Inflammation and tissue loss caused by periodontal pathogens is reduced by interleukin-1 antagonists.
Periodontal disease is a significant cause of tooth loss among adults. It is initiated by pathogenic bacteria, which trigger an inflammatory response that is effective in preventing significant microbial colonization of the gingival tissues. In some individuals, the reaction to bacteria may lead to an excessive host response, resulting in periodontal tissue destruction. Recent developments suggest that interleukin (IL)-1 genetic polymorphisms may identify certain individuals who have a predisposed susceptibility to periodontal breakdown and that elevated levels of IL-1 are found in individuals with periodontal disease. However, there is no direct evidence that IL-1 per se is responsible for the critical events that occur in periodontitis. We investigated the role of IL-1 in periodontal disease in a Macaca fascicularis primate model, using human soluble IL-1 receptor type I as a specific inhibitor. The results indicate that inhibition of IL-1 alone significantly reduces inflammation, connective tissue attachment loss, and bone resorption that are induced by periodontal pathogens.
Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Massachusetts 02118, USA.
Andrew J
AJ
Delima
Spyros
S
Karatzas
Salomon
S
Amar
Dana T
DT
Graves
D016301:Alveolar Bone Loss / Q000188:drug therapy / Q000382:microbiology; D000818:Animals; D016866:Bacteroidaceae Infections / Q000188:drug therapy* / Q000382:microbiology / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000382:microbiology; D007375:Interleukin-1 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D008252:Macaca fascicularis; D017622:Periodontal Attachment Loss / Q000188:drug therapy / Q000382:microbiology; D010510:Periodontal Diseases / Q000188:drug therapy* / Q000382:microbiology / Q000503:physiopathology; D016966:Porphyromonas gingivalis / Q000472:pathogenicity*; D017472:Receptors, Interleukin-1 / Q000008:administration & dosage / Q000627:therapeutic use*; D053573:Receptors, Interleukin-1 Type I; D016896:Treatment Outcome
D007375:Interleukin-1; D017472:Receptors, Interleukin-1; D053573:Receptors, Interleukin-1 Type I