Supervisors info:
Δερέκα Ξανθίππη, Αναπληρώτρια Καθηγήτρια, Τμήμα Οδοντιατρικής, Σχολή Επιστημών Υγείας, ΕΚΠΑ
Μπομπέτσης Γεώργιος, Επίκουρος Καθηγητής, Τμήμα Οδοντιατρικής, Σχολή Επιστημών Υγείας, ΕΚΠΑ
Κορομάντζος Παναγιώτης, Επίκουρος Καθηγητής, Τμήμα Οδοντιατρικής, Σχολή Επιστημών Υγείας, ΕΚΠΑ
Summary:
Aim: The purpose of this study is to: 1) assess the effect of surgical treatment of peri-implantitis on clinical parameters and levels of RANKL and OPG in the peri-implant crevicular fluid, and 2) compare these levels with levels of RANKL and OPG in the peri-implant crevicular fluid of healthy control implants.
Materials & Methodology: The research study involved a total of 27 subjects, of whom a) 13 subjects had healthy peri-implant tissues (HI), and b) 14 subjects had peri-implantitis implants (PI) which had already been treated with non-surgical treatment (as part of a parallel research study) and required surgical treatment of peri-implantitis. The surgical treatment of peri-implantitis applied included the following methods: a) patients whose implants were treated with an "access flap" to remove microbial biofilm from their threads (open flap debridement) (OFD) and b) patients whose implants were treated with implantoplasty (IMP). For implants treated with OFD, the biofilm and the hard deposits of calculus were removed using ultrasound devices with a special implant tip by PEEK (PIEZON® PI INSTRUMENT EMS), titanium-specific brushes (NiTi brush Regular) and Air-Flowing (AIRFLOW® EMS) using erythritol powder 14μm (EMS AIR-FLOW® PLUS Powder). For the implants treated with IMP, their threads were additionally polished with a medium-hardness diamond. The surgical technique used was selected by a randomization method. When intraoperatively was determined that peri-implant damage for optimal management was tolerable for a regenerative technique then this was performed and the implant was excluded from the study. The following clinical parameters were evaluated prior to and three months after surgical treatment: mean depth of peri-implant pocket, mean periodontal pocket depth and bleeding on probing (BOP). Moreover, peri-implant crevicular fluid was collected using 4 Durapore paper absorbent strips of 6mm length and 2mm width from the implants before surgical treatment and three months later to assess the levels of the biomarkers RANKL and OPG and the RANKL/OPG ratio via the ELISA (enzyme-linked immunosorbent assay) assay. Clinical measurements and peri-implant crevicular fluid collection were also performed during the initial examination (timepoint T0) and 3 months after non-surgical treatment (timepoint T1) in a parallel study.
Results: 10 implants were included in surgical therapy of peri-implantitis, while intraoperatively 2 implants were excluded. Thus, measurements 3 months after the surgical treatment of peri-implantitis (timepoint T2) were performed in 8 implants. All clinical and laboratory measurements at the timepoint T0 were statistically significantly greater than the corresponding values at the timepoint T2, however no statistically significant difference of BOP was observed. At the timepoint T1, the mean depth of the peri-implant pocket was 6,45mm (s.d.= 1,44mm) while at the timepoint T2 was 3,25mm (s.d.= 0,89mm), which is statistically significant (p-value<0,001). The mean periodontal pocket depth at the timepoint T1 was 3,07mm (s.d.= 0,60mm) while at the timepoint T2 was 2,51mm (s.d.= 0,55mm), which is statistically significant (p-value=0,004). BOP was detected in 62.50% of implants with peri-implantitis at the timepoint T2 with no statistically significant change in levels compared to timepoint T1. Respectively, mean RANKL levels were 3,86 pg/60sec (s.d.=5.62) at the timepoint T1 and 0,91 pg/60sec (s.d.=0.85) at the timepoint T2, mean OPG levels were 6,70 pg/60sec (s.d.=2.55) at the timepoint T1 and 6,56 pg/60sec (s.d.=7.08) at the timepoint T2, whereas the mean RANKL/OPG ratio was 0.65 (s.d.=0.94) at the timepoint T1 and 0.16 (s.d.=0.12) at the timepoint T2. No statistically significant changes in RANKL, OPG levels and ratio RANKL/OPG were observed following surgical treatment, although a tendency to decrease RANKL levels, stabilize OPG levels and decrease RANKL/OPG ratio was observed. At the timepoint T1, the mean depth of the peri-implant pocket in patients with healthy implants was statistically significantly lower than the corresponding pocket depth of the implants with peri-implantitis receiving non-surgical treatment (p-value<0,001). In contrast, non-statistically significant difference was observed between the mean periodontal pocket depth in the group of healthy implants and those with peri-implantitis at the timepoint T1. Also, the levels of OPG and the ratio of the RANKL/OPG do not differ statistically significantly (p-value=0,111 and 0.124 respectively), while a statistically significant difference was observed between the RANKL measurements (p-value=0,030). Statistically significant difference was also seen in the incidence of bleeding on probing between healthy implants and peri-implantitis implants at the timepoint T1 (p-value<0,001). The mean peri-implant pocket depth in the healthy implant group was 4,38mm (s.d.=0,87mm) while in peri-implantitis implants at the timepoint T2 was statisticallysignificantly lower (mean=3,25mm, s.d.=0,89mm, p-value=0,010). In contrast, no statistically significant difference in mean periodontal pocket depth was observed in healthy implants and in post-surgical implants (p-value=0,199). The mean ratio of RANKL/OPG measurements in healthy implants was 0.76 (s.d. =0.58) while after surgical treatment was 0.16 (s.d. =0.12), this difference being statistically significant (p-value=0,001). Correspondingly, statistically significantly lower post-surgical values compared to healthy implants were observed for the laboratory measurements of RANKL and OPG. A statistically significant difference was also seen in the incidence of bleeding on probing between healthy implants and implants after surgical treatment (p-value=0,001). No statistically significant correlation was found between clinical measurements of the mean peri-implant pocket depth and the mean periodontal pocket depth with the RANKL/OPG ratio. The correlation was tested separately in healthy implants and those with peri-implantitis, prior to and following different treatment modalities. In addition, a correlation was checked for the mean peri-implant pocket depth with RANKL and OPG measurements based on the status of the implants at different time points of measurement, and a statistically significant correlation was found between the mean depth of the peri-implant pocket and the OPG measurement in healthy implants (Correlation Factor= 0.58, p-value=0,037).
Conclusions: In conclusion and taking into account the limitations of this study:
a. Surgical treatment of peri-implantitis results in a statistically significant reduction in the mean depth of both the peri-implant and periodontal pockets, and no statistically significant variability of bleeding on probing was observed.
b. Three months after surgical treatment of peri-implantitis, statistically significantly lower levels were observed for the biomarkers RANKL, OPG and their RANKL/OPG ratio compared to baseline.
c. Surgical treatment did not appear to change the RANKL, OPG levels and their ratio at a statistically significant level compared to pre-surgical treatment, although a tendency to decrease RANKL levels, stabilize OPG levels and decrease RANKL/OPG ratio was observed.
d. Compared with healthy implants, surgically treated implants showed statistically significantly lower mean peri-implant pocket depth as well as RANKL, OPG and RANKL/OPG ratio levels.
e. No statistically significant correlation was found between clinical measurements of the mean peri-implant pocket depth and the mean periodontal pocket depth with the ratio of RANKL/OPG, and a statistically significant correlation was found between the mean peri-implant pocket depth and the measurement of OPG levels in healthy implants.
