Abstract
Objective
This study aims to identify risk factors for peri-implantitis in patients with implant-supported restoration, and explore the efficacy of subgingival sandblasting in modulating peri-implant microecology, so as to provide a basis for optimizing clinical management.
Methods
Ninety-six patients with early peri-implantitis treated from July 2022 to July 2024 were enrolled as the inflammation group and randomly subdivided into control, glycine-based subgingival sandblasting, and erythritol-based subgingival sandblasting groups (n = 32/group). Clinical outcomes were compared. Additionally, 102 patients without inflammation post-implant-supported restoration were selected as the non-inflammation group for independent risk factor analysis.
Results
Univariate analysis showed that peri-implantitis was related to 9 factors such as lower educational level, smoking, and diabetes (P < 0.05). Multivariate analysis further confirmed higher educational level (OR = 0.408) and regular dental cleaning (OR = 0.34) as protective factors, while implant sevice time ≥ 5 years (OR = 4.614) and insufficient keratinized mucosa width (OR = 3.267) as independent risk factors (all P < 0.05). Subgingival sandblasting (glycine/erythritol) significantly reduced plaque index (PLI), bleeding index (BI), and inflammatory factors (IL-6, IL-1β; P < 0.05). The erythritol group demonstrated superior long-term anti-inflammatory efficacy (e.g., IL-1β: 4.43 versus glycine 6.02 at 6 months; P < 0.001), though probing depth (PD) improvements attenuated beyond 6 months. Both subgingival sandblasting groups reported significantly higher patient satisfaction scores for aesthetic appearance and functional characteristics than controls (P < 0.05).
Conclusion
Peri-implantitis arises from interactions among oral hygiene, anatomical factors, and systemic conditions. Subgingival sandblasting effectively controls peri-implantitis progression by disrupting plaque biofilm and suppressing inflammation, with erythritol offering extended anti-inflammatory benefits. Sustained clinical outcomes needs adjunctive maintenance therapy alongside subgingival sandblasting.
ClinicalTrials.gov Identifier
NCT06998160(25th/April/2025) https://register.clinicaltrials.gov/prs/beta/records
Supplementary Information
The online version contains supplementary material available at 10.1186/s12903-025-06945-9.
Keywords: Peri-implantitis, Subgingival sandblasting, Risk factors, Inflammatory factors, Plaque index, Patient satisfaction
Introduction
In recent years, with the continuous progress of oral rehabilitation technology and the growing patient demands for aesthetic and functional restoration, dental implant therapy has been widely used in clinical practice for tooth replacement [1]. Implant-supported restoration can not only restore masticatory function and oral aesthetics, but also greatly improve the quality of life of patients. However, the rapid development of implant technology has revealed substantial challenges, notably the emergence of peri-implant diseases, mainly including peri-implant mucositis and peri-implantitis [2, 3]. These pathological conditions seriously compromise implant longevity and stability while posing a potential threat to overall oral health.
At present, some studies have reported that the incidence of peri-implant diseases is between 28% and 56%, which reminds us that while promoting implant therapy, we must attach great importance to the health status of peri-implant tissues [4]. The integrity of peri-implant tissues directly governs implantation success rates and long-term prosthetic functionality, serving as a key determinant of restorative outcomes [5]. Therefore, implants require more rigorous maintenance protocols than natural dentition due to their heightened susceptibility to rapidly progressive inflammatory reactions. Untreated peri-implantitis frequently escalates into irreversible bone resorption and implant instability, ultimately compromising survival rates. Etiologically, peri-implant diseases share pathogenic mechanisms with periodontal diseases, involving pathogenic plaque accumulation, dysregulated local inflammation, and aberrant host immune responses [6–8]. Dental plaque biofilm, formed on implant surfaces and surrounding soft and hard tissues under conditions of inadequate oral hygiene, decreased immunity, or local microenvironmental changes, acts as the primary etiological driver of inflammation [9–11]. Although periodontal treatment strategies provide valuable frameworks, the distinct material composition and surface topography of implants limit the application efficacy of traditional periodontal therapies [12, 13].
Despite its established role in periodontal therapy, mechanical scaling exhibits significant limitations in peri-implant plaque removal [14]. First of all, scalar instrumentation risks damaging implant surfaces, creating microgrooves that facilitate bacterial re-adhesion while destroying the protective titanium oxide film, potentially reducing implant biocompatibility. Furthermore, inadequate debridement efficacy in deep pockets often fails to achieve the purpose of completely removing microorganisms, resulting in repeated inflammation and affecting the therapeutic effect [15]. Recently, subgingival sandblasting, as a new periodontal treatment technique, has been paid increasing attention by clinicians [16–18]. Utilizing water-soluble glycine [19] or erythritol powders [20] with a mean particle size of 14–25 μm, subgingival sandblasting can not only efficiently remove dental plaques and calculi on implant surfaces, but also maintain implant surface integrity and minimize the damage to surrounding soft tissues. This technique’s procedural simplicity and enhanced patient comfort have driven its widespread international adoption for implant maintenance and peri-implant disease management, achieving favorable clinical results [21].
Currently, the prevention and treatment of peri-implant diseases in China is still in the exploratory stage, with particularly limited evidence regarding the long-term efficacy and mechanistic role of subgingival sandblasting in implant maintenance. Therefore, it is of great significance to systematically explore the factors affecting the occurrence of peri-implantitis and evaluate the role of subgingival sandblasting in maintaining peri-implant microecological balance for enhancing long-term implant survival. This study examines patients with early peri-implantitis who received treatment in our hospital from July 2022 to July 2024, comparing control, glycine-based subgingival sandblasting and erythritol-based subgingival sandblasting groups. Primary objectives include identifying independent risk factors for peri-implantitis while assessing the efficacy of subgingival sandblasting in plaque removal and microecological stabilization.
Data and methods
Study design and grouping
This study was designed as a single-center, randomized, controlled clinical trial with a 6-month follow-up period. A total of 198 participants were included and divided into two main cohorts: (1) non-inflammatory group (n = 102), consisting of patients who underwent implant-supported restoration without peri-implantitis; and (2) inflammation group (n = 96), comprising patients diagnosed with early peri-implantitis. The inflammation group was further randomly subdivided into three treatment arms: ultrasonic subgingival sandblasting group (control group), glycine-based subgingival sandblasting group, and erythritol-based subgingival sandblasting group (n = 32 in each). Randomization was performed using a computer-generated random number table. Due to the nature of the interventions, single-blinding was implemented wherein participants were blinded to treatment modalities, while operators were aware of group assignments.
General data
A total of 96 patients with early peri-implantitis treated in our hospital from July 2022 to July 2024 were selected as the inflammation group. All patients were randomly divided into control group, glycine-based subgingival sandblasting group, and erythritol-based subgingival sandblasting group (n = 32 per group).
Inclusion criteria comprised: (1) age ≥ 18 years; (2) implant placement in either the maxillary anterior or posterior region; (3) good oral hygiene status, with a full-mouth plaque score < 25% and willingness to maintain oral health throughout the follow-up; (4) no relevant pharmacological therapy during the month preceding enrollment; (5) good compliance and ability to follow the doctor’s advice and oral hygiene protocols; (6) no major systemic diseases, such as cardiac or renal insufficiency and hematological diseases; and (7) availability of complete clinical records.
Exclusion criteria were: (1) presence of mental or cognitive impairment impacting compliance; (2) diagnosis of malignant tumors; (3) documented coagulation dysfunction; and (4) lactating or pregnant women.
Concurrently, 102 patients who underwent implant-supported restoration (i.e., dental implant placement followed by prosthetic restoration with implant-supported crowns or bridges) in our hospital during the same period and exhibited no signs of peri-implantitis were selected as the non-inflammatory group. This study was approved by the Ethics Committee of our hospital, and all patients and their families provided informed consent by signing the appropriate documentation.
Treatment protocols
The control group was given ultrasonic subgingival sandblasting using a Swiss EMS ultrasonic therapy unit. Prior to treatment, both operator and patient wore safety goggles. Following oral rinse with a mouthwash, a mouth prop was positioned. Subgingival sandblasting was performed, with debridement time limited to ≤ 6 min for peri-implant sites and ≤ 5 s per tooth for non-implant areas.
The glycine-based subgingival sandblasting group underwent subgingival glycine powder air-polishing using that same ultrasonic unit. After safety eyewear placement and rinsing with a Mouthwash, a Mouth prop was inserted. The nozzle was positioned 1–2 mm subgingivally within the peri-implant sulcus. Sandblasting duration was restricted to ≤ 10 min for implant sites and ≤ 5 s per tooth for adjacent teeth, maintaining consistent water flow and power setting. Subsequently, the oral cavity was irrigated with normal saline for 20 s. Postoperative instructions emphasized implant hygiene techniques, peri-implant plaque control, and adherence to regular periodontal maintenance.
The erythritol-based subgingival sandblasting group received subgingival erythritol powder air-polishing following identical preparatory steps. The nozzle was angulated at 15–30° to the tooth axis and maintained 1–2 mm subgingivally. Treatment duration was capped at ≤ 10 min for implant surfaces and ≤ 5 s per natural tooth/periodontal pocket. A 30-second normal saline rinse ensured particle clearance. Postoperative care included prescription of antibacterial Mouthwash, interdental cleaning reinforcement, and avoidance of chromogenic substances for 24 h.
Evaluation indices
Assessment of peri-implant indices
Implant loosening was evaluated and recorded at baseline (preoperatively), 3 Months, and 6 Months postoperatively. The following peri-implant indices were compared between groups preoperatively and at 3 months postoperatively. The plaque index (PLI) was scored 0–3, where higher scores indicated greater plaque accumulation. Bleeding index (BI) was graded from 0 to 3, with increasing scores reflecting severer bleeding. Probing depth (PD) was measured to the nearest millimeter from the mucosal margin to the base of the peri-implant sulcus/pocket using a standardized pressure-sensitive periodontal probe. Attachment loss (AL) was calculated as PD minus the distance from the cementoenamel junction to the free gingival margin (mm).
Analysis of peri-implant inflammatory mediators
Gingival crevicular fluid (GCF) was collected at baseline (preoperatively), 3 Months, and 6 months postoperatively. The levels of interleukin-6 (IL-6), interleukin-17 (IL-17), and interleukin-1β (IL-1β) were detected by enzyme-linked immunosorbent assay (ELISA). Intergroup and intragroup comparisons of inflammatory mediator levels were performed across all timepoints.
Patient satisfaction assessment
A self-designed questionnaire (Supplementary File 1) was used to evaluate the satisfaction of patients with the treatment effect (including appearance, colour and lustre, character, and arrangement), and the scores were positively correlated with patient satisfaction.
Statistical methods
All statistical analyses were performed using Statistical Package for the Social Sciences (SPSS) version 26.0. Data conforming to a normal distribution were presented as mean ± standard deviation (
± s). Data that did not conform to the normal distribution were expressed as median and interquartile range [M (Q25, Q75)]. One-way analysis of variance (ANOVA) was used to compare normally distributed measurement data. Kruskal-Wallis one-way ANOVA was used to compare non-normally distributed measurement data. Counting data were expressed as frequency and percentage [n (%)], with chi-square (
) test for intergroup comparisons. Univariate and multivariate logistic regression analyses were applied to identify the factors affecting peri-implantitis occurrence. The statistical significance was set at P < 0.05.
Results
Univariate analysis of risk factors for peri-implantitis
Univariate analysis showed that the occurrence of peri-implantitis was correlated with a number of factors, among which lower educational level, smoking, drinking, diabetes, previous history of periodontal diseases, longer implant service time, overload from occlusal imbalance, insufficient keratinized mucosa width, and irregular dental cleaning were significantly correlated with peri-implantitis occurrence (P < 0.05, Table 1).
Table 1.
Univariate analysis of factors influencing the occurrence of peri-implantitis [n = 198, n (%)]
| Items | Non-inflammatory group (n = 102) |
Inflammatory group (n = 96) |
 |
P | |
|---|---|---|---|---|---|
| Gender | Male | 58 (56.86%) | 56 (58.33%) | 0.044 | 0.834 |
| Female | 44 (43.14%) | 40 (41.67%) | |||
| Age (years) | ≤ 60 | 77 (75.49%) | 61 (63.54%) | 3.343 | 0.067 |
| > 60 | 25 (24.51%) | 35 (36.46%) | |||
| Educational level | High school or below | 42 (41.18%) | 58 (60.42%) | 7.324 | 0.007 |
| University or above | 60 (58.82%) | 38 (39.58%) | |||
| Smoking | Yes | 39 (38.24%) | 59 (61.46%) | 10.670 | 0.001 |
| No | 63 (61.76%) | 37 (38.54%) | |||
| Drinking | Yes | 37 (36.27%) | 53 (55.21%) | 7.151 | 0.007 |
| No | 65 (63.73%) | 43 (44.79%) | |||
| Diabetes | Yes | 49 (48.04%) | 64 (66.67%) | 7.004 | 0.008 |
| No | 53 (51.96%) | 32 (33.33%) | |||
| Periodontal diseases | Yes | 49 (48.04%) | 71 (73.96%) | 13.916 | 0.000 |
| No | 53 (51.96%) | 25 (26.04%) | |||
| Implant service time (years) | ≤ 1 | 73 (71.57%) | 15 (15.63%) | 62.907 | 0.000 |
| 1 ~ 5 | 16 (15.69%) | 40 (41.67%) | |||
| ≥ 5 | 13 (12.75%) | 41 (42.71%) | |||
| Sleep bruxism | Yes | 41 (40.20%) | 49 (51.04%) | 2.346 | 0.126 |
| No | 61 (59.80%) | 47 (48.96%) | |||
| Implant occlusion | Normal | 59 (57.84%) | 28 (29.17%) | 16.510 | 0.000 |
| Overload | 43 (42.16%) | 68 (70.83%) | |||
| Keratinized mucosa width (mm) | ≥ 2 | 85 (83.33%) | 57 (59.38%) | 13.995 | 0.000 |
| < 2 | 17 (16.67%) | 39 (40.63%) | |||
| Implanting position | Maxillary anterior region | 52 (50.98%) | 62 (64.58%) | 3.746 | 0.053 |
| Maxillary posterior region | 50 (49.02%) | 34 (35.42%) | |||
| Regular dental cleaning | Yes | 71 (69.61%) | 42 (43.75%) | 13.497 | 0.000 |
| No | 31 (30.39%) | 54 (56.25%) | |||
Multivariate analysis of factors influencing peri-implantitis
The factors with statistical differences in univariate analysis were coded for regression modeling (assignment criteria detailed in Table 2). After adjusting for covariates, multivariate logistic regression analysis identified five independent influencing factors for peri-implantitis. Higher educational level (university or above) was a protective factor against inflammation development [odds ratio (OR) = 0.408]. Previous history of periodontal diseases significantly increased the risk of inflammation (OR = 3.084). The longer the implant service time, the higher the risk of inflammation (OR = 4.614). Insufficient keratinized mucosa width (< 2 mm) significantly predicted inflammation (OR = 3.267). Regular dental cleaning was a protective factor, and non-adherence to regular dental cleaning substantially increased susceptibility (OR = 2.902) (P < 0.05, Table 3).
Table 2.
Assignment table
| Variable | Assignment |
|---|---|
| Educational level | High school or below = 0, University or above = 1 |
| Smoking | No = 0, Yes = 1 |
| Drinking | No = 0, Yes = 1 |
| Diabetes | No = 0, Yes = 1 |
| Periodontal diseases | No = 0, Yes = 1 |
| Implant service time | ≤ 1 = 0, 1 ~ 5 = 1, ≥ 5 = 2 |
| Implant occlusion | Normal = 0, Overload = 1 |
| Keratinized mucosa width (mm) | ≥ 2 = 0, < 2 = 1 |
| Regular dental cleaning | Yes = 0, No = 1 |
Table 3.
Multivariate analysis of factors influencing the occurrence of peri-implantitis (n = 198)
| Factor | B | S.E | Wald | Sig | Exp (B) | 95% CI |
|---|---|---|---|---|---|---|
| Constant | −3.470 | 0.653 | 28.252 | 0.000 | 0.031 | - |
| Educational level | −0.896 | 0.405 | 4.899 | 0.027 | 0.408 | 0.185 ~ 0.902 |
| Smoking | 0.625 | 0.396 | 2.490 | 0.115 | 1.869 | 0.860 ~ 4.064 |
| Drinking | 0.213 | 0.402 | 0.280 | 0.597 | 1.237 | 0.563 ~ 2.719 |
| Diabetes | 0.527 | 0.425 | 1.539 | 0.215 | 1.694 | 0.737 ~ 3.897 |
| Periodontal diseases | 1.126 | 0.414 | 7.384 | 0.007 | 3.084 | 1.369 ~ 6.949 |
| Implant service time | 1.529 | 0.270 | 31.978 | 0.000 | 4.614 | 2.716 ~ 7.838 |
| Implant occlusion | 0.622 | 0.403 | 2.373 | 0.123 | 1.862 | 0.844 ~ 4.105 |
| Keratinized mucosa width | 1.184 | 0.438 | 7.321 | 0.007 | 3.267 | 1.386 ~ 7.703 |
| Regular dental cleaning | 1.065 | 0.405 | 6.921 | 0.009 | 2.902 | 1.312 ~ 6.419 |
Effects of subgingival sandblasting on peri-implant indices in patients with peri-implantitis
In this study, peri-implant indices (PLI, BI, PD, and AL) of patients in the control, glycine-based subgingival sandblasting, and erythritol-based subgingival sandblasting groups were compared at different time points. Both subgingival sandblasting techniques (glycine and erythritol) demonstrated superior efficacy versus ultrasonic subgingival sandblasting alone, effectively reducing peri-implant PLI and BI (P < 0.05 vs. baseline). These anti-inflammatory effects persisted at significantly reduced levels through the 6-month evaluation period. Concurrently, PD reductions reached statistical significance at 3 Months post-treatment, though the magnitude of improvement attenuated by the 6-month assessment (P < 0.05) AL measurements showed parallel trends, with both subgingival sandblasting groups maintaining superior stability compared to controls throughout follow-up (Table 4).
Table 4.
Effects of subgingival sandblasting on peri-implant indices in patients with peri-implantitis [n = 96, 
± s, M (Q25, Q75)]
| Index | Time point | Control group (n = 32) | Glycine-based subgingival sandblasting group (n = 32) | Erythritol-based subgingival sandblasting group (n = 32) | Statistic | P |
|---|---|---|---|---|---|---|
| PLI | Before treatmentb | 2 (2,3) | 2 (1.25,2.75) | 2 (1,2) | 5.791 | 0.055 |
| 3 months after treatmentb | 2 (1,2) | 1 (1,1)* | 1 (0,1)* | 20.081 | 0.000 | |
| 6 months after treatmentb | 2 (1,2) | 1 (1,1)* | 1 (1,1)* | 22.355 | 0.000 | |
| BI | Before treatmentb | 2 (2,2) | 2 (2,2) | 2 (2,2) | 0.791 | 0.673 |
| 3 months after treatmentb | 2 (1.5,2) | 1 (1,1)* | 1 (1,2)* | 23.730 | 0.000 | |
| 6 months after treatmentb | 2 (2,2) | 1 (1,1)* | 1 (1,2)* | 27.417 | 0.000 | |
| PD | Before treatmenta | 4.68 ± 1.62 | 4.52 ± 1.16 | 4.86 ± 1.29 | 0.493 | 0.612 |
| 3 months after treatmenta | 3.38 ± 0.80 | 3.97 ± 0.91* | 3.83 ± 0.69* | 4.593 | 0.013 | |
| 6 months after treatmenta | 3.52 ± 0.73 | 3.88 ± 0.51 | 3.71 ± 0.69 | 2.516 | 0.086 | |
| AL | Before treatmenta | 6.24 ± 1.70 | 6.12 ± 1.93 | 6.63 ± 1.63 | 0.732 | 0.484 |
| 3 months after treatmenta | 4.19 ± 1.09 | 3.75 ± 0.67 | 3.69 ± 1.41 | 1.947 | 0.148 | |
| 6 months after treatmenta | 4.14 ± 1.10 | 4.28 ± 0.73 | 3.73 ± 1.12 | 2.588 | 0.081 |
PLI Plaque Index, BI Bleeding Index, PD Probing Depth, AL Attachment Loss
a Kruskal-Wallis one-way ANOVA
b One-way ANOVA; Compared with control group
*P < 0.05
Biomarker responses to subgingival sandblasting in patients with peri-implantitis
In this study, the levels of inflammatory cytokines (IL-6, IL-17, IL-1β) in control, glycine-based subgingival sandblasting, and erythritol-based subgingival sandblasting groups were compared at different time points. At 3 months after treatment, the levels of IL-6, IL-17, and IL-1β in both sandblasting groups were significantly lower than those in the control group (P < 0.05), and the inhibitory effects of the erythritol group were better than those of the glycine group (P < 0.05). This therapeutic advantage persisted through the 6-month evaluation, where the erythritol group maintained significantly suppressed cytokine levels (P < 0.05). Control patients exhibited progressive inflammatory resurgence, evidenced by elevated IL-6 concentrations (Table 5).
Table 5.
Effects of subgingival sandblasting on CGF inflammatory mediators in patients with peri-implantitis [n = 96, 
± s, M (Q25, Q75)]
| Index | Time point | Control group (n = 32) |
Glycine-based subgingival sandblasting group (n = 32) |
Erythritol-based subgingival sandblasting group (n = 32) |
Statistic | P |
|---|---|---|---|---|---|---|
| IL−6 | Before treatmenta | 13.14 ± 0.76 | 12.92 ± 0.66 | 13.19 ± 0.59 | 1.498 | 0.229 |
| 3 months after treatmenta | 8.76 ± 0.39 | 5.69 ± 0.27* | 4.23 ± 0.24*# | 1800.519 | 0.000 | |
| 6 months after treatmenta | 8.48 ± 0.44 | 5.31 ± 0.38* | 3.82 ± 0.31*# | 1256.234 | 0.000 | |
| IL−17 | Before treatmenta | 6.85 ± 0.63 | 6.74 ± 0.61 | 6.95 ± 0.59 | 0.900 | 0.410 |
| 3 months after treatmenta | 5.35 ± 0.41 | 4.04 ± 0.61* | 3.73 ± 0.40*# | 101.435 | 0.000 | |
| 6 months after treatmentb | 5.14 (4.83,5.56) | 4.10 (3.91,4.22)* | 3.91 (3.91,3.67)* | 55.942 | 0.000 | |
| IL−1β | Before treatmenta | 14.68 ± 1.59 | 14.15 ± 1.34 | 14.57 ± 1.42 | 1.155 | 0.319 |
| 3 months after treatmenta | 8.87 ± 0.52 | 6.02 ± 0.45* | 4.41 ± 0.41*# | 769.622 | 0.000 | |
| 6 months after treatmentb | 8.98 (8.64,9.31)* | 6.02 (5.65,6.37)* | 4.43 (4.21,4.65)*# | 87.376 | 0.000 |
IL-6 Interleukin-6, IL-17 Interleukin-17, IL−1β Interleukin-1β
a, One-way ANOVA
b, Kruskal-Wallis one-way ANOVA; Compared with control group
*P < 0.05; Compared with glycine-based subgingival sandblasting group
#P < 0.05
Patient satisfaction scores
Comparative analysis of treatment satisfaction revealed significant differences among the control, glycine-based subgingival sandblasting, and erythritol-based subgingival sandblasting groups. In terms of appearance and character, the median satisfaction scores of both sandblasting groups were significantly higher than those of the control group (P < 0.05). There were no statistically significant differences in the scores of colour and lustre and arrangement among groups (P > 0.05) (Table 6).
Table 6.
Patient satisfaction scores [n = 96, M (Q25, Q75)]
| Items | Control group (n = 32) | Glycine-based subgingival sandblasting group (n = 32) | Erythritol-based subgingival sandblasting group (n = 32) | Kruskal-Wallis one-way ANOVA | P |
|---|---|---|---|---|---|
| Appearance | 3 (3, 4) | 4 (3, 4)* | 4 (3, 4)* | 10.624 | 0.005 |
| Colour and lustre | 3 (3, 4) | 3.5 (3, 4) | 3 (3, 4) | 1.930 | 0.381 |
| Character | 3 (3, 3) | 4 (3, 4)* | 4 (3, 4)* | 27.024 | 0.000 |
| Arrangement | 4 (3, 4) | 4 (3, 4) | 3.5 (3, 4) | 0.592 | 0.744 |
Compared with control group
*P < 0.05
Discussion
Influencing factors of peri-implantitis
Focusing on patients with early peri-implantitis, this study explored the underlying mechanisms by analyzing multiple contributing factors such as oral hygiene habits, general health status, and local anatomical conditions. Furthermore, it evaluated the efficacy of subgingival sandblasting in peri-implant microecological regulation. Univariate analysis showed that lower educational level, smoking, alcohol consumption, diabetes, a previous history of periodontal diseases, longer implant service time, overbite, insufficient keratinized mucosa width, and irregular dental cleaning were significantly associated with inflammation. This constellation of factors suggests that peri-implantitis arises not from a single microbial challenge but from the complex interplay of diverse internal and external factors. Lower educational level may diminish patient awareness and prioritization of to oral health maintenance [22]. Systemic conditions like diabetes may aggravate local plaque accumulation and mechanical damage by altering immune responses and impairing microcirculation within peri-implant tissues. In contrast, smoking, although not classified as a systemic disease, is a detrimental habit that may alter the oral microenvironment and impair local immunity, thereby facilitating inflammatory responses [23, 24]. Interestingly, our findings suggest a potential cumulative effect when lower educational level, systemic/metabolic comorbidities (such as diabetes), and poor oral hygiene habits co-exist, thereby synergistically increasing the risk of peri-implantitis. This highlights the multifactorial and interactive nature of this condition. Moreover, a history of periodontal diseases and insufficient keratinized mucosa width directly weakened the structural and functional integrity of the peri-implant soft tissue barrier, facilitating bacterial invasion and subsequent initiation of the host inflammatory response [25]. Collectively, these findings provide a theoretical basis for the development of personalized preventive measures in clinical practice.
Independent risk and protective factors
After assigning statistically significant factors in the univariate analysis, multivariate logistic regression analysis further identified five independent influencing factors for peri-implantitis. Higher educational level and regular dental cleaning emerged as protective factors, whereas a previous history of periodontal diseases, prolonged implant service duration, and insufficient keratinized mucosa width were confirmed as independent risk factors. Elevated literacy levels are often associated with enhanced health awareness and improved self-care habits, while regular dental cleaning can effectively reduce plaque formation. On the contrary, a previous history of periodontal diseases indicates pre-existing vulnerability due to compromised periodontal tissue integrity and chronic inflammatory susceptibility. Extended implant exposure predisposes to inflammation through cumulative plaque deposition and mechanical stress, while insufficient keratinized mucosa width compromises the defensive capacity of peri-implant tissues against bacterial invasion. These findings are consistent with the study of Murakami et al. [26–28]. Notably, our analysis suggests that patients with a prior history of periodontal diseases may require a greater keratinized mucosa width threshold to achieve comparable protective efficacy, indicating a possible biological interaction between these two risk factors. The multivariate analysis not only confirmed the independence of each factor, but also provides a quantitative framework for clinical risk assessment. This underscores the necessity for integrated health assessments, both preceding and following implant-supported restoration, coupled with intensified oral health education. High-risk cohorts, in particular, warrant tailored maintenance protocols to reduce the incidence of peri-implantitis.
Efficacy of subgingival sandblasting
This study further compared the peri-implant indices and inflammatory mediators among the control, glycine-based subgingival sandblasting, and erythritol-based subgingival sandblasting groups at different time points. Both sandblasting Modalities significantly reduced PI and Bi, indicating effective amelioration of local inflammation. At 3 months after treatment, both sandblasting techniques similarly suppressed key pro-inflammatory factors including IL-6, IL-17, and IL-1β. Notably, the erythritol group maintained significantly lower levels of inflammatory mediators through 6-month follow-up, demonstrating prolonged anti-inflammatory efficacy [29–31]. While PD showed immediate improvement, this effect attenuated beyond 6 months, indicating limited sustained impact on deep periodontal structures. Long-term stability therefore needs adjunctive mechanical debridement and maintenance protocols. Mechanistically, sandblasting not only plays a direct antibacterial role through mechanical removal of plaque biofilms, but also indirectly inhibits the release of pro-inflammatory factors and improves the peri-implant microenvironment, providing a simple and effective adjuvant treatment for peri-implantitis management.
To our knowledge, this study is among the few that compare glycine- and erythritol-based subgingival sandblasting in patients with early peri-implantitis using combined clinical and biochemical indicators (e.g., IL-6, IL-17, IL-1β). Our findings provide novel evidence for the superior long-term superiority of erythritol powder in maintaining local anti-inflammatory status, which has not been thoroughly investigated in similar population cohorts.
Clinical significance
In summary, this study shows that peri-implantitis pathogenesis involves a multifactorial interplay of oral hygiene practices, systemic diseases, unhealthy habits, and site-specific anatomical conditions. Consequently, effective clinical management necessitates multidimensional interventions targeting these diverse elements. Beyond fundamental strategies, including enhanced oral health education and regular dental cleanings, subgingival sandblasting emerges as a valuable adjunct for modulating the peri-implant microenvironment. This technique effectively reduces pathogenic biofilm load and pro-inflammatory mediator concentrations, thus improving clinical outcomes and patient-reported satisfaction with implant prostheses. In particular, erythritol-based sandblasting demonstrates outstanding long-term anti-inflammatory efficacy relative to glycine-based agents, highlighting its clinical utility for long-term peri-implant maintenance.
Limitations and future directions
However, this study still has several limitations. Its single-center design, limited sample size, and relatively short follow-up period precluded comprehensive assessment of patients’ systemic immune status and other possible systemic influencing factors. Moreover, although several factors showed statistical significance, the complex interactions among these variables warrant further validation with larger-scale studies incorporating stratified analyses. Future research should prioritize large-scale, multi-center cohorts with extended longitudinal follow-up to further verify the independent contributions of identified risk/protective factors, quantify the sustained efficacy of subgingival sandblasting, particularly erythritol-based protocols, and explore integrated therapeutic approaches, such as subgingival sandblasting combined with localized pharmacotherapy (e.g., antimicrobial agents) or laser-assisted therapy, for synergistic effects. Such evidence will establish refined and multidimensional clinical protocols for peri-implantitis management. Through comprehensive risk mitigation and rigorously maintained supportive care, clinicians can optimize the long-term functional and aesthetic outcomes of implant-supported restoration, thereby enhancing patient satisfaction and treatment longevity.
Supplementary Information
Acknowledgements
Not applicable.
Authors’ contributions
Author ContributionsTaohua Pan and Wei Meng contributed equally to the conceptualization and design of the study. Taohua Pan was primarily responsible for data collection and analysis, while Wei Meng played a key role in interpreting the results and drafting the manuscript. Minyi Zhang, Yan Xie both contributed to data analysis and interpretation, and participated in writing and revising the manuscript. They also provided valuable feedback on the study’s methodology and analysis. Zuoxian Chen, Meilu Zhou contributed to the project’s overall management and provided critical feedback on the study’s design and implementation. They also contributed to writing and revising the manuscript. Lifen Yin and Hui Xie contributed to the overall management of the project and provided critical feedback on the design and implementation of the research.All authors played significant roles in the development of the study and approved the final version of the manuscript.
Funding
This research is supported by Hunan Provincial Clinical Medical Technology Innovation Guidance Project (Grant No. 2021SK53303); Hunan Provincial Natural Science Foundation (Grant No. 2024JJ9542); Changsha Municipal Health Commission Scientific Research Program (Grant No. KJ-A2023015); Hunan Provincial Health Special Fund Project (Grant No. B2024-09).
Data availability
Data Availability StatementThe datas used and/or analyzed during the current study are available from the corresponding author.
Declarations
Ethics approval and consent to participate
This study was approved by the Human Ethics Committee of Changsha Stomatological Hospital (Approval number: 2023-023). All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Informed consent was obtained from all individual participants included in the study.
Consent for publication
All participants agreed to publish
Competing interests
The authors declare no competing interests.
Conflict of interest
The authors declare no conflict of interest, financial or otherwise.
Clinical trial registration statement
This clinical trial has been registered with ClinicalTrials.gov under the registration number NCT06998160. The registration provides detailed information about the study protocol, including objectives, methodology, and outcome measures.
Footnotes
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Kong HJ, Kim YL. Application of artificial intelligence in dental crown prosthesis: a scoping review. BMC Oral Health. 2024;24(1):937. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Roccuzzo A, et al. Peri-implantitis as the consequence of errors in implant therapy. Periodontol 2000. 2023;92(1):350–61. [DOI] [PubMed] [Google Scholar]
- 3.Ramanauskaite A, et al. Surgical interventions for the treatment of peri-implantitis. Clin Implant Dent Relat Res. 2023;25(4):682–95. [DOI] [PubMed] [Google Scholar]
- 4.Diaz P, et al. What is the prevalence of peri-implantitis? A systematic review and meta-analysis. BMC Oral Health. 2022;22(1):449. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Darby I. Risk factors for periodontitis & peri-implantitis. Periodontol 2000. 2022;90(1):9–12. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Schwarz F, et al. Surgical therapy of peri-implantitis. Periodontol 2000. 2022;88(1):145–81. [DOI] [PubMed] [Google Scholar]
- 7.Fu JH, Wang HL. Breaking the wave of peri-implantitis. Periodontol 2000. 2020;84(1):145–60. [DOI] [PubMed] [Google Scholar]
- 8.Roccuzzo M, Mirra D, Roccuzzo A. Surgical treatment of peri-implantitis. Br Dent J. 2024;236(10):803–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Wagner J, et al. Systematic review on diabetes mellitus and dental implants: an update. Int J Implant Dent. 2022;8(1):1. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Mo JJ, et al. Single-cell sequencing identifies inflammation-promoting fibroblast-neutrophil interaction in peri-implantitis. J Clin Periodontol. 2024;51(2):196–208. [DOI] [PubMed] [Google Scholar]
- 11.Chen L, et al. Titanium particles in peri-implantitis: distribution, pathogenesis and prospects. Int J Oral Sci. 2023;15(1):49. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Bi J, et al. Effect of air polishing on the treatment of Peri-Implant diseases: a systematic review and meta-analysis. J Oral Implantol. 2023;49(6):616–28. [DOI] [PubMed] [Google Scholar]
- 13.Huang N, et al. The clinical efficacy of powder air-polishing in the non-surgical treatment of peri-implant diseases: a systematic review and meta-analysis. Jpn Dent Sci Rev. 2024;60:163–74. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14.Rupp F, et al. Surface characteristics of dental implants: a review. Dent Mater. 2018;34(1):40–57. [DOI] [PubMed] [Google Scholar]
- 15.Dasgupta D, et al. Efficacy of implantoplasty in management of peri-implantitis: a systematic review. J Indian Prosthodont Soc. 2023;23(3):210–7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Onisor F, et al. Effectiveness and clinical performance of erythritol air-polishing in non-surgical periodontal therapy: a systematic review of randomized clinical trials. Medicina (Kaunas). 2022. 10.3390/medicina58070866. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Jentsch HFR, et al. Adjunctive air-polishing with erythritol in nonsurgical periodontal therapy: a randomized clinical trial. BMC Oral Health. 2020;20(1):364. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Nicola D, et al. Treatment of peri-implant mucositis: adjunctive effect of glycine powder air polishing to professional mechanical biofilm removal. 12 months randomized clinical study. Clin Implant Dent Relat Res. 2024;26(2):415–26. [DOI] [PubMed] [Google Scholar]
- 19.Leung K, et al. Decontamination of multispecies oral biofilm from rough implant surface by airflow with glycine. Clin Exp Dent Res. 2022;8(1):322–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Selimovic A, et al. Non-surgical treatment of peri-implantitis with and without erythritol air-polishing a 12-month randomized controlled trial. BMC Oral Health. 2023;23(1):240. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Hentenaar DFM, et al. Erythritol airpolishing in the non-surgical treatment of peri-implantitis: a randomized controlled trial. Clin Oral Implants Res. 2021;32(7):840–52. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Ramandeep G, et al. Oral health literacy among clients visiting a rural dental college in North India-a cross-sectional study. Ethiop J Health Sci. 2014;24(3):261–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Isola G. The impact of diet, nutrition and nutraceuticals on oral and periodontal health. Nutrients. 2020. 10.3390/nu12092724. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.Sczepanik FSC, et al. Periodontitis is an inflammatory disease of oxidative stress: we should treat it that way. Periodontol 2000. 2020;84(1):45–68. [DOI] [PubMed] [Google Scholar]
- 25.Levine M, Lohinai ZM. Resolving the contradictory functions of lysine decarboxylase and butyrate in periodontal and intestinal diseases. J Clin Med. 2021. 10.3390/jcm10112360. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Murakami S, et al. Dental plaque-induced gingival conditions. J Periodontol. 2018;89(Suppl 1):S17-27. [DOI] [PubMed] [Google Scholar]
- 27.Kimble R, et al. Association between oral health markers and decline in muscle strength and physical performance in later life: longitudinal analyses of two prospective cohorts from the UK and the USA. Lancet Healthy Longev. 2022;3(11):e777–88. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28.Cadenas de Llano-Perula M, et al. Risk factors for gingival recessions after orthodontic treatment: a systematic review. Eur J Orthod. 2023;45(5):528–44. [DOI] [PubMed] [Google Scholar]
- 29.Mensi M, et al. Clinical evaluation of air polishing with erythritol powder followed by ultrasonic calculus removal versus conventional ultrasonic debridement and rubber cup polishing for the treatment of gingivitis: a split-mouth randomized controlled clinical trial. Int J Dent Hyg. 2022;20(2):371–80. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Mensi M, et al. Efficacy of the additional use of subgingival air-polishing with erythritol powder in the treatment of periodontitis patients: a randomized controlled clinical trial. Part II: effect on sub-gingival Microbiome. Clin Oral Investig. 2023;27(6):2547–63. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.Yokoi H, et al. Erythritol can inhibit the expression of senescence molecules in mouse gingival tissues and human gingival fibroblasts. Nutrients. 2023. 10.3390/nu15184050. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
Data Availability StatementThe datas used and/or analyzed during the current study are available from the corresponding author.