Doppler Ultrasonographic Assessment of Healthy and Diseased Implant Sites and Predictors for the Resolution of Peri-implant Mucositis following Non-surgical Therapy: A Longitudinal Split-mouth Study

Abstract

Background: Peri-implant disease management continues to evolve, with increasing emphasis on early detection and monitoring to prevent and treat peri-implant disease. Conventional periodontal probing is the gold standard for diagnosis, however, high-frequency dental ultrasonography has emerged as an innovative diagnostic tool capable of assessing peri-implant lesions and tissue perfusion associated with inflammation. In addition, peri-implant crevicular fluid (PICF) biomarker analysis is another new diagnostic tool for peri-implant disease, shedding light onto the host inflammatory response to pathogenic bacteria. The aim of this longitudinal split-mouth study was to assess whether ultrasonographic and biomarker analysis can aid in early diagnosis of peri-implant disease and predict the outcomes of peri-implant mucositis (PM) treatment over a 1-year period. Methods: Twenty patients treated at the Harvard Dental Center with two non-adjacent implants (one healthy and one diagnosed with PM) were enrolled. Ultrasonographic and clinical parameters were assessed at baseline (T0), four weeks post-nonsurgical therapy (T1), and one year post-therapy (T2). Ultrasonographic measurements at midfacial and interproximal surfaces included tissue perfusion (via Doppler analysis), presence of a “lesion” (hypoechoic supracrestal area [HSA]), mucosal thickness (MT), buccal bone distance (BBD), buccal bone thickness (BBT), supracrestal tissue height (STH), and mesial and distal papilla height (PH). Clinical parameters included probing depth (PD), bleeding on probing (BOP), suppuration, keratinized mucosa width (KMW), plaque accumulation, and peri-implant soft tissue dehiscence (PSTD). Peri-implant crevicular fluid samples were collected from healthy and PM sites at T0 and T1 to quantify biomarkers associated with PM (bFGF, IL-1β, IL-6, IL-17, MMP-8, MMP-9, TNF-α, and VEGF). Patient reported outcome measures (PROMs) assessing esthetic satisfaction and discomfort during brushing (0–10 scale) were recorded at all time points. Non-surgical therapy was delivered to PM implants at T0, and oral hygiene instructions were reinforced. Patients were followed by their primary providers at three and six months. Fourteen of twenty participants completed the one-year follow-up. Clinical, ultrasonographic, and PROM assessments were repeated at T2. Results: At T1, ten of the twenty (50%) diseased implant sites exhibited complete resolution of inflammation. At T2, five of fourteen sites (35.7%) initially categorized as PM were diagnosed as healthy. The initial round of non-surgical therapy at diseased implants resulted in a significant reduction in coronal MT (p.05) and BOP (p.01). At T0, 75% of PM implants presented BOP at the mesiobuccal aspect, 65% at the midbuccal aspect, 65% at the distobuccal aspect, and 68.3% across all three buccal sites. At T1, relative BOP reduction was 46.7%, 38.5%, and 53.8% at the mesiobuccal aspect, midbuccal aspect, and distobuccal aspect, respectively (p.01 for all comparisons). From T0 to T2, relative BOP reduction was 36%, 29%, and 44% at the mesiobuccal aspect, midbuccal aspect, and distobuccal aspect, respectively (p.05 for all comparisons). Implant recession increased by a mean of 0.51 mm from T0 to T1 and 0.38 mm from T0 to T2. At T0, 19 healthy implant sites (95%) did not show ultrasonographic presence of an HSA (95%). The proportion of healthy sites without HSA was 80% at T1 and 78.6% at T2. In contrast, 90% of PM implants exhibited a detectable HSA at T0, while 80% and 64.3% of PM sites displayed an HSA at T1 and T2, respectively. The mean vertical extension of the HSA was 5.75 mm at T0, 3.2 mm at T1, and 3.9 mm at T2. The mean HSA area was 4.94 mm² at T0, 2.61 mm² at T1, and 3.11 mm² at T2. Color Doppler velocity and power Doppler intensity were significantly higher in PM sites compared to healthy sites at all time points (p.01) and correlated with HSA area (p.01), but not with other clinical parameters. Multilinear regression analysis revealed that baseline HSA area (p.01) and baseline power Doppler intensity (p.05) were significant predictors of PM resolution at one year. Baseline clinical parameters and biomarkers did not significantly correlate with resolution at T2. No significant differences in PROMs were observed between healthy and diseased sites at any time point. Conclusions: Echo-Doppler ultrasonography represents a valuable non-invasive tool for characterizing healthy and PM implant sites. Ultrasonographic parameters, including the presence of an HSA and Doppler-measured tissue perfusion, were associated with the clinical diagnosis of PM and showed potential predictive value for 1-year resolution following non-surgical therapy. In this cohort, non-surgical therapy resulted in modest resolution rates, highlighting variability in treatment response. Longer-term studies are required to validate these preliminary findings.