Letter to the Editor: Authors' Response
- Autores: Daniele Manfredini, Rossano Mura, Jari Ahlberg, Frank Lobbezoo
- Localización: Journal of periodontology, ISSN 0022-3492, Vol. 87, Nº. 1, 2016, págs. 3-4
- Idioma: inglés
- Enlaces
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Resumen
Authors’ response:
With interest, we have read the letter written by Dr. Perlitsh concerning our review article on the effects of bruxism on the periodontium.1 We appreciate his comments and consider them as sources of important input for our future studies on this topic. In particular, we understand his concern about the use of the term “unlikely,” which, at first sight, goes beyond the reviewed literature’s findings.
However, Dr. Perlitsh’s viewpoint that we failed to consider important findings from animal studies on the role of occlusal trauma for periodontal breakdown and from histologic studies on the topic is not backed up with evidence-based data. On the contrary, the literature on so-called “occlusal trauma” has increasingly marginalized its role as a risk factor for irreversible damage to healthy periodontal tissues in humans. Indeed, while some controversy still seems to exist as far as animal models are concerned,2 studies on humans have failed to show that occlusal trauma may cause long-term changes to the periodontium and tooth-supporting structures.3 Opinions that occlusion plays an etiological role in periodontal breakdown are kept alive by suggestions that occlusal adjustment should be part of the treatment protocol to reduce mobility of periodontally compromised teeth, based on clinical observations that such a combined occlusal and periodontal approach seems to offer additional clinical benefits relative to periodontal treatment alone. Notwithstanding that, the quality of the literature on this topic is poor.4,5 Furthermore, and even more importantly, it should be stressed that the possible presence of a clinical association between two phenomena (i.e., occlusal adjustment and reduction of tooth mobility) does not necessarily imply a causal relationship. The possible role of periodontal disease as a condition causing the tooth to suffer from occlusal trauma may be even more plausible than the opposite interpretation. Just to give a comparable example, it is a common clinical observation that acute pulpitis can cause occlusal supracontacts and that patients may experience some additional pain relief with those contacts’ removal. Does this mean that occlusal supracontacts are the cause of pulpitis? Of course, it doesn’t. And isn’t the hypothesis that teeth with periodontal disease may undergo positional changes, forcing them into a potentially traumatic occlusal condition, similarly plausible? According to our viewpoint as bruxism and orofacial pain experts, we feel that a lack of a true multidisciplinary approach to the topic is responsible for the decades-long controversy on the topic. It seems that some periodontists still take for granted some archaic uncontrolled studies on animals, without appraising that the literature on clinical pain models in humans has shown concrete differences between animals and humans that prevent us from unquestioningly accepting animal findings as sources of clinically useful information. The more recent histologic hypotheses put forward by Dr. Perlitsh are not an exception.
The most important examples concerning these differences come from clinical studies introducing iatrogenic occlusal interferences to healthy subjects. They show that an iatrogenic occlusal supracontact may cause only transient pain. As for bruxism, which is the actual topic of our review and this letter, such acute interferences are not able to trigger bruxism, likely due to the onset of pain avoidance, protective reflexes, or acquisition of different muscle engrams.6 That is a completely different reaction with respect to what has been hypothesized in previous studies on monkeys. In addition, such findings support the literature on the absence of a relationship between natural occlusion and bruxism.7,8 In short, it seems that Dr. Perlitsh has ignored the flaws and limitations of the rather unspecific and not-pertinent literature he has cited in support of his statements. We would like to invite him to consider two simple questions that the periodontal studies should be able to clarify to the scientific and clinical communities: 1) Have we been able to find a clinically plausible explanation to define chronic occlusal trauma in humans? 2) Are we sure that chronic occlusal trauma actually exists in the natural healthy dentition? According to current knowledge, answers to both questions are “No,” and high quality, difficult research is needed on these topics.
In addition, we should keep in mind that bruxism is not the same as occlusal trauma. Bruxism is an umbrella term grouping together multifaceted motor phenomena with different circadian manifestations, frequency, muscle contraction features, and etiology.9 So far, too many assumptions on bruxism have been based on self-reported “diagnosis,” which is suitable at best to detect possible bruxism. Diagnostic approaches allowing a definite measurement of bruxism activities are strongly required to draw definite conclusions on various bruxism topics and avoid relying on simple, unspecific, self-reported studies.10 Notwithstanding that, it is clinically plausible that the above-described avoidance reaction may prevent individuals from exacerbating or even performing bruxism behaviors over periodontally-damaged teeth.
All in all, it seems that citing untested animal or histologic models/hypotheses on occlusal trauma to jump to conclusions opposite to those of our review on bruxism and periodontium, as Dr. Perlitsh did, is an example of the old “broken-telephone” play for children. Too many assumptions concerning his line of reasoning simply lack evidence in support. With all respect, based on that, our conclusion that bruxism is not likely to cause chronic periodontal damage to healthy tooth-supporting structures is to be considered the most biologically plausible explanation for the relationship between the two phenomena.
