Progression of radiographic changes in the temporomandibular joints of patients with rheumatoid arthritis in relation to inflammatory markers and mediators in the blood.
The aim of this study was to investigate longitudinal radiographic changes in the temporomandibular joint (TMJ) with clinical involvement of rheumatoid arthritis (RA) and its relation to the blood level of inflammatory mediators and markers. Sixteen patients were investigated by computed tomography on two occasions 25-46 months apart. The radiographs were assessed independently for changes in presence of erosions, sclerosis, flattening, osteophytes, and subchondral pseudocysts. The serum (S) or plasma (P) concentrations of C-reactive protein (CRP), thrombocyte particle concentration, scrotonin (S-5-HT and P-5-HT), tumor necrosis factor alpha, interleukin-1 receptor antagonist, tumor necrosis factor soluble receptor type II, interleukin-1 soluble receptor type II (P-IL-1sRII) and interleukin 6 as well as the erythrocyte sedimentation rate (ESR) were measured. The radiographic status showed no consistent or significant change during the observation period, but the individual variation was considerable. The radiographic signs of erosion and sclerosis varied most. Regression of erosions was associated with high S-5-HT and P-IL-1sRII, while progression of erosions was associated with high P-5-HT. Regression of sclerosis was associated with an increase in P-5-HT and high ESR. Progression of flattening was associated with high CRP. In conclusion, this study indicates that the progression of radiographic changes that occurs in the TMJ of patients with well-controlled RA during a period of 25-46 months seems to be related to the blood levels of CRP, 5-HT, and IL-1sRII. However, only minor progression can be expected to occur, and with considerable individual variation.
Voog
Ulle
U
Department of Clinical Oral Physiology, Institute of Odontology, Karolinska Institutet, Huddinge, Sweden. ulle.voog@ofa.ki.se
Alstergren
Per
P
Eliasson
Sören
S
Leibur
Edvitar
E
Kallikorm
Riina
R
Kopp
Sigvard
S
D015703:Antigens, CD / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000000981:diagnostic imaging*; D001792:Blood Platelets / Q000473:pathology; D001799:Blood Sedimentation; D001845:Bone Cysts / Q000000981:diagnostic imaging; D002097:C-Reactive Protein / Q000032:analysis; D018450:Disease Progression; D005096:Exostoses / Q000000981:diagnostic imaging; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D053590:Interleukin 1 Receptor Antagonist Protein; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D010026:Osteosclerosis / Q000000981:diagnostic imaging; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors / Q000097:blood; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047889:Receptors, Tumor Necrosis Factor, Type II; D012701:Serotonin / Q000097:blood; D012795:Sialoglycoproteins / Q000097:blood; D013705:Temporomandibular Joint Disorders / Q000097:blood / Q000000981:diagnostic imaging*; D014057:Tomography, X-Ray Computed; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D015703:Antigens, CD; C507763:IL1RN protein, human; D018836:Inflammation Mediators; D053590:Interleukin 1 Receptor Antagonist Protein; D017472:Receptors, Interleukin-1; D053574:Receptors, Interleukin-1 Type II; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D012701:Serotonin; D002097:C-Reactive Protein