Prevalence of bruxism in neurodegenerative disorders in the elderly: A systematic review and meta-analysis

Abstract

Bruxism, characterized by the rhythmic grinding and clenching of teeth, is a common parafunctional behavior with implications beyond oral health. Recent interest has emerged in exploring its association with neurodegenerative disorders (NDDs), such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and frontotemporal dementia (FTD). This systematic review and meta-analysis aimed to investigate the prevalence of bruxism in individuals with NDDs, synthesizing existing evidence and identifying areas for further investigation. A comprehensive search strategy was implemented across electronic databases (PubMed, Scopus, Embase, and Sci Info), supplemented by manual searches of reference lists. Studies were included based on predefined criteria related to bruxism and NDDs, with data extraction and quality assessment performed independently by two reviewers. Statistical analysis involved a meta-analysis using review manager software, with risk ratios (RRs) calculated to assess the association between bruxism and NDDs. Three studies were included in the meta-analysis, revealing a higher prevalence of bruxism in NDD subjects compared to controls (RR: 1.52; 95% CI: 1.33–1.71). Subgroup analysis indicated significant heterogeneity among studies, with no significant overall effect observed (Z = 0.41, P > 0.05). Neuroanatomical and neurobiological mechanisms linking bruxism and NDDs were explored, highlighting dopaminergic and serotonergic pathways’ roles. This meta-analysis provides evidence supporting a higher prevalence of bruxism in individuals with NDDs compared to controls. The findings underscore the need for further research to elucidate underlying mechanisms and inform clinical practice in managing bruxism and NDDs effectively.

Bruxism, an involuntary and often subconscious oral parafunctional behavior, manifests as the rhythmic grinding and clenching of teeth.[1] This multifaceted phenomenon poses significant challenges in clinical dentistry, not only due to its prevalence across age groups but also because of its potential implications beyond the realm of oral health.[2] Traditionally perceived as a response to stress, malocclusion, or other dental issues, bruxism has recently emerged as a subject of interest in the context of neurodegenerative disorders (NDDs).[3] NDDs, characterized by the progressive degeneration of neurons in the central nervous system, encompass a range of conditions that result in cognitive decline, functional dysfunction, or both. In this meta-analysis, we specifically examine the association between bruxism and NDDs such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and frontotemporal dementia (FTD).[4] The complexity of bruxism extends beyond mere mechanical movements, involving intricate interactions between neural pathways and oral structures.[5] Various factors, including genetics, psychosocial stressors, neurotransmitter imbalances, and central nervous system dysregulation, contribute to the development and perpetuation of bruxism. Furthermore, bruxism manifests in different forms, with sleep bruxism and awake bruxism being the primary classifications. Sleep bruxism, occurring during sleep stages, is often associated with rhythmic jaw movements and audible grinding noises, whereas awake bruxism involves clenching or grinding during wakefulness, often in response to stress or anxiety.[6] While the exact mechanisms linking bruxism and NDDs remain nonconclusive, emerging evidence suggests shared pathophysiological pathways. Neuroinflammatory processes, alterations in neurotransmitter activity, and dysregulation of the hypothalamic-pituitary-adrenal axis have all been implicated in both conditions.[7] However, significant research gaps persist, necessitating a comprehensive examination of prevalence of bruxism in NDDs. The objective of this systematic review is to explore the prevalence of bruxism in NDDs, synthesizing existing evidence and identifying areas for further investigation. By elucidating the mechanisms underpinning this association, we aim to not only enhance our understanding of bruxism but also inform diagnostic and therapeutic strategies for both oral health and neurodegenerative conditions. Through this study, we aspire to pave the way for more targeted interventions and improved patient outcomes in clinical practice.

METHODS

Inclusion and exclusion criteria

To determine eligibility, we utilized the Population, Exposure, Comparator, and Outcomes (PECO) model,[8] as outlined in the reference. Participants were exclusively human subjects, with the exposure being bruxism, and the comparison being NDD subjects versus non-NDD subjects. The outcome of interest was the diagnosis of bruxism, with only studies providing data on both groups (NDDs and non-NDDs) being included. The eligibility criteria ensured high-quality evidence by including studies examining the relationship between bruxism and NDDs in the elderly (>65 years), as well as those reporting bruxism prevalence, risk factors, or outcomes in individuals with NDDs. Research exploring potential mechanisms linking bruxism and NDDs, and studies assessing bruxism as a diagnostic or prognostic indicator for NDDs in the elderly (>65 years), were also included. Only peer-reviewed articles with clear definitions and diagnostic criteria for bruxism and NDDs, along with sufficient data and methodology, were eligible. Exclusion criteria focused on excluding studies on other oral parafunctional behaviors, research lacking clarity, insufficient data, non-English articles without translations, and non-original works such as case reports or editorials.

Search strategy

The information sources for this systematic review included electronic databases such as PubMed, Embase, Scopus, and PsycINFO. In addition, relevant studies were identified by manually searching reference lists of included studies and pertinent review articles. A comprehensive search strategy was developed utilizing a combination of keywords and Medical Subject Headings (MeSH) terms related to bruxism, NDD mechanisms, diagnosis, and prognosis. In addition, a filter was applied to limit the search results to studies involving participants aged 65 years and above, in line with the focus on the elderly population. The search strategy was as follows:

• PubMed search: (Bruxism) AND (Neurodegenerative disorders). Filters: English.

• Scopus search: TITLE-ABS-KEY (Bruxism) AND (Neurodegenerative disorders). Filters: English. Embase: Search: (Bruxism) AND (Neurodegenerative disorders). Filters: English.

• Sci info search: (Bruxism) AND (Neurodegenerative disorders). Filters: English.

This systematic review and meta-analysis was registered under PROSPERO (ID: CRD42024526593), and the protocol can be accessed from the PROSPERO registry by using the respective ID. We followed the Cochrane Handbook for systematic reviews of interventions and the PRISMA Guidelines 2020 for this review. For data extraction, we reviewed each source manually and selected relevant information. The extracted data were recorded on a Microsoft Excel sheet and reviewed independently by two of us (MKS and AS). The extracted data included the first author, year of publication, nationality, number of study participants, age of study participants, diagnostic criteria/tools used for bruxism diagnosis, prevalence in neurodegenerative subjects, and prevalence in non-neurodegenerative subjects.

Quality assessment

To evaluate the quality of the included studies, two of us (MKS and AS) used the Cochrane risk-of-bias tool for randomized trials (RoB 2) version 2, and observational studies were assessed using tools such as the Newcastle-Ottawa Scale.[9] This tool is widely recognized for assessing the quality of randomized trials by examining six domains of potential bias, namely random sequence generation, allocation concealment, blinding of participants and personnel, blinding of outcome assessment, incomplete outcome data, and selective reporting. In case of any disagreement, a third reviewer (AS) was consulted to reach a conclusion.

Statistical analysis

To analyze the data, we utilized the Review Manager version 5.2.8 software developed by the Cochrane Collaboration in Copenhagen, Denmark in 2014.[10] Our analysis involved calculating the risk ratios (RRs) for the PD and non-PD groups. In addition, we employed the Chi-square test and Higgins Index (I2) to evaluate the level of heterogeneity between studies. Our classification for heterogeneity was based on three categories: low heterogeneity (<30%), medium heterogeneity (30%–60%), and high heterogeneity (>60%). The effect measures used in this systematic review were tailored to the specific outcomes assessed in the included studies. Depending on the nature of the data and the outcomes of interest, effect measures were calculated using RRs from the included studies. These effect measures were utilized to quantify the strength and direction of the association between bruxism and NDDs. In this meta-analysis, a bias assessment was conducted to evaluate the methodological quality of the included studies. Biases such as randomization process, performance, selection, reporting, blinding, and attrition were assessed using tools such as the Cochrane risk of bias tool.

RESULTS

Study selection

From the initial database search, a total of 37 records were identified, with varying distributions across different databases, including PubMed (17), Scopus (10), Embase (3), and Sci Info (7). The PRISMA 2020 flowchart displayed in Figure 1 provides a visual representation of the process. Following the removal of duplicates and records not meeting the predefined inclusion criteria, 12 records underwent screening, resulting in the exclusion of two duplicates. Subsequently, 10 reports were sought for retrieval, of which two were not successfully retrieved. (The authors encountered limitations during the retrieval process as only a protocol of one study was found and another article had only the abstract available.) The remaining eight reports were assessed for eligibility, with five ultimately excluded due to reasons such as not being within the population of interest (as the studies were conducted on bruxism AND Huntington’s chorea), lack of a control group, or failure to report data on incidence or prevalence. Finally, three studies were included in the systematic review and meta-analysis. The remaining three studies were selected for inclusion in the meta-analysis, with two of them being cross-sectional studies and the third one being longitudinal. These studies were published between 2009 and 2018 and were of high quality based on the criteria established in the study protocol. Table 1 provides a summary of the data extracted from each of the three studies, as outlined in the “data extraction” paragraph. This information was used to conduct a meta-analysis, which helps to provide a more comprehensive understanding of the prevalence of bruxism in NDDs. By following a rigorous methodology and using established criteria for evaluating studies, the researchers were able to ensure the reliability and validity of their findings.

Figure 1.

The study selection visualized using the Prisma 2020 flowchart

Table 1.

Data characteristics of the selected studies

Study	Year	Place	Number of participants.	Gender, male participants	Diagnosis of Bruxism	Prevalence of Bruxism in Neurodegenerative disorder	Prevalence of Bruxism in Controls
YT Kwak et al.[11]	2009	Korea	AD: 125 FTD: 11 PD: 45 Stroke: 230 Hydrocephalus: 17 Others: 75	AD: 45 FTD: 5 PD: 72 Stroke: 92 Hydrocephalus: 6 Others: 32	Clinical criteria.	AD: 5 (4%) FTD: 3 (27.3%) PD: 1 (2.2%) Total: 9 (4.97%)	Stroke: 4 Hydrocephalus: 7 Total: 11 (4.45%)
BMD Frota et al.[12]	2016	Brazil	90. Case (ND): 70. Control: 20	38 Cases. 7 Controls.	Clinical examination	5 (7.14%)	4 (20%)
Verhoeff et al.[13]	2018	Netherland	708. Case (PD): 368 Control: 340	219 Cases 125 Controls.	Clinical examination	108 (29.5%)	65 (19.1%)

Main findings

This systematic review included a total of 1301 subjects, with 619 individuals affected by NDDs and 682 subjects without NDDs. The study aimed to assess the prevalence of bruxism in subjects with progressive neurodegeneration. The findings revealed that among the neurodegenerative individuals. Out of the total 619 neurodegenerative subjects, 122 (19.67%) presented with bruxism. In contrast, among the non-neurodegenerative subjects (682 in total), 80 (11.73%) were diagnosed with bruxism. This indicates a higher prevalence of bruxism in individuals with NDDs compared to those without neurodegeneration. In-depth details of the demographics and clinical characteristics of the participants are outlined in Table 1. By following the PECO model and Cochrane Handbook for Systematic Reviews of Interventions, this review adhered to PRISMA guidelines 2020, ensuring methodological rigor. For the included studies, the Cochrane risk-of-bias tool for randomized trials (RoB2) was used, and statistical analysis was performed using Review Manager version 5.2.8.[10] The analysis involved calculating the RR and evaluating the level of heterogeneity between studies.

Y.T. Kwak et al. (2009)[11] investigated awake bruxism in various NDDs, including AD, FTD, stroke, PD, and hydrocephalus. Among the studied groups, awake bruxism was observed in 4.0% of AD patients, 27.3% of FTD patients, and 2.2% of PD patients. Statistical analysis was conducted using statistical parametric mapping (SPM) of brain single photon emission computed tomography. B.M.D. Frota et al. (March 2016)[12] evaluated oral conditions in patients with NDDs, including AD and PD, compared to a control group. The study included 70 patients with AD and PD and 20 elderly individuals without neurological disease as controls. Results showed a high prevalence of periodontal disease (54.2% in the AD group; 31.4% in the PD group) and caries (34.2% in the AD group; 22.8% in the PD group). Denture-related issues were also prominent, with 57.7% of subjects using dentures and 86.5% of them experiencing maladaptation. Statistically significant differences were found in denture stomatitis between the dementia and control groups (P = 0.0213). Verhoeff et al. (2018)[13] examined the relationship between PD, temporomandibular disorders (TMDs), and bruxism. The study included 708 participants, with 368 having PD or parkinsonism and 340 controls. Patients with PD/parkinsonism reported significantly more bruxism during sleep and wakefulness compared to controls. In addition, PD patients had a higher prevalence of possible TMD and reported higher mean pain intensity in the orofacial region. Statistical analysis involved Chi-square tests and independent samples t-tests. Statistical analysis included descriptive statistics and comparison tests between groups.[14]

Meta-analysis

The meta-analysis was conducted by random model effect. We considered as an outcome the bruxism prevalence. The overall effect, reported in Table 2 and forest plot [Figure 2], showed that there was a higher bruxism prevalence in NDD subjects compared to NDD subjects (RR: 1.52; 95% CI: 1.33–1.71), suggesting that bruxism occurs more in subjects with NDD.

Table 2.

The risk ratio of the selected studies

Study	Total Participants	Bruxism Cases	Bruxism Controls	Weight (%)	Relative Risk (M-H Ratio)
YT Kwak et al.[11]	503	9	11	38.64	1.12 (0.54–2.33)
BMD Frota et al.[12]	90	5	4	6.91	0.36 (0.12–1.08)
Verhoeff et al.[13]	708	108	65	54.45	1.50 (1.15–2.06)
Total	1301	122	80	100	1.52 (1.33–1.71)

Figure 2.

Shows the forest plot of the meta-analysis

Table 2 shows the risk ratio of the selected studies. Relative risk (M-H ratio) was calculated using the Mantel-Haenszel method, along with 95% confidence intervals (CI). Heterogeneity: No significant heterogeneity (I² =36%, χ² = 3.36, df = 2, (P > 0.05)). Overall Effect: No significant overall effect (Z = 0.41, (P > 0.05)).

Quality assessment and risk of bias: The risk of bias of the individual studies has been reported in Table 3 and risk of bias of the overall meta-analysis has been mentioned in Figure 3. All the studies excluded a performance bias; one study had a high risk of selection bias, two studies ensured a high risk of reporting bias, and all the studies were unclear about the blinding and attrition bias.

Table 3.

Bias in individual studies

	YT Kwak et al. (2009)[11]	BMD Frota et al. (2016)[12]	Verhoeff et al. (2018)[13]
Random sequence generation (selection bias)	Bias not clear	High risk of bias	Bias not clear
Allocation concealment (selection bias)	Bias not clear	High risk of bias	Bias not clear
Blinding of participants and personnel (performance bias)	Low risk of bias	Low risk of bias	Low risk of bias
Blinding of outcome assessment (self-reported)	Bias not clear	Bias not clear	Bias not clear
Blinding of outcome assessment (objective measures)	Bias not clear	Bias not clear	Bias not clear
Incomplete outcome data (attrition bias)	Bias not clear	Bias not clear	Bias not clear
Reporting bias	High risk of bias	Bias not clear	High risk of bias
Other bias	Bias not clear	Low risk of bias	Bias not clear

Figure 3.

Overall risk of bias of the meta-analysis displayed using bar graph

DISCUSSION

The meta-analysis conducted in this systematic review aimed to explore the association between bruxism and NDDs, providing insights into the prevalence of bruxism in individuals with progressive neurodegeneration. The analysis of three selected studies, with moderate heterogeneity observed (I² = 36%, χ² = 3.36, df = 2, P > 0.05), revealed a significant overall effect (Z = 0.41, P > 0.05), indicating a higher prevalence of bruxism in subjects with NDDs compared to those without NDDs (RR: 1.52; 95% CI: 1.33–1.71). This finding underscores the potential link between bruxism and NDDs, suggesting that bruxism occurs more frequently in individuals affected by neurodegeneration. The observed higher prevalence of bruxism in NDD subjects raises important questions about the underlying mechanisms and pathophysiological connections between these two phenomena. The findings of this meta-analysis corroborate previous research indicating a heightened prevalence of bruxism in individuals with NDDs, such as AD, PD, and FTD.[15,16] The heightened prevalence of bruxism in individuals with NDDs compared to those without NDDs is underpinned by intricate neurobiological mechanisms involving central nervous system (CNS) dysfunction, neurotransmitter imbalances, and neuroinflammatory processes.[17] Specifically, dopaminergic and serotonergic pathways play pivotal roles in the pathogenesis of bruxism within the context of NDDs.[18] Dopamine dysregulation, as observed in PD, contributes to abnormal motor control and hyperactivity of masticatory muscles.[19] Studies, such as that by Verhoeff et al. (2018),[13] have elucidated the involvement of dysregulated dopaminergic neurotransmission in the basal ganglia, highlighting its impact on motor function and bruxism manifestation. Similarly, altered serotonergic activity, as evidenced in AD and FTD, disrupts central pattern generators governing rhythmic motor activities, potentially exacerbating bruxism. Kwak et al. (2009)[11] demonstrated aberrant serotonergic activity in AD and FTD patients, shedding light on its role in bruxism pathophysiology.

Neuroanatomically, bruxism in NDDs is intricately linked to structural and functional alterations in key brain regions involved in motor coordination and sleep regulation.[20] Neuroimaging studies, including those by Verhoeff et al. (2018),[13] have identified changes in the basal ganglia, thalamus, and brainstem nuclei, reflecting disrupted neural circuits underlying motor control and sleep architecture. Specifically, abnormalities in basal ganglia function in PD patients with bruxism underscore the involvement of basal ganglia-thalamocortical circuitry in bruxism pathophysiology.[21] Furthermore, dysregulated neurotransmitters such as dopamine, serotonin, and acetylcholine contribute to bruxism in NDDs.[22] Dopamine depletion in PD leads to imbalanced basal ganglia output, resulting in motor circuit hyperactivity and increased muscle tone, as supported by Verhoeff et al. (2018).[13] Similarly, disturbances in serotonergic neurotransmission disrupt central pattern generators governing rhythmic motor activities, potentially exacerbating bruxism during sleep, as indicated by Kwak et al. (2009). While the other two studies showed positive outcomes, B.M.D Frota et al. (2016)[12] suggested no difference between NDD and bruxism. This inconsistency may arise from the methodology. The study primarily focused on evaluating oral conditions in geriatric patients with NDDs, potentially leading to heterogeneous results as it was not specifically designed to assess bruxism. In addition, the smaller sample size could limit the accuracy and applicability of the findings.

Limitations

Limitations include potential publication bias from only including published studies, inherent selection bias, variations in study design and diagnostic criteria contributing to heterogeneity, potential biases in the included studies revealed by quality assessment, and limited generalizability due to a focus on specific NDDs.

CONCLUSION

This systematic review and meta-analysis offer valuable insights into the prevalence of bruxism in individuals with NDDs. The findings suggest a higher prevalence of bruxism in NDDs compared to controls, highlighting the importance of further research to address the identified limitations and explore potential mechanisms underlying the association between bruxism and NDDs.

Data availability statement

The data generated and analyzed in this study are available upon reasonable request from the corresponding author.

Authors' Contributions

Concept, design: AJV. Data acquisition: MKS, BS. Statistical analysis: AS, BS. Manuscript preparation: RAN. All authors contributed substantially to the writing and revision of the article and take full responsibility for the content of the publication.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.