Abstract Background Burning mouth syndrome (BMS) is a complex chronic pain disorder that significantly impairs patients' quality of life. Low-level laser therapy (LLLT) uses infrared or near-infrared light to produce analgesic, anti-inflammatory, and biological stimulation effects. The aim of this systematic review is to evaluate the effect of LLLT on burning pain, quality of life, and negative emotions in patients with BMS. Methods The PubMed, Embase, Cumulative Index of Nursing and Allied Health Literature (CINAHL), Cochrane Library, Web of Science, and Scopus databases were searched up January 2023 to identify relevant articles. All randomized controlled trials that were published in English and examined the use of LLLT treatment for BMS were included. The methodological quality of the included trials was assessed using the Cochrane risk of bias tool for randomized controlled trials (RCTs). A meta-analysis was performed to evaluate burning pain, quality of life, and negative emotions. Sensitivity, subgroup, and funnel plot analyses were also carried out. Results Fourteen RCTs involving a total of 550 patients with BMS met the inclusion criteria. The results showed that LLLT (measured by the Visual Analog Scale; SMD: -0.87, 95% CI: -1.29 to -0.45, P < 0.001) was more effective for reducing burning pain than placebo LLLT or clonazepam. LLLT improved quality of life (evaluated by the Oral Health Impact Profile-14; SMD: 0.01, 95% CI: -0.58 to 0.60, P = 0.97) and negative emotions (evaluated by the Hospital Anxiety and Depression Scale; SMD: -0.12, 95% CI: -0.54 to 0.30, P = 0.59), but these effects were not statistically significant. Conclusions The meta-analysis revealed that LLLT may be an effective therapy for improving burning pain in patients with BMS, and producing a positive influence on quality of life and negative emotions. A long-term course of intervention, a larger sample size, and a multidisciplinary intervention design are urgently needed in future research. Trial registration PROSPERO registration number: CRD42022308770.
Objective:To investigate single nucleotide polymorphisms(SNP) of interleukin 12A gene with oral lichen planus(OLP) in Chinese Hans residing in East and South-east China,and to provide an important genetic basis in exploring the disease susceptibility and diverse clinical manifestation.Method:Two hundred and ninety-two patients with OLP and 686 healthy control subjects were recruited in Chinese Hans residing in East and South-east China.Genomic DNA was extracted and PCR products spanning five SNPs of the IL-12A gene at positions (rs3024415,rs2243123,rs583911,rs568408 and rs2243143) were analyzed.The genotype frequencies were calculated and analyzed.Result:①Polymorphism of rs568408,located at the 3'-UTR region was found to have a significant association with OLP(P =0.0427).②Polymorphism of rs583911 was also found to have a significant association with OLP(P =0.0085).③The allele frequencies of IL-12A-rs568408/A in the erosive OLP group were much higher than that in the healthy group(OR=1.76,95 % CI:1.133-2.732,P =0.011).Conclusion:The variation of IL-12A rs568408 gene polymorphisms seems to have some influence on the disease susceptibility and association with the severity of OLP in this Chinese cohort residing in East and South-east China.
Oral leukoplakia (OL) is the best-known potentially malignant disorder. A new binary system to grade dysplasia was proposed by WHO, but the biological significance in predicting malignant transformation risk is unknown. The objective of this study is to estimate the rate of malignant transformation in a long-term follow-up cohort, explore the usefulness of the new binary system of grading dysplasia and identify significant risk factors of OL malignant transformation in China.A total of 218 patients with clinical and histopathologic diagnosis of OL were retrospectively reviewed. They were selected among all archived files at the Department of Oral Mucosal Diseases, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine. The mean follow-up period was 5.3 years.Among 218 cases, 39 (17.9%) OL patients developed oral cancer, with a mean duration of 5.2 years. Cox regression analysis revealed that dysplasia was an independent risk factor for OL malignant transformation, but age, gender, lesion site, diet habit, smoking and ethanol intake were not risk factors. High-risk dysplastic OL was associated with a 4.57-fold (95% confidence interval, 2.36-8.84; P < 0.001) increased risk of malignant transformation, compared with low-risk dysplasia. Consistent with this result, high-risk dysplastic OL had significantly higher malignant incidence than low-risk dysplasia, particularly during the first 2-3 years of follow-up, by Kaplan-Meier analysis (Log-rank test, P < 0.001).The new binary system's function in predicting OL malignant transformation risk was investigated in this survey. The utilization of high-risk dysplasia as a significant indicator for evaluating malignant transformation risk in patients with OL was suggested, which may be helpful to guide treatment selection in clinical practice.
MicroRNA-27b (miR-27b) was recently found to be significantly downregulated in oral lichen planus (OLP). However, evidence of the function of miR-27b in OLP remains limited.Initially, miR-27b expression in OLP was verified using the quantitative real-time polymerase chain reaction (qRT-PCR). Functionally, gain-/loss-of-function studies were then conducted using miR-27b mimics/inhibitor to investigate cell growth in human oral keratinocytes (HOKs). Mechanistically, subsequent miRNA target analyses including a starBase database analysis and a luciferase reporter assay were performed to predict and validate the direct target, respectively. In addition, overexpression/knockdown assays of target(s) of miR-27b were performed to investigate its functional significance and qRT-PCR and western blotting were used to evaluate the target(s) of miR-27b mRNA and protein levels, respectively.MicroRNA-27b was significantly downregulated in OLP tissues when compared with healthy control tissues. Bioinformatics predicted that Polo Like Kinase 2 (PLK2) might be a potential target of miR-27b, while the luciferase reporter assay results showed the direct inhibition of the plk2-3'untranslated region by miR-27b. Moreover, functional analysis indicated that downregulated miR-27b caused an increase in cell growth in HOKs, and correspondingly, overexpression of PLK2 promoted HOK proliferation.There were aberrant expressions of miR-27b and PLK2 in OLP tissues. Decreased miR-27b may have induced cell proliferation by increasing the levels of PLK2 in HOKs, which provides a new perspective into the potential mechanisms underlying OLP development.
Abstract Objective We determined the bacterial community structure of the buccal mucosa in patients with oral lichen planus (OLP) and evaluated the potential association of Fusobacterium nucleatum with OLP. Subjects and Methods We collected buccal mucosal swab samples of patients with OLP ( n = 20) and healthy controls ( n = 10) and performed 16S rRNA gene sequencing and real‐time PCR to determine potentially different bacteria. Damaged and adjacent non‐damaged mucosal swab samples of 25 OLP patients were used to detect the amount of F. nucleatum by real‐time PCR. Results Compared with healthy controls, enrichment of Fusobacterium and Granulicatella was more abundant in patients with OLP ( p = .0146 and 0.0034). The abundance of Fusobacterium and F. nucleatum was significantly enriched on buccal mucosa of patients with OLP compared with healthy controls ( p = .0043 and 0.0235). Compared with adjacent non‐damaged buccal mucosa of OLP patients, the amount of F. nucleatum in the damaged mucosa was significantly increased ( p = .001). We examined third‐level KEGG pathways for bacteria on mucosal surface and found that genes controlling sporulation and ether lipid metabolism were enriched in patients with OLP. Conclusions A high amount of F. nucleatum may be associated with OLP. Further studies are required to investigate the precise association of F. nucleatum with OLP.
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