Soluble antagonists to interleukin-1 (IL-1) and tumor necrosis factor (TNF) inhibits loss of tissue attachment in experimental periodontitis

Background, aims: Periodontal disease is a significant cause of tooth loss among adults and is characterized by the alteration and permanent destructi on of the deeper periodontal tissues. Although the presence of pathologic m icrobes is required to trigger this process, the amplification and progress ion of the diseased state is believed to rely heavily on the production of host mediators in response to bacteria or their metabolic products. The inf lammatory response is effective in preventing large-scale colonization of t he gingival tissues by bacteria that lie in close proximity to the tooth su rface or within the gingival sulcus. It has been postulated that the host-r esponse in some individuals may lead to an over-reaction to invading oral p athogens resulting in the destruction of periodontal tissues. Methods: Several host-derived mediators are believed to contribute to this response. Two agents considered to be essential in periodontal destruction are interleukin-1 (IL-1) and tumor necrosis factor (TNF). We investigated t he role of IL-1 and TNF in the loss of connective tissue attachment in a Ma caca fascicularis is primate model of experimental periodontitis. Silk liga tures impregnated with the periodontal pathogen, Porphyromonas gingivalis w ere wrapped around the posterior teeth and the activity of IL-1 and TNF wer e inhibited by soluble receptors to these proinflammatory cytokines via loc al injection into interdental papillae. Results: Histomorphometric analysis indicates that IL-1 and TNF antagonists significantly reduced the loss of connective tissue attachment by approxim ately 51% and the loss of alveolar bone height by almost 91%, both of which were statistically significant. Conclusion: This investigation demonstrates that the loss of connective tis sue attachment and progression of periodontal disease can be retarded by an tagonists to specific host mediators such as IL-1 and TNF and may provide a potential treatment modality to combat the disease process.