Maximum Muscle Output and Electromyographic Activity of Masticatory Muscles in Persons With Parkinson's Disease. A Case–Control Study

ABSTRACT

Background

Parkinson's disease (PD) affects the motor system of the body; however, there is limited understanding of how the disease impacts the complex interaction of the masticatory muscles.

Objective

The purpose of this study is to investigate the maximum muscle output of the masticatory muscles during natural functions.

Methods

This clinical case–control study included persons with PD and age‐ and gender‐matched controls without PD. The masticatory muscle output was evaluated by bite force and bilateral surface electromyography. Electromyographic recordings were conducted from the anterior temporal, masseter and digastric muscles during chewing and maximum voluntary contraction (MVC) during maximal intercuspal biting (MVC biting) and maximal jaw opening (MVC opening). Statistical analyses included χ²‐test, Mann–Whitney U test and Spearman's rank correlation analysis (significance level p < 0.05).

Results

The study included 20 persons with PD (median age: 68.5 years) and 20 persons without PD (median age: 67 years). No significant differences were found between the groups in terms of demographics, teeth present, or bite force measurements. The activity in the masseter muscle was significantly lower in the PD group during MVC biting. The PD group utilised 82% of their masseter muscle MVC during chewing, whereas the control group used 49% of theirs. Additionally, a negative correlation was observed between the severity of PD and the bite force and digastric muscle activity during MVC opening.

Conclusion

These findings indicate that PD may alter the activity patterns of the masticatory muscles during function. This new understanding can be utilised to design targeted interventions aimed at improving orofacial function for this patient group.

1. Background

Parkinson's disease (PD) is a complex neurodegenerative condition that poses a significant burden on global healthcare systems and profoundly affects individuals' quality of life [1]. With approximately 2% of the global population aged over 65 affected, PD is one of the most prevalent age‐related conditions and is experiencing the most rapid growth among neurological disorders globally [1, 2, 3]. The number of people with PD is also expected to increase due to the general increase in the number of older adults in the future [1, 4]. PD is characterised by chronic degeneration and progressive changes in the central nervous system leading to the loss of dopaminergic neurons in the substantia nigra, resulting in a cascade of physiological disturbances [5]. The disease is clinically characterised by general motor symptoms, including slow and sluggish movements (hypo−/bradykinesia), involuntary shaking (rest tremor), stiffness and rigidity of the muscles, as well as instability and difficulty in walking [5].

Concurrently, PD induces motor changes that have profound effects on the musculoskeletal system, leading to significant functional limitations and impairment of the orofacial and stomatognathic system, which is essential for functions such as chewing and swallowing [6, 7, 8, 9]. Despite the acknowledgment of masticatory dysfunction in persons with PD, a notable lack of understanding remains regarding the exact impact of PD on masticatory muscles. Studies employing questionnaires on mastication have demonstrated impaired chewing function in persons with PD [10, 11, 12, 13, 14]. Additionally, some clinical studies have used objective measures of masticatory function in dentulous individuals with PD and reported similar findings [11, 15, 16]. Furthermore, a few studies have identified functional alterations in the masticatory system using electromyography [14, 17, 18, 19, 20]. However, there is limited literature on the specific impact of PD on masticatory muscles during maximum muscle output, and no electromyographic studies have investigated the intricate interactions between mandibular elevators (e.g., masseter and temporal) and depressors (e.g., anterior belly of digastric) during natural function. Furthermore, studies with appropriate control groups matched for gender, age and dental status are necessary, as these factors can significantly affect masticatory muscle performance. During mastication, the mandibular elevators and depressors work in intricate coordination to control precise chewing movements, maintain jaw stability and regulate the timing of occlusal contacts [21, 22, 23, 24, 25, 26, 27]. These interactions are complex, requiring neuromuscular coordination to balance the opposing forces involved in jaw opening and closing while adapting to varying food textures and resistances [25, 26]. PD‐associated neuromuscular impairments, characterised by bradykinesia, rigidity and tremor, are likely to disrupt these dynamics, but the extent and mechanisms of such disruptions remain unclear. While the challenges of chewing and swallowing in PD are well‐documented, the lack of detailed studies on how PD affects these neuromuscular interactions presents a critical gap in understanding.

Such research would help clarify the functional changes in the orofacial and stomatognathic systems caused by PD and determine whether the disease affects the activity patterns of the masticatory muscles due to differential impairment of neural activation. These findings could potentially enhance the diagnosis and treatment of muscular dysfunctions, allowing for more personalised therapeutic approaches to improve oral health, dietary intake and overall well‐being.

Hence, this study aims to explore the complex relationship of the orofacial and stomatognathic system during natural function in persons with PD, thereby uncovering the subtle functional patterns linked to the disease. The hypothesis is that PD alters the activity patterns of the masticatory muscles during natural orofacial functions, such as chewing and jaw opening.

2. Methods

2.1. Study Design, Setting and Participants

This clinical case–control study was conducted between May 2021 and December 2022 through a collaboration between the Department of Odontology at the University of Copenhagen, Denmark, and the Department of Neurology at Bispebjerg Hospital in Copenhagen. The PD participants were outpatients at the Department of Neurology and had been diagnosed with PD prior to participating in this study. Recruitment of age‐ and gender‐matched controls was initiated by enlisting the spouses of participants with PD to ensure comparable dental status, diet and socioeconomic background. To supplement this group, additional controls were subsequently recruited through flyers distributed at the hospital, university and public libraries.

Inclusion for both PD participants and controls required full understanding of participant information and cooperation during examinations, as well as the ability to travel to and from the Department of Odontology and to sit upright in a dental chair. Furthermore, PD participants had to be adequately medicated by the neurologist. Exclusion criteria for all participants were cognitive impairment hindering comprehension and cooperation, diagnosis of Sjögren's syndrome, presence of implanted electronic devices (e.g., pacemaker, DBS) and/or prior radiation therapy to the head/neck region.

The trial was registered at ClinicalTrials.gov (NCT05356845) and approved by the Regional Committee on Research Health Ethics of the Capital Region (H‐20047464) and the Danish Data Protection Agency (514‐0510/20‐3000).

2.2. Characteristics and Classification of Participants

For the participants with PD, a neurological examination and severity assessment were performed by a senior consultant in neurology (author MK) at the Department of Neurology at Bispebjerg Hospital in Copenhagen and included:

• –Duration of PD in years.
• –PD staging was assessed using the modified Hoehn and Yahr scale (H&Y) [28], which describes the progression of PD symptoms and evaluates both disability and impairment related to clinical disease progression. The scale consists of five stages, with stage one involving unilateral involvement only and stage 5 indicating being wheelchair‐bound or bedridden.
• –PD severity was assessed using the Unified Parkinson's Disease Rating Scale (UPDRS) [29]. The UPDRS evaluates various aspects of PD, including both non‐motor and motor experiences in daily life. This study utilised two segments of the UPDRS: UPDRS II (self‐evaluation of activities of daily living) and UPDRS III (clinician‐scored motor examination). UPDRS II comprises 13 items, with a score range from 0 to 52, with higher scores indicating more severe disability in motor experiences of daily living. This segment involves self‐assessment of motor aspects in daily activities, including speech, swallowing, hygiene, salivation and tremor. UPDRS III consists of 14 items, with a score range from 0 to 56, with higher scores indicating greater motor disability. This segment involves clinician‐scored evaluations of motor functions, including speech, diminished facial expressions, rigidity, tremor and bradykinesia/hypokinesia.

Subsequently, all participants underwent a dental and orofacial examination by author SB, a dentist with specialised training in clinical oral physiology and orofacial surface electromyography. During these examinations, the participants with PD were in their ‘on’ time, when their PD medications were effective, and their motor symptoms were reduced.

Firstly, a clinical oral examination was conducted regarding:

• –Number of teeth, including fixed prosthetic restorations.
• –Posterior occlusal contacts using the Eichner Index. This classification system assesses occlusal support based on the number and location of posterior tooth contacts, categorising patients into three groups: A (complete posterior support), B (partial support) and C (no posterior support) [30].
• –Maximum unassisted opening without pain in mm. This is achieved by measuring the distance between the incisal edges of the upper and lower central incisors while the mouth is fully open without pain, and then adding the vertical incisal overlap [31].
• –Presence of removable dentures.

Additionally, a systematic evaluation of temporomandibular disorders (TMD) was performed following the Diagnostic Criteria for TMD (DC/TMD), incorporating the Symptom Questionnaire (SQ) and full clinical examination from Axis I [31] and no significant differences were identified between the PD and control group [14].

2.3. Outcomes

Following the dental and orofacial examination, maximum muscle output was assessed. The outcome measures (illustrated in Figure 1) included the following:

FIGURE 1.

Outcome measures of maximum muscle output. MVC, maximum voluntary contraction; sEMG, surface electromyography.

2.3.1. Bite Force

The maximum bite force indicating the total mechanical force of the jaw elevator muscles was measured in Newton (N) by a recorder constructed according to Fløystrand et al. [32], i.e., a strain‐gauge transducer (A/S Mikro Elektronikk, 3191 Horten, Norway) for loads up to 1000 N in a housing (11 × 15 × 4 mm), connected to an amplifier with digital display and storage facilities for peak values (Newport Digital Meter model 204B‐3) [33, 34, 35]. The transducer was placed unilaterally on the first mandibular molar during a 1–2 s period of maximal biting and the peak bite force value was recorded twice on each side. Bite force was calculated as the average of these four measurements, expressed in Newtons.

2.3.2. Surface Electromyography (sEMG)

Simultaneous bilateral sEMG activity was recorded using surface electrodes on the anterior temporal muscles, masseter muscles and anterior belly of the digastric muscles during chewing, maximum intercuspal biting (MVC biting) and maximal jaw opening (MVC jaw opening).

The recordings were conducted with participants seated upright in a dental chair, with their heads unsupported. The temporal and masseter muscles are primary masticatory muscles, while the anterior digastric muscle is an accessory masticatory muscle. Thus, the anterior digastric muscle facilitates the opening of the mouth and contributes to the chewing process. Reusable, bipolar tin surface electrodes (10.0 × 3.0 × 1.5 mm) for the anterior temporal and masseter muscles and (5.0 × 3.0 × 1.5 mm) for the anterior belly of the digastric muscles with electrode paste (SAC2) were utilised to record muscle activity [23, 36]. The electrodes were taped and positioned 1 cm apart and perpendicular to the direction of muscle fibres after skin cleansing with alcohol to reduce electrode impedance. The electrodes for the anterior belly of the digastric muscles were placed just behind the lowest (most inferior) end of the mandibular symphysis. All EMG data were collected, amplified and filtered using an 8‐channel EMG system (8 amplifiers, DISA type 14C10 with gain at 500–10 000; high‐pass filter at 20–50 Hz and low‐pass filter at 1 kHz). The amplified and filtered EMG signals were digitised with 12‐bit resolution and a sample rate of 2.5 kHz (ADC board from Data Translation type DT3001). The recordings were processed using customised software (ODONTEMG by co‐author CET), which initially processes the averaged rectified value (ARV) of the raw EMG signal, and the ARV value (measured in μV) was used as an amplitude indicator during the various tasks.

sEMG activity was recorded during the following three tasks:

2.3.2.1. Chewing

For chewing, the peak ARV of five consecutive chewing cycles was measured using bites of 10 g peeled apple slices. The mean of peak ARV values over the five consecutive strokes was calculated. The chewing task was repeated, giving EMG measurements over two individual chewing sequences, each within a 10 s recording window [36]. Previous studies have demonstrated a well‐defined activation pattern in the anterior portion of the temporalis muscle; consequently, the right anterior temporalis muscle was selected as the reference muscle in our automated EMG measurement system [37, 38]. This muscle served as the reference for timing, with the chewing cycle automatically defined as the interval between the onset of activity in the right anterior temporalis during one closing phase and its onset in the subsequent closing phase.

2.3.2.2. MVC Biting

The participants were instructed to clench as hard as possible in the intercuspal position for 2 s [23]. The peak ARV value was identified. They were asked to repeat the biting, and the mean of the two peak ARV values was calculated.

2.3.2.3. MVC Jaw Opening

The participants were asked to open their jaws as forcefully as possible for 2 s. The peak ARV value was identified. They were asked to repeat the jaw opening, and the mean of the two peak ARV values was calculated.

Furthermore, the following outcome measures were calculated after the participants had completed their recording session:

2.3.2.4. Relative Contraction Level During Chewing Compared to MVC (%)

The relative contraction level for chewing in relation to MVC biting was calculated in percent (mean peak ARV value during chewing/mean peak ARV value during MVC biting (%)); thus, indicating the extent of muscle contraction during chewing relative to MVC biting.

2.3.2.5. Workload

The workload was calculated by integrating the area under the ARV curve of an averaged chewing cycle and dividing it by the cycle duration. This result is then divided by the MVC biting peak ARV value to obtain the relative workload in percent. The workload value can be seen as being equivalent to a static contraction during the entire chewing cycle.

The outcome measures are illustrated in Figure 1.

2.4. Statistics

2.4.1. Power Calculation

A prior study [11] indicated that PD persons have a 50% risk of experiencing orofacial symptoms, compared to a 10% risk in the control group. With a power of 80% and a significance level of 0.05, a sample size of 19 participants per group was required. Therefore, we included 20 PD participants and 20 controls [14].

2.4.2. Statistical Analysis

Statistical analysis was conducted using IBM SPSS Statistics 29. Initially, descriptive statistics were employed to analyse the characteristics of the study population, including age, gender, number of teeth, posterior occlusal contacts and maximum jaw opening. For PD participants, the analysis also encompassed PD status, including disease duration, H&Y staging and UPDRS II and III assessments.

To evaluate the reliability of the sEMG measurements, the Intraclass Correlation Coefficient (ICC) with 95% confidence intervals was calculated using a two‐way random‐effects model for consistency agreement. A threshold of ICC ≥ 0.75 was considered indicative of good reliability. ICCs were computed separately for each task (chewing, MVC biting and MVC jaw opening) and for each muscle (temporal, masseter and digastric), based on the ARV from repeated measures during the same task. The results demonstrated excellent reliability across all recordings. During chewing, ICCs were 0.94 (95% CI: 0.90–0.96) for the temporal muscles, 0.93 (95% CI: 0.89–0.96) for the masseter muscles and 0.91 (95% CI: 0.86–0.95) for the digastric muscles. For MVC biting, ICCs were 0.98 (95% CI: 0.96–0.99) for the temporal muscles and 0.97 (95% CI: 0.95–0.98) for the masseter muscles. During MVC opening, the ICC for the digastric muscle was 0.90 (95% CI: 0.83–0.94).

Due to the non‐normal distribution of the data, non‐parametric analyses were conducted using the Mann–Whitney U Test for continuous variables and the χ²‐test for categorical variables. The small number of participants made it unfeasible to adjust for multiple explanatory variables in regression analyses. Subsequently, the relationship between the neurological assessment for PD participants and the maximum muscle output was assessed by using Spearman's rank correlation coefficient (2‐tailed). Statistical significance was set at p < 0.05.

3. Results

The median age was 68.5 years for the PD group and 67.0 years for the control group (Table 1). Both groups had an equal gender distribution, with 6 males and 14 females in each. There were no significant differences between the PD and control groups in terms of age, gender, number of teeth, posterior occlusal contacts and maximum unassisted jaw opening without pain (Table 1). None of the PD participants had removable dentures, whereas one individual in the control group had a partial denture solely for aesthetic purposes, covering only the front teeth and not the posterior teeth. In the PD group, the duration of PD ranged from 3 to 23 years, with H&Y staging ranging from 1 to 4. The PD medication consisted of Levodopa, MAO‐B inhibitors, dopamine agonists, COMT inhibitors and anticholinergic agents.

TABLE 1.

The characteristics of the study population.

	PD	Control	p
Study population	20	20
Age in years
Median (range)	68.5 (35–80)	67.0 (35–83)	0.62 e
Gender
Male	6	6
Female	14	14	1.0 f
Number of teeth
Median (range)	27 (18–31)	27 (22–31)	0.84 e
Number of persons with Eichner index a
A	17	19
B	3	1	0.30 f
Maximum unassisted opening without pain in mm
Median (range)	50 (37–60)	54 (41–60)	0.15 e
Years with PD
Median (range)	10 (3–23)	—	—
H&Y b
Median (range)	3 (1–4)	—	—
UPDRS II c
Median (range)	12 (5–23)	—	—
UPDRS III d
Median (range)	19 (11–30)	—	—

^a Eichner index: a classification system based on the presence of occlusal contacts in the premolar and molar regions.

^b Modified Hoehn and Yahr scale.

^c Unified Parkinson's Disease Rating Scale II (Motor experience of daily living).

^d Unified Parkinson's Disease Rating Scale III (Motor function).

^e Mann–Whitney U test.

^f χ²‐test.

No significant difference in bite force measurements was found between the two groups (p = 0.17, Mann–Whitney U test); the PD group had a median bite force of 316 N (range: 150 N–672 N), while the control group had a median of 353 N (range: 172 N–701 N).

Figure 2 displays an example of sEMG recordings in the right and left anterior temporal, masseter and anterior belly of the digastric muscles for a person with PD during chewing, MVC biting and MVC opening.

FIGURE 2.

sEMG recordings of activity in the right (R) and left (L) anterior temporal (Temp), masseter (Mass.) and anterior belly of the digastric (Dig.) muscles for a person with PD during chewing, MVC biting and MVC opening.

There was no significant difference in muscle activity observed during chewing and MVC opening between the two groups (Table 2). However, the control group exhibited significantly higher masseter activity (170 μV) during MVC biting compared to the PD group (107 μV) (p = 0.01). This discrepancy was further underscored by the relative contraction level for the masseter during chewing compared to MVC biting; the PD group utilised 82% of their MVC while chewing, whereas the control group utilised 49% of their MVC while chewing (p = 0.02, Table 2). This occurrence is also observed in the workload during mastication, where a significantly greater percentage of muscle activity was exerted by masseter during mastication in the PD group compared to the control group (p = 0.01). The difference in EMG activity between the right and left sides of the muscles during MVC biting was also analysed with the Mann–Whitney U Test to determine if there was any asymmetry in muscle activity in the PD group. However, no significant difference was observed.

TABLE 2.

Difference in sEMG outcomes between PD participants and controls. Difference between groups is analysed with Mann–Whitney U test.

	PD	Control	p
Chewing a
Temporal, median (range)	66 (27–164)	49 (30–134)	0.20
Masseter, median (range)	74 (41–317)	82 (19–244)	0.74
Digastric, median (range)	61 (32–86)	65 (16–136)	0.38
MVC biting a
Temporal, median (range)	112 (34–339)	94 (42–232)	0.45
Masseter, median (range)	107 (27–780)	170 (83–382)	0.01
MVC opening a
Digastric, median (range)	177 (61–260)	198 (77–508)	0.27
Relative contraction level for chewing in relation to MVC biting in %
Temporal, median (range)	55 (40–124)	59 (22–148)	0.96
Masseter, median (range)	82 (25–159)	49 (15–132)	0.02
Workload in %
Temporal, median (range)	19 (10–31)	19 (7–54)	0.45
Masseter, median (range)	26 (9–48)	16 (6–35)	0.01

Abbreviations: MVC, maximum voluntary contraction; sEMG, surface electromyography.

^a Measured in μV for ARV (average rectified value). Bold values, p value under 0.05 and are therefore significant.

Table 3 illustrates the correlation between the duration and severity of PD within the PD group and the bite force and muscle activity during MVC biting for the temporal and masseter muscles, as well as MVC opening for the digastric muscle. No correlation was observed regarding the temporal and masseter muscle activity and progression of the disease. However, a significant strong negative correlation was observed between the activity of the digastric muscle during maximum jaw opening and PD progression, assessed by UPDRS III with a correlation coefficient of −0.80 (p < 0.001). There was no significant correlation found between digastric muscle activity and H&Y staging or disease duration; however, there was a tendency for association between UPDRS II and the activity of the digastric muscle as the p‐value was just above the significance level (p = 0.07). Furthermore, a significant moderate negative correlation was observed between bite force and H&Y staging (correlation coefficient: −0.59, p = 0.013) and UPDRS III (correlation coefficient: −0.62, p = 0.008) (Table 3).

TABLE 3.

Association within the PD participants between duration and severity of PD, and bite force and muscle activity for the anterior temporal and masseter muscles during MVC biting and for the anterior belly of the digastric muscle during MVC opening.

	Duration of PD	H&Y a	UPDRS II b	UPDRSIII c
Bite force
Spearman's rho (95% CI)	−0.25 (−0.66; 0.27)	−0.59 (−0.85; −0.11)	−0.39 (−0.74; 0.13)	−0.62 (−0.86; −0.16)
p‐value	0.33	0.013	0.12	0.008
MVC biting, temporal muscle
Spearman's rho (95% CI)	−0.17 (−0.57; 0.30)	−0.11 (−0.53; 0.35)	−0.19 (−0.58; 0.29)	−0.27 (−0.64; 0.20)
p‐value	0.47	0.65	0.44	0.25
masseter muscle
Spearman's rho (95% CI)	0.17 (−0.30; 0.57)	0.39 (−0.08; 0.72)	0.23 (−0.25; 0.61)	0.36 (−0.12; 0.70)
p‐value	0.48	0.09	0.34	0.12
MVC opening digastric muscle
Spearman's rho (95% CI)	−0.16 (−0.56; 0.31)	−0.35 (−0.69; 0.13)	−0.41 (−0.73; 0.06)	−0.80 (−0.93; −0.50)
p‐value	0.51	0.14	0.07	< 0.001

Note: CI: 95% Confidence intervals based on Fisher's r to z transformation. Standard error is based on formula by Bonett and Wright.

^a Modified Hoehn and Yahr scale.

^b Unified Parkinson's Disease Rating Scale II (Motor experience of daily living).

^c Unified Parkinson's Disease Rating Scale III (Motor function). Bold values, p value under 0.05 and are therefore significant.

4. Discussion

The findings reveal alterations in orofacial function among persons with PD, thus supporting the hypothesis that PD affects the activity patterns of the masticatory muscles during natural orofacial functions. Our results showed no significant difference in bite force measurements and muscle activity during chewing between the PD and control group; however, a negative correlation was observed between the severity of PD and bite force, suggesting a decline in the total mechanical force of the jaw elevator muscles as the motor abilities of the body deteriorate. The control group exhibited significantly higher masseter activity during MVC intercuspal biting compared to the PD group. This discrepancy underscores the increased relative contraction rate for the masseter muscle during chewing in PD participants, suggesting that persons with PD utilise a greater percentage of their MVC while chewing compared to controls. In the case of the PD group, our findings suggest that the masseter muscle is required to exert a higher workload compared to the control group. This could be due to compensatory mechanisms that occur because of PD‐related impairments in other muscles involved in mastication. As PD is characterised by motor difficulties like bradykinesia and rigidity, which can affect motor control, the masseter muscle may take on a greater role in the chewing process to compensate for decreased efficiency in other areas of the masticatory system. Furthermore, the study found a significant negative correlation between the severity of PD and the activity of the digastric muscle during maximum jaw opening. This suggests that as the disease progresses, the functionality of the digastric muscle diminishes, indicating a deterioration in the ability to open the jaw forcefully.

Muscle activity in the anterior temporal muscles, masseter muscles and anterior belly of the digastric muscles during chewing did not show significant differences between the PD and control groups.

These findings align with previous research on the same study population [14], where electromyographic analysis showed no differences in the chewing cycle length or swallowing duration [14]. However, clinical assessments of masticatory efficiency revealed a significant difference: individuals with PD took longer (25 s) to chew and swallow a standardised apple slice compared to the control group (19 s) [14]. Similarly, the control group could swallow 19 mL of water per second, while the PD group managed only 11 mL per second [14]. Other clinical studies also report significant differences in mastication [11, 15, 16]. This could suggest that even if the chewing cycles are not severely affected, various other factors that are critical for chewing may still be impacted, leading to reduced masticatory function. Previous questionnaire‐based research has also indicated impaired chewing abilities in persons with PD [10, 11, 12, 13, 14]. Interestingly, our study found no significant difference in bite force measurements, which contradicts findings from other studies [20, 39]. However, it is worth noting that these studies did not describe the dental status of the groups or were conducted on participants with removable prosthesis.

The temporal and masseter muscles contain a mix of muscle fibre types, including Type I and Type II fibres [23, 40, 41]. Type I fibres are fatigue‐resistant and used for prolonged, low‐intensity contractions, while Type II fibres generate the powerful, rapid contractions required for biting and grinding food. The exact proportion of these fibre types may vary among individuals and be influenced by factors such as age, diet and dental health. The masseter and temporal muscle mostly consist of Type I fibres, but the proportion of Type I fibres is higher in the masseter muscle [23, 40, 41]. Skeletal muscle biopsies from persons with PD in various muscle groups have shown characteristic changes, including an increase in the percentage and size of Type I fibres and a reduction in the size and percentage of Type II fibres [42]. This could explain why our results show no difference in muscle activity during chewing but a difference in MVC, which requires more activation from Type II fibres. The significant reduction in EMG activity observed in the masseter muscle, but not the temporalis, could be attributed to the initially smaller proportion of Type II fibres in the masseter, making it more susceptible to the reduction of these fibres. Additionally, the digastric muscle predominantly consists of Type II fibres [40], which could also explain why its activity declines as the disease progresses. Furthermore, it is important to consider that the digastric muscle also functions as a pharyngeal muscle, and thus the reduced muscle activity as the disease progresses could contribute to the most reported orofacial motor symptom, which is dysphagia [14]. Previous studies have shown that training of the orofacial muscles for this patient group enhances both objective and subjective orofacial function [13, 16]. Investigating the specific muscle fibres that benefit from such training would be an interesting area for further research.

The characteristics of the two groups were largely similar, with no significant differences observed in factors affecting orofacial function, including the number of teeth, occlusion, maximum jaw opening capacity, DC/TMD diagnoses [14] and removable denture status. Furthermore, the PD participants were examined during their ‘On’ times, which is when medication should be most effective and motor symptoms minimised. Despite this optimal period, there were still notable differences in outcomes. Thus, the observed differences in maximum muscle output may primarily be attributed to PD itself, as observed in individuals with muscular dystrophy [43], or to the combined impact of PD and the side effects of its medications on the orofacial muscles. Additionally, considering that PD patients often experience a decline in dental health [10, 44, 45], potentially resulting in poor occlusion, which can further impair function, this is a significant concern. Consequently, we are likely underestimating the problems within the group. The strength of this study rests on the uniformity of these factors among the participants, a characteristic that, to the best of our knowledge, is not present in other studies [19, 20]. While other studies have explored rehabilitation with prosthetics [39, 46], they have not specifically focused on individuals with intact dentition and minimal dental treatment needs. Despite the advancements presented in this study, several limitations warrant consideration. The small sample size, while adequate for an initial exploration, necessitates expansion for broader generalisability and for obtaining significant results. Additionally, the cross‐sectional nature of this study precludes causal inferences, underscoring the need for longitudinal studies to track the progression of orofacial dysfunctions over time. Moreover, there was considerable variability in the disease severity among participants with PD, potentially introducing a bias that we were unable to mitigate and adjust for. Another limitation was that the investigator was not blinded during the recordings. However, all analyses, including peak values, ARV, identification of the five chewing cycles, and workload, were automatically generated by the software, ensuring the investigator had no influence on the automated process. Additionally, the use of sEMG presents challenges in accurately isolating the activity of the anterior belly of the digastric muscle. Due to its close anatomical proximity to adjacent muscles, distinguishing the anterior digastric's activity from that of surrounding muscles can be difficult. As a result, the recorded sEMG signal may potentially be reflecting the combined activity of the entire suprahyoid muscle group, rather than isolating the anterior belly of the digastric muscle specifically.

Overall, this study sheds light on the intricate relationship between PD and the function of the orofacial and stomatognathic system. Through the employment of objective measurements such as bite force and electromyographic activity, this study addresses a critical gap in the literature, offering a more nuanced understanding of how PD impacts orofacial muscles during chewing, biting and jaw opening. Regular physical exercise is important for people with PD for several reasons. It can significantly improve motor symptoms such as bradykinesia, rigidity, balance, coordination and overall mobility [47, 48, 49]. Additionally, exercise helps preserve physical function, including muscle strength, flexibility and endurance, thus enhancing quality of life [47, 48, 49]. Furthermore, exercise promotes neuroplasticity, which may lead to cognitive benefits [49]. Therefore, future research should concentrate on refining orofacial exercises designed to enhance orofacial motor symptoms such as rigidity, coordination and muscle strength, thereby helping in maintaining orofacial function. These targeted interventions can optimise muscle performance for specific orofacial tasks and be integrated into standardised training programmes, such as those provided by a physiotherapist, occupational therapist or specialised dentist.

Interdisciplinary collaboration, particularly between neurology and dentistry, will be critical in developing comprehensive and multidisciplinary care strategies [50, 51]. Ultimately, improving our understanding of the orofacial and stomatognathic implications of PD holds promise for improving not only oral health and nutritional intake but also overall well‐being, thereby mitigating the broader impacts of this challenging disease.

Author Contributions

Sara Baram contributed to design, data acquisition including EMG recording, statistical analysis, data interpretation, drafted and critically revised the manuscript. Carsten Eckhart Thomsen contributed to design, EMG and critically revised the manuscript. Esben Boeskov Øzhayat contributed to conception, design and critically revised the manuscript. Merete Karlsborg contributed to design, recruited the participants and critically revised the manuscript. Merete Bakke contributed to conception, design, data interpretation and critically revised the manuscript. All authors gave final approval and agreed to be accountable for all aspects of the work.

Conflicts of Interest

The authors declare no conflicts of interest.

Peer Review

The peer review history for this article is available at https://www.webofscience.com/api/gateway/wos/peer‐review/10.1111/joor.14044.

Data Availability Statement

The dataset used and/or analysed during the current study is available from the corresponding author upon reasonable request, but a transfer of data must comply with the General Data Protection Regulation (GDPR) of the European Union (EU).