无核细胞性紫癜儿童牙周附着丧失:两名男性兄弟姐妹的病例报告。

Bárbara Soldatelli Ballardin, Suelen aCroline Rodrigues, Magda Feres, Cassius Carvalho Torres-Pereira, Geisla Mary Silva Soares
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引用次数: 0

摘要

目的:报告两名被诊断为先天性无核细胞性紫癜(AP)的兄弟姐妹(2岁和4岁)的牙周状况,他们接受了异基因造血干细胞移植(HSCT)并发展为具有口腔表现的移植物抗宿主病(GVHD)。方法:通过体格检查和病历资料获取临床病史。患者在移植后2个月开始出现GVHD的体征和症状时接受临床和微生物学评估,并在移植后8/15个月进行监测。采用预防措施和口腔卫生指导进行治疗。每例患者取两份龈上生物膜标本,采用棋盘DNA-DNA杂交法进行分析。结果:乳牙列患者出现严重的牙周附着缺失(CAL)并伴有牙周组织萎缩。他们还在口腔黏膜、嘴唇和舌头上出现GVHD病变。发现有龋齿、牙龈炎和重度生物膜沉积。生物膜样品的微生物学特征显示出高水平和比例的牙周病原体,如放线菌聚集菌。结论:报告的病例提示,AP患儿严重牙周CAL可能是AP和/或GVHD相关的非典型表现,其可能因含有牙周病原体(尤其是放线菌)的生物膜的存在而加重。
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Periodontal Attachment Loss in Children with Amegakaryocytic Purpura: Case Reports of Two Male Siblings.

Aims: To report the periodontal condition of two siblings (ages 2 and 4) diagnosed with congenital Amegakaryocytic Purpura (AP), who underwent allogeneic hematopoietic stem cell transplant (HSCT) and developed graft-versus-host disease (GVHD) with oral manifestations.

Methods: Clinical history was obtained through physical examination and medical records. Patients received clinical and microbiological assessment at 2 months post-HSCT, when they started to show signs and symptoms of GVHD and were monitored at 8/15-months post-transplant. They were treated by means of prophylaxis and oral hygiene instruction. Two supragingival biofilm samples were collected from each patient and analyzed by Checkerboard DNA-DNA hybridization.

Results: Patients developed severe periodontal clinical attachment loss (CAL) in deciduous dentition associated with recession of the periodontal tissues. They also presented GVHD lesions in the oral mucosa, lips and tongue. Caries lesions, gingivitis, and heavy biofilm deposits were identified. The microbiological profile of biofilm samples presented high levels and proportions of periodontal pathogens, such as Aggregatibacter actinomycetemcomitans.

Conclusion: The cases presented suggested that severe periodontal CAL in children with AP may be an atypical manifestation associated with AP and/or GVHD, which may be aggravated by the presence of a dysbiotic biofilm containing periodontal pathogens, especially A. actinomycetemcomitans.

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