A microtomographic and histopathological evaluation of dental cements as late-stage peri-implant complication in a rat model.

Cement mediated peri-implantitis accounts for 1.9-75% of dental implant failures associated with peri-implant diseases. This study evaluated the biological impact of dental cements on osseointegrated implants using Lewis rats. Twenty-two rats were distributed into 6 groups: negative control (NC) soft diet (SD), and hard diet (HD); positive control SD and HD (n = 3); Implant + bio-ceramic Cement (BC) SD and HD which included contralateral Sham sites (n = 5). Titanium implants were placed on either side of the maxillae and allowed to heal for 14 days. Later, both sides of experimental groups underwent a re-entry surgery to simulate clinical cementation. The right side received 0.60 mg of BC. At 14 days post cement application, maxillae were harvested for clinical, microtomographic, and histological evaluations. Clinical and microtomographic evaluations indicated evidence of extensive inflammation and circumferential bone resorption around BC implants in comparison to NC. Histology revealed cement particles surrounded by inflammatory infiltrate in the implant area accompanied by biofilm for SD groups. Both sides of BC indicated intensive bone resorption accompanied by signs of osteolysis when compared to NC. Cemented groups depicted significantly lower bone to implant contact when compared to NC. In conclusion, residual cement extravasation negatively impacted osseointegrated implants after re-entry surgeries.

Experimental Model of Ligature-Induced Peri-Implantitis in Mice.

Dental implants have a high success and survival rate. However, complications such as peri-implantitis (PI) are highly challenging to treat. PI is characterized by inflammation in the tissues around dental implants with progressive loss of supporting bone. To optimize dental implants' longevity in terms of health and functionality, it is crucial to understand the peri-implantitis pathophysiology. In this regard, using mouse models in research has proven clear benefits in recreating clinical circumstances. This study aimed to describe an experimental model of ligature-induced peri-implantitis in mice and determine whether there is effectiveness in inducing this disease, given the observed bone and tissue changes. The experimental peri-implantitis induction comprehends the following steps: teeth extraction, implant placement, and ligature-inducted PI. A sample of eighteen 3-week-old C57BL/6J male mice was divided into two groups, ligature (N=9) and control non-ligature (N=9). The evaluation of clinical, radiographical, and histological factors was performed. The ligature group showed significantly higher bone loss, increased soft tissue edema, and apical epithelial migration than the non-ligature group. It was concluded that this pre-clinical model can successfully induce peri-implantitis in mice.

CXCL5/CXCL8 induces neutrophilic inflammation in peri-implantitis.

OBJECTIVE AND BACKGROUND: This research aimed to examine the role of C-X-C motif chemokine ligand 5 (CXCL5) and C-X-C motif chemokine ligand 8 (CXCL8; also known as IL-8) in neutrophilic inflammation triggered by peri-implantitis and to shed light on the underlying mechanisms that link them to the development of this condition. MATERIALS: This study included 40 patients who visited the Department of Periodontology at Kyungpook University Dental Hospital. They were divided into two groups based on their condition: healthy implant (HI) group (n = 20) and peri-implantitis (PI) group (n = 20). Biopsy samples of PI tissue were collected from the patients under local anesthesia. HI tissue was obtained using the same method during the second implant surgery. To construct libraries for control and test RNAs, the QuantSeq 3' mRNA-Seq Library Prep Kit (Lexogen, Inc., Austria) was used according to the manufacturer's instructions. Samples were pooled based on representative cytokines obtained from RNA sequencing results and subjected to Reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Hematoxylin and eosin staining, and immunohistochemistry (IHC) analysis were performed to visually assess expression levels and analyze tissue histology. Student's t-test was employed to conduct statistical analyses. RESULTS: Initially, heatmaps were used to examine gene expression variations between the HI and PI groups based on the results of RNA sequencing. Notably, among various cytokines, CXCL5 and CXCL8 had the highest expression levels in the PI group compared with the HI group, and they are known to be associated with inflammatory responses. In the gingival tissues, the expression of genes encoding cytokines such as interleukin (IL)-1ß, tumor necrosis factor-alpha (TNF)-α, interleukin (IL)-6, and CXCL5/CXCL8 was assessed via RT-qPCR. The mRNA expression level of CXCL5/CXCL8 significantly increased in the PI group compared with the HI group (p < .045). Contrarily, the mRNA expression level of interleukin 36 receptor antagonist (IL36RN) significantly decreased (p < .008). IHC enabled examination of the distribution and intensity of CXCL5/CXCL8 protein expression within the tissue samples. Specifically, increased levels of CXCL5/CXCL8 promote inflammatory responses, cellular proliferation, migration, and invasion within the peri-implant tissues. These effects are mediated through the activation of the PI3K/Akt/NF-κB signaling pathway. CONCLUSIONS: This study found that the PI sites had higher gene expression level of CXCL8/CXCL5 in the soft tissue than HI sites, which could help achieve more accurate diagnosis and treatment planning.

Peri-implantitis and maxillary sinus membrane thickening: A retrospective cohort study.

OBJECTIVE: The objective of this study is to investigate the association of peri-implantitis (PI) and sinus membrane thickening and to assess the resolution of membrane thickening following intervention (implant removal or peri-implantitis treatment) aimed at arresting PI. MATERIALS AND METHODS: Forty-five patients with 61 implants in the posterior maxillary region were retrospectively included in the study. Twenty-four patients were diagnosed with peri-implantitis (PI) and 21 had peri-implant health (PH). Cone-beam computed tomography (CBCT) scans were evaluated to assess maxillary sinus characteristics, including membrane thickening, sinus occupancy and ostium patency. The CBCT scans taken 6 months after intervention aimed at arresting disease (implant removal or treatment of PI) in the PI group were also appraised and compared to baseline scans. RESULTS: At baseline, all parameters evaluating membrane thickness disorders yielded significant differences between groups (p < .001). Patients with posterior maxillary implants diagnosed with PI were 7× more likely to present membrane thickening compatible with pathology when compared to patients with healthy implants (OR = 7.14; p = .005). Furthermore, the likelihood was 6x greater in implants diagnosed with PI to exhibit moderate membrane thickening (OR = 6.75, p = .001). The patients receiving interventions aimed at arresting PI experienced significant enhancement in all radiographic parameters related to the sinus cavity at the 6-month follow-up (p < .001), though these variations were similarly independent of whether treatment consisted of PI treatment or implant removal. CONCLUSIONS: Maxillary sinus membrane thickening and the permeability/obstruction of the ostium are frequently associated with the presence of PI in posterior implants. Interventions targeting disease resolution effectively reduce membrane thickness to levels compatible with maxillary sinus health.

Ultrastructural and immunohistochemical evaluation of hyperplastic soft tissues surrounding dental implants in fibular jaws.

In reconstructive surgery, complications post-fibula free flap (FFF) reconstruction, notably peri-implant hyperplasia, are significant yet understudied. This study analyzed peri-implant hyperplastic tissue surrounding FFF, alongside peri-implantitis and foreign body granulation (FBG) tissues from patients treated at the Department of Oral and Maxillofacial Surgery, Seoul National University Dental Hospital. Using light microscopy, pseudoepitheliomatous hyperplasia, anucleate and pyknotic prickle cells, and excessive collagen deposition were observed in FFF hyperplastic tissue. Ultrastructural analyses revealed abnormal structures, including hemidesmosome dilation, bacterial invasion, and endoplasmic reticulum (ER) swelling. In immunohistochemical analysis, unfolded protein-response markers ATF6, PERK, XBP1, inflammatory marker NFκB, necroptosis marker MLKL, apoptosis marker GADD153, autophagy marker LC3, epithelial-mesenchymal transition, and angiogenesis markers were expressed variably in hyperplastic tissue surrounding FFF implants, peri-implantitis, and FBG tissues. NFκB expression was higher in peri-implantitis and FBG tissues compared to hyperplastic tissue surrounding FFF implants. PERK expression exceeded XBP1 significantly in FFF hyperplastic tissue, while expression levels of PERK, XBP1, and ATF6 were not significantly different in peri-implantitis and FBG tissues. These findings provide valuable insights into the interconnected roles of ER stress, necroptosis, apoptosis, and angiogenesis in the pathogenesis of oral pathologies, offering a foundation for innovative strategies in dental implant rehabilitation management and prevention.

Immune cell composition and inflammatory profile of human peri-implantitis and periodontitis lesions.

Peri-implantitis (PI) and periodontitis (PD) are common oral inflammatory diseases, which seem to exhibit critical differences in some of their molecular features. Thus, we assessed the immune cell composition of PI and PD lesions and the corresponding inflammatory profile in soft tissues and crevicular fluid. PI, PD, and control patients were recruited (n = 62), and soft tissue biopsies were collected during surgery. Crevicular fluid around implant or tooth was collected. The proportions of major immune cell populations in tissues were analyzed by flow cytometry, and the inflammatory profile in tissue and crevicular fluid by a multiplex immunoassay. No significant difference was seen between PI and PD lesions in the proportions of immune cells. PI tissues showed an increased frequency of B cells in comparison with control tissues, along with higher levels of IL-1ß, TNF-α, IL-4, and BAFF in tissue and crevicular fluid. Moreover, TNF-α, IL-17A, and BAFF were higher in PI tissues, but not in PD, than in control tissues. The immune cell composition did not differ significantly between PI and PD, but an enhanced inflammatory profile was seen in PI tissue. PI lesions were enriched in B cells, and displayed increased levels of IL-1ß, TNF-α, IL-4, and BAFF in both tissue and crevicular fluid.

Sustained Release of Salicylic Acid for Halting Peri-Implantitis Progression in Healthy and Hyperglycemic Systemic Conditions: A Gottingen Minipig Model.

To develop a peri-implantitis model in a Gottingen minipig and evaluate the effect of local application of salicylic acid poly(anhydride-ester) (SAPAE) on peri-implantitis progression in healthy, metabolic syndrome (MS), and type-2 diabetes mellitus (T2DM) subjects. Eighteen animals were allocated to three groups: (i) control, (ii) MS (diet for obesity induction), and (iii) T2DM (diet plus streptozotocin for T2DM induction). Maxillary and mandible premolars and first molar were extracted. After 3 months of healing, four implants per side were placed in both jaws of each animal. After 2 months, peri-implantitis was induced by plaque formation using silk ligatures. SAPAE polymer was mixed with mineral oil (3.75 mg/µL) and topically applied biweekly for up to 60 days to halt peri-implantitis progression. Periodontal probing was used to assess pocket depth over time, followed by histomorphologic analysis of harvested samples. The adopted protocol resulted in the onset of peri-implantitis, with healthy minipigs taking twice as long to reach the same level of probing depth relative to MS and T2DM subjects (∼3.0 mm), irrespective of jaw. In a qualitative analysis, SAPAE therapy revealed decreased levels of inflammation in the normoglycemic, MS, and T2DM groups. SAPAE application around implants significantly reduced the progression of peri-implantitis after ∼15 days of therapy, with ∼30% lower probing depth for all systemic conditions and similar rates of probing depth increase per week between the control and SAPAE groups. MS and T2DM conditions presented a faster progression of the peri-implant pocket depth. SAPAE treatment reduced peri-implantitis progression in healthy, MS, and T2DM groups.

Detection and comparison of neutrophil extracellular traps in tissue samples of peri-implantitis, periodontitis, and healthy patients: A pilot study.

OBJECTIVE: The aim of this study was to detect and compare the tissular expression of neutrophil extracellular traps (NETs) in peri-implant and periodontal samples of patients with peri-implantitis, periodontitis, and controls. MATERIALS AND METHODS: An observational study was performed on patients with peri-implantitis, periodontitis, and controls. Peri-implant and/or periodontal clinical examinations were performed on each participant. Tissue samples were collected during tooth/implant extraction for clinical reasons. Electron microscopy analysis, Picro-Sirius red staining, immunohistochemical (CD15), and immunofluorescence (citrullinated H3 and myeloperoxidase) techniques were performed to detect NET-related structures and the degree of connective tissue destruction, between the study groups. RESULTS: Sixty-four patients were included in the study: 28 peri-implantitis, 26 periodontitis, and 10 controls, with a total of 51 implants, 26 periodontal teeth, and 10 control teeth. Neutrophil release of nuclear content was observed in transmission electron microscopy. Immunohistochemical analysis showed a greater CD15 expression in both peri-implantitis and periodontitis compared to controls (p < 0.001), and peri-implantitis presented lower levels of connective tissue and collagen compared to both periodontitis (p = 0.044; p < 0.001) and controls (p < 0.001). Immunofluorescence showed greater citH3 expression in peri-implantitis than the one found in both periodontitis (p = 0.003) and controls (p = 0.048). CONCLUSIONS: A greater presence and involvement of neutrophils, as well as a greater connective tissue destruction were observed in cases of peri-implantitis. A higher expression of NET-related markers was found in mucosal samples of peri-implantitis compared to periodontitis and controls.

Comparative Assessment of Catalase Levels in Peri-Implant Health and Disease.

Peri-implant disease pathogenesis is similar to periodontal disease pathogenesis resulting in production of pro-inflammatory mediators. These mediators alter the redox balance leading to decrease in antioxidants, among which catalase is one of the enzymatic antioxidants. The aim of the study was to compare the levels of catalase in peri-implant health and disease. The present observational study was carried out from June 2022 to December 2022 in the Department of Implantology, Saveetha Dental College and Hospitals, Chennai, India. A total of 60 patients with peri-implant health (Group 1; n = 20), peri-implant mucositis (Group 2; n = 20) and peri-implantitis (Group 3; n = 20) were enrolled. Unstimulated salivary samples were collected and subjected to ELISA for catalase analysis. Catalase levels were then compared between the groups using ANOVA. The mean catalase level in peri-implant health, peri-implant mucositis, peri-implanti-tis were 25.07 ± 0.44 U/mL, 18.5 6 ± 0.65 U/mL, and 11.25 ± 0.76 U/mL respectively. The difference between the three groups were statistically significant (P < 0.05). Catalase level decreases with severity of peri-implant diseases. Therefore, catalase can be used as a diagnostic marker for peri-implant diseases.

Correlation of C-Reactive Protein and Severity of Peri-Implant Diseases.

Peri-implant disease pathogenesis is similar to periodontal disease pathogenesis resulting in production of pro-inflammatory mediators. These mediators are released during the inflammation phase, among which C-reactive protein (CRP) is one of the acute phase reactants. The aim of the study was to correlate the levels of CRP with the severity of peri-implant diseases. The present observational study was carried out from June 2022 to December 2022 in the Department of Implantology, Saveetha Dental College and Hospitals, Chennai, India. A total of 60 patients with peri-implant health (n = 20), peri-mucositis (n = 20) and peri-implantitis (n = 20) were enrolled. Unstimulated salivary samples were collected and subjected to latex agglutination assay for CRP analysis. CRP levels were then correlated with severity of peri-implant diseases. The mean CRP level in peri-implant health, peri-implant mucositis, peri-implantitis were 0.25 ± 0.36 mg/dl, 3.56 ± 0.85 mg/dl and 5.07 ± 0.74 mg/dl, respectively. Pearson correlation coefficient analysis revealed a strong positive correlation between CRP and peri-implant parameters suggesting that the CRP level increased as the severity of peri-implant disease increased. CRP level increases with severity of peri-implant diseases and there exists a positive correlation between CRP level and peri-implant parameters. Therefore, CRP can be used as a diagnostic marker for peri-implant diseases.

Proximal Periodontal Support Adjacent to Untreated Peri-implantitis Lesions: A Cross-Sectional Analysis.

PURPOSE: To assess site-related features of peri-implantitis occurring adjacent to teeth and its association with the proximal periodontal bone level. MATERIALS AND METHODS: Periapical radiographs were collected from partially edentulous patients exhibiting peri-implantitis adjacent to teeth. The following variables were quantified: intrabony defect width (DW), implant marginal bone loss (MBLi), tooth marginal bone loss (MBLt), implant-tooth distance (ITd), intrabony defect angulation (DA), adjacent periodontal bone peak height (ABPh), and implant-tooth angulation (ITa). A correlation matrix using the Spearman correlation coefficient was created to explore the dependence of these variables. Univariate linear regression analysis was carried out by means of generalized estimating equations (GEE), using MBLt as dependent variable. RESULTS: Overall, 61 patients and 84 implants were included in this study, consisting of a total of 105 implant sites facing adjacent teeth. This resulted in 515 linear and 194 angular measurements. A total of 11 different statistically significant associations were demonstrated between the different variables analyzed. Moreover, the univariate regression analysis revealed significant positive associations between MBLt and MBLi (P = .013) and between MBLt and periodontitis (PD) (P = .014). These associations were confirmed in the multivariate model. CONCLUSIONS: Teeth adjacent to untreated peri-implantitis lesions are associated with proximal loss of periodontal support. This finding is more remarkable in scenarios that display short implant-tooth distance.

Titanium particles in peri-implantitis: distribution, pathogenesis and prospects.

Peri-implantitis is one of the most important biological complications in the field of oral implantology. Identifying the causative factors of peri-implant inflammation and osteolysis is crucial for the disease's prevention and treatment. The underlying risk factors and detailed pathogenesis of peri-implantitis remain to be elucidated. Titanium-based implants as the most widely used implant inevitably release titanium particles into the surrounding tissue. Notably, the concentration of titanium particles increases significantly at peri-implantitis sites, suggesting titanium particles as a potential risk factor for the condition. Previous studies have indicated that titanium particles can induce peripheral osteolysis and foster the development of aseptic osteoarthritis in orthopedic joint replacement. However, it remains unconfirmed whether this phenomenon also triggers inflammation and bone resorption in peri-implant tissues. This review summarizes the distribution of titanium particles around the implant, the potential roles in peri-implantitis and the prevalent prevention strategies, which expects to provide new directions for the study of the pathogenesis and treatment of peri-implantitis.

Evaluation of IL-4, MIP-1α, and MMP-9 gene expression levels in peri-implant tissues in peri-implantitis.

This case-control study evaluated the gene expression levels of interleukin (IL)-4, macrophage inflammatory protein type 1 alpha (MIP-1α), and metalloproteinase (MMP)-9, factors involved in the formation of giant cells in healthy peri-implant tissue and peri-implantitis. Thirty-five subjects (15 healthy and 20 with peri-implantitis), who met the inclusion and exclusion criteria, were included in this study. The peri-implant tissue biopsies were subjected to total RNA extraction, DNAse treatment, and cDNA synthesis. Subsequently, the reaction of real-time PCR was performed to evaluate the gene expression levels of IL-4, MIP-1α, and MMP-9 concerning the reference gene. IL-4 gene expression showed higher (18-fold) values in the Peri-Implantitis Group of Patients when compared with the Healthy (Control) Group (p<0.0001). Although MIP- 1α and MMP-9 gene expression levels were higher in diseased implants, they showed no significant differences (p=0.06 and p=0.2337), respectively. Within the limitations of this study, the results showed that in tissues affected by peri-implantitis, only levels of Il-4 were increased when compared with tissues in the control group.

Application of Immediate Implant Placement Techniques in Peri-implantitis Modeling.

OBJECTIVES: To explore the use of immediate implant placement technique in peri-implantitis modeling, shorten the modeling period, and obtain similar effects. MATERIALS AND METHODS: Eighty rats were divided into 4 groups: immediate placement (IP), delayed placement (DP), IP-ligation (IP-L) and DP-ligation (DP-L). In the DP and DP-L groups, implants were placed 4 weeks after tooth extraction. In the IP and IP-L groups, implants were placed immediately. Four weeks later, the implants were ligated to induce peri-implantitis in the DP-L and IP-L groups. RESULTS: Nine implants were lost (3 in the IP-L and 2 each in the IP, DP, and DP-L group). The bone level decreased after ligation, and the buccal and lingual bone levels were lower in IP-L versus DP-L. The implant pullout strength was decreased after ligation. Micro-CT showed bone parameters were decreased after ligation, and the percent bone volume was higher in IP versus DP. Histology showed that the percent of CD4 + cells and IL-17 + cells was increased after ligation and higher in IP-L versus DP-L. CONCLUSIONS: We successfully introduced immediate implant placement into the modeling of peri-implantitis and observed similar bone resorption and more soft tissue inflammation in a shorter time.

AdipoAI suppresses osteoclastogenesis by activating AdipoR1/APPL1: An in vivo experimental study in diabetes-associated peri-implantitis.

AIM: Diabetics experience severe peri-implant inflammatory bone damage. We aimed to provide powerful evidence supporting the novel adiponectin receptor agonist AdipoAI in treating diabetes-associated peri-implantitis. MATERIALS AND METHODS: Twenty-four ZDF-Leprfa/Crl rats were randomly allocated to three groups (N = 8). After feeding with a high-fat diet to establish diabetic rats, experimental peri-implantitis was induced by implanting titanium rods (1.5 mm diameter and 20 mm length) contaminated with Staphylococcus aureus into the femurs. Radiographic evaluation, microCT, histological analyses and qRT-PCR were used to detect inflammatory infiltration and bone destruction. In vitro, the inhibition by AdipoAI of osteoclastogenesis, including the number and function of osteoclasts, was investigated by TRAP staining, immunofluorescence, qRT-PCR and Western blotting. Immunofluorescence, qRT-PCR and Western blotting were also utilized to explore AdipoR1, APPL1, NF-κB and Wnt5a-Ror2 signalling molecules in this process. One-way ANOVA with Tukey's post hoc test was used to compare the data. RESULTS: AdipoAI reduced inflammation and bone destruction caused by peri-implantitis in diabetic rats, which were manifested by a reduction in F4/80-positive macrophage infiltration by 72%, the number of osteoclasts by 58% and the levels of cytokines (p < .05) in disease group. In vitro, 1 µM AdipoAI decreased the number of osteoclasts to 51%, inhibited F-actin ring formation and reduced the levels of related markers (p < .05). Mechanistically, AdipoAI activated AdipoR1/APPL1 and conversely suppressed the phosphorylation of IκB-α, nuclear translocation of P65 and the Wnt5a-Ror2 signalling pathway (p < .05). CONCLUSIONS: AdipoAI suppressed osteoclastogenesis in diabetes-associated peri-implantitis by inhibiting the NF-κB and Wnt5a-Ror2 pathways via the AdipoR1/APPL1 axis.

[Comparison of three methods for establishing rat peri-implantitis model].

OBJECTIVE: To compare the efficiency and effect of establishing rat peri-implantitis model by traditional cotton thread ligation and local injection of Porphyromonas gingivalis lipopolysaccharide (LPS) around the implant, as well as the combination of the two methods. METHODS: Left side maxillary first molars of 39 male SD rats were extracted, and titanium implants were implanted after four weeks of healing. After 4 weeks of implant osseointegration, 39 rats were randomly divided into 4 groups. Cotton thread ligation (n=12), local injection of LPS around the implant (n=12), and the two methods combined (n=12) were used to induce peri-implantitis, the rest 3 rats were untreated as control group. All procedures were conducted under 5% isoflurane inhalation anesthesia. The rats were sacrificed 2 weeks and 4 weeks after induction through carbon dioxide asphyxiation method. The maxilla of the rats in the test groups were collected and marginal bone loss was observed by micro-CT. The gingival tissues around the implants were collected for further real time quantitative PCR (RT-qPCR) analysis, specifically the expression of tumor necrosis factor-alpha (TNF-α) as well as interleukin-1ß (IL-1ß). The probing depth (PD), bleeding on probing (BOP) and gingival index (GI) of each rat in the experimental group were recorded before induction of inflammation and before death. RESULTS: After 4 weeks of implantation, the osseointegration of implants were confirmed. All the three test groups showed red and swollen gums, obvious marginal bone loss around implants. After 2 weeks and 4 weeks of inflammation induction, PD, GI and BOP of the three test groups increased compared with those before induction, but only BOP was statistically significant among the three test groups (P < 0.05). At the end of 2 weeks of inflammation induction, marginal bone loss was observed at each site in the cotton thread ligation group and the combined group. At each site, the bone resorption in the combined group was greater than that in the cotton thread ligation group, but the difference was not statistically significant (P > 0.05), bone resorption was observed at some sites of some implants in LPS local injection group. At the end of 4 weeks of inflammation induction, marginal bone loss was observed at all sites in each group. The marginal bone loss in the cotton thread ligation group and the combined group was greater than that in the LPS local injection group, and the difference was statistically significant (P < 0.05). At the end of 2 weeks and 4 weeks of induction, the expression of TNF-α and IL-1ß in the test groups were higher than those in the control group (P < 0.05). CONCLUSION: Compared with local injection of LPS around the implant, cotton thread ligature and the two methods combined can induce peri-implantitis in rats better and faster.

Detecting lymphadenopathy affected by peri-implantitis using diffusion-weighted magnetic resonance imaging.

PURPOSE: This study aimed to assess peri-implantitis-induced lymphadenopathy on diffusion-weighted imaging (DWI). METHODS: This retrospective study was conducted from October 2017 to March 2020 in patients with and without peri-implantitis who underwent magnetic resonance imaging (MRI). Patients in the peri-implantitis group had radiographically confirmed loss of alveolar bone > 2.0 mm and clinical findings such as bleeding on probing, suppuration of tissues surrounding the teeth, probing-pocket depth of > 4 mm, pain on implant function, and clinical implant mobility, whereas those without peri-implantitis had none of the abovementioned clinical findings. The Mann-Whitney U test was used to compare groups, using lymph node (LN) short-axis diameters and apparent diffusion coefficients (ADCs) as the criterion variables and presence or absence of peri-implantitis as the explanatory variable. Receiver operating characteristic (ROC) analysis was done to investigate the effectiveness of LN size and ADC use in detecting peri-implantitis-induced lymphadenopathy. Statistical significance was established at P < 0.05. RESULTS: There were 66 lymph nodes from 12 patients analyzed. The mean LN size and ADC were significantly higher in patients with peri-implantitis than in those without (P < 0.01). ROC curve analysis showed cut-off LN sizes of 4.78 and 4.84 mm and cut-off ADCs of 1.12 and 1.09 for lymphadenopathy affected by peri-implantitis corresponding to levels IB and II, respectively. CONCLUSIONS: Cervical lymphadenopathy may be an inflammatory finding associated with peri-implantitis.

Bone defect development in experimental canine peri-implantitis models: a systematic review.

PURPOSE: To provide a systematic overview of preclinical research regarding bone defect formation around different implant surfaces after ligature-induced peri-implantitis models in dogs. Two focused questions were formulated: 'How much bone loss can be expected after a certain time of ligature induced peri-implantitis?' and 'Do different implant types, dog breeds and study protocols differ in their extent of bone loss?' MATERIALS AND METHODS: A systematic literature search was conducted on four databases (MEDLINE, Web of Science, EMBASE and Scopus). Observations, which consisted of bone defects measured directly after ligature removal in canine models, were included and analysed. Two approaches were used to analyse the relatively heterogeneous studies that fulfilled the inclusion criteria. First, separate simple linear regressions were calculated for each study and implant surface, for which observations were available across multiple time points. Second, a linear mixed model was specified for the observations at 12 weeks after ligature initiation, and assessing the potential influencing factors on defect depth was explored using lasso regularisation. RESULTS: Thirty-six studies with a total of 1082 implants were included after. Bone loss was determined at different time points, either with clinical measurements radiographically or histologically. Different implant groups [e.g. turned, sand-blasted-acid-etched (SLA), titanium-plasma-sprayed (TPS) and other rough surfaces] were assessed and described in the studies. A mean incremental defect depth increase of 0.08 mm (SD: -0.01-0.28 mm) per week was observed. After 12 weeks, the defect depths ranged between 0.7 and 5 mm. Based on the current data set, implant surface could not be statistically identified as an essential factor in defect depth after 12 weeks of ligature-induced peri-implantitis. CONCLUSION: Expectable defect depth after a specific time of ligature-induced peri-implantitis can vary robustly. It is currently impossible to delineate apparent differences in bone loss around different implant surfaces.

The role of foreign body response in peri-implantitis: What is the evidence?

Historically, there has been broad consensus that osseointegration represents a homeostasis between a titanium dental implant and the surrounding bone, and that the crestal bone loss characteristic of peri-implantitis is a plaque-induced inflammatory process. However, this notion has been challenged over the past decade by proponents of a theory that considers osseointegration an inflammatory process characterized by a foreign body reaction and peri-implant bone loss as an exacerbation of this inflammatory response. A key difference in these two schools of thought is the perception of the relative importance of dental plaque in the pathogenesis of crestal bone loss around implants, with obvious implications for treatment. This review investigates the evidence for a persistent foreign body reaction at osseointegrated dental implants and its possible role in crestal bone loss characteristic of peri-implantitis. Further, the role of implant-related material release within the surrounding tissue, particularly titanium particles and corrosion by-products, in the establishment and progression in peri-implantitis is explored. While it is acknowledged that these issues require further investigation, the available evidence suggests that osseointegration is a state of homeostasis between the titanium implant and surrounding tissues, with little evidence that a persistent foreign body reaction is responsible for peri-implant bone loss after osseointegration is established. Further, there is a lack of evidence for a unidirectional causative role of corrosion by-products and titanium particles as possible non-plaque related factors in the etiology of peri-implantitis.

Does implant location influence the risk of peri-implantitis?

Peri-implantitis is characterized by nonreversible and progressive loss of supporting bone and is associated with bleeding and/or suppuration on probing. Peri-implant disease is considered as the main etiologic factor related to implant failure. Peri-implant disease has a pathogenesis similar to that of periodontal disease, both being triggered by an inflammatory response to the biofilm accumulation. Although the prevalence of peri-implantitis has been evaluated by several clinical studies with different follow-ups, there are currently little data on the impact of implant location and the prevalence of peri-implantitis. The aim of this review, therefore, was to summarize the evidence concerning the prevalence of peri-implantitis in relation to implant location and associated risk predictors. Even though most studies evaluating the prevalence of peri-implantitis in relation to implant location are cross-sectional or retrospective, they suggest that the occurrence of peri-implantitis is most prevalent in the anterior regions of the maxilla and mandible. Moreover, it seems that there is a higher prevalence of peri-implantitis in the maxilla than in the mandible.