A Novel Non-invasive Mouthpiece Model for Evaluating Oral Hypofunction: Focus on Mastication and Stomatognathic Dynamics.

BACKGROUND/OBJECTIVES: Studies have examined the mechanisms of oral hypofunction by investigating the relationship between the number of remaining teeth, bite force, mastication ability, and lateral induction factors influencing chewing pathways. However, many previous studies have not consistently assessed the same individuals across all these factors, leaving key contributing factors unaddressed. This study aimed to develop a reliable oral hypofunction model using non-invasive mouthpieces. We hypothesized that it is possible to reproduce a model of oral hypofunction in healthy individuals using a mouthpiece by modifying occlusal contact areas and lateral induction factors.

METHODS

A total of 10 healthy adults (five men and five women; mean age: 28.4 ± 1.5 years old) with normal occlusion and no stomatognathic abnormalities participated in this study. Experiments were conducted under four conditions: (1) no mouthpiece; (2) a mouthpiece with large occlusal contact areas and canine guidance; (3) a mouthpiece with large occlusal contact areas but no canine guidance; and (4) a mouthpiece with small occlusal contact areas and no canine guidance. The outcomes assessed were maximum bite force, occlusal contact area, mastication ability, and salivation.

RESULTS

A strong positive correlation was identified between occlusal contact area and maximum bite force (p < 0.001). Furthermore, occlusal contact was positively correlated with mastication ability (p < 0.001). The glucose concentration of the filtered solution decreased significantly from Condition I (mean: 203.3 (SD = 42.7) mg/dl) to Condition IV (mean: 90.2 (SD = 14.2) mg/dl) (Figure 9). The presence of lateral induction factors, such as canine guidance, demonstrated a significant influence on these outcomes (p < 0.05).

CONCLUSIONS

The findings align with those of previous studies and validate the use of this mouthpiece model for simulating oral hypofunction. This model, adaptable for use in healthy individuals, supports larger-scale studies under controlled conditions to better elucidate the mechanisms underlying oral hypofunction.