{Reference Type}: Journal Article
{Title}: Notch down-regulation and inflammatory cytokines and RANKL overexpression involvement in peri-implant mucositis and peri-implantitis: A cross-sectional study.
{Author}: Milinkovic I;Djinic Krasavcevic A;Nikolic N;Aleksic Z;Carkic J;Jezdic M;Jankovic S;Milasin J;
{Journal}: Clin Oral Implants Res
{Volume}: 32
{Issue}: 12
{Year}: Dec 2021
{Factor}: 5.021
{DOI}: 10.1111/clr.13850
{Abstract}: <B>OBJECTIVE: </B>Notch signaling pathway, known to influence bone resorption in several oral diseases, has not been analyzed in peri-implantitis yet. Therefore, the aims of the present study were to determine the levels of Notch cascade, bone remodeling mediators, and pro-inflammatory cytokines, in conjunction with clinical parameters, in subjects with peri-implant mucositis and peri-implantitis.<BR><B>METHODS: </B>Clinical parameters: peri-implant probing depth, bleeding on probing, suppuration on probing, and plaque index (PI) were recorded. Samples were collected from 130 participants, divided into peri-implantitis (PI), peri-implant mucositis (PM), and healthy implants (HI) group. Relative expression levels (REL) of Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-α, IL-17, IL-1β, IL-6, RANKL, and OPG mRNA were determined by reverse transcriptase-real-time polymerase chain reaction. Quantitation of Notch 1, Il-17, and IL-6 proteins was performed using ELISA assays.<BR><B>RESULTS: </B>All clinical parameters were significantly higher in PI compared to HI. Significant decrease of Notch 1, and higher REL of Hey 1, IL-1β, IL-6, and RANKL were found in PI compared to HI. PM showed significant increase of IL-1β REL in comparison with HI. In PI versus PM, significantly higher REL was found for Hey 1, TNF-α, IL-17, IL-1β, IL-6, and RANKL. Additionally, higher protein concentrations of IL-6 and IL-17 were detected in PI versus PM and versus HI group.<BR><B>CONCLUSIONS: </B>The combined effect of Notch 1 down-regulation and elevated expression of some key inflammation modulators might result in osteoclast activity increase and subsequent osteolysis in peri-implantitis.