Difference between revisions of "Is dopaminergic medication dose associated with self-reported bruxism in Parkinson's disease? A cross-sectional, questionnaire-based study"

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(Created page with "{{transl}} {{FR | Title = Is dopaminergic medication dose associated with self-reported bruxism in Parkinson’s disease? A cross-sectional, questionnaire-based study | author1 = M. C. Verhoeff | author2 = M. Koutris | author3 = M. K. A. van Selms | author4 = A. N. Brandwijk | author5 = M. S. Heres | author6 = H. W. Berendse | author7 = K. D. van Dijk | author8 = F. Lobbezoo | author9 = | author10 = | Source = https://pubmed.ncbi.nlm.nih.gov/32918624...")
 
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==== Data analysis ====
==== Data analysis ====
Aggregation of medication usage per participant was achieved through the use of the levodopa equivalent daily dosage (LEDD) [22, 23]. According to Tomlinson, the LEDD is a ‘summation of the calculated conversion factors of each individual antiparkinsonian drug, aligned to 100 mg immediate release levodopa’ [22] (see Table ​Table11 for an example). All LEDD scores were calculated by two independent examiners (NB and MH). When no consensus was reached between the two examiners (N = 169), a third examiner (MV) calculated the LEDD separately. When consensus was reached, this LEDD score was used. When no consensus was reached or doubt occurred between the three examiners, a neurologist experienced with calculating LEDD scores was contacted (KvD) (N = 35). Most of the time, a conflict occurred because participants did not report that a medicine with slow release was used instead of immediate release. However, based on the dosage and frequency of the intake, it could be determined if immediate release or slow release was taken. Also, handwriting mistakes were made (e.g., 2,75 mg instead of 275 mg a day). The following general agreement was made: when medication usage was ambiguous or the medication list was not completed, participants were excluded from the data analysis (N = 166). Imputation methods were not used because of the amount of missings (> 20%) and the non-random distribution of the missings, which is in line with the recommendations when to use imputation methods [24].
Aggregation of medication usage per participant was achieved through the use of the levodopa equivalent daily dosage (LEDD) [22, 23]. According to Tomlinson, the LEDD is a ‘summation of the calculated conversion factors of each individual antiparkinsonian drug, aligned to 100 mg immediate release levodopa’ [22] (see Table 1 for an example). All LEDD scores were calculated by two independent examiners (NB and MH). When no consensus was reached between the two examiners (N = 169), a third examiner (MV) calculated the LEDD separately. When consensus was reached, this LEDD score was used. When no consensus was reached or doubt occurred between the three examiners, a neurologist experienced with calculating LEDD scores was contacted (KvD) (N = 35). Most of the time, a conflict occurred because participants did not report that a medicine with slow release was used instead of immediate release. However, based on the dosage and frequency of the intake, it could be determined if immediate release or slow release was taken. Also, handwriting mistakes were made (e.g., 2,75 mg instead of 275 mg a day). The following general agreement was made: when medication usage was ambiguous or the medication list was not completed, participants were excluded from the data analysis (N = 166). Imputation methods were not used because of the amount of missings (> 20%) and the non-random distribution of the missings, which is in line with the recommendations when to use imputation methods [24].
 
 
'''Table 1'''
[[File:Verhoeff 1.jpg|alt=|left|thumb|Table1 Anexampleofa medication list, aligned to 100 mg of immediate release levodopa with the use of conversion factors of different types of dopaminergic medication]]
 


[[File:Verhoeff 1.jpg|alt=|left|thumb|'''Table1:''' Anexampleofa medication list, aligned to 100 mg of immediate release levodopa with the use of conversion factors of different types of dopaminergic medication]]


An example of a medication list, aligned to 100 mg of immediate release levodopa with the use of conversion factors of different types of dopaminergic medication
An example of a medication list, aligned to 100 mg of immediate release levodopa with the use of conversion factors of different types of dopaminergic medication


Descriptives were calculated for gender, age, time since PD diagnosis, and LEDD. Besides, the prevalence was calculated for awake bruxism and sleep bruxism. Additionally, for the dependent variables awake bruxism and sleep bruxism, multiple logistic regression models were built and odds ratios with confidence intervals were calculated. First, the unadjusted associations with gender, age, time since PD diagnosis, LEDD, TMD pain, jaw locks, and self-reported tooth wear were determined. Variables that showed at least a weak association (p < 0.10) with the outcome variables ‘awake bruxism’ or ‘sleep bruxism’ were included in the multiple logistic regression models. Through the step-by-step approach, the individual variables with the weakest association with the dependent variable were removed from the model (p-to-exit value), until all independent variables showed at least a p value < 0.05 in the final model. ORs smaller than 1.5 and ORs above 5 were considered as small and large clinical effect sizes, respectively [25]. All analyses were performed using the IBM SPSS Statistics 26 software package (IBM Corp, Armonk, NY, USA). Probability levels of less than 0.05 were considered statistically significant.
Descriptives were calculated for gender, age, time since PD diagnosis, and LEDD. Besides, the prevalence was calculated for awake bruxism and sleep bruxism. Additionally, for the dependent variables awake bruxism and sleep bruxism, multiple logistic regression models were built and odds ratios with confidence intervals were calculated. First, the unadjusted associations with gender, age, time since PD diagnosis, LEDD, TMD pain, jaw locks, and self-reported tooth wear were determined. Variables that showed at least a weak association (p < 0.10) with the outcome variables ‘awake bruxism’ or ‘sleep bruxism’ were included in the multiple logistic regression models. Through the step-by-step approach, the individual variables with the weakest association with the dependent variable were removed from the model (p-to-exit value), until all independent variables showed at least a p value < 0.05 in the final model. ORs smaller than 1.5 and ORs above 5 were considered as small and large clinical effect sizes, respectively [25]. All analyses were performed using the IBM SPSS Statistics 26 software package (IBM Corp, Armonk, NY, USA). Probability levels of less than 0.05 were considered statistically significant.
[[File:Verhoeff 2.jpg|thumb|Table 2: Demographic information and prevalences of the independent variables (including missings) of the included participants with PD (N = 395)]]


=== Results ===
=== Results ===
In Table ​2 the demographic characteristics of the participants are presented. The prevalences of possible awake bruxism and sleep bruxism in patients with PD were 46.0% and 24.3%, respectively (see Table ​Table2).
[[File:Verhoeff 2.jpg|thumb|'''Table 2:''' Demographic information and prevalences of the independent variables (including missings) of the included participants with PD (N = 395)]]In Table ​2 the demographic characteristics of the participants are presented. The prevalences of possible awake bruxism and sleep bruxism in patients with PD were 46.0% and 24.3%, respectively (see Table2).
 
[[File:Verhoeff 3.jpg|left|thumb|Table 3: Single and multiple regression analysis of variables associated with possible sleep bruxism in patients with PD (N = 283). The associated p value and odds ratio (OR) with 95% confidence interval (CI) are presented]]
 
In this study, the LEDD appeared not to be associated with awake or sleep bruxism (see Tables ​Tables33 and ​and4).4). The results of the single and multiple logistic regression analyses for possible awake bruxism and sleep bruxism are shown in Tables ​Tables33 and ​and4,4, respectively. The unadjusted associations for awake bruxism showed a possible association (p < 0.10) with age (odds ratio (OR) 0.94; 95% CI 0.92–0.97), sleep bruxism (OR 11.50; 95% CI 6.02–21.99), TMD pain (OR 6.78; 95% CI 3.97–11.58), jaw locks (OR 3.83; 95% CI 1.91–7.71), and tooth wear (OR 4.98; 95% CI 3.03–8.17). In the multiple regression analysis, only sleep bruxism (OR 8.82; 95% CI 3.56–20.40), TMD pain (OR 4.51; 95% CI 2.31–8.79), and tooth wear (OR 1.87; 95% CI 1.02–3.43) remained significant. The unadjusted associations for sleep bruxism showed a possible association (p < 0.10) with female gender (OR 2.24; 95% CI 1.36–3.68), age (OR 0.94; 95% CI 0.91–0.96), awake bruxism (OR 11.50; 95% CI 6.02–21.99), TMD pain (OR 4.65; 95% CI 2.74–7.88), jaw locks (OR 3.81; 95% CI 1.96–7.41), and tooth wear (OR 16.64; 95% CI 7.26–38.13). According to the multiple regression model, the following variables were significantly associated with the report of sleep bruxism: awake bruxism (OR 9.48; 95% CI 4.24–21.19) and tooth wear (OR 12.49; 95% CI 4.97–31.38). Besides, a trend towards a significant association of sleep bruxism with TMD pain was shown (p-to-exit value 0.057). For both awake and sleep bruxism models, no statistically significant difference was found between the observed and predicted probabilities, according to the Hosmer and Lemeshow test (p = 0.92 and 0.85, respectively), concluding that both models fit the observed data.
 
 
 


[[File:Verhoeff 4.jpg|thumb|''R''2 = .48(Nagelkerke), 0.32 (Cox and Snell). ''X''2 (2) = 109.5, ''p'' < 0.001]]
[[File:Verhoeff 3.jpg|left|thumb|'''Table 3:''' Single and multiple regression analysis of variables associated with possible sleep bruxism in patients with PD (N = 283). The associated p value and odds ratio (OR) with a 95% confidence interval (CI) are presented]]


In this study, the LEDD appeared not to be associated with awake or sleep bruxism (see ​Tables 3 ​and 4). The results of the single and multiple logistic regression analyses for possible awake bruxism and sleep bruxism are shown in ​Tables 3 and ​and4, respectively. The unadjusted associations for awake bruxism showed a possible association (p < 0.10) with age (odds ratio (OR) 0.94; 95% CI 0.92–0.97), sleep bruxism (OR 11.50; 95% CI 6.02–21.99), TMD pain (OR 6.78; 95% CI 3.97–11.58), jaw locks (OR 3.83; 95% CI 1.91–7.71), and tooth wear (OR 4.98; 95% CI 3.03–8.17). In the multiple regression analysis, only sleep bruxism (OR 8.82; 95% CI 3.56–20.40), TMD pain (OR 4.51; 95% CI 2.31–8.79), and tooth wear (OR 1.87; 95% CI 1.02–3.43) remained significant. The unadjusted associations for sleep bruxism showed a possible association (p < 0.10) with female gender (OR 2.24; 95% CI 1.36–3.68), age (OR 0.94; 95% CI 0.91–0.96), awake bruxism (OR 11.50; 95% CI 6.02–21.99), TMD pain (OR 4.65; 95% CI 2.74–7.88), jaw locks (OR 3.81; 95% CI 1.96–7.41), and tooth wear (OR 16.64; 95% CI 7.26–38.13). According to the multiple regression model, the following variables were significantly associated with the report of sleep bruxism: awake bruxism (OR 9.48; 95% CI 4.24–21.19) and tooth wear (OR 12.49; 95% CI 4.97–31.38). Besides, a trend towards a significant association of sleep bruxism with TMD pain was shown (p-to-exit value 0.057). For both awake and sleep bruxism models, no statistically significant difference was found between the observed and predicted probabilities, according to the Hosmer and Lemeshow test (p = 0.92 and 0.85, respectively), concluding that both models fit the observed data.
=== Discussion ===
=== Discussion ===
The first aim of the present study was to determine the prevalence of possible awake bruxism and sleep bruxism in a population of PD patients. The results showed a respective prevalence of 46.0% and 24.3% for these conditions. The second aim was to investigate possible associations between the dose of dopaminergic medication and the presence of awake and sleep bruxism. The results showed that in a PD population, the levodopa equivalent daily dosage (LEDD) was not associated with the self-reports of awake and sleep bruxism. Hence, the hypothesis formulated in the introduction, viz., that there is an association between awake bruxism/sleep bruxism and dopaminergic medication, could not be accepted. Furthermore, this study examined whether other factors were significantly associated with self-reported awake and sleep bruxism. Co-occurrence of both awake bruxism and sleep bruxism was observed. Besides, there was an association with tooth wear and both circadian manifestations of bruxism. Finally, awake bruxism was also found to be associated with TMD pain.
[[File:Verhoeff 4.jpg|thumb|'''Table 4:''' ''R''<sup>2</sup> = .48(Nagelkerke), 0.32 (Cox and Snell). ''X''<sup>2</sup> (2) = 109.5, ''p'' < 0.001]]The first aim of the present study was to determine the prevalence of possible awake bruxism and sleep bruxism in a population of PD patients. The results showed a respective prevalence of 46.0% and 24.3% for these conditions. The second aim was to investigate possible associations between the dose of dopaminergic medication and the presence of awake and sleep bruxism. The results showed that in a PD population, the levodopa equivalent daily dosage (LEDD) was not associated with the self-reports of awake and sleep bruxism. Hence, the hypothesis formulated in the introduction, viz., that there is an association between awake bruxism/sleep bruxism and dopaminergic medication, could not be accepted. Furthermore, this study examined whether other factors were significantly associated with self-reported awake and sleep bruxism. Co-occurrence of both awake bruxism and sleep bruxism was observed. Besides, there was an association with tooth wear and both circadian manifestations of bruxism. Finally, awake bruxism was also found to be associated with TMD pain.


==== Prevalence of awake and sleep bruxism ====
==== Prevalence of awake and sleep bruxism ====
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