Van Dyke T E, Horoszewicz H U, Cianciola L J, Genco R J
Infect Immun. 1980 Jan;27(1):124-32. doi: 10.1128/iai.27.1.124-132.1980.
Polymorphonuclear leukocyte (PMNL) chemotaxis studies of 32 patients with localized juvenile periodontitis (periodontosis or LJP), 10 adult patients with a history of LJP (post-LJP), 8 patients with generalized juvenile periodontitis (GJP), and 23 adults with moderate to severe periodontitis were performed: (i) to determine the prevalence of a PMNL chemotaxis defect in a large group of LJP patients; (ii) to study PMNL chemotaxis in patients with other forms of severe periodontal disease; and (iii) to determine if the PMNL chemotaxis defect seen in LJP patients is a cell-associated defect or is mediated by humoral factors. The effect of periodontal treatment on PMNL chemotaxis was studied in nine LJP patients. The chemotactic response was measured with the Boyden chamber procedure, and patient's peripheral PMNL were compared with those of control subjects, using endotoxin-activated serum, bacterial factor, N-formylmethionyl-leucylphenylalanine, and leukocyte-derived chemotactic factor as the standard chemoattractants. Based upon statistical analysis of chemotaxis assays, most carried out on at least two and often three or more separate occasions, 26 of 32 LJP patients, 7 of 10 post-LJP patients, and 5 of 8 GJP patients exhibited cellular defects of chemotaxis, whereas only 2 of 23 of the patients with adult periodontitis exhibited depressed chemotaxis. Elevated PMNL chemotaxis was occasionally found in subjects with juvenile periodontitis (2 of 32 with LJP and two of eight with GJP); however, it was found in a significant number (10 of 23) of patients with adult periodontitis. In eight of nine LJP patients, depressed PMNL chemotaxis was observed before and after periodontal therapy. The results indicate that the PMNL chemotaxis defect observed in juvenile periodontitis is due to a cell-associated defect of long duration. These studies suggest that the PMNL plays a major protective role against periodontal infection and that the cellular chemotactic defects and may predispose subjects to LJP.
对32例局限性青少年牙周炎(牙周变性或LJP)患者、10例有LJP病史的成年患者(LJP后)、8例广泛性青少年牙周炎(GJP)患者以及23例中重度牙周炎成年患者进行了多形核白细胞(PMNL)趋化性研究:(i)确定一大组LJP患者中PMNL趋化性缺陷的患病率;(ii)研究其他形式重度牙周疾病患者的PMNL趋化性;(iii)确定LJP患者中所见的PMNL趋化性缺陷是细胞相关缺陷还是由体液因子介导。对9例LJP患者研究了牙周治疗对PMNL趋化性的影响。用博伊登小室法测量趋化反应,以内毒素激活血清、细菌因子、N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸和白细胞衍生趋化因子作为标准趋化剂,将患者外周血PMNL与对照受试者的进行比较。基于对趋化性测定的统计分析,大多数测定至少在两个且通常在三个或更多不同时间进行,32例LJP患者中的26例、10例LJP后患者中的7例以及8例GJP患者中的5例表现出趋化性细胞缺陷,而23例成年牙周炎患者中只有2例表现出趋化性降低。青少年牙周炎患者偶尔发现PMNL趋化性升高(32例LJP患者中的2例和8例GJP患者中的2例);然而,在相当数量(23例中的10例)的成年牙周炎患者中也发现了这种情况。9例LJP患者中有8例在牙周治疗前后均观察到PMNL趋化性降低。结果表明,青少年牙周炎中观察到的PMNL趋化性缺陷是由于长期存在的细胞相关缺陷。这些研究表明,PMNL在抵抗牙周感染中起主要保护作用,并且细胞趋化性缺陷可能使受试者易患LJP。