title: Diacerein: a potential therapeutic drug for periodontal disease.
abstract: Periodontal diseases are chronic inflammatory diseases characterized by the destruction of the tooth-supporting structures. They are the most prevalent form of bone pathology in humans and act as a modifying factor of the systemic health of patients. Accumulating evidence has provided insight into mechanisms of periodontal inflammation revealing that oral pathogens induce inflammatory cascades, including a variety of cytokines produced by different cell types, which promotes host-mediated tissue destruction. Cytokine networks established in diseased periodontal tissues are extremely complex, and substances regulating immuno-inflammatory reactions and signaling pathways, in addition to traditional periodontal treatment, could potentially be targeted as an approach for prevention and treatment of periodontal diseases. Diacerein, a purified anthraquinone derivative, was derived originally from plants with profound anti-inflammatory and analgesic activities. Its wide range of biological activities have been applied and discussed for several decades; however, studies of diacerein have mainly concentrated on effects on joint-derived tissues/cells, which suggest a beneficial role in osteoarthritis treatment. Diacerein reduces association of the IL-1 receptor to form heterodimer complexes, repressing IL-1 and its related downstream events and impairing active IL-1 release due to the inhibition of the IL-1-converting enzyme (ICE). To date, there are no reports describing the therapeutic effect of diacerein for treatment of periodontitis. Given the involvement of inflammation and occurrence of tissue destruction in periodontal disease, we propose that diacerein might be a promising biological drug for periodontal disease due to its therapeutic advantages. In addition, we hypothesize that the underlying mechanisms might involve the capacity of diacerein to selectively inhibit signal transduction to affect the cytokine profiles and, consequently, produce the outcome of ameliorating disease breakdown.
authors.affiliation: Department of Periodontology, School of Dentistry, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan. ndmcandy@ndmctsgh.edu.tw
authors.forename: Ren-Yeong
authors.initials: RY
authors.lastname: Huang
authors.forename: Sheng-Hua
authors.initials: SH
authors.lastname: Lu
authors.forename: Kwan-Wei
authors.initials: KW
authors.lastname: Su
authors.forename: Jen-Kun
authors.initials: JK
authors.lastname: Chen
authors.forename: Wen-Hui
authors.initials: WH
authors.lastname: Fang
authors.forename: Wei-Neng
authors.initials: WN
authors.lastname: Liao
authors.forename: Sih-Yu
authors.initials: SY
authors.lastname: Chen
authors.forename: Yi-Shing
authors.initials: YS
authors.lastname: Shieh
mesh_terms: D000880:Anthraquinones / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D020170:Caspase 1; D006801:Humans; D007375:Interleukin-1 / Q000276:immunology*; D018448:Models, Immunological; D010510:Periodontal Diseases / Q000188:drug therapy* / Q000276:immunology*; D010519:Periodontium / Q000187:drug effects / Q000276:immunology*
chemical_list: D000880:Anthraquinones; D000893:Anti-Inflammatory Agents; D007375:Interleukin-1; C025292:diacerein; D020170:Caspase 1