Masticatory Function and Corticomotor Plasticity Across the Lifespan: Implications for Older Adults—A Scoping Review

Highlights

What are the main findings?

• Masticatory function influences corticomotor excitability and activity in the distributed sensorimotor network, including the primary motor cortex, indicating participation in activity-dependent neuroplasticity.
• Tooth loss, ageing, and diminished oral sensory input are associated with changes in cortical organisation, while masticatory training and dental rehabilitation lead to alterations in neural activation and corticomotor responsiveness.

What are the implications of these findings?

• Prosthodontic rehabilitation and oral motor training could be effective neurobiological interventions promoting adaptive cortical reorganisation and sensorimotor functions, though more long-term studies are needed to confirm sustained effects.
• Maintaining masticatory function may correlate with improved cognitive and functional outcomes in ageing populations, hinting at a significant role in healthy ageing, although causal and long-term neuroprotective effects have yet to be proven.

Abstract

Background/Objectives: Mastication is a complex sensorimotor function involving coordination between the brainstem central pattern generator and supraspinal systems, particularly the primary motor cortex (M1). Evidence suggests a link between masticatory activity and corticomotor plasticity, but findings remain fragmented. This scoping review aimed to synthesise the human evidence on the relationships among mastication, tooth loss, dental rehabilitation, ageing, and corticomotor plasticity, with emphasis on M1 mechanisms. Methods: Following PRISMA-ScR guidelines, systematic searches were conducted in MEDLINE/PubMed, Scopus, and Web of Science using terms related to mastication, neuroplasticity, motor cortex, ageing, and rehabilitation. Eligible studies included human experimental, clinical, and observational research employing neuroimaging or neurophysiological methods. Data were extracted and synthesised using a Population–Concept–Context framework across eight conceptual domains. Results: Twenty-two heterogeneous studies (fMRI, TMS, EMG, psychophysical, histological) were included. Mastication consistently activated distributed sensorimotor networks, including M1 and the primary somatosensory cortex (S1). Peripheral sensory input and dental mechanoreception were linked to structural and functional adaptations. Corticomotor excitability was modulated by chewing, oral-motor learning, and rehabilitative interventions. Ageing was associated with altered but preserved cortical responsiveness. Associations between mastication and cognition were reported, though largely cross-sectional. Overall, findings suggested a relationship linking peripheral input, sensorimotor integration, and corticomotor plasticity, but methodological variability limited causal inference. Conclusions: Mastication is linked to modifiable corticomotor activity and supports experience-dependent neuroplasticity. However, the evidence remains largely associative and methodologically heterogeneous. Neural adaptations appear to be preserved with ageing but are influenced by systemic and environmental factors. Longitudinal, multimodal research is needed to clarify the mechanisms, causality, and clinical relevance, particularly in rehabilitation contexts.

1. Introduction

Mastication is a complex sensorimotor process generated through the interaction of the brainstem central pattern generator (CPG) with supraspinal motor control, particularly from the primary motor cortex (M1). The CPG produces the individualised, repetitive rhythmic jaw movement, but this activity is not purely automatic or reflexive. Cortical input from M1 modulates the brainstem-generated pattern to accommodate voluntary intent, food properties, learning, and changes in the oral environment [1]. Experimental and neuroimaging studies demonstrate increased cortical activation during voluntary or task-modified chewing, highlighting the role of M1 in refining and adapting masticatory behaviour [2,3].

The capacity of the nervous system to adapt to experience is described as neuroplasticity, defined as activity-dependent modification of neural structure and function [4]. Corticomotor plasticity refers to experience-dependent changes within M1, including modulation of cortical excitability, motor output, and motor representations. These plastic changes typically emerge first at a functional level, through alterations in synaptic efficacy and neural excitability and may progress to longer-term reorganisation with sustained stimulation [5]. Motor behaviours that combine repetitive activity with rich sensory input, such as mastication, are therefore plausible drivers of use-dependent plasticity.

Mastication provides a multimodal sensorimotor stimulus, integrating motor output with afferent input from oral and maxillofacial structures (muscles, temporomandibular joints, periodontal ligaments, and oral mucosa), alongside adaptive and learning-related processes. Variations in food texture, dietary consistency, and oral conditions further shape this integration. Tasks requiring adaptation, precision and error correction, such as chewing with new dental prostheses, have been proposed to engage these plastic processes, although the extent and mechanisms of such effects remain incompletely defined.

Alterations in masticatory function, including tooth loss and reduced chewing activity, are associated with changes in corticomotor output and sensory-driven plasticity. Early effects are typically functional, whereas prolonged reductions in input may contribute to reorganisation of cortical representations and connectivity [6,7,8]. Neuroimaging and neurophysiological studies indicate that impaired oral function is associated with altered cortical activation, while dental rehabilitation and prosthodontic interventions have been reported to partially restore aspects of cortical organisation and motor control [9,10]. However, these findings are derived from heterogeneous methodologies and should be interpreted cautiously in terms of causality and clinical impact.

Neuroplastic capacity is maintained across the lifespan, although its efficiency and expression change with ageing. Age-related adaptations include slower synaptic modification, increased bilateral cortical recruitment, and greater reliance on distributed neural networks. Despite this, older adults retain the capacity for adaptive plasticity, particularly with sufficiently intensive, sustained or enriched stimulation. Mastication operates at an individualised chewing rate with a consistent frequency across the lifespan. As a repetitive sensorimotor behaviour under partial voluntary control, it has been suggested as one such stimulus, although evidence in ageing populations remains variable [11]. Conversely, impaired oral function may diminish afferent input critical for maintaining corticomotor integrity. Tooth loss and reduced masticatory performance in older adults are associated with changes in both peripheral function and central neural circuits, including corticomotor pathways originating in M1 [12,13,14].

According to the World Health Organisation framework for healthy ageing, maintaining functional performance is a key clinical objective [15]. Adequate masticatory efficiency and patient-reported chewing ability are therefore central outcomes for prosthodontic interventions, given their relevance to nutrition and overall health.

Despite growing interest, the evidence linking mastication and neuroplasticity in humans remains fragmented, indirect, and methodologically heterogeneous. Differences in study design, neuroimaging and neurophysiological techniques, and participant characteristics limit comparability and hinder definitive conclusions about mechanisms and clinical relevance. In particular, it remains unclear how changes in masticatory activity and oral sensory input relate specifically to corticomotor plasticity within M1, how consistently these effects are observed across populations (especially older adults), and to what extent dental rehabilitation induces measurable, functionally meaningful neural adaptation.

Accordingly, this review is guided by the hypothesis that masticatory function and oral rehabilitation are associated with corticomotor plasticity in humans, particularly within M1, reflecting emerging but heterogeneous evidence and limited causal clarity. It therefore aims to synthesise human evidence on mastication, tooth loss, dental rehabilitation, and ageing in relation to corticomotor plasticity, identifying consistent patterns, methodological limitations, and key gaps to facilitate future research.

2. Materials and Methods

This scoping review was carried out following the PRISMA Extension for Scoping Reviews (PRISMA-ScR) to offer a clear and organised overview of the existing evidence instead of a detailed quantitative analysis. The methodological approach was primarily descriptive and interpretive. The publication of the present scoping review is in accordance with the Operating Regulations of the Research Ethics Committee, School of Dentistry, Aristotle University of Thessaloniki, Greece (https://dent.auth.gr/epitropi-deontologias/, accessed date 18 May 2026) and was not prospectively registered.

The search strategy was developed in accordance with PRISMA-ScR guidelines to support transparency and reproducibility. Electronic database searches were conducted in major biomedical databases, such as MEDLINE/PubMed, Scopus, and Web of Science. Search combined Medical Subject Headings (MeSH) and key MeSH terms included “Mastication”, “Chewing”, “Neuroplasticity”, “Motor Cortex”, “Ageing”, and “Rehabilitation”, alongside terms describing corticomotor plasticity and oral-motor interventions. Reference lists of included studies were also screened to identify additional relevant literature. The flow diagram illustrates the progression from 1402 records identified to 22 studies ultimately included in the final scoping review after removal of duplicates, screening, full-text assessment, and additional records identified through reference searching. (Figure 1).

The research was confined to human studies to enhance clinical relevance. Studies involving animal models were excluded owing to differences in neuroanatomical organisation and voluntary control of mastication, as the translational applicability varies. Eligible studies comprised original clinical or experimental research conducted in human populations that examined masticatory function or closely related oral sensorimotor processes in relation to motor cortical activity or neuroplasticity. Given the exploratory scope of the review, studies were included if they provided indirect or proxy measures of corticomotor function, such as oral-motor tasks, chewing-related paradigms, or sensorimotor adaptations relevant to mastication, even if mastication was not the sole experimental task. Studies were required to employ neurophysiological and/or neuroimaging methodologies and to be published in English.

Exclusion criteria included studies that did not assess cortical involvement, as well as case reports, editorials, and narrative reviews. Investigations focusing exclusively on non-oral pathologies or not providing outcomes interpretable in relation to masticatory or oral sensorimotor function were also excluded.

Study selection was performed by two independent reviewers (PG, VB), who screened the available evidence for eligibility using the predefined inclusion and exclusion criteria. Any disagreements between reviewers were resolved through discussion and consultation with a third reviewer (VA).

Data extraction was conducted using a structured framework to ensure consistency across studies. The following variables were systematically charted: Authors (Year), Conceptual Domain, Study Design, Population, Intervention/Activity, Neuro-methodology, Key Neuroplasticity Indicators, Age and Modifying Factors, Clinical/Functional Implications, and Core Contribution.

Given the exploratory nature of the review, a Population–Concept–Context (PCC) framework was adopted. The population of interest comprised adults and older adults with natural dentition, partial tooth loss, or complete edentulism. The central concept was the relationship between mastication (and related oral sensorimotor processes) and corticomotor plasticity, particularly within M1. The context included experimental, clinical, and rehabilitation settings involving masticatory activity, dental interventions (such as dentures or implant-supported prostheses), or oral-motor training. Comparisons and outcomes were not narrowly predefined but were instead mapped across studies, reflecting the heterogeneity of methodologies and endpoints (such as cortical activation, excitability, or functional performance measures)

A structured, analytical framework was employed to organise and interpret the evidence; however, it was developed iteratively during the review process rather than being predefined. The eight analytical domains used to categorise the evidence were derived post hoc from recurring themes across the included studies. Studies addressing multiple domains were classified under the relevant categories.

Given the heterogeneity of study designs and methodologies, appraisal approaches were applied as appropriate to each study type. The outcomes of this process informed the synthesis and interpretation of the findings, thereby enabling a more nuanced understanding of the evidence base.

3. Results

The framework provided an appraisal approach in addressing the distributed, multilevel nature of mastication by encompassing interconnected components spanning peripheral mechanisms, central neural processes, and clinical outcomes. It facilitated the identification of patterns, knowledge gaps, and reported associations across study domains that enabled a coherent synthesis while preserving the complexity of mastication-related neuroplasticity.

Across domains, studies employed heterogeneous methodologies, including histology, psychophysics, neuroimaging (fMRI), neurophysiology (TMS, EMG), and behavioural and cognitive assessments, representing a multimodal but methodologically diverse evidence base. Age-related differences and sensory/motor modifiers were reported in several studies, particularly regarding tooth loss and prosthetic rehabilitation. Findings are presented as reported within individual studies (

Table 1. Corticomotor Plasticity in Mastication—Structured Evidence Synthesis: Conceptual framework: Peripheral → Sensorimotor → Corticomotor → Rehabilitation → Clinical/Translational → Ageing → Cognitive associations.

No	Author (Year)	Domain	Design/Population	Activity/Evidence	Methods/Outcomes	Key Finding
1	Garzino 1996 [16]	Peripheral	Obs histology adults implant n = 36	Implant loading	PGP9.5 nerve density	↑ peripheral nerve fibres
2	Ramieri 2004 [17]	Peripheral	Comparative adults dentate/edentulous n = 29	Tooth loss/rehab	GAP-43 marker	Neural marker changes post rehab
3	Onozuka 2002 [2]	Sensorimotor	Exp healthy adults n = 17	Chewing	fMRI BOLD M1/S1	Multiregional activation
4	Tamura 2003 [3]	Sensorimotor	Obs healthy adults n = 30	Jaw movement	fMRI M1	Motor cortex activation
5	Onozuka 2003 [9]	Sensorimotor	Exp adults n = 32	Chewing gum	fMRI cortical network. Bilateral increase in BOLD signals	Distributed activation
6	Svensson 2013 [18]	Sensorimotor	Exp teeth and implant fixedprosthesis users n = 20	Chewing implant use	EMG kinematics	Motor strategy adaptation
7	Xiao 2017 [19]	Corticomotor	Obs adults n = 20	Jaw/tongue movement	fMRI somatotopy	Distinct M1 maps
8	Stipancic 2021 [20]	Corticomotor	Exp adults motor learning n = 20	Dual oromotor task	Kinematics motor learning	Task-dependent modulation
9	Simione 2018 [21]	Corticomotor	tDCS study adults n = 10	tDCS + chewing	Neurostimulation + kinematics	Task-specific excitability
10	Kobayashi 2020 [22]	Corticomotor and Ageing	Cross-sec dentate/edentulous n = 37	Teeth tapping	fMRI connectivity	Dentition affects networks
11	Iida 2020 [23]	Corticomotor and Temporal Dynamics, Predictive Markers	Repeated measures adults n = 16	Jaw training	TMS MEP	↑ excitability
12	Boscato 2022 [7]	Rehab	RCT bruxers n = 28	Clenching + NGF	TMS MEP/maps	Altered plasticity in bruxism
13	Costa 2024 [24]	Rehab	RCT adults n = 28	Mandibular device	TMS MEP	↑ excitability/maps
14	Hara 2026 [25]	Rehab	Intervention dental patients n = 46	Electrical stimulation	EMG chewing	Improved chewing function
15	Habre-Hallage 2012 [26]	Clinical Translational	Cross-sec implant pts n = 19	Mechanical stimulation	fMRI S1/S2	Implant-related activation
16	Narita 2025 [27]	Clinical Trans-lational	Exp adults n = 7	Food texture chewing	Neuroimaging	Texture modulates cortex
17	Ishii 2024 [28]	Clinical Trans-lational	Exp adults n = 9	Chewing/visual food	fMRI	Multisensory activation
18	Yajima 2017 [29]	Corticomotor and Ageing	Cohort elderly n = 140	Tongue strength	Functional tests	Oral function health
19	Kashiwazaki 2024 [30]	Corticomotor and Ageing	RCT older adults n = 130	Gum chewing	Functional oral tests	Improved oral function
20	Moriya 2011a [31]	Corticomotor and Cognitive	Cross-sec elderly n = 208	Masticatory ability	Cognitive tests	Assoc with cognition
21	Moriya 2011b [32]	Corticomotor and Cognitive	Cross-sec elderly n = 381	Chewing ability	Strength/body measures	Assoc with function
22	Lee 2025 [33]	Corticomotor and Cognitive	Cross-sec young adults n = 52	Hard vs soft chewing	fMRI	Cognitive region activation

).

3.1. Peripheral Sensory Plasticity

Reduced Oral Sensory Input and Peripheral Adaptation

Peripheral sensory input was consistently examined as a contributor to oral-motor control. Histological and experimental studies reported structural changes in oral sensory tissues following mechanical loading or rehabilitation. For example, implant-supported rehabilitation was associated with increased expression of peripheral nerve markers, including PGP 9.5 immunoreactivity [16] and GAP-43 expression [17]. These results reported neural and tissue changes at the periphery that occur during mechanical stimulation.

Conversely, research on the loss of periodontal mechanoreceptors has shown impaired force control during biting and food manipulation tasks. These results suggested a link between decreased afferent feedback and changes in motor performance, though they do not directly prove the involvement of central neuroplastic mechanisms.

Overall, the evidence indicates that peripheral sensory input influences oral motor performance and is reported in association with downstream sensorimotor processing, especially in situations of sensory deprivation like tooth loss.

3.2. Sensorimotor Integration

Sensory Modulation of Distributed Motor Networks

Functional neuroimaging studies reported activation of M1, S1, SMA, and insular cortices during chewing and voluntary oral-motor tasks [2,3,9]. These studies consistently demonstrated distributed cortical engagement during mastication-related behaviours. The M1 was described as generating and refining descending motor commands to brainstem circuits, integrating somatosensory feedback to regulate central pattern generators.

Manipulation of sensory input (such as food hardness or occlusal variation) was associated with changes in cortical activation patterns and motor strategies. These findings indicated task-dependent modulation of sensorimotor networks in response to peripheral input.

TMS and EMG studies reported coupling between sensory afferent input and motor output [18]. Hemispheric dominance during chewing varies with handedness, suggesting lateralised processing and individual variability in motor strategy development. However, these studies primarily demonstrated functional connectivity and task-dependent modulation rather than structural reorganisation. Taken together, the evidence described sensorimotor integration as a dynamic process linking oral sensory input to motor output during chewing tasks.

3.3. Corticomotor Plasticity

Task-Related Modulation of M1 Excitability

Corticomotor plasticity reflects experience-dependent adaptability of M1 through dynamic interactions across distributed sensorimotor networks. Cortical mapping studies confirm distinct M1 representations for jaw and tongue muscles, establishing the somatotopic organisation of oral-motor control [19]. Studies using TMS and fMRI have reported that repetitive oral-motor tasks and chewing paradigms were associated with changes in motor-evoked potentials (MEPs), intracortical inhibition, and cortical activation patterns [20,21]. These findings indicated that corticomotor excitability was modulated by repetitive masticatory activity under experimental conditions.

Ageing modifies the magnitude and focality of these responses. Older adults exhibited attenuated BOLD activation during oral-motor tasks, with compensatory recruitment of distributed cortical networks maintaining functional output [22]. These findings reflected age-associated differences in activation patterns rather than loss of cortical responsiveness.

Importantly, these adaptations were reported alongside maintained task-related cortical responses. TMS, fMRI, and EMG evidence demonstrated that corticomotor plasticity remains modifiable in older adults, as reported in intervention-based study contexts [23]. These age-related modifications highlighted preserved adaptive capacity rather than loss of plasticity. However, variability in the study design and outcome measures limited direct comparison across the studies.

3.4. Rehabilitation and Neural Reorganisation

Effects of Oral Rehabilitation and Targeting Training

Intervention studies reported changes in MEP amplitude, EMG coordination, and cortical activation following mandibular advancement therapy, prosthodontic rehabilitation, or masticatory training [7,20,23,24].

These findings suggested that oral-motor training and prosthodontic interventions were associated with measurable changes in corticomotor excitability and motor performance. Electrical stimulation during dental or facial interventions was also reported to be associated with changes in masticatory function [25].

Overall, the included studies described associations between rehabilitation interventions and neurophysiological changes; however, causal mechanisms were not consistently established across studies.

3.5. Clinical and Translational Evidence

Functional Relevance of Mastication-Related Neural Responses

Mechanical stimulation of osseointegrated implants was associated with cortical activation in the S1 and M1 regions [26], which the included studies interpreted as evidence of sensory–motor integration. Additional studies reported M1 activation during various chewing and jaw-movement tasks [24,27,28].

These findings demonstrated that masticatory-related behaviours are consistently associated with cortical activation in motor and sensory regions, as reported across experimental and clinical study settings. These findings described associations between prosthodontic rehabilitation, masticatory tasks, and measured neurophysiological outcomes. However, evidence linking these activation patterns directly to long-term clinical outcomes remains limited.

3.6. Influence of Ageing

Age-Related Differences in Masticatory Function and Neural Response

Ageing was associated with reduced tongue strength and functional decline in oral-motor performance in a cohort of older adults, with associations reported between tongue strength, health status, and mortality risk [29]. Neuroimaging and neurophysiological studies reported reduced MEP modulation and altered functional connectivity during oral-motor tasks in older populations [22].

Despite these differences, studies consistently reported a preserved ability to generate task-related cortical responses. This was reported alongside observations of bilateral and distributed cortical recruitment patterns. Training and prosthetic adaptation studies reported that older adults still exhibit measurable changes in motor performance and cortical activity following intervention [30].

3.7. Cognitive–Motor Associations

Association Between Mastication and Cognitive Function

Observational studies reported associations between masticatory ability and cognitive performance in older adults [31], as well as functional independence in community-dwelling populations [32].

Neuroimaging studies reported activation of prefrontal and hippocampal regions during the chewing of harder foods [33]. The evidence remains insufficient to determine whether these changes in older adults reflected the same mechanisms observed in younger populations. The findings suggested an association between mastication-related activity and activation of brain regions involved in cognition; however, most evidence is cross-sectional or task-based, limiting causal inference and providing no clear indication that mastication directly influences cognitive outcomes.

3.8. Temporal Dynamics-Based Predictive Markers

Early Functional Changes and Training Response

TMS-based studies reported that changes in MEP amplitude during the early phases of oral-motor training were associated with later changes in task performance [23,24].

These findings suggested that early neurophysiological changes may reflect training-related adaptation within the experimental paradigms. However, the evidence remains limited to small numbers of intervention studies, and broader predictive models for rehabilitation timing have not been established.

4. Discussion

Mastication is a distributed sensorimotor process that integrates brainstem pattern-generating networks, peripheral sensory feedback, and corticomotor circuits in the M1, thereby supporting activity-dependent neuroplasticity across the lifespan. Current evidence suggests an associative, mechanistically plausible relationship between mastication and neural adaptation, rather than a fully established causal role in broader neuroplastic or cognitive outcomes.

This integrative, PRISMA-ScR guided scoping review synthesised human evidence to clarify how the masticatory process relates to tooth loss, dental rehabilitation, and ageing, and how these factors modulate neural interactions, linking peripheral and central pathways to functional and structural brain-chewing outcomes. The findings supported an emerging integrative framework in which mastication-related activity is associated with neuroplastic processes, while emphasising the influence of confounding factors and the predominantly associative nature of the evidence.

Specifically, the present review critically evaluated human evidence linking masticatory function with neuroplastic changes in the M1, situating these effects within a broader sensorimotor–cognitive framework. Rather than treating mastication as a purely peripheral or biomechanical process, the findings align with contemporary neuroplasticity models that emphasise distributed, experience-dependent reorganisation across sensory, motor, associative, and cognitive networks [4,5,34]. Within the adopted framework, mapping the evidence supported a structured interpretive approach, enabling the integration of descriptive findings with mechanistic, functional, and translational insights, thereby clarifying how mastication-related neuroplasticity emerges across interconnected neural and clinical domains [35].

However, the overall evidence base remains heterogeneous, largely indirect, and methodologically variable, and therefore supports association-based interpretations rather than definitive causal conclusions regarding brain health outcomes.

The included studies collectively supported a multilevel association in which peripheral sensory integrity, sensorimotor integration, corticomotor excitability, and higher order cognitive engagement operate as interdependent components of oral-motor neuroplasticity. This interpretation was consistent with integrative neuroscience frameworks that advocate for multimodal synthesis across levels of analysis rather than isolated regional effects [36]. Critically, the strength of evidence varies substantially across domains, with stronger mechanistic support for sensorimotor and corticomotor processes, and weaker, predominantly associative evidence for cognitive outcomes.

4.1. Peripheral Sensory Integrity as a Foundation for Central Plasticity

The evidence aligned with the principle that peripheral sensory input is associated with central plasticity processes. Histological studies demonstrated increased nerve fibre density and growth-associated markers following implant loading [16,17], consistent with sensory-driven plasticity mechanisms described across the nervous system [37,38]. Conversely, behavioural and psychophysical studies illustrated that reduced periodontal feedback is associated with impaired force regulation and motor precision [18].

Notably, some studies reported associations between tooth loss and altered central neural measures, including hippocampal changes [2,39], but these findings are primarily indirect and do not establish causal pathways from mastication to cognitive decline.

Ageing further modulates these associations through reduction in synaptic efficiency, neurovascular coupling, and afferent input [14,40,41]. Taken together, this evidence supports the interpretation that sensory-preserving interventions (such as prosthodontics, implant rehabilitation, and oral stimulation) may help maintain oralmotor performance, particularly in older adults [42].

Moreover, the preservation of neuroplastic capacity in older adults highlights the potential of prosthodontic rehabilitation and targeted masticatory training as clinically relevant, neurobiologically grounded strategies to support oral-motor function and functional resilience. However, these approaches should be considered promising rather than definitive, as further controlled and longitudinal studies are required to confirm their broader effects on neural and cognitive adaptation.

4.2. Sensorimotor Integration as a Distributed Cortical Process

Neuroimaging and neurophysiological studies consistently demonstrated that mastication engages distributed sensorimotor networks involving M1, S1 and supplementary motor area (SMA), insula, and frontoparietal regions [2,3,18,43]. These patterns align with established models of distributed networks. Other explanations may also account for these findings. Mastication may, therefore, again represent an indicator of broader health and functional capacity, suggesting that the observed associations reflect systemic and functional influences rather than a direct causal relationship [36,44].

Variations in food hardness, occlusion, and prosthetic status modulated cortical activation and motor strategies, supporting adaptive sensorimotor integration [45]. This aligns with graded sensorimotor gain control models in which afferent input influences cortical recruitment [18,46].

Age-related reductions in efficiency and lateralisation were observed alongside preserved network engagement [9,22,42,46], suggesting compensatory rather than degenerative mechanisms, although longitudinal causal evidence remains limited.

Clinically, these findings support task-specific oral-motor training and prosthodontic design that enhances sensory feedback [47,48,49], although evidence for long-term functional superiority remains limited and heterogeneous.

4.3. Corticomotor Plasticity and Task-Specific Reorganisation

TMS and fMRI studies demonstrated that mastication is associated with task-dependent modulation of corticomotor excitability and M1 representation [18,19]. These findings align with broader use-dependent plasticity models observed in motor systems.

Changes in MEP amplitude and intracortical inhibition likely reflected synaptic-level modulation [50,51]. However, most studies were short-term, small-sample interventions, limiting inference about sustained or clinically meaningful cortical reorganisation.

Age-related attenuation of focal plasticity accompanied by broader recruitment patterns across motor and cognitive domains was observed [27,52]. While this supports preserved adaptability, the magnitude of plastic change varies considerably across studies and may depend on baseline health, dentition, and task design rather than age alone [53,54].

4.4. Rehabilitation, Reversibility, and Monitoring Plasticity

Prosthodontic rehabilitation and oral-motor training were associated with changes in corticomotor excitability [2,6,7,8,24]. These findings suggested that oral interventions may modulate neural function in addition to restoring mechanical performance.

However, the strength of evidence varied across intervention types: stronger for short-term neurophysiological modulation (such as TMS/MEP changes) and weaker for long-term functional or structural brain outcomes.

TMS and EEG studies provided mechanistic insight into cortical modulation [55], and early neurophysiological markers (such as MEP changes) may reflect short-term neural responsiveness [56,57]. Nevertheless, predictive validity for long-term rehabilitation outcomes remains to be established.

4.5. Clinical and Translational Relevance Across the Lifespan

Osseoperception studies demonstrated cortical responses to mechanical stimulation of implants [26], indicating central processing of prosthetic input.

Neuroimaging and meta-analytic evidence confirm consistent M1 involvement across oro-motor behaviours [28,58,59].

Epidemiological and imaging studies indicated meaningful associations between masticatory function and cognitive measures, brain activation, and broader health outcomes [10,60,61]. Although largely based on cross-sectional or short-term designs, these findings provide supportive evidence for a potential link between mastication and cognitive processes. Activation of prefrontal and hippocampal regions during more demanding chewing tasks, such as chewing harder food [25,27,33,62,63,64,65], further suggests engagement of cognitive networks, pointing toward a plausible contribution of mastication to brain function, while longer-term effects remain to be clarified.

4.6. Cross-Domain Integration of Evidence vs. Limitations

Across domains, the evidence supports a multilevel (peripheral–M1–behavioural) but primarily associative model of mastication-related neuroplasticity. Peripheral sensory input, sensorimotor integration, and corticomotor excitability appear closely interconnected, whereas cognitive associations are more variable and indirect. Behavioural and rehabilitative interventions may induce measurable neurophysiological changes; however, their translation into sustained functional or cognitive benefits has not been sufficiently demonstrated. Age-related differences reflect preserved adaptability rather than a loss of plasticity; however, ageing alone does not fully explain these changes, as the magnitude and functional relevance of plasticity are likely modulated by health status, baseline function, and environmental factors [1,14,27,28].

These interpretations should be considered in the light of important methodological limitations. The evidence base is characterised by small sample sizes, short intervention durations, and heterogeneity in neuroimaging, neurophysiological protocols, and outcome measures, which limit comparability and constrain integrative synthesis. Consequently, causal inference and mechanistic continuity remain limited, suggesting that observed associations may reflect broader systemic influences rather than direct effects of mastication. Importantly, the review design involved a trade-off: restricting inclusion to human studies enhanced clinical relevance and translational applicability, but limited access to detailed mechanistic insights typically derived from animal models [37,65,66,67]. Finally although consistent with the scoping review methodology under PRISMA-ScR, no formal risk-of-bias assessment was conducted (Appendix A).

This conceptual framework, which connects the full range of human data pathways linking mastication and brain function, has enabled a clear synthesis of related mechanisms and clinical factors, highlighting meaningful associations using the PRISMA checklist (Supplementary Material, Table S1). It emphasises the importance of future research using longitudinal, multimodal approaches that include neuroimaging, neurophysiological, and behavioural data, along with standardised intervention methods. More studies focusing on ageing and clinical groups as well as the roles of sensory input, masticatory features, and cognitive engagement are necessary to improve understanding of the underlying mechanisms and to develop targeted, evidence-based rehabilitation strategies.

5. Conclusions

Mastication is a sensorimotor process involving brainstem, sensory, and corticomotor networks, with evidence indicating an associative—rather than causal—relationship with neuroplasticity. In older adults, maintained plasticity suggests that prosthodontic rehabilitation and specific masticatory training could enhance oral-motor function, although the broader neural effects remain unclear. More longitudinal, multimodal, and standardised research is needed to better understand these mechanisms and their clinical significance.