Clinical investigation of botulinum toxin (prabotulinumtoxin A) for bruxism related to masseter muscle hypertrophy: A prospective study.

This study aims to confirm the effectiveness and safety of a prabotulinumtoxin type A (praBTX-A) injection in patients with bruxism and masseter hypertrophy. The study included patients who ground or clenched their teeth while sleeping and had computed tomography (CT) scans that showed a maximum thickness of the masseter muscle of 15 mm or more. The praBTX-A was administered bilaterally into the masseter muscles; 15 U/side for group 1, 25 U/side for group 2, and 35 U/side for group 3. CT scans and bruxism questionnaires were conducted before and eight weeks after the injection. Thirty-seven patients were enrolled, but three dropped out due to loss of follow-up. After injection, masseter thickness decreased to 15.1 ± 2.0 mm for group 1, 14.3 ± 2.9 mm for group 2, and 13.4 ± 1.8 mm for group 3 (p = 0.043). Group 3 showed a statistically significant lower masseter thickness compared to group 1 (p = 0.039). Both subjective and objective frequencies of bruxism decreased for all groups, but there were no significant differences in either subjective (p = 0.396) or objective frequencies (p = 0.87) between the groups after the injection. The results of this study suggest that praBTX-A injection is a safe and effective treatment for bruxism and masseter hypertrophy. A dosage of 35 IU/side can effectively decrease masseter thickness and relieve bruxism symptoms. Even the minimum dosage of 15 IU/side can contribute to improvements in bruxism symptoms. This investigation provides valuable information for managing bruxism that is associated with hypertrophic masseter muscles.

Immune Tolerance of Human Dental Pulp-Derived Mesenchymal Stem Cells Mediated by CD4⁺CD25⁺FoxP3⁺ Regulatory T-Cells and Induced by TGF-ß1 and IL-10.

PURPOSE: Most studies on immune tolerance of mesenchymal stem cells (MSCs) have been performed using MSCs derived from bone marrow, cord blood, or adipose tissue. MSCs also exist in the craniofacial area, specifically in teeth. The purpose of this study was to evaluate the mechanisms of immune tolerance of dental pulp-derived MSC (DP-MSC) in vitro and in vivo. MATERIALS AND METHODS: We isolated DP-MSCs from human dental pulp and co-cultured them with CD4⁺ T-cells. To evaluate the role of cytokines, we blocked TGF-ß and IL-10, separately and together, in co-cultured DP-MSCs and CD4⁺ T-cells. We analyzed CD25 and FoxP3 to identify regulatory T-cells (Tregs) by fluorescence-activated cell sorting (FACS) and real-time PCR. We performed alloskin grafts with and without DP-MSC injection in mice. We performed mixed lymphocyte reactions (MLRs) to check immune tolerance. RESULTS: Co-culture of CD4⁺ T-cells with DP-MSCs increased the number of CD4⁺CD25⁺FoxP3⁺ Tregs (p<0.01). TGF-ß or/and IL-10 blocking suppressed Treg induction in co-cultured cells (p<0.05). TGF-ß1 mRNA levels were higher in co-cultured DP-MSCs and in co-cultured CD4⁺ T-cells than in the respective monocultured cells. However, IL-10 mRNA levels were not different. There was no difference in alloskin graft survival rate and area between the DP-MSC injection group and the non-injection group. Nonetheless, MLR was reduced in the DP-MSC injected group (p<0.05). CONCLUSION: DP-MSCs can modulate immune tolerance by increasing CD4⁺CD25⁺FoxP3⁺ Tregs. TGF-ß1 and IL-10 are factors in the immune-tolerance mechanism. Pure DP-MSC therapy may not be an effective treatment for rejection, although it may module immune tolerance in vivo.