Review of murine models reveals that masticatory dysfunction and high-fat diet impair salivary and gastrointestinal hormone signaling, suggesting occlusal stability supports metabolic health.
Purpose Recent evidence highlights a bidirectional relationship between oral function and systemic metabolic diseases, particularly type 2 diabetes mellitus. Although orthodontics has traditionally emphasized craniofacial aesthetics and functional occlusion, basic research increasingly links masticatory function to neuroendocrine and metabolic homoeostasis. The primary purpose of this comprehensive review is to clarify the impacts of high-fat diet (HFD) exposure and masticatory dysfunction – induced by bilateral maxillary molar extraction (BMME) – on the stomatognathic and gastrointestinal systems.Materials and methods To address this objective, we synthesized recent basic research findings from murine models, focusing on transgenerational HFD exposure, experimental T2DM models, and occlusal loss.Results Transgenerational high-fat diet exposure alters craniofacial morphology, including increased total skull length in males, and programmes high-salt taste preference through angiotensin II receptor type 1 upregulation. Type 2 diabetes mellitus is associated with time-dependent purinergic receptor upregulation and incretin receptor downregulation in submandibular glands. The combined effects of occlusal loss and type 2 diabetes mellitus further downregulate incretin receptors in the submandibular glands and reduce gastric ghrelin expression with mucosal hypertrophy.Conclusion Supported by quantitative and human epidemiological evidence, this review suggests that stable occlusion through orthodontic and prosthodontic interventions may support systemic metabolic management.
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Takashi Ono (2026) studied this question.
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