Cytokine profiles in peripheral blood and whole blood cell cultures associated with aggressive periodontitis, juvenile idiopathic arthritis, and rheumatoid arthritis.
BACKGROUND
Cytokines play a key role in the pathogenesis of inflammatory diseases. An obvious question is whether patients with aggressive periodontitis, juvenile idiopathic arthritis, or rheumatoid arthritis share blood cytokine profiles distinguishing them from individuals free of disease.


METHODS
The study population consisted of Danish white adults, <35 years of age, diagnosed with localized aggressive periodontitis (LAgP; N = 18), generalized aggressive periodontitis (GAgP; N = 27), juvenile idiopathic arthritis (JIA; N = 10), or rheumatoid arthritis (RA; N = 23) and healthy individuals with no systemic or oral diseases (control [CTRL]; N = 25). Enzyme-linked immunosorbent assays were used to determine the levels of interleukin (IL)-1alpha, IL-1beta, IL-1 receptor antagonist (IL-1Ra), IL-6, IL-10, tumor necrosis factor (TNF)-alpha, and lymphotoxin (LT)-alpha in peripheral blood (plasma) and unstimulated and stimulated whole blood cell cultures from the same blood collection. Autoantibodies (aAb) to IL-1alpha and IL-6 were quantitated by radioimmunoassay.


RESULTS
Similar patterns of slightly higher IL-10 levels in plasma were found for GAgP and RA patients and in unstimulated cultures for GAgP, RA, and JIA patients. Interestingly, unstimulated cultures also demonstrated similar patterns of higher TNF-alpha levels for these three groups of patients. Similar group patterns of periodontitis patients (LAgP and GAgP) included increased IL-1Ra levels in stimulated cultures, which also showed similar group patterns of arthritis patients (JIA and RA) with respect to higher IL-1alpha and lower LT-alpha levels. Low titers of aAb to IL-1alpha and IL-6 were found in almost all individuals.


CONCLUSIONS
Patients with aggressive periodontitis and types of arthritis presented with similar components of blood cytokine profiles distinguishing them from individuals free of disease.
Havemose-Poulsen
Anne
A
Department of Periodontology, School of Dentistry, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. ah@odont.ku.dk
Sørensen
Lars Korsbaek
LK
Stoltze
Kaj
K
Bendtzen
Klaus
K
Holmstrup
Palle
P
D000293:Adolescent; D000328:Adult; D001171:Arthritis, Juvenile / Q000097:blood* / Q000145:classification; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000145:classification; D001323:Autoantibodies / Q000097:blood; D001773:Blood Cells / Q000737:chemistry*; D002478:Cells, Cultured; D016207:Cytokines / Q000097:blood*; D005884:Gingival Hemorrhage / Q000145:classification; D006801:Humans; D007375:Interleukin-1 / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008233:Lymphotoxin-alpha / Q000097:blood; D017622:Periodontal Attachment Loss / Q000145:classification; D010518:Periodontitis / Q000097:blood* / Q000145:classification; D010949:Plasma; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D013585:Synovitis / Q000145:classification; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D001323:Autoantibodies; D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D008233:Lymphotoxin-alpha; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10