title: Immunohistochemical study of interleukin-1beta and interleukin-1 receptor antagonist in an antigen-induced arthritis of the rabbit temporomandibular joint.
abstract: BACKGROUND
  In temporomandibular joint (TMJ) arthritis, there is limited knowledge of the relationship between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1ra), as well as the source of these cytokines. We investigated the development of an antigen-induced arthritis in the rabbit TMJ immunohistochemically.
  
  
  METHODS
  Unilateral TMJ arthritis was induced in 32 adult New Zealand White rabbits. From 6 h to 12 weeks after induction of arthritis, topology of IL-1beta and IL-1ra were observed.
  
  
  RESULTS
  The acute stage of induced arthritis lasted for one week after induction, thereafter it became chronic. In the early phase of the acute stage, infiltrating inflammatory cells, as well as synovial cells, produced IL-1beta and IL-1ra. In the late phase of the acute stage, the main source of these cytokines was subsynovial fibroblasts. In this phase of arthritis, IL-1beta and IL-1ra did not appear to be produced by synovial cells. From the early to intermediate phase of the chronic stage, proliferating synovial cells produced IL-1beta and IL-1ra. In this phase of the arthritis, these cytokines were also observed in a cluster formation in chondrocytes.
  
  
  CONCLUSIONS
  This arthritis model shows a staging of the joint inflammation process with time. IL-1beta and IL-1ra are produced by a certain kind of cells depending on the stage of inflammation.
authors.affiliation: First Department of Oral and Maxillofacial Surgery, Kyushu Dental College, Kokurakita, Kitakyushu, Japan. h-manabu@kyu-dent.ac.jp
authors.forename: Manabu
authors.initials: M
authors.lastname: Habu
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Tominaga
authors.forename: Miho
authors.initials: M
authors.lastname: Sukedai
authors.forename: Per
authors.initials: P
authors.lastname: Alstergren
authors.forename: Susumu
authors.initials: S
authors.lastname: Ohkawara
authors.forename: Sigvard
authors.initials: S
authors.lastname: Kopp
authors.forename: Jinichi
authors.initials: J
authors.lastname: Fukuda
mesh_terms: D000208:Acute Disease; D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology* / Q000473:pathology; D002455:Cell Division; D019902:Chondrocytes / Q000276:immunology / Q000473:pathology; D002908:Chronic Disease; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000276:immunology; D005355:Fibrosis; D007150:Immunohistochemistry; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000032:analysis*; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D009504:Neutrophils / Q000473:pathology; D010950:Plasma Cells / Q000473:pathology; D011817:Rabbits; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*; D012795:Sialoglycoproteins / Q000032:analysis*; D013583:Synovial Membrane / Q000276:immunology / Q000473:pathology; D013705:Temporomandibular Joint Disorders / Q000276:immunology* / Q000473:pathology
chemical_list: D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D017472:Receptors, Interleukin-1; D012795:Sialoglycoproteins