Marcaccini Andrea M, Meschiari César A, Sorgi Carlos A, Saraiva Maria C P, de Souza Ana M, Faccioli Lúcia H, Tanus-Santos José E, Novaes Arthur B, Gerlach Raquel F
Department of Morphology, Stomatology, and Physiology, School of Dentistry of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
J Periodontol. 2009 Apr;80(4):594-602. doi: 10.1902/jop.2009.080561.
Periodontal disease has been associated with many chronic inflammatory systemic diseases, and a common chronic inflammation pathway has been suggested for these conditions. However, few studies have evaluated whether periodontal disease, in the absence of other known inflammatory conditions and smoking, affects circulating markers of chronic inflammation. This study compared chronic inflammation markers in control individuals and patients with periodontal disease and observed whether non-surgical periodontal therapy affected inflammatory disease markers after 3 months.
Plasma and serum of 20 controls and 25 patients with periodontal disease were obtained prior to and 3 months after non-surgical periodontal therapy. All patients were non-smokers, they did not use any medication, and they had no history or detectable signs and symptoms of systemic diseases. Periodontal and systemic parameters included probing depth, bleeding on probing, clinical attachment level, hematologic parameters, as well as the following inflammatory markers: interleukin (IL)-6, high-sensitivity C-reactive protein (hs-CRP), CD40 ligand, monocyte chemoattractant protein (MCP)-1, soluble P-selectin (sP-selectin), soluble vascular adhesion molecule (sVCAM)-1, and soluble intercellular adhesion molecule (sICAM)-1.
There were no differences in the hematologic parameters of the patients in the control and periodontal disease groups. Among the tested inflammatory markers, IL-6 concentrations were higher in the periodontal disease group at baseline compared to the controls (P = 0.006). Therapy was highly effective (P <0.001 for all the analyzed clinical parameters), and a decrease in circulating IL-6 and hs-CRP concentrations was observed 3 months after therapy (P = 0.001 and P = 0.006, respectively). Our results also suggest that the CD40 ligand marker may have been different in the control and periodontal disease groups prior to the therapy (P = 0.009).
In apparently otherwise healthy patients, periodontal disease is associated with increased circulating concentrations of IL-6 and hs-CRP, which decreased 3 months after non-surgical periodontal therapy. With regard to the CD40 ligand, MCP-1, sP-selectin, sVCAM-1, and sICAM-1, no changes were seen in the periodontal disease group between baseline and 3 months after therapy.
牙周疾病与许多慢性炎症性全身性疾病相关，并且有人提出这些疾病存在共同的慢性炎症途径。然而，很少有研究评估在不存在其他已知炎症性疾病和吸烟的情况下，牙周疾病是否会影响慢性炎症的循环标志物。本研究比较了对照组个体和牙周疾病患者的慢性炎症标志物，并观察了非手术牙周治疗3个月后是否会影响炎症性疾病标志物。
在非手术牙周治疗前及治疗后3个月获取20名对照组个体和25名牙周疾病患者的血浆和血清。所有患者均不吸烟，未使用任何药物，且无全身性疾病的病史或可检测到的体征和症状。牙周和全身参数包括探诊深度、探诊出血、临床附着水平、血液学参数以及以下炎症标志物：白细胞介素（IL）-6、高敏C反应蛋白（hs-CRP）、CD40配体、单核细胞趋化蛋白（MCP）-1、可溶性P选择素（sP-selectin）、可溶性血管细胞黏附分子（sVCAM）-1和可溶性细胞间黏附分子（sICAM）-1。
对照组和牙周疾病组患者的血液学参数无差异。在检测的炎症标志物中，牙周疾病组基线时的IL-6浓度高于对照组（P = 0.006）。治疗非常有效（所有分析的临床参数P <0.001），治疗3个月后观察到循环IL-6和hs-CRP浓度降低（分别为P = 0.001和P = 0.006）。我们的结果还表明，治疗前对照组和牙周疾病组的CD40配体标志物可能存在差异（P = 0.009）。
在其他方面显然健康的患者中，牙周疾病与循环中IL-6和hs-CRP浓度升高相关，非手术牙周治疗3个月后这些浓度降低。关于CD40配体、MCP-1、sP-selectin、sVCAM-1和sICAM-1，牙周疾病组在基线至治疗后3个月期间未见变化。
