Changes of masseter muscle thickness during orthodontic treatment with fixed appliances: a prospective controlled study in growing children

Abstract

Objectives

To examine the effects of orthodontic treatment with fixed appliances on masseter muscle thickness in growing children.

Subjects and method

Forty children with a mean pre-treatment age of 12.9 ± 1.19 years with mild to moderate malocclusions were treated with fixed appliances. Forty untreated children served as the control group, with a mean age of 9.14 ± 0.91 years at the start of the study. Masseter muscle thickness was measured by ultrasonography at treatment start and 1 year later in the patient group, and at equivalent times in the control group. Differences within and between the groups were evaluated using paired and independent sample t-tests, respectively. Multiple regression analysis was conducted to examine associations between different variables, including age, gender, and treatment.

Results

Masseter thickness at the beginning of the study was smaller (P = .004) in the control group (10.57 ± 1.04 mm) than in the treatment group (11.26 ± 1.03 mm), an observation that can be partly explained by the initial age difference between the groups. One year later, masseter muscle thickness increased in the control group (0.38 ± 0.50 mm, P < .001) while no statistically significant changes were found in the treatment group (−0.08 ± 0.55 mm, P = .37). The observed change in masseter muscle thickness in the two groups presented statistically significant differences (0.46 ± 0.11 mm, P < .001).

Conclusions

Masseter muscles in growing children normally increase in thickness annually. Fixed appliance treatment seems to hinder this growth during a 1-year treatment period. This information should be considered when assessing the progress and stability of the orthodontic treatment of certain malocclusions.

Introduction

Fixed orthodontic appliances are commonly used in children to treat a wide range of malocclusions. The application of orthodontic force induces a cascade of events that lead to the remodelling of the alveolar bone and the periodontal ligament (PDL) and to subsequent tooth movement [1, 2]. Periodontal mechanoreceptors are highly sensitive tactile sensors located within the PDL that provide sensory feedback to the central nervous system about tooth loads via afferent nerve fibres. These inputs contribute to the regulation of muscle activity that generates masticatory forces and jaw movements [3, 4]. Changes in the mechanical environment due to application of orthodontic forces can alter the oral neuromuscular system, including masticatory muscle function [5, 6].

The masseter muscle is a key representative of the group of jaw elevator muscles [7, 8]. Various imaging modalities have been used to assess masseter muscle size, such as computed tomography (CT) [9–11] and magnetic resonance imaging (MRI) [12, 13], but despite their accuracy they cannot be routinely used due to ethical or practical constraints. However, helping to overcome these constraints, the superficial position of the masseter muscle makes it easy to access and to measure by means of ultrasonography. This method offers several advantages as it has no documented accumulated biological impact, it is rapid and cost-effective and the equipment can be easily handled. The accuracy and the validity of ultrasonography in measuring masseter muscle thickness have been confirmed in several human studies [14, 15]. Muscle thickness gives an indication of the functional capacity of the muscle [16] and for the masseter muscle, it has been shown that it is well related to its electromyographic (EMG) activity [17, 18] and it has been significantly correlated to measurements of occlusal bite force [18–20].

Clinical studies on masticatory muscle performance shortly after the application of orthodontic forces point to a reduced muscle activity during function, as measured by EMG [21–23]. Since the activity of a muscle indicates its mechanical force output, prolonged reduction in masticatory muscle function may subsequently influence the masticatory muscle structure, which could explain the reported decreased bite force at least during the initial stages of orthodontic treatment [24–26].

Indeed, a decrease in the thickness of the masseter muscle was reported in the treatment of Class II malocclusion with functional appliances after ∼1 year of appliance use [27, 28]. Furthermore, treatment with removable bite-blocks in long-faced growing subjects reduces masseter muscle thickness compared with untreated subjects with similar characteristics [29].

Though such prospective studies provide significant insights into the association between masseter muscle thickness and orthodontic treatment, they have primarily focused on orthopaedic appliances that are used either for a short treatment time and/or on a part-time daily basis. In contrast, fixed orthodontic appliances exert continuous forces during a significantly longer treatment time and are widely used to correct various types of malocclusions in growing children. However, research studies concerning the effects of fixed appliances on masseter muscle have often been retrospective [30, 31], have mostly focused on adults [30–32], and the techniques applied are either inappropriate for routine use, as with cone-beam computed tomography (CBCT) [31], or provide information that has a transient character for the muscle condition, as with EMG activity measurements [30, 32, 33].

The aim of the present study was therefore to prospectively examine the effect of orthodontic treatment with fixed appliances on masseter muscle thickness in growing individuals, on a group of subjects 1 year after the start of treatment compared with a group of untreated subjects. The null hypothesis was that no difference exists in the changes of masseter muscle thickness in growing children treated with fixed appliances 1 year after their insertion, as compared with the untreated growing subjects.

Materials and methods

Trial design

The present study is a prospective longitudinal controlled clinical trial and was approved by the local research ethics board (protocol number 00195). The reporting of the study was based on the STROBE guidelines for observational studies [34]. The sample consisted of two groups: (i) children planned to be treated with fixed appliances in both dental arches and (ii) an untreated control group of children. The children in the treatment group were examined at two time points, namely prior to treatment (T0), and ∼1 year after the placement of fixed appliances (T1). The children in the control group that were not in need for immediate orthodontic treatment were examined at the same time interval without any orthodontic intervention.

Setting, participants, and intervention

All participants were recruited from a private orthodontic office over a 3-year period (2021–24). Informed consent was received from parents following a detailed explanation of the purposes of the study and the procedures that would be followed throughout the study.

The treatment group consisted of 40 children who met the following eligibility criteria:

• Growing patients in the permanent dentition.

• No previous fixed or interceptive orthodontic intervention (such as headgear or space maintainers).

• Mild to moderate malocclusions (all Angle classifications included)

• No need for extraction during orthodontic treatment.

• Absence of anterior crossbite, posterior crossbite, scissor bite, tooth agenesis, craniofacial syndromes, and/or clefts, temporomandibular disorders, muscular pathologies.

The control group consisted of 40 children who were primarily selected from siblings, relatives, and friends of existing patients and staff of the orthodontic clinic. The inclusion criteria were the same as described for the treatment group with an additional requirement, i.e. no immediate need for orthodontic treatment. Consequently, younger children were included in the control group to meet this criterion, as it was not feasible to identify older children without any objective treatment need. It is important to stress that the subjects of the control group had no absence and no mobility of the deciduous molars during the study period.

In the treatment group, all patients were treated with fixed edgewise appliances (018″ slot, Roth prescription) in both dental arches. Adjustments of the appliances were scheduled approximately every 4–6 weeks. By the time of the measurements at T1, all children under treatment had reached a stage where 16 × 22 stainless steel wires had been placed in both dental arches. Auxiliaries during treatment such as palatal/lingual fixed arches and intermaxillary elastics were used in some patients.

The control group did not receive any kind of orthodontic intervention during the study.

Masseter muscle thickness measurements

The thickness of the masseter muscles was measured based on the method proposed by Kiliaridis and Kälebo [14], at two time points: before treatment (T0) and 1 year later (T1), during fixed appliance treatment. Similar recordings were performed in the control group with a 1-year interval and in the absence of treatment.

All examinations were conducted by the same operator using a real time scanner (Pie Medical Scanner 480) with a 7.5 MHz linear array transducer. Imaging and measurements were performed bilaterally with the subject seated in an upright position and without head support. The masseter muscles were measured under contraction (maximal clenching in the intercuspal position).

For the treatment group, on the day of masseter muscle thickness measurements at T1, these were performed prior to the activation of the appliances in order to avoid any discomfort or force-related inhibition during clenching.

The site of measurement was the thickest part of the masseter muscle close to the level of the occlusal plane, approximately in the middle of the mediolateral distance of the ramus (Fig. 1). Care was taken to ensure that the transducer was perpendicularly orientated to the mandibular ramus, since oblique scanning would increase the muscle thickness values measured. A generous amount of gel was applied to minimize tissue compression.

Figure 1.

Left: Transverse ultrasound scan of masseter muscle in contraction. The upper line represents the outer fascia of the masseter muscle, the lower line represents the lateral surface of mandibular ramus and the vertical dotted line shows the measured masseter muscle thickness. Right: Masseter muscle thickness measurement by means of ultrasonography, using a real time scanner with a 7.5 MHz linear array transducer.

Imaging and measurements were performed twice on each side with a few minutes interval between the two recordings. The final thickness per side was calculated as the mean of the two measurements. The measurements were taken directly from the image at the time of scanning with a read-out distance to the nearest 0.1 mm. Scans were printed on film paper using a video printer (model P66E; Mitsubishi, Japan).

Sample size calculation

A sample size calculation was performed using G*Power analysis software [35] based on the changes in masseter muscle thickness in the fixed appliance group, using an alpha significance level of .05 and a beta of 90% for a two-tailed t-test. Based on a previous study that found a 0.4 mm (SD: 0.7) change of the masseter muscle thickness with the full-time use of functional appliances during a 1-year period [27], a minimum of 35 participants in each group was required to reveal statistically significant differences. To ensure the desired sample size due to possible drop-outs, we decided to include 40 children in each group.

Statistical methods

All statistical analyses were performed using the SPSS statistical package (version 29.0; IBM, Chicago, USA). Data were checked and confirmed for normal distribution in order to implement parametric tests. The level of significance was set at P < .05. Paired sample t-tests were used within each group to investigate differences in the masseter muscle thickness between the right and left sides and also to evaluate masseter thickness changes between T0 and T1. Independent sample t-tests were used to compare changes in the masseter muscle thickness between the two groups. Backward multiple regression analysis was conducted to investigate the influence of age, gender, exact interval between T0 and T1, and study group, on the masseter muscle thickness change throughout the study period. Since there was a considerable age difference between the two groups, regression analysis was also performed to examine the influence of age, and subsequently the gender influence on the initial masseter muscle thickness. Multiple regression analysis was also performed within the treatment group, to investigate the possible association of the use of intermaxillary elastics in some treated patients and masseter muscle thickness change.

Error of the measurements

Reliability between the recordings for masseter muscle thickness was examined by double measurements in 15 adult subjects that agreed to participate in the study of the method error (mainly parents of the orthodontic patients), within a 2-week interval. The absence of dentofacial pain and any kind of dental intervention for 2 weeks was a necessary condition for their participation.

Random error was calculated using Dahlberg's formula [36] while systematic error was assessed with paired t-tests [37]. Results showed no significant systematic error (P > .05) and random error was found to be 0.31 mm.

Results

Sample demographics

The study included a total of 80 participants, of which 40 belonged to the treatment group and 40 to the untreated control group. The patients in the treatment group with fixed edgewise appliances had a mean age of 12.9 years (SD: 1.19) at the start of the study, while the control group had a mean age of 9.14 years (SD: 0.91) at the start of the study. The gender distribution in the treatment group was 14 males and 26 females while in the control group it was 17 males and 23 females. All patients who started the study also completed it, without any drop-outs in either study group.

Ultrasound measurements of masseter muscle thickness under contraction were performed just before the placement of fixed appliances in the treatment group (T0) and approximately a year later (T1) with the orthodontic appliances in place (time interval: 1.12 ± 0.15 years). Similar recordings were made for the untreated children in the control group over a comparable interval period (1.23 ± 0.22 years).

Masseter muscle thickness showed no statistically significant difference (P > .05) between the right and left sides for both groups and for each time point, therefore for each individual the mean thickness of the right and left side was used.

Masseter muscle thickness measurements

Ultrasonographic masseter muscle thickness measurements for both treatment and control groups are shown in Table 1 and Fig. 2.

Table 1.

Masseter muscle thickness measurements in mm (T0 = at the start of the study period, T1 = at the end of the study period, and T1-T0 = time interval of ∼1 year).

	Treatment group		Control group		Difference between the groups
	Mean ± SD	P	Mean ± SD	P	Mean ± SD	95% CI	P
T0	11.26 ± 1.03		10.57 ± 1.04		0.69 ± 0.23	−1.11 to −0.21	.004*
T1	11.18 ± 1.17		10.95 ± 1.08		0.23 ± 0.25	−0.64 to 1.23	.36
T1-T0	−0.08 ± 0.55	.37	0.38 ± 0.50	<.001*	0.46 ± 0.11	0.42 to 1.34	<.001*

^* P < .05.

Figure 2.

Box plots showing changes in masseter muscle thickness (MMT) in millimetres between the first and the second measurements, in the treatment and control groups. The lower border of the box represents the first quartile, the upper border the third quartile, and the line within the box the median. Whiskers represent maximum and minimum values. The horizontal line at zero percent represents a line below which the measurement showed a decrease, and above which the measurement showed an increase of masseter muscle thickness during the 1-year study period.

In the treatment group, no statistically significant changes were found in the thickness of the masseter muscles 1 year after fixed appliance placement (−0.08 ± 0.55 mm, P = .37). In contrast, in the control group, the masseter muscle thickness increased over the same period (0.38 ± 0.50 mm, P < .001). The difference between the overall changes of masseter muscle thickness during the study period between the two groups was statistically significant (0.46 ± 0.11 mm, P < .001).

At baseline (T0), masseter muscles were thinner in the control group than in the treatment group (difference: 0.69 ± 0.23 mm, P < .05). However, upon the second recording at T1 the groups no longer exhibited a statistically significant difference between them in terms of masseter muscle thickness (0.23 ± 0.25 mm, P = .36).

Associations

The difference in masseter muscle thickness changes during the study period between the two groups was increased in favour of the control group (0.46 ± 0.11 mm, P < .001). To further investigate this finding, a multiple regression analysis using a backward elimination model was performed with masseter muscle thickness change (MMT CHANGE) as the dependent variable and the following independent variables: (i) duration of study (TIME INTERVAL (T1-T0); (ii) age of subjects at baseline (AGE T0); (iii) males or females (GENDER); and (iv) control or treatment group (GROUP). Among these factors, orthodontic treatment with fixed appliances (GROUP) was the only significant predictor for masseter muscle thickness changes during the 1-year study period (Table 2).

Table 2.

Multiple regression analysis to test the significance of: (a) duration of study (TIME INTERVAL (T1-T0), (b) age of subjects at baseline (AGE T0), (c) males or females (GENDER), and (d) control or treatment group (GROUP), on the change of masseter muscle thickness (MMT change) during the study period.

Variables	Coefficient b	Standard error	Significance (P value)
TIME INTERVAL (T1-T0)	0.004	0.326	.990
AGE T0	0.011	0.057	.858
GENDER	−0.060	0.122	.642
GROUP	−0.468	0.118	.046*

Regression equation from the final model of the backward multiple regression process: (Y) = b₀ − b₁ × GROUP.

MMT CHANGE = 0.389–0.468 × GROUP.

Dependent variable (Y): Masseter muscle thickness change during study period, in mm (MMT CHANGE).

b₀  = constant, b₁ = regression coefficient.

Independent variable: GROUP (control-treatment).

Excluded variables: TIME INTERVAL (T1-T0), AGE T0, GENDER.

*P < .05.

Significance of the model: R = 0.41 (correlation coefficient), R² = 16.8% (percentage of explained variance), P < .001.

A notable finding at baseline (T0) was the significantly thinner masseter muscles in the control group (10.57 ± 1.04 mm) compared with the treatment group (11.26 ± 1.03 mm). The children in the control group were considerably younger than in the treatment group. Moreover, the two groups were not matched for gender. Therefore, a multiple regression analysis model was performed, to examine the potential influence of the age at baseline (AGE T0) and gender (GENDER), on the initial masseter muscle thickness (MMT T0).

The results showed that the model was statistically significant, indicating that older children and particularly boys, appeared to have thicker masseter muscles in the beginning of the study (Table 3).

Table 3.

Multiple regression analysis to test the significance of the age of the subjects at baseline (AGE T0) as well as gender (GENDER) on initial masseter muscle thickness (MMT T0).

Variables	Coefficient b	Standard error	Significance (P value)
AGE T0	0.116	0.054	.03*
GENDER	−0.480	0.241	.05*

Regression equation: (Y) = b₀ + b₁ × AGE T0 − b₂ × GENDER.

MMT T0 = 9.933 + 0.116 × AGE T0 −0.480 × GENDER.

Dependent variable (Y): Masseter muscle thickness at baseline, in mm (MMT T0).

b₀  = constant, b₁, b₂ = regression coefficients.

Independent variables: age (yrs) at baseline (AGET0), GENDER (0 = Males, 1 = Females).

*P < .05.

Significance of the model: R = 0.31 (correlation coefficient), R² = 9.8% (percentage of explained variance), P = .019.

In the treatment group, intermaxillary elastics were used in some patients after aligning and levelling. Though the onset of the elastics use was shortly prior to the second masseter thickness measurement, only half of the children (N = 21) made use of these auxiliaries, therefore we performed a multiple regression analysis to assess whether the use of intermaxillary elastics affected the masseter muscle thickness change in the treatment group, including also the gender and the initial age of the patients as independent factors. The findings were not statistically significant for any of the variables that were included in the model, suggesting that the change of masseter muscle thickness within a year was not influenced by intermaxillary elastic wear (Table 4).

Table 4.

Multiple regression analysis in the treatment group, to test the significance of the use of intermaxillary elastics (ELASTICS), the age of treated subjects at baseline (AGE T0) and the gender (GENDER) on the change of masseter muscle thickness (MMT change) during the study period.

Variables	Coefficient b	Standard error	Significance (P value)
AGE T0	0.040	0.078	.612
GENDER	0.009	0.194	.965
ELASTICS	−0.260	0.188	.176

Regression equation from the multiple regression process:

(Y) = b₀ + b₁ × AGE T0 + b₂ × GENDER − b₃ × ELASTICS.

MMT CHANGE = −0.462 + 0.040 × AGE T0 + 0.009 × GENDER −0.260 × ELASTICS.

Dependent variable (Y): Masseter muscle thickness change during study period, in mm (MMT CHANGE).

b₀ = constant, b₁b_2,b₃ = regression coefficients.

Independent variables: AGE T0, GENDER, ELASTICS.

Significance of the model:

R = 0.23 (correlation coefficient), R² = 5.5% (percentage of explained variance), P > .05.

Discussion

The present prospective longitudinal study shows that in growing individuals undergoing orthodontic treatment with fixed appliances over a 1-year period, the thickness of the masseter muscles does not increase as compared with the untreated children where the masseter muscle increases in thickness over the same period as part of the normal growth process. Thus, the null hypothesis could be rejected.

Our findings are in agreement with a previous study that compared masseter muscle thickness before and after fixed appliance treatment, which reported a reduction in the thickness of the muscle following treatment [31]. That study however has some limitations, as it was retrospective in nature and was conducted only on adult females, measuring masseter muscle thickness by means of CBCT.

Several research studies on the changes of bite force and masseter muscle EMG activity during fixed appliance treatment also report conclusions similar to ours. Bite force is positively correlated with masseter muscle thickness and the number of occlusal contacts [18, 38], and fixed appliances seem to decrease both occlusal forces and contacts at least during the first year of treatment [25, 26]. The activity of the masseter muscles also seems to be influenced by fixed appliance treatment although findings show some inconsistency, with some studies presenting a decrease in EMG activity during treatment [21, 32] while others show either an increase in EMG activity, if Class II elastics are also used [33], or an initial decrease followed by a later recovery of masseter muscle activity [39]. The greater variability of these findings could be attributed to the sensitivity of the EMG method [40] and to the different designs of each of the cited studies.

Looking into findings using ultrasonography to measure masseter muscle thickness in growing children undergoing various orthodontic treatments, some studies examine transverse and vertical malocclusions and their correction [29, 41]. Children with unilateral functional crossbite have thinner pre-treatment masseter muscles on the affected compared with the unaffected side, but after correction of the crossbite either with a quad helix fixed appliance or a Hyrax-type expander, the muscle thickness gradually equalizes between the two sides [41]. Notably, following transverse expansion where masseter thickness became comparable between the two sides, insertion of a posterior bite-block for full-time use in dolichofacial growing subjects, seems to result in a significant decrease in masseter muscle thickness as compared with an untreated control group [29]. Our study excluded patients with transverse discrepancies in order to prevent potential baseline differences in masseter thickness between sides within the same individual, since this could complicate the analysis of the results.

Prospective studies investigating masseter muscle thickness in growing children that used removable functional appliances for the correction of Class II division 1 malocclusion [27, 28] have reported a decrease in masseter muscle thickness during treatment, while the control group exhibits normal growth, giving support to our comparable findings. Specifically, in the study of Kiliaridis et al. [27] the masseter muscles in the treated group were thinner by a mean of 0.4 mm (SD: 0.7) at the end of the observation period (mean: 13.5 months), while untreated controls showed an increase in muscle thickness of ∼0.6 mm (SD: 0.2). In the study of Antonarakis and Kiliaridis [28], masseter muscle thickness was reduced by 0.1 mm (SD: 1.1) in the treatment group and increased by 0.5 mm (SD 0.5) in the control group. The overall change in masseter muscle thickness during the study period between the treatment and control groups was significantly different in both the above-mentioned studies. It is worth to mention that the stability of the treatment results was associated to the masseter muscle thickness [42].

While our study involved children with mild to moderate malocclusions the observed 0.46 mm difference in masseter muscle thickness between the treatment and control groups is noteworthy, especially since fixed appliance treatment often continues for longer than 1 year, something that could aggravate this difference.

The mode of action differs between fixed and functional appliances. Functional appliance treatment is directly influenced by the masticatory muscles and their myotatic reflexes, namely active muscle contraction in combination with the viscoelastic properties of muscles that produce the desired orthodontic or orthopaedic force, resulting in the correction of the malocclusion [43]. Fixed orthodontic appliances on the other hand act solely through the movement of teeth and it seems that the light yet constant changes in the interdental occlusal relationships during the treatment, in combination with the induced orthodontic pain, likely influence the neuromuscular equilibrium via the afferents located within the PDL [5, 6]. This process results in reduced activity of the masseter muscles [21, 22], that could further lead to a mild atrophy of the muscle, as demonstrated by its inability to reach the normal growth increment, as compared with untreated subjects.

Interestingly, our fixed appliance treatment group had a similar masseter muscle thickness decrease (−0.08 ± 0.55 mm) as the functional appliance treatment group of the Antonarakis and Kiliaridis study (−0.1 ± 1.1 mm) during a comparable time period [28]. One might expect a more pronounced decrease of masseter muscle thickness in the functional appliance group due to the acute mandibular displacement and its different mode of action. A possible explanation for the similar findings however could be that fixed appliances exert continuous forces, while functional appliances are only worn on a part-time basis. This assumption is supported by the fact that in the treatment group with removable functional appliances in the Kiliaridis et al. study [27] the decrease of masseter muscle thickness was more evident (−0.4 ± 0.7 mm), perhaps in part because the patients were instructed to use their twin-block appliance almost on a full-time basis.

Ultrasound imaging of the masseter muscle is a safe, simple and reliable clinical tool for measuring its thickness, provided a standard method is followed [14, 15, 44]. In the present study we recorded masseter muscle thickness under contraction (maximal intercuspation) since it is a more reproducible measurement compared with the muscle in its relaxed state, where the muscle is more susceptible to transducer pressure artefacts [45, 46]. Occlusal contacts are associated with the muscle's thickness and function [18, 47], therefore another reason for measuring the masseter muscle in contraction was because the contracted condition reflects how the muscle actually works in relation to the ongoing occlusal changes during fixed orthodontic treatment, making this measurement functionally relevant for the present study.

A key limitation of our study was the lack of a matched control group particularly regarding age. This decision was made as part of the study design and resulted in an age difference between groups, which was accounted for in the statistical analysis.

Younger children made up the control group that were in no immediate need of orthodontic treatment. Recruiting older children with treatment needs that would have to remain untreated for at least a year would raise ethical concerns. Alternatively, identifying older children without an objective orthodontic treatment need for participation in a longitudinal study proved impractical. Furthermore, including individuals without any treatment need could add another confounding variable due to potential differences in masseter muscle thickness related to malocclusion status [48].

Consequently, at baseline the mean masseter muscle thickness in the younger control group (10.57 ± 1.04 mm) was statistically significantly smaller than that in the older treatment group (11.26 ± 1.03 mm). Regression analysis indicated a significant age association (P < .05) and a borderline gender effect (P = .05), with ∼10% of the initial masseter muscle thickness variance explained by these factors, i.e. older children and particularly boys having thicker masseter muscles. Indeed, growing individuals have an age-related masseter muscle thickness increase [49, 50] while gender effects are not always clear, meaning that even if boys consistently have thicker masseter muscles than girls at similar ages, this difference is not always statistically significant [51, 52].

Despite age differences between the groups, regression analysis revealed that changes in masseter thickness during the study period were significantly associated only with the presence or absence of orthodontic treatment which accounted for 17% of the variance in masseter muscle thickness changes, suggesting that the growth suppression observed is not attributable to age alone. Additionally, our control group demonstrated a mean annual growth of 0.38 mm, aligning with former studies that report growth increments between 0.3 and 0.6 mm in similar age ranges [20, 27, 49]. These findings reinforce the biological validity of our control data and add indirect support that the inhibited growth observed in the treatment group is a treatment-related effect rather than a maturational trajectory.

Another methodological consideration is the use of auxiliary appliances such as transpalatal and lingual arches, and intermaxillary elastics in some of the treated patients. While these auxiliaries could theoretically influence occlusal force transmission and masticatory muscle activity, their use was limited, applied based on specific clinical needs and implemented either in the early or late stages of the study period. Regarding the intermaxillary elastics, since almost half of the treated children started their use after ∼9 months of the treatment start, we conducted a multiple regression analysis within the treatment group, which did not reveal any effect of the use of intermaxillary elastics in masseter muscle thickness change.

The principal strength of this study is its prospective longitudinal design along with the use of a control group, and the inclusion of children with various mild to moderate malocclusions corrected by fixed appliances, an aspect not previously examined in a prospective way. Additionally, the sample size and the lack of drop-outs ensured a statistical power of more than 90%, thus reducing the possibility of type II error even further.

From a clinical perspective, the results of the present study underscore the importance of monitoring tooth movements and occlusal changes during fixed orthodontic treatment. Given the fact that masseter muscle thickness has been associated with bite force, occlusal stability, and vertical facial growth control [18, 53], it is possible that the inhibited muscle growth observed in the treatment group may affect long-term functional adaptation and stability in some patients especially those with lower initial muscle thickness.

Nonextraction fixed mechanotherapy generally reduces overbite [54]. Moreover, thinner masseter muscles are associated with an increased vertical growth pattern [55]. This consideration could be relevant when selecting mechanics that could exacerbate vertical dimension changes or compromise muscular equilibrium. Therefore, it is advisable for the clinician to be cautious during orthodontic treatment with fixed appliances, as masseter muscle changes could play some role in the treatment progress and the final results.

Future studies could investigate whether the masseter muscle thickness recovers after the completion of fixed orthodontic treatment, returning to its normal growth trajectory as well as its association with orthodontic post-treatment stability. Studies using EMG and bite force measurements point to a normalization of masseter muscle activity and force output post-treatment [26, 56], yet structural changes remain to be explored.

Conclusion

The thickness of the masseter muscle in growing children normally increases over time. However, fixed appliance treatment seems to interfere with normal masseter muscle growth, restraining the increase in its thickness during a 1-year treatment period. This information should be taken into consideration when evaluating the progress and stability of the treatment of certain malocclusions.

Funding

None declared.

Data availability

All data generated and/or analysed for the current study will be made available from the corresponding author upon reasonable request.