金德勒综合征的异常口腔表现:病例报告和文献综述。

IF 3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Frontiers in oral health Pub Date : 2024-09-05 eCollection Date: 2024-01-01 DOI:10.3389/froh.2024.1430698
Rahul Bhandary, Geethu Venugopalan, Padmaraj Hegde
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引用次数: 0

摘要

金德勒综合征(Kindler Syndrome,KS)是一种罕见的常染色体隐性遗传性皮肤病,以先天性尖锐疱疹为特征,通常在婴儿期发病,随后出现特征性的皮肤色素沉着和光敏性皮肤病。这些临床表现源于 FERMT-1(Fermitin 家族同源物 1)的突变,该基因编码 kindlin-1,kindlin-1 是一种定位于角朊细胞局灶粘附的蛋白质。Kindlin-1在整合素受体激活过程中起着关键作用,而整合素受体激活对细胞粘附和迁移至关重要。大多数 KS 病例都表现出 kindlin-1 表达减少或缺失,导致整合素激活缺陷以及细胞粘附和迁移过程受损。细胞粘附性受损最终导致 KS 出现水疱表型。KS 的口腔表现经常被漏报和误诊,可能导致治疗延误或错误。此外,由于表皮屏障功能受损和牙周健康受损,糖尿病(DM)会进一步加剧 KS 的严重程度。这种并发症会产生协同效应。牙周感染通常会通过一种依赖于 caspase-3 的机制被 DM 加剧,从而导致上皮细胞和成纤维细胞凋亡。DM 导致的细胞凋亡增强和上皮屏障功能丧失进一步阻碍了组织修复过程。因此,与 KS 相关的皮肤和口腔并发症在糖尿病患者中变得更加严重。我们报告了一例独特的糖尿病青少年 KS 病例,该病例表现为口腔大面积化脓性肉芽肿和广泛的牙周破坏,并对文献进行了全面回顾,探讨了目前对 KS 口腔表现的认识,强调了其诊断不足以及 DM 加重病情的可能性。该病例强调,需要提高对 KS 口腔表现的认识,尤其是糖尿病患者。早期诊断和多学科方法对于KS相关的皮肤和口腔并发症的最佳治疗至关重要。
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Unusual oral manifestation of Kindler syndrome: a case report and review of literature.

Kindler syndrome (KS) is a rare autosomal recessive genodermatosis characterized by congenital acral blistering, that typically presents in infancy and is followed by the development of characteristic poikilodermatous pigmentation and photosensitivity in later life. These clinical manifestations arise from mutations in the FERMT-1 (Fermitin family homologue 1) that encodes kindlin-1, a protein localized to focal adhesions in keratinocytes. Kindlin-1 plays a crucial role in integrin receptor activation, which is essential for cell adhesion and migration. Most KS cases exhibit reduced or absent kindlin-1 expression, leading to defective integrin activation and impaired cell adhesion and migration processes. This impaired cell adhesion ultimately results in the blistering phenotype observed in KS. Oral manifestations of KS are frequently under-reported and misdiagnosed, potentially leading to delayed or incorrect treatment. Furthermore, diabetes mellitus (DM) can further exacerbate the severity of KS due to impaired epidermal barrier function and compromised periodontal health. This co-morbidity creates a synergistic effect. Periodontal infection, often exacerbated by DM through a caspase-3-dependent mechanism, can cause apoptosis of epithelial cells and fibroblasts. This enhanced apoptosis and loss of epithelial barrier function due to DM further hinder tissue repair processes. Consequently, both cutaneous and oral complications associated with KS become more severe in diabetic patients. We report a unique case of a diabetic adolescent with KS presenting with a massive oral pyogenic granuloma and extensive periodontal destruction with a comprehensive review of the literature exploring the current understanding of oral manifestations in KS, emphasizing their under-diagnosis and potential for exacerbation by DM. This case emphasizes the need for increased awareness of oral manifestations in KS, especially in diabetic patients. Early diagnosis and a multidisciplinary approach are crucial for optimal management of cutaneous and oral complications associated with KS.

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