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Aim: Our previous study revealed that the C-C motif chemokine receptor 2 (CCR2) is a promising target for periodontitis prevention and treatment. However, CCR2 is a receptor with multiple C-C motif chemokine ligands (CCLs), including CCL2, CCL7, CCL8, CCL13 and CCL16, and which of these ligands plays a key role in periodontitis remains unclear. The aim of the present study was to explore the key functional ligand of CCR2 in periodontitis and to evaluate the potential of the functional ligand as a therapeutic target for periodontitis., Materials and Methods: The expression levels and clinical relevance of CCR2, CCL2, CCL7, CCL8, CCL13 and CCL16 were studied using human samples. The role of CCL2 in periodontitis was evaluated by using CCL2 knockout mice and overexpressing CCL2 in the periodontium. The effect of local administration of bindarit in periodontitis was evaluated by preventive and therapeutic medication in a mouse periodontitis model. Microcomputed tomography, haematoxylin and eosin staining, tartrate-resistant acid phosphatase staining, real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, bead-based immunoassays and flow cytometry were used for histomorphology, molecular biology and cytology analysis., Results: Among different ligands of CCR2, only CCL2 was significantly up-regulated in periodontitis gingival tissues and was positively correlated with the severity of periodontitis. Mice lacking CCL2 showed milder inflammation and less bone resorption than wild-type mice, which was accompanied by a reduction in monocyte/macrophage recruitment. Adeno-associated virus-2 vectors overexpressing CCL2 in Ccl2 -/- mice gingiva reversed the attenuation of periodontitis in a CCR2-dependent manner. In ligation-induced experimental periodontitis, preventive or therapeutic administration of bindarit, a CCL2 synthesis inhibitor, significantly inhibited the production of CCL2, decreased the osteoclast number and bone loss and reduced the expression levels of proinflammatory cytokines TNF-α, IL-6 and IL-1β., Conclusions: CCL2 is a pivotal chemokine that binds to CCR2 during the progression of periodontitis, and targeting CCL2 may be a feasible option for controlling periodontitis., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Objectives: This study aimed to investigate the relationship between microbial communities and the severity of peri-implant mucosal bleeding in peri-implant mucositis., Materials and Methods: Submucosal plaque samples were collected from 54 implants divided into the healthy implant (HI) group, peri-implant mucositis (PM) group, and peri-implantitis (PI) group. Sequencing of 16S rRNA was performed using the Illumina MiSeq platform. Alpha diversity (i.e., Shannon and Chao index) and beta diversity were used to measure microbial diversity within and between microbial communities, respectively. Differences in microbial taxa between groups were assessed via linear discriminate analysis effect size. Correlation between the modified sulcus bleeding index (mSBI) and microbial dysbiosis index (MDI) was examined using Spearman correlation analysis and linear models., Results: The submucosal bacterial richness (Chao index) was positively correlated with the mean mSBI in the PM group. As the mean mSBI increased in the PM group, the beta diversity became closer to that of the PI group. In the PM group, the abundances of 47 genera were significantly correlated with the mean mSBI, and the MDI was positively associated with the mean mSBI. Fourteen of the forty-seven genera were discriminative taxa between the HI and PI groups, and the abundances of these biomarkers became closer to those in the PI group in the progression of peri-implant disease., Conclusions: A higher mSBI value corresponded to a higher risk of microbial dysbiosis in peri-implant mucositis. The biomarkers identified may be useful for monitoring the progression of peri-implant disease., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Changes in alveolar bone dimension after tooth extraction may affect placement of the subsequent implant, resulting in ridge deficiency that can adversely impact long-term implant stability or aesthetics. Alveolar ridge preservation (ARP) was effective in reducing the amount of ridge resorption following tooth extraction. There is sparse evidence regarding the benefit of ARP at periodontally compromised molar extraction sockets. This study will be a randomized trial to assess the soft tissue contour, radiographical, and histological changes of ARP at molar extraction sites in order to compare severe periodontitis cases with natural healing results and determine the most beneficial and least traumatic clinical treatment for such patients., Methods: This research is designed as a two-group parallel randomized controlled trial. The total number of tooth extraction sites will be 70 after calculation with power analysis. Teeth will be randomly assigned to two groups with the test group conducting ridge preservation and the control group healing naturally. Periodontal examination, cone beam-computed tomography (CBCT) data, and stereolithographic (STL) files obtained by intraoral scanning will be collected through the follow-up period, and bone biopsy samples would be obtained during implant surgery. The primary outcomes are the vertical and horizontal change of alveolar ridge measured on CBCT images, soft tissue contour changes evaluated by superimposing the digital impressions, alterations of mucosa thickness (as measured by superimposing the CBCT data and STL files), histological features of implant sites and periodontal parameter changes. The secondary outcomes are patient-reported post-operative reaction and conditions of simultaneous bone graft or sinus lifting procedures during implantation., Discussion: This study will provide information about hard and soft tissue dimension changes and histomorphology evaluation following ARP and natural healing in periodontally compromised molar sites, which may contribute to complement the missing information of ARP at periodontally compromised molar extraction sockets., Trial Registration: Chinese Clinical Trial Register (ChiCTR) ChiCTR2200056335. Registered on February 4, 2022, Version 1.0., (© 2022. The Author(s).)

Aim: CCR2 plays important roles in many inflammatory and bone metabolic diseases, but its specific role in periodontitis is unknown. In the present study, we aimed to explore the role of CCR2 in the progression of periodontitis and evaluate the effect of cenicriviroc (CVC) on periodontitis., Materials and Methods: The expression of CCR2 was studied in patients with periodontitis and in ligation-induced murine model of periodontitis. The role of CCR2 in promoting inflammation and bone resorption in periodontitis was evaluated in Ccr2 -/- mice and wild-type mice. The effect of CVC in the prevention and treatment of periodontitis was evaluated by systemic and local medication. Microcomputed tomography, haematoxylin and eosin staining, tartrate-resistant acid phosphatase staining, quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and flow cytometry were used for histomorphology, molecular biology, and cytology analysis, respectively., Results: In this study, we demonstrated that CCR2 was highly expressed in human and murine periodontitis and that CCR2 deficiency was associated with decreased inflammatory monocyte and macrophage infiltration and inflammatory mediators, osteoclast number and alveolar bone resorption. Prevention and treatment with CVC significantly reduced the severity of periodontitis, regardless of whether it was administered systemically or locally., Conclusions: CCR2 plays an important role in the development and progression of periodontitis, and CVC is a potential drug for the prevention and treatment of periodontitis., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Objectives: To assess alveolar bone changes and treatment modality alterations after ridge preservation on maxillary molar extraction sockets with severe periodontitis, compared to natural healing., Material and Methods: Thirty-six maxillary infected-molar teeth either receiving ridge preservation (RG group) or undergoing natural healing (NT group) were investigated. Cone-beam computed tomography (CBCT) scanning was performed immediately after surgery (the baseline) and repeated 6 months later to measure the linear and volumetric changes of the sockets., Results: Based on radiographic measurements, alveolar bone width decreased by 1.58 ± 4.61 mm in the NT group but increased by 3.74 ± 4.17 mm in the RG group (p < 0.05). Significant increases in ridge height at the center of both the NT (7.54 ± 4.54 mm) and RG (9.20 ± 3.26 mm) groups were observed. Mean sinus pneumatization was 0.19 ± 0.45 mm in the RG group and 0.59 ± 0.63 mm in the NT group (p < 0.05). The relative increase in total ridge volume was 8.0% and 35.5% in the NT and RG group, respectively (p < 0.05). Implant placement with additional sinus augmentation procedure was performed in 16.7% of the RG group cases, whereas 50% in the NT group cases., Conclusions: Ridge preservation in the maxillary molar extraction sockets with severe periodontitis can improve alveolar ridge dimensions and decrease the necessity of advanced regenerative procedures at implant placement compared to natural healing., Clinical Relevance: Ridge preservation on maxillary molar extraction sockets with severe periodontitis maintained the vertical bone height more efficiently and resulted in less need for sinus augmentation procedures at 6 months compared to natural healing., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: Information regarding the reaction of bone augmentation in terms to sinus mucosa thickness of periodontally compromised molar extraction sites is limited. This retrospective study aimed to analyze the effect of ridge preservation procedures following the extraction of molars with severe periodontitis on the healing pattern of adjacent maxillary sinus mucosal membranes., Methods: Thirty-one periodontally compromised maxillary molar teeth either receiving ridge preservation (test group, n = 20) or undergoing spontaneous healing (control group, n = 11) were investigated. Cone-beam computed tomography (CBCT) scanning was performed before the extraction procedure and repeated 6 months later. The mucosa thickness (MT) of the adjacent periodontally compromised molar tooth was measured from CBCT images before tooth extraction and after 6 months of healing at nine assigned measurement points. The data were analyzed at α = 0.05., Results: The prevalence of pre-extraction maxillary sinus mucosal thickening was 60.0% and 63.6% in the test and control groups, respectively. The average MT of the thickened sinus mucosa before tooth extraction was 3.78 ± 2.36 mm in the test group and 4.63 ± 3.20 mm in the control group (P = 0.063). The mean mucosal thickening reductions in the thickened MT subjects after 6 months of healing were 2.20 ± 2.05 mm (test group) and 2.64 ± 2.70 mm (control group), P = 0.289. The differences of MT between the time prior to extraction and after 6 months of healing were statistically significant within both groups (P < 0.05)., Conclusions: Following extraction of molars with severe periodontitis, a reduction in swelling of the Schneiderian membrane has been observed regardless of the addition of a DBBM socket graft. However, a mucosal thickness > 2 mm was still frequently observed.

The efficacy of the socket preservation procedure using deproteinized bovine bone mineral, bioabsorbable collagen membrane, and collagen sponge on molar extraction sites with severe periodontitis was assessed at 6 postoperative months, before implant placement. Results revealed excellent soft tissue healing without loss of keratinized tissue and no statistically significant differences in socket marginal bone changes in 20 molar extraction sockets. High levels of primary implant stability were recorded. Socket preservation using a minimally invasive surgical technique provides good soft and hard tissue healing as well as anticipated stability of implant placement at sites of extracted molars with severe periodontitis.

Aim: To investigate the role of platelets during the development of ligature-induced experimental periodontitis in mice., Materials and Methods: Experimental periodontitis was induced by placement of sterilized 5-0 cotton ligatures around the maxillary and mandibular second molars of C57BL/6 wild-type mice. Flow cytometry was used to analyse platelet activation and platelet-leucocyte aggregate formation, and histologic analysis was used to evaluate inflammation and localization of platelets and leucocytes in periodontal tissues during the development of experimental periodontitis and in experimental periodontitis with and without antiplatelet drug treatment., Results: Experimental periodontitis induced platelet activation and platelet-leucocyte interaction. Platelets and leucocytes gradually infiltrated in inflammatory gingival tissues during the development of experimental periodontitis. The inhibition of platelet activation via drug therapy led to significant inhibition of leucocyte migration and marked reduction in periodontal inflammation., Conclusion: This study revealed that platelets are critical for inflammation and tissue injury in periodontitis and serve as mediators of inflammation in periodontal tissue., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Objective: Ferritin, an iron-binding protein, is ubiquitous and highly conserved; it plays a crucial role in inflammation, which is the main symptom of periodontitis. Full-length cDNA library analyses have demonstrated abundant expression of ferritin in human periodontal ligament. The aims of the present study were to explore how ferritin is regulated by local inflammation, and to investigate its functions and mechanisms of action in the process of periodontitis., Methods: Human gingival tissues were collected from periodontitis patients and healthy individuals. Experimental periodontitis was induced by ligature of second molars in mice. The expression of ferritin light polypeptide (FTL) and ferritin heavy polypeptide (FTH) were assessed by immunohistochemistry. Meanwhile, after stimulating human periodontal ligament cells (HPDLCs) with P. gingivalis -lipopolysaccharide (LPS), interleukin (IL)-6, and tumor necrosis factor-α (TNF-α), the expression of FTH and FTL were measured. Then, IL-6 and IL-8 were measured after incubation with different concentrations of apoferritin (iron-free ferritin) and several intracellular signaling pathway inhibitors, or after knockdown of the transferrin receptor., Results: Both FTH and FTL were substantially higher in inflamed periodontal tissues than in healthy tissues. The location of the elevated expression correlated well with the extent of inflammatory infiltration. Moreover, expression of FTH and FTL were enhanced after stimulation with P. gingivalis -LPS, IL-6, TNF-α. Apoferritin induced the production of IL-6 and IL-8 in a dose-dependent manner partly through binding to the transferrin receptor and activating ERK/P38 signaling pathways in HPDLCs., Conclusions: Ferritin is up-regulated by inflammation and exhibits cytokine-like activity in HPDLCs inducing a signaling cascade that promotes expression of pro-inflammatory cytokines associated with periodontitis., (© 2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.)

Background: Studies of the extracted infected-molar ridge preservation are limited., Purpose: To compare alterations of hard and soft tissue in infected-molar sockets receiving ridge preservation compared with natural healing., Materials and Methods: Thirty-five infected-molar extraction sites either preserving with Bio-Gide membrane covered the Bio-Oss material or receiving natural healing procedure as controls. The soft tissue profile was evaluated before tooth extraction and after 6-month healing. Cone-beam computed tomography scans were taken immediately and 6 months after extraction. Vertical and horizontal bone changes were assessed radiographically. Data were analyzed with Mann-Whitney U test and α = 0.05., Results: No significant differences in soft tissue and vertical bone changes in the medium region of the sockets were found (P > .05). Buccal bone changes in the mesial and distal sites in the test group were significantly lower than the control group (P < .05). Ridge width increased from 0.21mm to 5.30mm at 1mm apical from the crest in the test and reduced from 0.12 mm to 1.00 mm in the control groups., Conclusion: Ridge preservation at periodontally compromised molar extraction sites might compensate for ridge width and buccal bone resorption that occurs with natural healing alone., (© 2018 Wiley Periodicals, Inc.)

Aim: This study aimed to assess hard and soft tissue contour changes following micro crestal flap‐alveolar ridge preservation (MCF‐ARP) and natural healing (NH) in periodontally compromised molar extraction sites and to analyse the feasibility and need for bone augmentation during implant therapy. Materials and Methods: Fifty‐six patients with 70 sites were randomized into two groups at the site level (35 sites from 31 patients in the test group and 35 sites from 29 patients in the control group). Among whom, four patients contributed one tooth to the control group and one tooth to the test group. Hard tissue indicators were measured using cone beam computed tomography performed before tooth extraction and 6 months after surgery. Soft tissue contour changes were assessed using intraoral scanning performed before and immediately after surgery and also 2 weeks and 1, 3 and 6 months after surgery. Results: Six months after surgery, the MCF‐ARP group showed less resorption in buccal bone height (p =.032) and greater augmentation in central bone height (p =.001) and ridge width (p =.009). The mean, vertical and horizontal collapse of buccal soft tissue contour in the MCF‐ARP group were 0.95 mm (p =.010), 0.61 mm (p =.019) and 0.56 mm (p =.013) less than that in the NH group, respectively. There were significantly (p =.007) fewer sites in the MCF‐ARP group than in the NH group (0% vs. 26.7%) for staged bone augmentation and more sites that could be treated with simple implant procedure in the MCF‐ARP group than in the NH group (71.9% vs. 56.6%). Conclusions: Compared with NH, MCF‐ARP reduced bone resorption in periodontally compromised molar extraction sites and maintained the buccal soft tissue contour. MCF‐ARP reduces the need for complex bone augmentation procedures in implant therapy. Trial registration: Chinese Clinical Trial Register (ChiCTR) ChiCTR2200056335. Registered on 4 February 2022, Version 1.0. [ABSTRACT FROM AUTHOR]

Aim: CCR2 (C‐C chemokine receptor type 2) plays a crucial role in inflammatory and bone metabolic diseases; however, its role in peri‐implantitis remains unclear. This study aimed to explore whether CCR2 contributes to peri‐implantitis and the treatment effects of cenicriviroc (CVC) on peri‐implant inflammation and bone resorption. Materials and Methods: The expression of CCR2 was studied using clinical tissue analysis and an in vivo peri‐implantitis model. The role of CCR2 in promoting inflammation and bone resorption in peri‐implantitis was evaluated in Ccr2−/− mice and wild‐type mice. The effect of CVC on peri‐implantitis was evaluated using systemic and local dosage forms. Results: Human peri‐implantitis tissues showed increased CCR2 and CCL2 levels, which were positively correlated with bone loss around the implants. Knocking out Ccr2 in an experimental model of peri‐implantitis resulted in decreased monocyte and macrophage infiltration, reduced pro‐inflammatory cytokine generation and impaired osteoclast activity, leading to reduced inflammation and bone loss around the implants. Treatment with CVC ameliorated bone loss in experimental peri‐implantitis. Conclusions: CCR2 may be a potential target for peri‐implantitis treatment by harnessing the immune‐inflammatory response to modulate the local inflammation and osteoclast activity. [ABSTRACT FROM AUTHOR]

aimed to determine whether and to what extent there are transcriptional differences between periodontitis and peri-implantitis in the same susceptible host. Background: As an immune-mediated inflammatory disease resulting in aggressive bone resorption around dental implants, peri-implantitis constitutes a major threat to dental implants' long-term success. Compared to periodontitis, its etiological molecular mechanism remains elusive. Currently, there are few investigations on these two diseases at the transcriptional level within the same basal environment. Methods: Ligature-induced peri-implantitis and periodontitis were generated in the same mice. Gingival tissues of healthy, periodontitis, and peri-implantitis sites from the same oral cavity were collected and used for RNA sequencing. Differentially expressed genes (DEGs) were screened between periodontitis/peri-implantitis and healthy sites. Enrichment analysis of DEGs was performed. The comprehensive immune landscape was annotated by seq-ImmuCC. Hub genes from peri-implantitis-specific DEGs were filtered using the STRING database and Cytoscape. Validation of the selected hub genes was performed on the GEO106090 dataset (gingival tissues from six periodontitis patients, six peri-implantitis patients, and six healthy controls). Results: The results indicated that peri-implantitis and periodontitis exhibited significantly distinct transcriptional signatures, with the complement and coagulation cascade pathways and osteoclast differentiation predominating in peri-implantitis mucosa. Compared with periodontitis, peri-implantitis sites exhibited elevated macrophage proportions and relatively enriched macrophage activation and bone loss. Hub genes were selected, and IL1B, CCL3, and CLEC4E were significantly highly expressed in human peri-implantitis mucosa. Conclusion: The study suggests that the interplay between macrophages and bone resorption seems to be more robust than in periodontitis. IL1B, CCL3, and CLEC4E may be considered promising therapeutic targets for peri-implantitis. These critical biological processes and identified genes may contribute to the etiology of peri-implantitis, which is unique from periodontitis. This work may make way for deeper exploration and contribute significantly to the treatment and prevention of peri-implantitis. [ABSTRACT FROM AUTHOR]

Background: The information of the association between residual alveolar bone height and mucosal thickening is sparse. This study aimed to explore the effect of maxillary molar periodontal status on sinus mucosal thickening using cone-beam computed tomography (CBCT).Methods: One hundred ninety-four CBCT images were evaluated for the following parameters: age, sex, alveolar bone loss, maximum mucosal thickness (maxMT), minimum residual alveolar bone height (minRABH), and vertical infrabony pockets. The presence of mucosal thickening (maxMT > 2 mm) of the maxillary sinus was recorded. The parameters that could influence the dimensions of the maxillary sinus membrane were assessed. The data were analyzed using logistic regression, and multivariate linear regression with the significant level at α = 0.05.Results: Mucosal thickening was present in 32% of the analyzed CBCT images and increased in frequency as the periodontal status of the corresponding molar progressed from mild (2.6%) to moderate (14.9%) to severe (75.5%). Mucosal thickness was significantly increased in cases of moderate (odds ratio = 5.73, P < 0.05) and severe (odds ratio = 82.06, P < 0.001) alveolar bone loss. Multivariate linear regression revealed that alveolar bone loss and minRABH had a statistically significant influence on maxMT (P < 0.05).Conclusions: Alveolar bone loss and minRABH were significantly associated with mucosal thickening of the maxillary sinus. [ABSTRACT FROM AUTHOR]