REVIEW

 

Phenotypes and Clinical Genotypes of Bruxism Patients: A Systematic Review

 

 

RB Velasquez^I; RA Zambrano^II; GA Ulloa^III; AA Sierra^IV; TM Rodriguez^V; LB Chauca^VI; MA Serrano^VII

^IDepartment Prosthesis School of Dentistry, Universidad de Las Americas (UDLA) , Av. Colón y 6. Diciembre CP 170523, + 593023981000 ext 3060,Quito, Ecuador; https://orcid.org/0000-0001-5660-3941
^IIDoctor in Dentistry Oral Rehabilitation Speciality, School of Dentistry, Universidad de las Americas (UDLA) , Av. Colón y 6. Diciembre CP 170523, + 593023981000 ext 3060, Quito, Ecuador; EMAIL: anabel.zambrano@udla.edu.ec; https://orcid.org/0000-0001-8922-5043
^IIIDoctor in Dentistry Oral Rehabilitation Speciality , School of Dentistry, Universidad de las Americas (UDLA) , Av. Colón y 6. Diciembre CP 170523, + 593023981000 ext 3060, Quito, Ecuador; ana.ulloa@udla.edu.ec https://orcid.org/0000-0001-9275-5133
^IVDoctor in Dentistry Oral Rehabilitation Speciality , School of Dentistry, Universidad de las Americas (UDLA) , Av. Colón y 6. Diciembre CP 170523, + 593023981000 ext 3060, Quito, Ecuador;. alexander.sierra@udla.edu.ec. https://orcid.org/0000-0001-5753-6963
^VDr. Dentistry Resident, Faculty of Dentistry. University of Las Americas. UDLA. Campus Colón. +593958916317 CP 170523 Quito-Ecuador. maria.rodriguez.tates@udla.edu.ec; https://orcid.org/0000-0002-4764-0764
^VIPeriodontics and Implantology Oral Research. College Dentistry. Universidad de Guayaquil, Ecuador. Email: luischauk@hotmail.com / luis.chaucab@ug.edu.ec.; https://orcid.org/0000-0002-8713-951X
^VIIPhD. Msc Doutora em Odontologia na Area de Dentistica Restuaradora. Departamento de Investigación de Prótesis Dental. Facultad de Odontología. Universidad de Las Américas. UDLA. Campus Colón. +5930239981000 ext.3060. CP 170523 Quito-Ecuador. alexandra.mena@udla.edu.ec. https://orcid.org/0000-0001-6358-8145

Correspondence

 

 

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ABSTRACT

BACKGROUND: Bruxism is a phenomenon where psychological and exogenous biological factors act in greater percentage. Several genetic polymorphisms have been described in GABAA receptors, and some have been associated with motor limitations, such as the rs1805057 polymorphism of the GABRB1 gene (GABAA), which found a haplotype associated with a lower limitation in movement in acute pain processes. The aim to identify the clinical phenotypes in bruxism patients
METHODS: Eligibility criteria were as follows: observational studies, case control studies, odds ratios, bruxism, patients, and a keyword search that included [[bruxism]], OR [[temporomandibular joint disorders]] OR [[sleep bruxism]], OR [[awake bruxism]], OR [[polymorphism]] or [[GABAA]], or [[serotonin]] , using the Boolean operators AND, OR and NOT
RESULTS: Were included 210 identified records in databases; 50 records from other sources; 117 records were deleted after determining they were duplicates; 42 studies were included in qualitative synthesis ; finally, who met inclusion requirements 5 studies were included in synthesis. The comparison of global DNA methylation profiles in patients with bruxism shows a possible genetic influence on their etiology, indicating that patients with HTR2A rs2770304 alleles are at increased risk
CONCLUSION: the HTR2A rs2770304 allele leads to an increased risk of bruxism

Keywords: bruxism, temporomandibular joint disorders, phenotype, genotype, methylation.

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INTRODUCTION

Initial genetic evidence of bruxism is based on questionnaires and surveys, and evidence indicates that 20% to 50% of patients have at least one close family member reporting that there is a genetic relationship.¹ Several genetic polymorphisms have been described in GABAA receptors. Some have been associated with motor limitations, such as the rs1805057 polymorphism of the GABRB1 gene (GABAA), which found a haplotype associated with a lower limitation in movement in acute pain processes²; this subunit would act as an endogenous muscle relaxant with a greater inhibitory GABAergic action, reducing muscle spasm and allowing greater movement the chewing muscles.³ Another case is the rs4906902 polymorphism of the GABRB3 gene (GABAA), which has been associated with the presence of a complex syndrome characterized by skeletal muscle pain.⁴ Mishra et al., postulated that at least 10-15 genes relate to phenotypes of anxiety. The most studied genes in this regard are serotonin transporter genes (receptors), and their relation to anxious personality ranges. The medium rafe brain serotonin system is related to mood modulation, anxiety, emotions, and cognition. In addition, the serotonergic system has been investigated in molecular genetics relating it to emotional behavior, variations in the SLC6A4 gene of the serotonin receptor (SERT) have been associated with more than twelve different traits of human behavior and other pathologies.⁴⁵ Bruxism is characterized by biological, psychological, and exogenous factors presenting as frequent clinical signs: repetitive movements of the jaw causing the teeth⁶ to squeak, micro trauma to chewing muscles and cervical pain skull mandibular. The prevalence of bruxism was⁸ to 31.4%, with the highest percentage in men⁷, neuromuscular activity accompanied by teeth grinding with three-dimensional mandibular movements. In 2017, the International Bruxism Assessment Council defined conceptual differences between sleep bruxism and awake bruxism. The new definitions are as follows. Masticatory muscle activity during sleep is characterized as rhythmic (phasic) or non-rhythmic (tonic), not a movement disorder or a sleep disorder, in healthy individuals, which is known as sleep bruxism.⁸ Awake bruxism is a masticatory muscle activity during wakefulness that is characterized by repetitive, sustained dental contact and mandibular hypermobility. An etiologically, emerging evidence suggests that psychology, biologic, and exogenous risk indicators have greater involvement than morphologic factors.⁹ Havingidentified the HTR2A rs2770304 allele related to bruxism, a comprehensive evaluation system can be created to facilitate the diagnosis and subsequent clinical management of the patient.¹⁰ Symptomatology found in patients with bruxism include the following: headache, neck pain, TMJ pain, limitation of mouth opening, joint noises, fatigue, and deviation in mouth opening. The following risk factors are considered as predisposing factors: macro and micro trauma¹¹, skeletal changes of the face, occlusal contact, hyperactivity of chewing or cervical muscles, changes in TMJ¹², hormonal and genetic factors, and psychological factors.¹³ The aim to identify the clinical phenotypes in bruxism patients

 

MATERIALS AND METHODS

This systematic review was registered with PROSPERO with the registration number CRD42020164836.

 

RESULTS

 

Table 1

 

 

Table 2

 

 

Table 3

 

Eligibility criteria were as follows: observational studies, case- control studies, odds ratios, bruxism, patients "with temporomandibular disorders , and a keyword search that included [[bruxism]], OR [[sleep bruxism]] , AND [[Sleep Bruxism]], , OR [[chewing]],OR [[oral parafunctional habits]], OR [[oral habits]] OR [[Facial pain]] or [[temporomandibular joint disorders]] AND [[Temporomandibular Joint Dysfunction Syndrome]] OR [[myofascial pain]] OR [[syndromes]] AND [[myalgia ]] AND [[osteoarthritis ]] OR [[arthralgia ]] OR [[orofacial pain]] OR [[TMD]] O [[temporomandibular disorder]] OR[[polymorphism]] OR [[GABAA]],OR [[serotonin]], OR [[Case Control Studies ]],OR [[Odds Ratio Studies]] using the Boolean operators AND, OR and NOT. The Scopus, Ebsco, PubMed, Medline Embase, the Cochrane Library, the Web of Science databases were searched; alternate databases that were searched included Scielo, Latindex, and Redalyc. Using the Prisma research protocol, the flowchart sequentially explains the selected information. Complete articles published were included as follows: were included 210 identified records in databases; 50 records from other sources; 117 records were deleted after determining they were duplicates; 42 studies were included in qualitative synthesis ; finally who met inclusion requirements 5 studies were included in synthesis. (Fig. 1) The authors (BVVR, AZ, AU, LCH, BS.) independently selected the titles and summaries, excluded duplicates and irrelevant articles that did not contain keywords or fell within the inclusion criteria and considered only full text articles. The date and names of all authors were included in the final review article. If the articles did not meet the inclusion and exclusion criteria as complete articles, case controls, odds ratio were resolved by the third and fourth evaluator (VC, MR) those who considered the results obtained in the studies and the methodology to confirm or eliminate the articles. The data extraction procedure was evaluated according to the criteria of all authors. Articles are classified by the author/year, study objective, study type, methodology, results (standard mean and deviation) and conclusions.

 

DISCUSSION

The circadian manifestations of bruxism are associated with characteristic personality traits (stress)^13,14 as well as alterations in neurotransmitters and their pathways.¹⁵

Therefore, the neurotransmitters of the central nervous system as its genes are related to bruxism^16,18 considering its pathogenesis by serotonin , which is responsible for the circadian rhythm, maintaining arousal, and regulating the response to stress, muscle tone and respiration, the typical manifestations associated with BRX.¹⁹ Abe et al., 20 studied the polymorphisms (HTR1A (rs6295), HTR2A (rs1923884, rs4941573, rs6313, rs2770304) and HTR2C) relating them to serotoninergic transmission produced in sleep bruxism, finding three SNPs within the HTR2A gene (rs6313, rs2770304 and rs4941573) associated with SB in Japanese individuals, but did not explore other circadian manifestations.^21.23 The process of selecting patients with SB included screening, clinical examination, and the nightly use of an electromyography device for masseter muscle We could not determine whether in the study control group people had signs of Bruxism. In the review carried out, evaluations were observed that coincided with the selection process of the SB individuals used, there were some differences in the general diagnostic method.

Patients recruited to participate in the study were referred by physicians and dentists in the community and at the university, with a presumptive diagnosis of bruxism 25 Patients were then evaluated by a specialist in temporomandibular disorders^{26, 28} and classified into bruxism circadian manifestations (sleep bruxism, weak up bruxism , and sleep bruxism, weak up bruxism ). This examination was performed in the control group as well to exclude the presence of bruxism. ²⁹

 

Figure

 

Therefore, to our knowledge, our work constitutes systematic review study that associated and examined the relationship between all circadian manifestations of bruxism and genetic polymorphisms within the serotonergic system.³⁰ We found significant differencesin the rs27703045 SNP (HTR2A) between the SB group and the control group, where carriers of allele C showed an increased risk of SB compared to the control group. Grigoriadis, A et al.,³¹ found differences in the rs27703045 SNP but compared genotypes of patients with SB with the control group. The HTR2A gene encodes 5-hydroxytryptamine (5-HT) 2A receptors. This family of receptors coupled with the G protein located in the brain involves physiological functions such as memory, sleep, nociception, eating and rewarding. However, these receptors have also been associated with depression³² and epilepsy.³³ Serotonin receptors can directly or indirectly, depolarize or hyperpolarize, neurons by changing ion conductance and/or their concentrations within the cell; therefore, it is not surprising that serotonin is able to alter excitability in most serotonergic networks.³⁴ No information is available regarding the clinical importance of the Rs2770304 SNP, and this variant is known to be within the intrinsic regions of HTR2A. Previous reports have determined that inactivation of 5-HT2A receptors enhances depressive effects³⁵, and in animal models, inactivation of these receptors increased susceptibility to epileptic chemicals and electrical products.^{36, 37}

The findings show that the HTR2A rs6313 SNP was associated with an increased risk of SB in Japanese individuals. Therefore, it is possible that the HTR2A gene plays a role in SB physiopathology as well.^{38, 39} HTR2A rs2770304 allele C studies showed an increased risk of patients with SB compared to the control group ^{40, 41, 42} whereas a decrease in the function of the 5-HT 2A receptor could be associated with depression and epilepsy. 43 Along with the intrinsic location of the rs2770304 SNP, it is noted that carriers of allele C^{44, 45} showed receptor expression of 5-HT 2A; the function of receptors can also decrease in these individuals with episodes of BRX during sleep.^{46, 47} Future research should be conducted to test this hypothesis, including functional studies and/or gene expression trials, to achieve a better understanding of the genetic basis of BRX circadian manifestations.⁴⁸ Although the diagnostic methods used in studies have limitations, they can be improved with the use of polysomnographic (PSG) and electromyography devices. Studies indicate that to recognize SB, the use of PSG is highly recommended by doctors and dentists within the gold standard of diagnostic research. Some authors note that the unstable nature of SB will also be reflected in fluctuations in the result variables of PSG recordings.^{49, 50} In most studies, SB patients are asked to spend the night in a sleep monitoring laboratory. This action would detract from the validity of the procedure. The first night the patient will be adapting to, changes in the environment, which can alter the results. The re commendation is to first make a recording of only PSG to inhibit the patient to sleep under experiences and conditions different from their normal conditions. Observations indicate that variables associated with rapid eye movement take longer to stabilize ^51,52 which appears to be a process extending to the fourth night. The PSG is described as a technique that is only suitable for small waiting times between diagnostic evaluation that takes between 5 and 6 months in the United States and around the world, with noted limitations for the control policies and ethics committees that each country has. The etiology of bruxism is multifactorial; this SNP is one of the mechanisms in volved in the circadian manifestations of BRX. ⁵³

 

CONCLUSION

The clinical phenotype identified by the authors is the HTR2A rs2770304 allele the risk of bruxism patients.

 

AUTHOR CONTRIBUTIONS

BVR, AZR, AUG, and ASA were involved in the conception and design of this study. BVR, LCHB, AMS, MRT were involved in the analysis and interpretation of the data. All authors were involved in drafting the manuscript. All authors reviewed and approved the final manuscript and agree to be held accountable for all aspects of the work

 

ETHICAL APPROVAL

Approved by the Bioethics committee (CEISHSOLCAQ. OBS.19.125)

 

FINANCING

All funds for publications used to support this work were allocated by UDLA.

 

ACKNOWLEDGEMENTS

The authors would like to express their special thanks to the UDLA (University of Las Americas).

 

CONFLICT OF INTEREST

The authors have explicitly stated that there are no conflicts of interest in this article.

 

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Correspondence:
RB Velasquez
Prosthetic Research Department. School of Dentistry Universidad de Las Americas ( UDLA). Av. Colón y 6. Diciembre CP 170523, Quito-Ecuador.
Tel: + 593023981000 ext 3060, + 593984938162; Email: byron.velasquez@udla.edu.ec/drvelasquezron@gmail.com

 

 

 

Author Contribution:
1. Conceptualitation: Byron Velasquez Ron
2. Data curation: Alexandra Mena Serrano/Luis Chauca
3. Formal Analysis: Byron Velásquez Ron, Anabel Zambrano, Ana Ulloa, Alexander Sierra, Maria Rodriguez Tates
4. Acquicition of funds: Byron Velasquez Ron, Alexandra Mena Serrano
5. Research: Byron Velásquez Ron, Anabel Zambrano, Ana Ulloa, Alexander Sierra, Maria Rodriguez Tates, Luis Chauca, Alexandra Mena Serrano.
6. Methodology: Byron Velásquez Ron, Alexandra Mena Serrano
7. Proyect administration: Byron Velásquez Ron
8. Means : Byron Velásquez Ron, Anabel Zambrano, Ana Ulloa, Alexander Sierra, Maria Rodriguez Tates, Luis Chauca
9. Software:
10. Supervición: Byron Velásquez Ron, Alexandra Mena Serrano
11. Validation: Byron Velásquez Ron, Anabel Zambrano, Ana Ulloa, Alexander Sierra, Maria Rodriguez Tates, Luis Chauca, Alexandra Mena Serrano
12. Visualitation: Byron Velásquez Ron, Alexandra Mena Serrano
13. Drafting - Byron Velasquez Ron, Anabel Zambrano, original draft: Ana Ulloa, Alexander Sierra, Maria Rodriguez Tates, Luis Chauca, Alexandra Mena Serrano.
14. Drafting - Byron Velásquez Ron, Anabel Zambrano, review and edition Ana Ulloa, Alexander Sierra, Luis Chauca, Maria Rodriguez Tates, Alexandra Mena Serrano