Role of TNF-α and Its Receptors in Pericoronitis

Abstract

The classic stimulus for cellular cytokine production is bacterial lipopolysaccharide (endotoxin). It was therefore hypothesized that tumor necrosis factor-alpha (TNF-alpha) may be responsible for pericoronitis. TNF-alpha and its receptors were detected by immunohistochemical staining in third molar pericoronitis in ten patients and ten healthy control samples. The percentage of TNF-alpha 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-1beta and vascular cell adhesion molecule-1 was found as a biological indicator of TNF-alpha ligand-receptor interaction. Explanted tissues acquired destructive potential upon TNF-alpha stimulation, whereas TNF-alpha 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-alpha, with pathogenic and potential therapeutic relevance.

Common Matrix Metalloproteinases ( M MP - 8, -9, -25, and -26) Cannot Explain Dentigerous Cyst Expansion

“…The proinflammatory cytokines have also been demonstrated to be able to evoke the bone destructing potential of the HDF's around asymptomatic and clinically innocent looking third molars [8]. This inflammatory reservoir has also suggested being a possible initiator in the transformation into a bone destructive lesion [8]. Our findings supports this only to some extent, since there was no significant difference between the expressions of bone destruction related MMPs between the HDF's and DC's.…”

“…This may also have clinical relevance since rationale for symptomless wisdom tooth removal is often justified by radiologic findings and suspected future osteolytic complications; this is not justified based on HDF and DC MMP profiles. Interestingly, it seems that the initiator may be the inflammation itself rather than epithelial remnants of the follicle since it has also been demonstrated that HDF supernatants start to express high levels of MMP-9 if stimulated with TNF-α [8]. However, our new findings suggest that in the case of DC the more bone destructive nature cannot be explained by higher expression of MMPs in the proliferating epithelial interface between cyst and bone leaving the mechanisms to be discovered.…”

“…This is an interesting finding since most of the MMPs can be produced by inflammatory cells [17] and chronic inflammation quite often involves also the asymptomatic third molars [18]. The proinflammatory cytokines have also been demonstrated to be able to evoke the bone destructing potential of the HDF's around asymptomatic and clinically innocent looking third molars [8]. This inflammatory reservoir has also suggested being a possible initiator in the transformation into a bone destructive lesion [8].…”

“…Connective tissue capsule of HDF have been earlier considered to be mainly free of inflammatory cells except in the case of pericoronitis. Interestingly some results, however, suggest that the destructive potentiality is also present in the healthy follicles mediated by proinflammatory cytokines and their receptors [8]. This is an interesting finding since the risk/ benefit ratio for the prophylactic extraction of un-or partially erupted wisdom tooth is under constant discussion in clinical practice.…”

Effects of treatment on soluble tumour necrosis factor receptor type 1 and 2 in chronic periodontitis

“…The clinical condition and the progression mechanism of pericoronitis are similar to those of periodontitis. Beklen et al (2005) reported that the transmembrane TNFR1 and 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. They concluded that TNF‐ α and its receptors may play an important and active role in pericoronitis.…”