Bont LG, Stegenga B. Pathology of temporomandibular joint internal
derangement and osteoarthrosis. Int J Oral Maxillofac Surg 1993;22(2):
71-4.
32. Milam SB. Articular disk displacements and degenerative temporoman-
dibular joint disease. Sessle BJ, Bryant PS, Dionne RA, eds. Temporo-
mandibular disorders and related pain conditions. Seattle: IASP Press;
1995. p. 89-12.
33. Milam SB, Zardeneta G, Schmitz JP. Oxidative stress and degenerative
temporomandibular joint disease: a proposed hypothesis. J Oral
Maxillofac Surg 1998;56:214-23.
34. Saxton JM, Donnelly AE, Roper HP. Indices of free-radical-mediated
damage following maximum voluntary eccentric and concentric
muscular work. Euro J Appl Physiol Occup Physiol 1994;8(3):189-93.
Gremillion 47