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Role of TNF- and Its Receptors in Pericoronitis

¹ Department of Medicine/Invärtes medicin, Helsinki University Hospital, Helsinki, Finland;
² Institute of Biomedicine/Anatomy, University of Helsinki, Helsinki, Finland;
³ Medico-social Centre, Dental Clinic, Bogazici University, Istanbul, Turkey;
⁴ Finnish Student Health Service, Helsinki, Finland;
⁵ ORTON Orthopaedic Hospital of the Invalid Foundation, Helsinki, Finland; and
⁶ COXA Hospital for Joint Replacement, Tampere, Finland

^* corresponding author, yrjo.konttinen{at}helsinki.fi, Biomedicum Helsinki, PO Box 700 (Haartmaninkatu 8), FIN-00029 HUS, Finland

The classic stimulus for cellular cytokine production is bacterial lipopolysaccharide (endotoxin). It was therefore hypothesized that tumor necrosis factor- (TNF-) may be responsible for pericoronitis. TNF- and its receptors were detected by immunohistochemical staining in third molar pericoronitis in ten patients and ten healthy control samples. The percentage of TNF- positive cells was high in pericoronitis (p = 0.0317). TNF receptors TNF-R1 and TNF-R2 were found in macrophage- and fibroblast-like cells, vascular endothelial cells in post-capillary venules, and basal epithelial cells in pericoronitis, but were only weakly expressed in controls. Increased expression of interleukin-1ß and vascular cell adhesion molecule-1 was found as a biological indicator of TNF- ligand-receptor interaction. Explanted tissues acquired destructive potential upon TNF- stimulation, whereas TNF- blockers controlled it in inflamed tissues. These findings suggest that, in pericoronitis, inflammatory and resident cells produce and respond to potent pro-inflammatory cytokine TNF-, with pathogenic and potential therapeutic relevance.

KEY WORDS: pericoronitis • tumor necrosis factor-alpha • TNF-R1 • TNF-R2