Johnson R B, Serio F G
Department of Periodontics, University of Mississippi School of Dentistry, Jackson 39216-4505, USA.
J Periodontol. 2001 Sep;72(9):1254-7. doi: 10.1902/jop.2000.72.9.1254.
Plasma leptin concentrations are reported to be elevated in patients with inflammatory diseases. There is no consensus concerning the biological mechanism for this phenomenon. To date, tissue leptin concentrations have not been assessed within normal or inflamed gingiva. The purpose of this study was to assess concentrations of human leptin within healthy and diseased gingiva to define its possible role in periodontal disease progression.
Healthy (non-hemorrhagic gingiva adjacent to a < or =3 mm gingival sulcus) and inflamed gingiva (hemorrhagic gingiva adjacent to a > or =3 mm periodontal pocket) were studied. Leptin, vascular endothelial growth factor (VEGF; to assess potential vascular expansion), and interleukin-6 (IL-6; to assess periodontal disease activity and severity) concentrations were assessed within solubilized gingival biopsies by enzyme-linked immunosorbent assay. Data were grouped by sulcular depth and compared by factorial analysis of variance, regression analysis, and Scheffé comparisons.
Leptin concentrations were highest within gingiva adjacent to a < or =3 mm sulcus and progressively declined within gingiva adjacent to a > or =3 mm sulcus. VEGF concentrations were highest within gingiva adjacent to 4 to 6 mm pockets and nearly equivalent in healthy (< or =3 mm sulcus) and severely diseased gingiva (>6 mm sulcus). IL-6 was positively correlated and leptin negatively correlated with adjacent probing depth; IL-6 concentration was significantly higher and leptin significantly lower in gingiva adjacent to >6 mm pockets compared to sites adjacent to <6 mm pockets (P<0.001).
Human leptin is present within healthy and marginally inflamed gingiva and decreases in concentration as the adjacent probing depth increases. When leptin concentrations decreased (> or =3 mm sulcus), VEGF concentrations increased, suggesting that leptin could be released from gingiva coincident to vascular expansion. Thus, gingiva, in addition to adipose tissue, could be a source of circulating leptin in patients with periodontal disease. This possibility requires further investigation.
据报道，炎症性疾病患者的血浆瘦素浓度会升高。关于这一现象的生物学机制尚无定论。迄今为止，尚未在正常或发炎的牙龈组织中评估瘦素浓度。本研究的目的是评估健康和患病牙龈中人类瘦素的浓度，以确定其在牙周病进展中的可能作用。
对健康牙龈（牙龈沟≤3mm相邻的非出血性牙龈）和发炎牙龈（牙周袋≥3mm相邻的出血性牙龈）进行研究。通过酶联免疫吸附测定法评估可溶性牙龈活检组织中的瘦素、血管内皮生长因子（VEGF；用于评估潜在的血管扩张）和白细胞介素-6（IL-6；用于评估牙周病的活动和严重程度）浓度。数据按龈沟深度分组，并通过方差分析、回归分析和谢费比较进行比较。
在牙龈沟≤3mm相邻的牙龈中，瘦素浓度最高，而在牙龈沟≥3mm相邻的牙龈中逐渐下降。VEGF浓度在4至6mm牙周袋相邻的牙龈中最高，在健康（≤3mm牙龈沟）和严重患病牙龈（>6mm牙龈沟）中几乎相等。IL-6与相邻探诊深度呈正相关，瘦素与相邻探诊深度呈负相关；与<6mm牙周袋相邻的部位相比，>6mm牙周袋相邻牙龈中的IL-6浓度显著更高，瘦素浓度显著更低（P<0.001）。
人类瘦素存在于健康和轻度发炎的牙龈中，并且随着相邻探诊深度的增加而浓度降低。当瘦素浓度降低（≥3mm牙龈沟）时，VEGF浓度增加，这表明瘦素可能与血管扩张同时从牙龈中释放出来。因此，除脂肪组织外，牙龈可能是牙周病患者循环瘦素的来源之一。这一可能性需要进一步研究。
