From bruxism to genetics

The concept of bruxism, from a colloquial point of view, has been and is a generic denomination referring to the situation suffered by those patients who claim to grind or clench their teeth and who present dental wear that require an acrylic splint for their containment, normally of night use. From a more academic point of view, much has been written about its causes, both those triggered by an excitation of the central nervous system and those triggered by the peripheral nervous system in the oral cavity. The effects of bruxism on dental structures, masticatory muscles and temporomandibular joint are collected as part of what we call temporomandibular dysfunction (TMD).

However, when a patient asks us what is the cause and treatment for bruxism, we may answer: “well, improving occlusion will help and lower the degree of stress too, but there is little more we can do”. Like many colleagues in the profession, I have always been concerned about when we could answer this question in a more convincing way. In other words, as professionals we treat its consequences (dental wear, myofascial pain…) and sometimes we are even successful in treating causal factors such as occlusion (through occlusal adjustment with selective grinding, orthodontics or restorations and rehabilitations), but a large number of cases seem to mislead us… and, of course, their causes.

Bruxism is something that has always generated a profound debate in the field of dentistry. As a student, I was interested in the different positions between the gnatological schools around their relationship with ideal occlusions (that of canine guides, group function, bibalanced occlusion…) and their relationship in the so-called TMD. Subsequently, the exercise of specialization in orthodontics revealed to me the infinity of malocclusions subject to multiple variables and to which, as a professional, one seeks to provide the best solution, but it must be taken into account that there is a lack of proportionality between the degrees of malocclusion and severity in the presentation of signs and symptoms, both when referring to bruxism and to the TMD itself, an issue that deserves special attention.

Another aspect that marked my way of observing malocclusions and TMD was taking into account other factors such as: the presence of erosions not subject to exogenous factors and where the endogenous acid medium due to gastroesophageal reflux constitutes the main etiological agent; coexistence with lesions of the oral mucosa, digestive, autoimmune pathologies, family history of some types of cancer…; observe signs of the malocclusions that we frequently treat in orthodontics such as agenesis, supernumerary teeth, alterations in size, structure and tooth position; and finally the psychological profile and sleep disturbances. All these factors (and some others) are well known, but how to fit them in or relate them is not so well known. The key to beginning to understand the links between these factors and their observation at different stages of life was an approach to the world of genetics. Pleiotropy, that word totally unknown to me, made me understand the profession in a completely new way, a different and broader way of thinking and relating to patients.

The term pleiotropy refers to how one gene is responsible for multiple phenotypic effects. This becomes more relevant when a mutation occurs in that gene and these different phenotypes are expressed in apparently unrelated systems and in different stages of life. But, how to fit this vision in clinical development without falling into the temptation of understanding that every sign is related to a significant mutation? Perhaps, by establishing ties with those medical disciplines that can help us fit all the pieces together in the right measure. Genetics will give us one part of the solution and epigenetics the other.

A relevant fact has to do with the presentation of a series of articles that were published between 2018 and 2019 by Li Yuanyuan et al. with a notable impact, both due to the sample size and the applied methodology, and which I interpret, due to its results, as a goodbye to the traditional concept of temporomandibular dysfunction by providing a more multidisciplinary medical vision. Together, they evaluated the relationship between chronic temporomandibular dysfunction, dental erosions, and gastroesophageal reflux, as well as the mediation of sleep or mental disorders in this relationship. Their conclusions deserve a read.

I like to keep in mind that what we do not know is greater than clinging to the security of dogmas, although without falling into absolute relativism, that doubts everything, I seek out and try to approach those research groups that base their research processes on the methodology known as evidence-based medicine, as well as the clinical eye of veterans, which is no small thing, since ultimately we are dedicated to performing treatments.

Broadening the horizon of causal relationships with a more interdisciplinary medical approach may allow us in the future to understand what is called bruxism in a more open way.

Bruxism is not just a dental problem.