A cross-sectional study: correlation of forehead morphology and dentoskeletal malocclusion in Chinese people.

BACKGROUND: The lateral profile is an important indicator of facial attractiveness. This study explored the general characteristics of the forehead profile and protrusion, and their relationship with related factors in structure and development. METHODS: Four hundred fourteen Chinese participants in the Yangtze River Delta region were involved. Including 206 males (17.15 ± 7.68 years old) and 208 females (18.35 ± 8.06 years old); 94 children (8.54 ± 2.21 years old, ranging from 4 to 12 years old), 166 adolescents (14.83 ± 1.50 years old, ranging from 13 to 17 years old), and 154 adults (25.52 ± 4.89, 18 years or older). The frontal section of the forehead was used to explore its shape. The straight distance between the vertical line of the FH plane through the nasal root point and its parallel line, which is tangential to the forehead, indicates the forehead prominence. Frontal sinus width was measured using the method described by Mahmood. RESULTS: The general shape of the forehead was straight and slightly bulged near the eyebrow arch in males but rounder in females. The average forehead protrusion in males was higher than that in females in adults. Significant differences in forehead protrusion between the dentoskeletal classifications and growth phases were notable. Frontal protrusion significantly correlated with frontal sinus depth, especially in males, adults, Class I, and those whose convex points were located in the lower section of the forehead. CONCLUSIONS: Age, race, and sex affect the forehead protrusion and frontal sinus width. Forehead protrusion may be an indicator of dentoskeletal deformities in the early stage. And dentoskeletal deformities may impair the correlation between the frontal sinuses and forehead protrusion during development. TRIAL REGISTRATION: This retrospective, cross-sectional study was reviewed and approved by the Research Ethical Committee (T2020008), and registered at ClinicalTrial.gov with an identified number (ChiCTR2100041913).

Electrical stimulation prevents condyle and subchondral degeneration following the masseter atrophy.

OBJECTIVE: There is a strong relationship between masticatory muscle atrophy and condyle degeneration. Although electrical stimulation (ES) is an effective treatment for muscle atrophy, its influence on the underlying condyle is unclear. This study aimed to investigate whether ES can prevent condyle degradation during the stage of masseter muscle atrophy. MATERIALS AND METHODS: Six-week-old rats were randomly divided into the control, botulinum toxin (BTX), or BTX + ES group. BTX was injected into the bilateral masseters of rats to induce masseter atrophy. The left-side masseters without ES treatment were served as BTX group, and the right-side masseters received ES with different parameters (5 mA/10 Hz, 5 mA/50 Hz, 6 mA/10 Hz, 6 mA/50 Hz, 7 mA/10 Hz, and 7 mA/50 Hz) were served as BTX + ES groups. After 4 weeks, micro-CT and qualitative or quantitative analysis of osteogenesis, chondrogenesis, and angiogenesis-related genes in condyles were conducted. RESULTS: ES, especially at 7 mA/50 Hz, significantly attenuated masseter atrophy, condyle degeneration, and subchondral bone loss. Moreover, the upregulation of related proteins, including collagen 1, osteocalcin, bone morphogenetic protein 2, collagen 2a, and vascular endothelial growth factor were observed. CONCLUSION: ES partly rescued condylar degeneration and subchondral bone loss following masseter atrophy.

Response of human periodontal ligament to orthodontic force using superb microvascular imaging.

INTRODUCTION: Remodeling of the periodontal ligament (PDL) during orthodontic tooth movement is closely related to the vascularity of the PDL, which has not been thoroughly investigated in humans. This study aimed to measure the width and vascular parameters of human PDL using superb microvascular imaging for the first time. METHODS: Patients aged 18-25 years were selected for participation. The intervention was randomly allocated from the maxillary canines to the first molars on both sides using 50 g or 150 g of force. The width and vascular parameters of the PDL were measured using superb microvascular imaging at different time intervals (baseline, 30 minutes, and 1, 3, 7, and 14 days). RESULTS: Before the intervention, the width of the PDL ranged from 0.14 to 0.25 mm, and the vascular index ranged from 9.40% to 13.54%. After applying orthodontic forces, the cervical and middle PDL widths increased. The vascular index decreased slightly in 30 minutes, decreased to a minimum value after 1 day, increased to the maximum in 3-7 days, and returned to baseline values in 14 days. The values of other vascular parameters showed similar trends. CONCLUSIONS: The width and vascular parameters of the PDL changed slightly after force application, underwent changes in the period of reconstruction for 3-7 days, and eventually returned to baseline in 14 days.

Exploring the mechanism of diabetic cardiomyopathy treated with Qigui Qiangxin mixture based on UPLC-Q/TOF-MS, network pharmacology and experimental validation.

Despite its effectiveness in treating diabetic cardiomyopathy (DCM), Qigui Qiangxin Mixture (QGQXM) remains unclear in terms of its active ingredients and specific mechanism of action. The purpose of this study was to explore the active ingredients and mechanism of action of QGQXM in the treatment of DCM through the comprehensive strategy of serum pharmacology, network pharmacology and combined with experimental validation. The active ingredients of QGQXM were analyzed using Ultra-performance liquid chromatography coupled with quadrupole time of flight mass spectrometry (UPLC-Q/TOF-MS). Network pharmacology was utilized to elucidate the mechanism of action of QGQXM for the treatment of DCM. Finally, in vivo validation was performed by intraperitoneal injection of STZ combined with high-fat feeding-induced DCM rat model. A total of 25 active compounds were identified in the drug-containing serum of rats, corresponding to 121 DCM-associated targets. GAPDH, TNF, AKT1, PPARG, EGFR, CASP3, and HIF1 were considered as the core therapeutic targets. Enrichment analysis showed that QGQXM mainly treats DCM by regulating PI3K-AKT, MAPK, mTOR, Insulin, Insulin resistance, and Apoptosis signaling pathways. Animal experiments showed that QGQXM improved cardiac function, attenuated the degree of cardiomyocyte injury and fibrosis, and inhibited apoptosis in DCM rats. Meanwhile, QGQXM also activated the PI3K/AKT signaling pathway, up-regulated Bcl-2, and down-regulated Caspase9, which may be an intrinsic mechanism for its anti-apoptotic effect. This study preliminarily elucidated the mechanism of QGQXM in the treatment of DCM and provided candidate compounds for the development of new drugs for DCM.