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HERRERA ET AL .
noted. When excluding from pooled data analysis of cohort and case – control studies, the results were consistent with no statistical hetero- geneity. No difference in PPD (SMD: 0.25; 95% CI [ 0.63; 0.13]; p = .20; I 2 : 0%; based on 107 implants), whereas a significant differ- ence in BOP (SMD: 1.5; 95% CI [ 1.93; 1.06]; p < .0001; I 2 : 0%; based on 107 implants) and MBL changes (SMD: 0.33; 95% CI [ 0.55; 0.11]; p = .003; I 2 : 0%; based on two studies, 66 implants) were noted between PIKM-augmented sites versus non-augmented sites. Only two studies reported the occurrence of PIDs (Frisch et al., 2015; Roccuzzo et al., 2016). The first study defined peri- implantitis as the presence of BOP, PPD ≥ 5 mm, and a radiographic bone loss ≥ 3.5 mm (Frisch et al., 2015). During a mean follow-up of 12 years, three groups receiving FGG, CTG or no intervention were compared. No statistical differences were found between groups. The second study, a 10-year prospective cohort, observed a significantly higher rate of PIDs for dental implants with PIKM deficiency com- pared with implants surrounded by PIKM (51.4% vs. 12.7%; p < .0001) (Roccuzzo et al., 2016). The authors also reported a signifi- cantly lower soreness for implants surrounded by PIKM or placed in the alveolar mucosa receiving FGG compared with implants sur- rounded by alveolar mucosa and not receiving FGG (Roccuzzo et al., 2016). Consistency Results are based on heterogeneous studies with, most of the time, small sample sizes and short follow-ups. Consistency is low. Balance of benefit and harm Not assessed. However, the decision-making process concerning sur- gical procedures to augment PIKM should consider the general risks associated with periodontal and implant surgery. Overall certainty of the evidence Low. No study design provided direct evidence. Results are inferred from studies with various working hypotheses that were not originally developed to test the effectiveness of peri-implant soft tissue aug- mentation procedures on the prevention of peri-implant diseases over time. Care must be taken regarding the interpretation of the study results due to the high clinical heterogeneity of the included studies. Most of the studies described clinical peri-implant outcomes in the short term (6 – 12 months follow-up), whereas only two observational studies reported the occurrence of peri-implant diseases over a 10-year (low risk of bias) and 12-year (high risk of bias) follow-up. However, a reduced width of keratinized tissue is associated with an increased prevalence of peri-implantitis, plaque accumulation, soft tissue inflammation, mucosal recession, MBL and greater patient dis- comfort (Ramanauskaite et al., 2022). The effectiveness of increasing PIKM as a preventive measure for peri-implant diseases requires lon- gitudinal studies designed with a long-term follow-up, to evaluate the outcome of interest (i.e., peri-implant diseases).
R5.8. In patients with healthy peri-implant tissues, does augmentation of peri-implant soft tissues lower the likelihood of incident peri-implant diseases?
PICOS question addressed by an SR
R5.8: Evidence-based recommendation In patients who have dental implants with an absence or deficiency of keratinized/attached mucosa, and where the patient experiences discomfort on brushing, increasing peri-implant keratinized/attached mucosal width to maintain peri-implant health may be considered . Supporting literature (Carra et al., 2023) Quality of evidence Low Grade of recommendation GradeO — $ Strength of consensus Consensus (0% of the group abstained due to potential CoI)
Background
Intervention
The risk factor is the deficiency of PIKM (PIKM < 1, 2 or 3 mm according to the studies), and the preventive intervention is the aug- mentation of PIKM by a free gingival graft (FGG).
Available evidence
Number and design of included studies Six of the studies included in the SR and meta-analysis (three RCTs, one NRCT, one case – control and one cohort study) were considered. They compared peri-implant tissue health parameters between sites with a deficiency in PIKM and receiving an FGG to increase PIKM width versus no intervention. No study was specifically designed to assess the impact of FGG on the prevention of peri-implant diseases. Risk of bias According to RoB-II-RCT, the three RCTs presented some concerns. According to RoBins-NRTC, the selected study was at moderate risk of bias. According to NOS: the two studies were at low risk of bias. Effect sizes and their clinical relevance Indirect evidence based on the evaluation of peri-implant health parameters in the short term showed a non-significantly different PPD between the PIKM-augmented and non-augmented sites but a significantly lower clinical soft tissue inflammation index (BOP/GI) (standardized mean difference [SMD] = 1.18; 95% CI [ 1.85; 0.51]; p = .0006; I 2 : 69%) around the dental implants receiving FGG to augment PIKM. Concerning the mean MBL, based on data from four studies, a significant difference in favour of PIKM-augmented sites (SMD: 0.25; 95% CI [ 0.45; 0.05]; p = .01; I 2 : 62%) was also
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