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GUEST EDITORIAL |
Institute of Dentistry, University of Turku, Lemminkäisenkatu 2, SF 20520 Turku, Finland; pealan{at}utu.fi
The discussion about TMD etiology may be the longest debate in dentistry. Why does this debate still continue? I believe an answer can be found by analyzing the design of TMD studies against the principles of etiological epidemiology (Rothman and Greenland, 1998).
Both parties of the debate refer to empirical evidence. High-quality studies of occlusal adjustment in TMD patients are still too few to permit firm conclusions to be drawn (Forssell et al., 1999; Tsukiyama et al., 2001), but the use of occlusal splints seems to relieve TMD symptoms (Forssell et al., 1999). Success in therapy, however, is proof neither for nor against an etiological theory.
Where is the Evidence Suggesting that Occlusion and TMD are not Associated?
The observation that many subjects have "occlusal abnormality" without TMD has clearly encouraged reviewers to conclude that occlusal factors have no significant etiological role (Clark, 1991; DeBoever et al., 2000). Results of experimental interference studies are also seen as strong evidence for the same conclusion (Tsukiyama et al., 2001).
It is possible, however, that the reviews by Clark (1991), Clark et al. (1999), DeBoever et al. (2000), and Tsukiyama et al. (2001) have overlooked some methodological errors in studies on TMD etiology: (1) use of data which are not suitable for etiological generalizations, (2) confusion between the concepts "sufficient cause" and "causal factor", and (3) confounders in studies of artificial interference.
Generalizations
There are two types of generalizations in epidemiology. Rothman and Greenland (1998) have pointed out that studies aiming at generalization to the target population require representative samples, whereas powerful tests of competing hypotheses require selected samples. The majority of the epidemiological studies of association between occlusal factors and TMD have not made this decisive distinction but have used samples representing non-selected populations. It is therefore possible that the variation has been insufficient for effective comparisons between subjects with and those without a certain trait. For a critical study design, one must select subjects with occlusion totally free from any kind of interference, and compare them with subjects with interference. If this is impractical by selection, the needed variation can be produced by adjustment (Kirveskari et al., 1992, 1998).
Sufficient Cause vs. Causal Factor
Clark’s (1991) comment that "a high percentage of patients who have a naturally occurring ‘occlusal abnormality’ do not exhibit TM disorder" discloses that a distinction between the concepts "sufficient cause" and "causal factor" has not been made. This criticism applies also to the review by DeBoever et al. (2000). The conclusion should have read: "The literature does not give strong support for the opinion that occlusion is a sufficient cause for TMD." (emphasis added)
All diseases and disorders are multifactorial in practice. The most common example in dentistry is dental caries. Not mutans streptococci alone and not a sugar-rich diet alone lead to dental decay; they are both needed in addition to a certain weakness in host resistance. Analogously, if both stress and occlusal factors are needed for TMD to develop, then occlusal factors are a causal factor but not a sufficient cause for TMD. Occlusion could be excluded as a causal factor if the absence or presence of occlusal interferences does not affect the incidence rate of TMD in longitudinal studies (Kirveskari et al., 1998).
Confounder in Artificial Interference Studies
The trials with experimental interference are considered powerful (Tsukiyama et al., 2001). Interestingly, the usually virtuous principle of including only subjects healthy at baseline can be a confounder in the present case. Healthy adult subjects have demonstrated the ability to tolerate their natural interferences. Therefore, they can also be expected to adapt to artificial interference. What would happen if the study subjects were former TMD patients? In the trial by LeBell et al. (2002), the former patients did not adapt to the artificial interference as well as did healthy controls.
To conclude, studies which have not disclosed associations between occlusion and TMD may not have fulfilled sound methodological criteria. Lack of evidence has been interpreted as evidence of lacking association. In spite of the fact that it has been much more difficult for the occlusal hypothesis to survive in the trials by Kirveskari et al. (1992 (1998) and Le Bell et al. (2002), these studies have not succeeded in finding evidence against the occlusal hypothesis. Therefore, the rejection of the occlusal hypothesis cannot be justified with the present empirical evidence.
Received May 14, 2002; Accepted May 13, 2002
REFERENCES
Clark GT (1991). Etiologic theory and the prevention of temporomandibular disorders. Adv Dent Res 5:60–66.[Abstract]
Clark GT, Tsukiyama Y, Baba K, Watanabe T (1999). Sixty-eight years of experimental occlusal interference studies: what have we learned? J Prosthet Dent 82:704–713.[Medline]
DeBoever J, Carlsson G, Klineberg I (2000). Need for occlusal therapy and prosthodontic treatment in the management of temporomandibular disorders. Part I. Occlusal interferences and occlusal adjustment. J Oral Rehabil 27:367–379.[Medline]
Forssell H, Kalso E, Koskela P, Vehmanen R, Puukka P, Alanen P (1999). Occlusal treatments in temporomandibular disorders: a qualitative systematic review of randomised controlled trials. Pain 83:549–560.[Medline]
Kirveskari P, Alanen P, Jämsä T (1992). Association between craniomandibular disorders and occlusal interferences in children. J Prosthet Dent 67:692–696.[Medline]
Kirveskari P, Jämsä T, Alanen P (1998). Occlusal adjustment and the incidence of demand for temporomandibular disorder treatment. J Prosthet Dent 79:433–438.[Medline]
Le Bell Y, Jämsä T, Korri S, Niemi P, Alanen P (2002). The effect of artificial occlusal interferences depends on previous experience of temporomandibular disorders. Acta Odontol Scand (in press).
Rothman K, Greenland S (1998). Modern epidemiology. 2nd edition. Philadelphia: Lippincott–Raven, pp. 133-134.
Tsukiyama Y, Baba K, Clark GT (2001). An evidence-based assessment of occlusal adjustment as a treatment for temporomandibular disorders. J Prosthet Dent 86:57–66.[Medline]
This article has been cited by other articles:
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  C. S. Greene Occlusion and temporomandibular disorders (TMD): still unsolved question? J. Dent. Res., November 1, 2002; 81(11): 732 - 732. [Full Text] [PDF]
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