Hall technique crowns and children's masseter muscle activity: A surface electromyography pilot study

Background: Hall technique crowns (HTCs) alter the occlusion temporarily, potentially affecting jaw muscles, particularly the masseter – the primary jaw-closing muscle. Aim: To assess masseter muscle activity (MMA) in children treated with a unilateral HTC. Design: In 12 children treated with a single HTC, bilateral MMA was recorded with surface electromyography (sEMG) for ten cycles of Rest Position (RP) and Maximum Voluntary Clenching (MVC) over 20 seconds immediately pre-HTC cementation (Pbase), immediately post-HTC cementation (Pimmed), at 2 weeks post-HTC cementation (P2w) and at 6 weeks post-HTC cementation (P6w). t test, ANOVA and post hoc statistics were used (P < .05). Results: As expected, MMA was low at rest and increased during maximal jaw clenching (P < .0001). MMA (mean ± SD) increased significantly (P < .001) between RP and MVC at: Pbase [from 1.60 μV·s (±0.96) to 5.40(±2.30)]; Pimmed [1.57(±1.15) to 3.75(±1.87)]; P2w[1.39(±0.54) to 5.54(±1.45)] and finally P6w [1.46(±0.56) to 6.45(±2.56)]. Rest MMA at Pbase, Pimmed, P2w and P6w remained unchanged (P = .18) whereas Pbase clench MMA reduced by a third at Pimmed (P < .001), returned to and exceeded baseline levels at P2w (P = .822) and P6w (P < .001), respectively. Conclusions: This pilot study showed that Hall technique crowns may affect masseter muscle activity in children. Clench MMA was reduced immediately post-treatment but returned to and later exceeded baseline levels at 2 and 6 weeks, respectively. Rest MMA remained unchanged

D-2-hydroxyglutarate supports a tolerogenic phenotype with lowered major histocompatibility class II expression in non-malignant dendritic cells and acute myeloid leukemia cells

D-2-hydroxyglutarate (D-2-HG) accumulates in primary acute myeloid leukemia (AML) patients with mutated isocitrate dehydrogenase (IDH) and other malignancies. D-2-HG suppresses antitumor T cell immunity but little is known about potential effects on non-malignant myeloid cells. Here we show that D-2-HG impairs human but not murine dendritic cell (DC) differentiation, resulting in a tolerogenic phenotype with low major histocompatibility (MHC) class II expression. In line, IDH-mutated AML blasts exhibited lower expression of HLA-DP and were less susceptible to lysis by HLA-DP-specific T cells. Interestingly, D-2-HG reprogrammed metabolism towards increased lactate production in DCs and AML besides its expected impact on DNA demethylation. Vitamin C accelerated DNA demethylation, but only the combination of vitamin C and glycolytic inhibition lowered lactate levels and supported MHC class II expression. Our results indicate an unexpected link between the immunosuppressive metabolites 2-HG and lactic acid and suggest a potentially novel therapeutic strategy with combinations of anti-glycolytic drugs and epigenetic modulators (hypomethylating agents) or other therapeutics for the treatment of AML