Cytokine expression in rat molar gingival periodontal tissues after topical application of lipopolysaccharide

Abstract

It is well known that proinflammatory cytokines produced by host cells play an important role in periodontal tissue destruction. However, the localization of the cytokines in in vivo periodontal tissues during development of periodontal disease has not been determined. Immunohistochemical expression of proinflammatory cytokines including IL-1α, IL-1β, and TNF-α was examined at 1 and 3 h, and 1, 2, 3, and 7 days after topical application of lipopolysaccharide (LPS; 5 mg/ml in physiological saline) from E. coli into the rat molar gingival sulcus. In the normal periodontal tissues, a small number of cytokine-positive epithelial cells were seen in the junctional epithelium (JE), oral sulcular and oral gingival epithelium, in addition to macrophages infiltrating in the subjunctional epithelial area and osteoblasts lining the alveolar bone surface. Epithelial remnants of Malassez existing throughout periodontal ligament were intensely positive for IL-1β but negative for the other two cytokines. At 3 h after the LPS treatment, almost all cells in the JE were strongly positive for the cytokines examined. In addition, several cytokine-positive cells, including neutrophils, macrophages, and fibroblasts, were seen in the subjunctional epithelial connective tissue. At day 2, expression of the cytokines in the JE gradually decreased, while cytokine-positive cells in the connective tissue increased in number. Positive stain-ing of the cytokines was seen in osteoclasts and preosteoclasts which appeared along the alveolar bone margin in this period. The number of cytokine-positive cells decreased by day 7. These findings indicate that, in addition to macrophages, neutrophils, and fibroblasts, the JE cells are a potent source of TNF-α, IL-1α, and IL-1β reacting to LPS application, and suggest that JE cells may play an important role in the first line of defense against LPS challenge, and the proinflammatory cytokines transiently produced by various host cells may be involved in the initiation of inflammation and subsequent periodontal tissue destruction.

Interleukin‐1α and tumor necrosis factor‐α expression during the early phases of orthodontic tooth movement in rats

“…It was clearly demonstrated that the gingival epithelium was constitutively stained for both IL-1a and TNF-a. This observation is in agreement with previous data (15,22,31) and implies some degree of inflammation in the rat gingiva under normal conditions. When orthodontic forces were applied, there was not only increased gingival staining reaction for the above cytokines, but also extension of the staining in the subjunctional area, including the PDL and the alveolar bone below the gingiva, indicating a substantial inflammatory reaction over a greater area.…”

Lipoxin suppresses inflammation via the TLR4/MyD88/NF‐κB pathway in periodontal ligament cells

“…For this purpose, the levels of TNFα and IL-4 were analyzed in which TNFα:IL-4 ratio was used as predictor of inflammation (Tsurumi, Que, Ryan, Tompkins, & Rahme, 2016). The results showed that incubation of human PDLCs with LPS resulted in higher TNFα release, which corroborated with data from previous studies (Miyauchi et al, 2001;Morsczeck, Dress, & Gosau, 2012;Yamaji et al, 1995;Yoshimura et al, 1987).…”

Effect of soluble receptors to interleukin‐1 and tumor necrosis factor alpha on experimentally induced root resorption in rats

“…This is also reflected by receptor distribution, as monocytes have relatively abundant p55 and p75 TNF receptors (8). In a study on cytokine expression in rat molar periodontal tissues after local application of inflammation-challenging lipopolysaccharide, Miyauchi et al (44) found TNFa expression in macrophages, as well as in preosteoclasts and osteoclasts on the alveolar bone surface. Another reason for the different potencies between the blocking of IL-1 and TNFa may lie in a possible agonistic activity of soluble IL-1 receptors by which compensatory events could be induced.…”