Letter to the Editor: Re: Bruxism is Unlikely to Cause Damage to the Periodontium: Findings from a Systematic Literature Assessment
- Autores: Max J. Perlitsh
- Localización: Journal of periodontology, ISSN 0022-3492, Vol. 87, Nº. 1, 2016, págs. 1-2
- Idioma: inglés
- Enlaces
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Resumen
To the Editor:
Re: Bruxism is Unlikely to Cause Damage to the Periodontium: Findings from a Systematic Literature Assessment. Manfredini D, Ahlberg J, Mura R, and Lobbezoo F. (J Periodontol 2015;86:546-555).
I read the article by Manfredini et al., with great interest and compliment the authors for the comprehensive literature search undertaken for this paper. Over 4,040 articles were screened on the subject of bruxism. This clearly demonstrates the ongoing, widespread scientific interest in parafunctional movements of the mandible as a significant etiological factor affecting the health of the periodontium. The central aim of the Manfredini study was to answer the question “Is there any evidence that bruxism may cause periodontal damage per se”? The conclusion of the authors as presented in the title of the paper is that “bruxism is unlikely to cause damage to the periodontium.” My view is that the word “unlikely” is taken to mean NOT likely, and is an unsupported and premature conclusion based on the following: 1) the limited data presented and the methodologic limitations of the studies; 2) the scientific logic used; and 3) the omission of relevant recent knowledge from other domains of research. Acceptance of such a conclusion has profound negative implications for the diagnosis and treatment of patients and the training of practitioners.
Limited Data Presented and Methodologic Limitations of the Studies Cited The authors identified only six out of over 4,040 studies as having relevance and sufficient scientific merit to address their question. Even these few studies however, do not have objective, systematically obtained measures of the independent variable of bruxism, i.e. its type, extent, and duration as measured independently from the often vaguely described self-reports of patients. The authors themselves concluded that: “Unfortunately, the scarce quantity and quality of the reviewed literature prevented sound conclusions….particularly sleep bruxism assessment requires more high-quality studies.” Furthermore, the measures of the dependent variable, periodontal breakdown, are not consistent or precise across the studies, and the samples themselves are not comparable based on clinical status. Because the focus of the review was to relate bruxism to tissue breakdown, samples should be defined and the tissue damage measured accordingly. Finally, if there had been an adequate set of studies that met acceptable standards, a meta-analysis would have been performed enabling a valid assessment of the effects of bruxing on the periodontium and its relationship to periodontal disease.
Scientific Logic Used Correlational data of contemporaneous events, as were presented in the studies, do not enable a determination of causality. The research standard for determining causality is that predictive studies with precise experimental controls, and objective measurements of the independent and dependent variables are the required basic conditions. Such conditions minimize the erroneous attribution of irrelevant variance in the assessment of causality. In the research cited in the review, no longitudinal or predictive studies were conducted. Indeed, the reviewers candidly reported this and displayed other design limitations for each of the six studies. Further, in the practice of science there is general consensus that the absence of statistically significant relationships between variables does not lead to the inevitable conclusion that differences do not exist, certainly not before other relevant variables have been controlled for and demonstrated to almost exclusively account for the outcomes.
Periodontal disease processes are complex and a preferred research model for understanding the disease would be to address the complexity of causal factors, the examination of the disease process over time, and the contributions of environmental, genetic and systemic variables. Thus, asking the question of whether bruxing as a “per se” cause is itself a detour from a comprehensive analysis of the complex, interactive nature of the disease process, in which bruxing may well have a contributing role for a subset of patients.
Omission of Relevant Knowledge from Other Domains of Research Bruxism is in the category of variables that can produce trauma from occlusion. The extensive histologic research studies of trauma from occlusion undertaken from 1950 to 1980 should not be ignored. These studies clearly demonstrated damage to the periodontium in human and animal tissues. My 1980 paper1 attempted an integration of the existing understanding of the independent or codestructive interaction of plaque-induced immunoinflammatory changes and trauma from occlusion. The paper described a systematic approach to the interpretation of tooth mobility. The evidence led to the formulation that “the tensions and pressures of excessive occlusal forces transmitted to the periodontal ligament produce molecular and physicochemical alteration of the ground substance and fibrous component of this tissue. This results in qualitative and quantitative changes seen histologically as a typical response to injury with atrophic, degenerative, and necrotic changes in the periodontal ligament.”1 Studies of microdamage to the periodontal complex have been conducted in recent years that used the most advanced microscopy technologies to focus on mechanical, structural, biochemical, cellular, and molecular variables. These technologies include: immunohistochemistry and cryomicrotomy, atomic force microscopy (AFM), nano-transmission x-ray microscopy, microcomputed tomography, microprobe x-ray fluorescence analysis, and mechanical heterogeneity related to AFM-based nano-indentation.2-4 These studies demonstrated the plastic nature of the periodontium when teeth were subjected to a variety of loads that generated a mixed mode of tension and compression strain fields, similar to forces caused by bruxism. These studies found many significant types of changes, i.e. microdamage to the periodontium. These changes were characterized by: 1) mechanical, structural, and chemical discontinuities localized at the interfaces of the periodontal ligament with cementum and alveolar bone; 2) microscale “bony protrusions” that were interpreted to be the result of non-physiologic functional demands at the anchored ends of the periodontal ligament to bone and the periodontal ligament to cementum interfaces; 3) swelling of the hygroscopic collagen fibers of the periodontal ligament in response to hydrostatic pressure changes; and 4) the stretching and realignment of collagen fibers in the direction of the over-loading occlusal forces. Further, and very importantly, tissue alterations have been observed that resulted in significant mineral formation or resorption with 5) adaptive or non-physiologic narrowing or widening of the periodontal ligament space. Similar changes are seen radiographically at the mesial and distal aspects of teeth with extreme wear facets caused by bruxism and may reflect the earliest damage to the periodontium from parafunctional movements of the mandible.
All of these alterations impact Sharpey’s fiber system of tooth support that has recently been recognized as a novel bone matrix regulatory system.5 With advanced alveolar bone loss, there is loss of the Sharpey’s fiber support system resulting in significant tooth mobility. The fleeting tooth contacts that occur in food mastication then become a source of secondary trauma from occlusion. The intense forces of bruxism can become additive to this injury.
Another source of damage to the periodontium can be found in the extensive studies of the effects of orthodontic tooth movement. The complex chemical cascade impacting the periodontal tissues is graphically portrayed in these studies. The controlled forces of tension and compression applied to stimulate bone resorption and bone formation (similar to bruxing forces) often cause microdamage to the periodontal tissues beginning with blood flow changes resulting in tissue hypoxia and tissue cytokine release.6 The conclusion that bruxism is unlikely to cause damage to the periodontium is based on methodologically flawed and incomplete research protocols. Bruxism should not be dismissed from the attention of practitioners as doing so would have faulty preventive and treatment implications for patient care as well as negative implications for the adequacy of the training of practitioners. Until proven otherwise, tooth mobility associated with widening of the periodontal ligament should remain a definitive clinical sign of the possible active role of trauma from occlusion acting independently or codestructively with bacterially induced immunoinflammatory changes. The interpretation of these definitive clinical signs as acceptable physiologic and functional adaptations is questionable. Recent research findings at the cellular and molecular levels provide abundant and convincing evidence for clinicians that microdamage to the periodontium is caused by trauma from occlusion. The clinical implication of such evidence is that bruxism, which may result in tooth mobility, should not be ignored in the prevention and treatment of periodontal disease. If the goal of periodontal therapy is regeneration and maintenance of the normal architectural integrity of the periodontium then these deviations from the normal need to be considered in diagnosis and treatment.
The author reports no conflict of interest related to this letter.
