Pulpal and periapical diseases are characterized by inflammation. The cytokine IL-6 is a major mediator of the host response to tissue injury and infection. This study examined the level of interleukin-6 (IL-6) in six inflamed human pulps and six human periapical lesions of endodontic origin using ELISA. Pulp samples from eight clinically impacted teeth were used as controls. The periapical samples exhibited significant levels of IL-6 (mean = 78.1 +/- 9 pg/mg protein) as did inflamed pulpal tissues mean = 36 +/- 3.9 pg/mg protein) compared to healthy pulp mean = 0.01 +/- 0.02 pg/mg protein). These data indicated that IL-6 was produced and released locally in the inflamed pulpal and periapical lesions.

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Immunopathologic reactions play a significant role in inflammatory diseases of dental pulp. Interleukin-1beta (IL-1beta) is recognized as a key player in mediating cellular immune response. In this study, we measured the content of IL-1beta and its effect on collagen synthesis in cultures of fibroblasts derived from healthy and diseased dental pulps. We found that diseased pulp fibroblasts contain 2.5-fold greater amounts of IL-1beta and synthesized 80% greater amounts of collagen compared with healthy pulp fibroblasts. However, exogenous IL-1beta failed to stimulate collagen synthesis by diseased fibroblasts, whereas collagen synthesis by healthy pulp fibroblasts was stimulated by more than 2-fold. These observations imply that pulp disease induces abnormalities associated with fibroblast response toward IL-1beta.

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