PHAGOCYTIC-CELLS IN PERIODONTAL DEFENSE - PERIODONTAL STATUS OF PATIENTS WITH CHRONIC GRANULOMATOUS-DISEASE OF CHILDHOOD
PHAGOCYTIC-CELLS IN PERIODONTAL DEFENSE - PERIODONTAL STATUS OF PATIENTS WITH CHRONIC GRANULOMATOUS-DISEASE OF CHILDHOOD
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DOI：
10.1902/jop.1985.56.10.611
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发表时间：
1985-01-01
影响因子：
4.3
通讯作者：
SIMPSON, DM
中科院分区：
文献类型：
--
作者：
COHEN, MS;LEONG, PA;SIMPSON, DM
中性粒细胞的定性和定量异常都与严重的牙周炎有关。从青少年和快速进展性牙周炎患者的外周血和牙龈中采集的中性粒细胞中均报告了趋化性、吞噬作用和细菌杀灭的缺陷。儿童慢性肉芽肿病（CGD）是一种罕见的遗传性疾病，与皮肤、肝脏、淋巴结和其他器官的严重、危及生命的化脓性感染有关。来自患有CGD的个体的中性粒细胞和单核细胞缺乏产生氧还原/产物（如H2 O2和超氧阴离子）所必需的酶，因此不能杀死许多种类的细菌和真菌。然而，没有详细的研究，这些患者的牙周组织已进行。因此，本研究纳入了5例年龄范围为17 - 32岁的患者。根据完整的牙科记录，纳入了另外1例（第6例）患者。所有患者的中性粒细胞均表现出O2代谢缺陷，所有患者均具有与CGD一致的慢性复发性血小板增多症病史。所有患者均接受抗生素预防治疗。几名患者的口腔溃疡性病变的病因不明。牙周组织检查显示，三名患者有牙龈炎，一个有局部早期牙周炎，一个有广泛的早期至中度牙周炎。牙周病的严重程度与患者的年龄和当地的病因因素一致。尽管患者存在白细胞缺陷，但没有患者有幼年、重度或快速进展疾病的证据。这些发现表明了以下可能性：（1）由PMN杀死细菌的非氧化机制足以保护牙周病原体，（2）牙周组织的生物体产生浓度足以促进CGD嗜中性粒细胞功能的H2 O2，（3）抗生素预防防止与牙周炎相关的致病性口腔植物群的获得和/或繁殖，和（4）嗜中性粒细胞的氧化机制在促进与某些形式的牙周炎相关的组织损伤中是重要的。这些观察结果为牙周炎的病理生理学提供了线索。
Both qualitative and quantitative neutrophil abnormalities have been associated with severe forms of periodontitis. Defects in chemotaxis, phagocytosis and bacterial killing have been reported among both peripheral blood and gingival neutrophils harvested from patients with juvenile and rapidly progressive periodontitis. Chronic granulomatous disease of childhood (CGD) is a rare, inherited disorder associated with the occurrence of severe, life-threatening, suppurative infections of skin, liver, lymph nodes and other organs. Neutrophils and monocytes from individuals with CGD lack enzymes necessary for the production of oxygen reduction/products such as H2O2 and superoxide anion, and therefore are unable to kill many species of bacteria and fungi. However, no detailed study of the periodontium of these patients has been undertaken. Accordingly, five patients whose ages ranged from 17 to 32 years were included in this study. An additional (sixth) patient was included based on complete dental records. Neutrophils from all patients demonstrated defective O2 metabolism, and all patients had histories of chronic recurrent abscesses consistent with CGD. All patients were receiving antibiotic prophylaxis. Several patients had ulcerative lesions of the oral cavity of unknown etiology. Examination of the periodontium revealed that three patients had gingivitis, one had localized early periodontitis, and one had generalized early-to-moderate periodontitis. The severity of periodontal disease was consistent with patient age and local etiologic factors. No patients had evidence of juvenile, severe or rapidly-progressing disease in spite of their leukocyte defects. These findings suggest the following possibilities: (1) nonoxidative mechanisms of bacterial killing by PMNs are sufficient to protect against periodontal pathogens, (2) organisms of the periodontium make H2O2 in concentrations sufficient to contribute to the function of CGD neutrophils, (3) antibiotic prophylaxis prevents acquisition and/or multiplication of pathogenic oral flora associated with periodontitis and (4) oxidative mechanisms of neutrophils are important in promoting the tissue damage associated with some forms of periodontitis. These observations offer clues to the pathophysiology of periodontitis.