Johnson R B, Serio F G, Dai X
Department of Periodontics, University of Mississippi School of Dentistry, Jackson 39216-4505, USA.
J Periodontol. 1999 Aug;70(8):848-52. doi: 10.1902/jop.1999.70.8.848.
Tissues become hemorrhagic and edematous coincident to periodontal diseases; however, there is little information concerning the biologic mechanisms which may produce these changes. Vascular endothelial growth factor (VEGF) is a macromolecule which enhances blood vessel growth and permeability. However, there is no information concerning gingival VEGF concentrations within normal or diseased gingiva. The purpose of this study was to assess changes in gingival concentrations of VEGF during initiation and progression of periodontal diseases and compare them to changes in the number of blood vessel profiles and concentration of recognized markers of periodontal disease severity (interleukin-6[IL-6]).
Normal (non-hemorrhagic gingiva adjacent to a < or =3 mm gingival sulcus) and inflamed gingiva (hemorrhagic gingiva adjacent to a < or =3 mm, 4 to 6 mm, or >6 mm periodontal pocket) were studied. VEGF and IL-6 concentrations were assessed by ELISA and the number of blood vessels determined by histomorphometric techniques. Data were placed into one of the following groups: < or =3 mm, normal; < or =3 mm, diseased; 4 to 6 mm, diseased; and >6 mm, diseased. These groups were compared by factorial ANOVA and Scheffe comparisons. In addition, groups were compared by simple and multiple regression and regression ANOVA to determine possible correlations between them.
VEGF and IL-6 concentrations were significantly lower within normal than within diseased gingiva. The number of blood vessel profiles and mean IL-6 concentrations were highest in diseased tissues adjacent to >6 mm sulci and were significantly correlated with sulcular depth (P <0.001). In contrast, VEGF concentrations were highest within diseased gingiva adjacent to 4 to 6 mm periodontal pockets (P <0.001) and were not correlated with sulcular depth.
VEGF may be a factor in initiation and progression of gingivitis to periodontitis, possibly by promoting expansion of the vascular network coincident to progression of the inflammation.
组织出血和水肿与牙周疾病同时发生；然而，关于可能导致这些变化的生物学机制的信息很少。血管内皮生长因子（VEGF）是一种促进血管生长和通透性的大分子。然而，关于正常或患病牙龈中牙龈VEGF浓度的信息却没有。本研究的目的是评估牙周疾病发生和发展过程中牙龈VEGF浓度的变化，并将其与血管轮廓数量的变化以及公认的牙周疾病严重程度标志物（白细胞介素-6[IL-6]）的浓度变化进行比较。
研究了正常（与≤3mm牙龈沟相邻的非出血性牙龈）和发炎牙龈（与≤3mm、4至6mm或>6mm牙周袋相邻的出血性牙龈）。通过酶联免疫吸附测定（ELISA）评估VEGF和IL-6浓度，并通过组织形态计量学技术确定血管数量。数据分为以下几组：≤3mm，正常；≤3mm，患病；4至6mm，患病；>6mm，患病。通过析因方差分析和谢费比较对这些组进行比较。此外，通过简单和多元回归以及回归方差分析对组进行比较，以确定它们之间可能的相关性。
正常牙龈中的VEGF和IL-6浓度显著低于患病牙龈。血管轮廓数量和平均IL-6浓度在与>6mm龈沟相邻的患病组织中最高，并且与龈沟深度显著相关（P<0.001）。相比之下，VEGF浓度在与4至6mm牙周袋相邻的患病牙龈中最高（P<0.001），并且与龈沟深度无关。
VEGF可能是牙龈炎发展为牙周炎的起始和进展过程中的一个因素，可能是通过促进与炎症进展同时发生的血管网络扩张来实现的。
