Abstract
Soluble tumor necrosis factor receptors 1 and 2 (sTNF-R1 and sTNF-R2) are reported to protect against excessive TNF-α, a primary mediator of systemic responses to infection. This study aimed to investigate the levels of TNF-α, sTNF-R1, and sTNF-R2 in saliva and to verify whether their dynamics are associated with periodontal health. The study population comprised 28 adult patients. Probing pocket depth, clinical attachment level, and bleeding on probing were assessed, and periodontal inflamed surface area (PISA) was calculated. Stimulated saliva was collected before the oral examinations. The levels of TNF-α, sTNF-R1, sTNF-R2, and total protein (TP) in saliva samples were determined. There were significant positive correlations between TNF-α, sTNF-R1, and sTNF-R2 to TP (/TP) in stimulated saliva. Moreover, there were significant positive correlations between PISA and sTNF-R2/TP. Stepwise multiple regression analysis revealed that PISA was significantly associated with sTNF-R2/TP in saliva; however, TNF-α/TP was not significantly associated with PISA. In conclusion, this study demonstrates that significant relationships exist between the salivary levels of TNF-α and sTNF-R1, and that salivary sTNF-R2 is associated with the expansion of inflamed periodontal tissue.
Highlights
Tumor necrosis factor-α (TNF-α) is a major mediator of inflammation and inflammationrelated diseases [1]
The effects of TNF-α are mediated by two membrane receptors, TNF receptor type 1 (TNF-R1) and TNF receptor type 2 (TNF-R2), that are carried on the surface of the target cell [3]
TNF-R1 is expressed in a variety of cells, and its overexpression is involved in the induction and exacerbation of inflammatory responses, whereas TNF-R2 is expressed in a limited number of cells, such as endothelial, epithelial, immune, and fibroblasts, and is involved in disease remission [5,6]
Summary
Tumor necrosis factor-α (TNF-α) is a major mediator of inflammation and inflammationrelated diseases [1]. It acts as a pro-inflammatory cytokine that plays a central role in immune regulation and a variety of inflammatory responses during destructive periodontal disease [2]. The effects of TNF-α are mediated by two membrane receptors, TNF receptor type 1. (TNF-R1) and TNF receptor type 2 (TNF-R2), that are carried on the surface of the target cell [3]. These two receptors bind TNF-α with high affinity; they have different localizations and physiological effects [4]. TNF-R1 is expressed in a variety of cells, and its overexpression is involved in the induction and exacerbation of inflammatory responses, whereas TNF-R2 is expressed in a limited number of cells, such as endothelial, epithelial, immune, and fibroblasts, and is involved in disease remission [5,6].
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