title: Temporomandibular joint pressure pain threshold is systemically modulated in rheumatoid arthritis.
abstract: OBJECTIVE
  To investigate the relative importance of systemic and local inflammatory mediators (serotonin: 5-HT; tumor necrosis factor: TNF; soluble interleukin-1 receptor II: IL-1sRII) in the modulation of temporomandibular joint (TMJ) pressure pain threshold in patients with seropositive or seronegative rheumatoid arthritis (RA) and to investigate to what extent TMJ pressure pain threshold is related to other TMJ pain parameters.
  
  
  METHODS
  Sixty patients with seropositive RA for rheumatoid factor and 74 patients with seronegative RA involving the TMJ were investigated regarding synovial fluid and plasma levels of IL-1sRII, 5-HT, and TNF as well as erythrocyte sedimentation rate, C-reactive protein, thrombocyte particle count, and rheumatoid factor in blood. TMJ resting pain, movement pain, tenderness, and palpebral pain reflex to digital palpation and TMJ pressure pain threshold were examined.
  
  
  RESULTS
  Statistical analyses indicated that TMJ pressure pain threshold was only correlated to systemic factors. TMJ movement pain was in turn mainly correlated to systemic mediators in the seropositive patients but to local mediators in the seronegative patients where synovial fluid IL-1sRII was positively correlated to TMJ pain on mouth opening. Seropositive patients had higher systemic inflammatory activity but lower TMJ movement pain intensities than seronegative patients.
  
  
  CONCLUSIONS
  The results indicate that TMJ pressure pain threshold is modulated by systemic rather than local inflammatory mediators and suggest that it is unrelated or only weakly related to other TMJ pain entities in RA patients. A rheumatoid factor-dependent systemic modulation, in combination with local factors, seems to account for TMJ pain in RA patients.
authors.affiliation: Karolinska Institutet, Clinical Oral Physiology, Huddinge, Sweden. per.alstergren@ki.se
authors.forename: Per
authors.initials: P
authors.lastname: Alstergren
authors.forename: Lars
authors.initials: L
authors.lastname: Fredriksson
authors.forename: Sigvard
authors.initials: S
authors.lastname: Kopp
mesh_terms: D001172:Arthritis, Rheumatoid / Q000503:physiopathology*; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000032:analysis; D005157:Facial Pain / Q000503:physiopathology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis / Q000097:blood; D008297:Male; D008875:Middle Aged; D010147:Pain Measurement; D017288:Pain Threshold / Q000502:physiology*; D010173:Palpation; D019152:Paracentesis; D010976:Platelet Count; D011312:Pressure; D016059:Range of Motion, Articular / Q000502:physiology; D053574:Receptors, Interleukin-1 Type II / Q000032:analysis / Q000097:blood; D012217:Rheumatoid Factor / Q000097:blood; D012701:Serotonin / Q000032:analysis / Q000097:blood; D013582:Synovial Fluid / Q000737:chemistry; D013705:Temporomandibular Joint Disorders / Q000503:physiopathology*; D048069:Tumor Necrosis Factors / Q000032:analysis / Q000097:blood
chemical_list: D018836:Inflammation Mediators; D053574:Receptors, Interleukin-1 Type II; D048069:Tumor Necrosis Factors; D012701:Serotonin; D002097:C-Reactive Protein; D012217:Rheumatoid Factor