Impact of surface chemical treatment in surgical regenerative treatment of ligature-induced peri-implantitis: A canine study.

BACKGROUND: Implant surface decontamination is a critical step in peri-implantitis treatment. The aim of this study was to assess the effect chemotherapeutic agents have on reosseointegration after treatment on ligature-inducted peri-implantitis. METHODS: Six male canines had 36 implants placed and ligatures were placed around them for 28 weeks to establish peri-implantitis. The peri-implant defects were randomly treated by 1 of 3 methods: 0.12% chlorhexidine (CHX test group), 1.5% sodium hypochlorite (NaOCl test group), or saline (Control group). Sites treated with NaOCl and CHX were grafted with autogenous bone, and all sites then either received a collagen membrane or not. Histology sections were obtained at 6 months postsurgery to assess percentage of reosseointegration. RESULTS: Thirty-five implants were analyzed (CHX: 13; NaOCl: 14; Control:8). NaOCl-treated sites demonstrated reosseointegration with direct bone-to-implant-contact on the previously contaminated surfaces (42% mean reosseointegration), which was significantly higher than Controls (p < 0.05). Correspondingly, clinical improvement was noted with a significant reduction in probing depth from 5.50 ± 1.24 mm at baseline to 4.46 ± 1.70 mm at 6-months postsurgery (p = 0.006). CHX-treated sites demonstrated a nonsignificant reosseointegration of 26% (p > 0.05); however, in the majority of cases, the new bone growth was at a distance from the implant surface without contact. Probing depths did not improve in the CHX group. The use of membrane did not influence reosseointegration or probing depths (all p > 0.05). CONCLUSION: Titanium implants with peri-implantitis have the capacity to reosseointegrate following regenerative surgery. However, treatment response is contingent upon the chemotherapeutic agent selection. Additional chemical treatment with 1.5% NaOCl lead to the most favorable results in terms of changes in defect depth and percentage of reosseointegration as compared to CHX, which may hinder reosseointegration.

Palatal Augmentation Technique: A Predictable Method to Increase the Palatal Connective Tissue at Donor Sites- A Consecutive Case Series.

The palatal masticatory mucosa between the canine and first molar is the main source of connective tissue graft (CTG) for use in periodontal plastic surgery. The purpose of this study was to evaluate the palatal augmentation technique (PAT) to increase the palatal connective tissue donor area using a collagen sponge inserted between the palatal flap and bone. The 26 patients enrolled in this study were referred for root coverage and ridge augmentation procedures. All patients lacked adequate donor palatal tissue thickness. The PAT uses a full-thickness flap and insertion of a sterile lyophilized bovine collagen sponge between the flap and bone. The palatal thickness was clinically assessed before and after collagen sponge insertion. A manual probe was inserted in the mucosal surface perpendicular to the long axis of each tooth approximately 6 mm from the gingival margin. Probing depth (PD) and recession (REC) were also recorded. Treatment with PAT resulted in a statistically significant increase in the palatal thickness. The overall mean increase was from 2.03 mm before surgery to 3.57 mm after surgery, with no major alterations in PD and REC. Healing proceeded uneventfully and occurred by primary intention. PAT appeared to be a predictable procedure to create connective tissue donor graft in deficient areas and had uneventful postoperative healing.

Innate immune receptor expression in peri-implant tissues of patients with different susceptibility to periodontal diseases.

BACKGROUND: Although inflammation mediates the pathogenesis of periodontal diseases, the effects of innate immune responses on implant therapies have not been evaluated. Innate immune receptors, including toll-like-receptors (TLRs) and the receptor for advanced glycated end-products (RAGE), are upregulated within inflamed gingiva and are responsible for initiation of detrimental host responses. The aim of this study is to compare the expression of TLR2, TLR4, and RAGE in gingival tissues from participants susceptible to periodontitis and participants not susceptible to periodontitis before and after implant therapy. METHODS: Periodontally healthy participants received implant therapy for non-periodontal edentulism. Participants susceptible to periodontitis were diagnosed with chronic periodontitis prior to implant therapy. Gingival biopsies were collected from edentulous ridges before implant installation and from peri-implant mucosa 2 months after treatment. Histology, real-time PCR, and Western blot were used to evaluate levels of inflammatory infiltrate, TLR2, TLR4, and RAGE expression. RESULTS: Before implant therapy, elevated levels of RAGE were detected in gingival tissues from participants susceptible to periodontitis when compared to those from participants with healthy periodontiums, whereas no differences in the expression of TLR2 or TLR4 were detected. After implant therapy, there was an upregulation of RAGE and TLR4 levels that coincided with a downregulation of TLR2 levels in biopsies from participants susceptible to periodontitis. Levels of RAGE and TLR4 remained unchanged in biopsies from participants with healthy periodontiums, whereas TLR2 levels were significantly upregulated. Histologically, post-implant biopsies from participants susceptible to periodontitis displayed higher levels of inflammatory infiltrate. CONCLUSION: Elevated levels of inflammatory potential were found after implant therapy in participants susceptible to periodontitis.

Porphyromonas gingivalis-nucleoside-diphosphate-kinase inhibits ATP-induced reactive-oxygen-species via P2X7 receptor/NADPH-oxidase signalling and contributes to persistence.

Ligation of P2X7 receptors with a 'danger signal', extracellular ATP (eATP), has recently been shown to result in production of intracellular reactive-oxygen-species (ROS) in macrophages. We show that primary gingival epithelial cells (GECs) produce sustained, robust cellular ROS upon stimulation by eATP. The induction of ROS was mediated by P2X7 receptor signalling coupled with NADPH-oxidase activation, as determined by pharmacological inhibition and RNA interference. Furthermore, Porphyromonas gingivalis, an oral opportunistic pathogen, upregulated the antioxidant glutathione response, modulated eATP-induced cytosolic and mitochondrial ROS generated through P2X7 /NADPH-oxidase interactome, and subsequently blocked oxidative stress in GECs via temporal secretion of a P. gingivalis effector, nucleoside-diphosphate-kinase (Ndk). An ndk-deficient P. gingivalis mutant lacked the ability to inhibit ROS production and persist intracellularly following eATP stimulation. Treatment with recombinant Ndk significantly diminished eATP-evoked ROS production. P. gingivalis infection elicited a strong, time-dependent increase in anti-oxidativemitochondrial UCP2 levels, whereas ndk-deficient mutant did not cause any change. The results reveal a novel signalling cascade that is tightly coupled with eATP signalling and ROS regulation. Ndk by P. gingivalis counteracts these antimicrobial signalling activities by secreting Ndk, thus contributing to successful persistence of the pathogen.

The role of hyperglycemia in mechanisms of exacerbated inflammatory responses within the oral cavity.

Immune modulating factors are necessary for pathogen clearance, but also contribute to host tissues damage, as those seen in periodontal diseases. Many of these responses can be exacerbated by host conditions including type 2 diabetes [T2D], where toll-like receptor 4 [TLR4] and the receptor for advanced glycated end products [RAGE] play a significant role. Here we investigate causality associated with the increase in inflammatory markers observed in periodontally diseased patients with T2D using multi-variant correlation analysis. Inflammation associated with periodontal diseases, characterized by elevated pro-inflammatory cytokines, innate immune receptor expression, and cellular infiltrate was exacerbated in patients with T2D. In addition, a feed forward loop regulated by poor glycemic control was associated with a loss of mucosal barrier integrity and accumulation of innate immune receptor ligands resulting in an exacerbation of ongoing inflammation, where RAGE and TLR4 cooperated to induce responses in oral epithelial cells, which were exacerbated by hyperglycemia.

Crestal bone changes around implants with reduced abutment diameter placed non-submerged and at subcrestal positions: a 1-year radiographic evaluation.

BACKGROUND: There is limited information about two-part implants placed in subcrestal positions. The aim of this study is to retrospectively evaluate the 1-year outcome of implants placed non-submerged and in a subcrestal position. METHODS: Records of 50 consecutive partially edentulous patients restored with dental implants were reviewed. For each implant, radiographs from the surgical appointment were compared to those from the 1-year follow-up visit and evaluated regarding: 1) the degree of subcrestal positioning of the implant, 2) changes of marginal hard tissue height over time, and 3) if the marginal hard tissue could be detected on the implant platform at the follow-up visit. RESULTS: The overall survival rate from baseline to the last recorded follow-up visit was 100%. At the surgery, the implants were placed, on average, 1.37 mm (mesial) and 1.28 mm (distal) subcrestally. The mean marginal loss of hard tissues was 0.11 +/- 0.30 mm. There were no statistical significant differences regarding the loss of marginal hard tissues between mesial and distal surfaces or the maxilla versus the mandible. There was no statistical significant correlation regarding the degree of subcrestal implant position and loss of marginal mineralized hard tissue (r = 0.15; P >0.05). The mineralized hard tissue on the implant shoulder was found in 69% of the implants at the 1-year follow-up visit. CONCLUSIONS: The present study reported a minimal loss of mineralized hard tissue around dental implants placed non-submerged and at subcrestal positions. In addition, these implants had hard tissue healing that extended onto the implant shoulders on most of the observed implants.

ATP-dependent activation of an inflammasome in primary gingival epithelial cells infected by Porphyromonas gingivalis.

Production of IL-1beta typically requires two-separate signals. The first signal, from a pathogen-associated molecular pattern, promotes intracellular production of immature cytokine. The second signal, derived from a danger signal such as extracellular ATP, results in assembly of an inflammasome, activation of caspase-1 and secretion of mature cytokine. The inflammasome component, Nalp3, plays a non-redundant role in caspase-1 activation in response to ATP binding to P2X(7) in macrophages. Gingival epithelial cells (GECs) are an important component of the innate-immune response to periodontal bacteria. We had shown that GECs express a functional P2X(7) receptor, but the ability of GECs to secrete IL-1beta during infection remained unknown. We find that GECs express a functional Nalp3 inflammasome. Treatment of GECs with LPS or infection with the periodontal pathogen, Porphyromonas gingivalis, induced expression of the il-1beta gene and intracellular accumulation of IL-1beta protein. However, IL-1beta was not secreted unless LPS-treated or infected cells were subsequently stimulated with ATP. Conversely, caspase-1 is activated in GECs following ATP treatment but not P. gingivalis infection. Furthermore, depletion of Nalp3 by siRNA abrogated the ability of ATP to induce IL-1beta secretion in infected cells. The Nalp3 inflammasome is therefore likely to be an important mediator of the inflammatory response in gingival epithelium.