目的:本系统评价研究了诊断,预后,以及与阻生第三磨牙相关的牙源性角化囊肿(DCs)和牙源性角化囊肿(OKCs)中免疫组织化学标记的治疗意义。
方法:在包括MEDLINE/PubMed在内的主要数据库中采用了全面的搜索策略,EMBASE,和WebofScience,从数据库成立到2024年3月。关键词和医学主题标题(MeSH)术语,如“牙囊囊肿”,“牙源性角化囊肿”,“免疫组织化学”,\"Ki-67\",和“p53”被使用。遵循PRISMA2020指南,以确保方法的严谨性。纳入标准包括对人类和动物的研究,提供与DC和OKC相关的明确诊断或特定体征和症状。来自免疫组织化学的蛋白质表达结果,免疫抗体,蛋白质组学,或蛋白质表达方法。
结果:在最初确定的159项研究中,138符合纳入标准。我们的分析强调了Ki-67的表达显着升高(22.1%±4.7vs.10.5%±3.2,p<0.001),p53(15.3%±3.6vs.5.2%±1.9,p<0.001),和Bcl-2(18.4%±3.2vs.与DC相比,OKC中的8.7%±2.4,p<0.001),表明较高的增殖指数,细胞应激增加,并增强了OKCs的抗凋亡机制。此外,OKC中PCNA水平较高(25.6%±4.5vs.12.3%±3.1,p<0.001)。基因突变,特别是在PTCH1基因中,在OKC中经常观察到,强调他们的攻击行为和潜在的恶性肿瘤。
结论:研究结果强调了免疫组织化学标记在区分DC和OKC中的重要作用。Ki-67,p53,Bcl-2和PCNA在OKC中的水平升高,表明生长和复发的可能性更高。遗传见解,包括PTCH1突变,进一步支持个性化治疗方法的需要。这些标志物提高了诊断的准确性,并为有针对性的治疗策略提供了信息。可能改变口腔颌面外科的患者管理。
OBJECTIVE: This systematic review investigates the diagnostic, prognostic, and therapeutic implications of immunohistochemical markers in dentigerous cysts (DCs) and odontogenic keratocysts (OKCs) associated with impacted third molars.
METHODS: A comprehensive search strategy was employed across major databases including MEDLINE/PubMed, EMBASE, and Web of Science, from the inception of the databases to March 2024. Keywords and Medical Subject Heading (MeSH) terms such as \"dentigerous cysts\", \"odontogenic keratocysts\", \"immunohistochemistry\", \"Ki-67\", and \"p53\" were used. The PRISMA 2020 guidelines were followed to ensure methodological rigor. Inclusion criteria encompassed studies on humans and animals providing definitive diagnoses or specific signs and symptoms related to DCs and OKCs, with results on protein expression derived from immunohistochemistry, immune antibody, proteomics, or protein expression methods.
RESULTS: Of the 159 studies initially identified, 138 met the inclusion criteria. Our analysis highlighted significantly higher expressions of Ki-67 (22.1% ± 4.7 vs. 10.5% ± 3.2, p < 0.001), p53 (15.3% ± 3.6 vs. 5.2% ± 1.9, p < 0.001), and Bcl-2 (18.4% ± 3.2 vs. 8.7% ± 2.4, p < 0.001) in OKCs compared to DCs, indicating a higher proliferative index, increased cellular stress, and enhanced anti-apoptotic mechanisms in OKCs. Additionally, PCNA levels were higher in OKCs (25.6% ± 4.5 vs. 12.3% ± 3.1, p < 0.001). Genetic mutations, particularly in the PTCH1 gene, were frequently observed in OKCs, underscoring their aggressive behavior and potential malignancy.
CONCLUSIONS: The findings emphasize the significant role of immunohistochemical markers in distinguishing between DCs and OKCs, with elevated levels of Ki-67, p53, Bcl-2, and PCNA in OKCs suggesting a higher potential for growth and recurrence. Genetic insights, including PTCH1 mutations, further support the need for personalized treatment approaches. These markers enhance diagnostic accuracy and inform targeted therapeutic strategies, potentially transforming patient management in oral and maxillofacial surgery.