title: Induction of osteoclast-like cells derived from the synovial lavage fluids of patients with temporomandibular joint disorders.
abstract: OBJECTIVE
  Although biochemical studies have examined the synovial fluid (SF) of patients with temporomandibular joint (TMJ) disorders (TMDs), the details of the molecular mechanism of bone destruction and remodeling remain unknown. In this study, we induced and characterized osteoclast-like cells from the SF of patients with TMD and investigated the participation of these cells in the pathogenesis of TMD.
  
  
  METHODS
  We collected SF cells from patients with TMD after a pumping procedure, cultured osteoclast-like cells, and examined their characteristics, including osteoclast markers and bone resorption activities. In addition, we obtained fibroblastic cells from the SF of TMD patients by continuous sub-culturing. Using these fibroblastic cells, we examined fibroblast markers using immunocytochemical staining and analyzed the receptor activator of nuclear-factor-kappaB ligand (RANKL) mRNA levels. Detection of soluble form of RANKL (sRANKL) in the SF was measured by enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  Osteoclast-like cells were induced from the SF cells of patients with TMD by adding recombinant human (rh) macrophage colony stimulating factor (M-CSF) and either 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] or prostaglandin E2 (PGE2). These multinucleated giant cells were positive for tartrate-resistant acid phosphatase (TRAP) and had the ability to absorb bone. The fibroblastic cells from the SF of TMD patients were positive for fibroblast markers and RANKL mRNA was up-regulated. Detection of sRANKL in SF of patient group was significantly higher than control group.
  
  
  CONCLUSIONS
  The results suggest that the joint-infiltrating SF cells from TMD patients play important roles in the pathogenesis of these disorders, which is characterized by progressive bone destruction or remodeling.
authors.affiliation: Division of Oral and Maxillofacial Reconstructive Surgery, Kyushu Dental College, 2-6-1 Manazuru, Kitakyushu, Fukuoka 803-8580, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Takano
authors.forename: W
authors.initials: W
authors.lastname: Ariyoshi
authors.forename: T
authors.initials: T
authors.lastname: Kanno
authors.forename: E
authors.initials: E
authors.lastname: Fukuhara
authors.forename: H
authors.initials: H
authors.lastname: Ichimiya
authors.forename: T
authors.initials: T
authors.lastname: Matayoshi
authors.forename: T
authors.initials: T
authors.lastname: Goto
authors.forename: T
authors.initials: T
authors.lastname: Takahashi
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000032:analysis; D001862:Bone Resorption / Q000473:pathology*; D002117:Calcitriol / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D002478:Cells, Cultured; D003115:Colony-Stimulating Factors / Q000494:pharmacology; D015232:Dinoprostone / Q000494:pharmacology; D005260:Female; D005347:Fibroblasts / Q000378:metabolism*; D015726:Giant Cells / Q000201:enzymology / Q000378:metabolism; D006801:Humans; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010010:Osteoclasts / Q000201:enzymology / Q000378:metabolism*; D053245:RANK Ligand / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D053246:Receptor Activator of Nuclear Factor-kappa B / Q000378:metabolism*; D013582:Synovial Fluid / Q000166:cytology*; D000071681:Tartrate-Resistant Acid Phosphatase; D013705:Temporomandibular Joint Disorders / Q000378:metabolism* / Q000473:pathology
chemical_list: D015415:Biomarkers; D003115:Colony-Stimulating Factors; D007527:Isoenzymes; D053245:RANK Ligand; D012333:RNA, Messenger; D053246:Receptor Activator of Nuclear Factor-kappa B; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase; D002117:Calcitriol; D015232:Dinoprostone