Abstract Objective Peri‐implantitis has been attributed to a myriad of factors, including microleakage at the abutment‐implant interface. Implant abutment access channel sealing materials (IACSM) are readily used in implant dentistry, with little evidence on their effect on microleakage. This study aims to evaluate the effect of IACSM on the microbial composition in the implant access channel and the peri‐implant sulcus. Methods A total of n = 8 patients (64 implants) were included in this single‐blinded, randomized controlled trial, whereas four different materials (cotton, polytetrafluoroethylene [PTFE], synthetic foam, or polyvinyl siloxane [PVS]) were randomly placed as an IACSM. Following 6 months, microbial analysis was completed on the IACSM and samples from the peri‐implant sulci via PCR and high‐throughput sequencing. Bacterial samples on the IACSM and in the peri‐implant sulci were classified according to Socransky's microbial complexes. Results There was a preponderance of early colonizing bacteria within the IACSM, while the peri‐implant sulci were dominated by Orange complex bacteria. The proportion of Red and Orange complex members on the IACSM was significantly less than in the peri‐implant sulci. The proportion of Green, Yellow, and Blue complex members found on the IACSM was significantly greater than in the peri‐implant sulci. Atopobium , a diverse species not included in the microbial complexes, was frequently detected in the peri‐implant sulcus samples. Conclusions No detectable effects of IACSM on the microbial community in the peri‐implant sulcus or on the IACSM were identified. Variation of bacterial species was most dependent on the individual patient. No significant differences were found in the periodontal parameters between the different treatment groups.
ABSTRACT Maintenance of blood DC homeostasis is essential to preventing autoimmunity while controlling chronic infection. However, the ability of bacteremic pathogens to directly regulate blood DC homeostasis has not been defined. One such bacteremic pathogen, Porphyromonas gingivalis, is shown by our group to survive within mDCs under aerobic conditions and therein, metastasize from its oral mucosal niche. This is accompanied by expansion of the blood mDC pool in vivo, independently of canonical DC poietins. We presently know little of how this bacteremic pathogen causes blood DC expansion and the pathophysiological significance. This work shows that optimum differentiation of MoDCs from primary human monocytes, with or without GM-CSF/IL-4, is dependent on infection with P. gingivalis strains expressing the DC-SIGN ligand mfa-1. DC differentiation is lost when DC-SIGN is blocked with its ligand HIV gp120 or knocked out by siRNA gene silencing. Thus, we have identified a novel, noncanonical pathway of DC differentiation. We term these PDDCs and show that PDDCs are bona fide DCs, based on phenotype and phagocytic activity when immature and the ability to up-regulate accessory molecules and stimulate allo-CD4+ T cell proliferation when matured. The latter is dependent on the P. gingivalis strain used to initially “educate” PDDCs. Moreover, we show that P. gingivalis-infected, conventional MoDCs become resistant to apoptosis and inflammatory pyroptosis, as determined by levels of Annexin V and caspase-8, -3/7, and -1. Taken together, we provide new insights into how a relatively asymptomatic bacteremia may influence immune homeostasis and promote chronic inflammation.
Abstract An estimated 80 million U.S. adults have one or more types of cardiovascular diseases (CVD) with the total cost to the U.S. for 2009 estimated to be $475.3 billion. Atherosclerosis (ATH) is the single most important contributor to CVD; however, only 50% of ATH patients have currently identified risk factors. Chronic periodontitis (CP), a common inflammatory disease, is linked to an increased CVD risk. Dendritic cells (DCs) which infiltrate arterial walls and destabilize atherosclerotic plaques, have been implicated in CVD. While the source of atherogenic DCs is presently unclear, we propose that dermal DCs from peripheral inflamed sites, such as CP tissues are a source. We therefore designed a clinical study to elicit, quantitate and isolate DCs in the peripheral blood of otherwise healthy CP patients. Ten patients with CP were consented according to IRB standards and enrolled in the study. Peripheral blood collected at baseline and 24 hrs after mechanical debridement (MD) was used to identify and sort blood DCs. After PBMC separation, DCs were labeled with DC-SIGN-APC and BDCA-1-PE and quantitated by FACS analysis. We found that after MD there was a 5-6% increase in the numbers of blood DCs in this patient population. This increase in the blood may represent mobilization of DCs from bone marrow stores, as well as from CP tissues. We are presently analyzing the DC transcriptome of sorted DCs to identify markers of atherogenesis.
Tardive dyskinesia (TD) is an involuntary movement disorder of neurologic origin caused by the use of neuroleptic drugs known as dopamine receptor antagonists. The condition may adversely affect prosthodontic interventions and their possible merits. In this case history description, the rigor of scrupulous history-taking and clinical evaluation of patients with TD or neurologic disorders is emphasized. The successful prosthodontic management of a 74-year-old completely edentulous TD patient is presented, with the conclusion that a prosthodontic intervention may aid symptom reduction and contribute to improvement in a TD patient's quality of life.
Background: Glycogen storage diseases (GSDs) are genetic disorders that result from defects in the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types. It also manifests with impaired neutrophil chemotaxis and neutropenic episodes which results in severe destruction of the supporting dental tissues, namely the periodontium. Although GSD Type Ib cannot be cured, associated symptoms and debilitating oral manifestations of the disease can be managed through collaborative medical and dental care where early detection and intervention is of key importance. This objective of the case report was to describe a child with GSD Ib and its associated oral manifestations with microbial, immunological and histological appearances. Case Presentation: An eight-year-old Hispanic male with a history of GSD type Ib presented with extensive intraoral generalized inflammation of the gingiva, ulcerations and bleeding, and intraoral radiographic evidence of bone loss. Tannerella forsythia was readily identifiable from the biofilm samples. Peripheral blood neutrophils were isolated and a deficient host response was observed by impaired neutrophil migration. Histological evaluation of the soft and hard tissues of the periodontally affected primary teeth showed unaffected dentin and cementum. Conclusions: This case illustrates the association between GSD Ib and oral manifestations of the disease. A multi-disciplinary treatment approach was developed in order to establish healthy intraoral conditions for the patient. Review of the literature identified several cases describing GSD and its clinical and radiographic oral manifestations; however, none was identified where also microbial, immunological, and histological appearances were described.
ABSTRACT Several intracellular pathogens, including a key etiological agent of chronic periodontitis, Porphyromonas gingivalis , infect blood myeloid dendritic cells (mDCs). This infection results in pathogen dissemination to distant inflammatory sites (i.e., pathogen trafficking). The alteration in chemokine-chemokine receptor expression that contributes to this pathogen trafficking function, particularly toward sites of neovascularization in humans, is unclear. To investigate this, we utilized human monocyte-derived DCs (MoDCs) and primary endothelial cells in vitro , combined with ex vivo -isolated blood mDCs and serum from chronic periodontitis subjects and healthy controls. Our results, using conditional fimbria mutants of P. gingivalis , show that P. gingivalis infection of MoDCs induces an angiogenic migratory profile. This profile is enhanced by expression of DC-SIGN on MoDCs and minor mfa-1 fimbriae on P. gingivalis and is evidenced by robust upregulation of CXCR4, but not secondary lymphoid organ (SLO)-homing CCR7. This disruption of SLO-homing capacity in response to respective chemokines closely matches surface expression of CXCR4 and CCR7 and is consistent with directed MoDC migration through an endothelial monolayer. Ex vivo -isolated mDCs from the blood of chronic periodontitis subjects, but not healthy controls, expressed a similar migratory profile; moreover, sera from chronic periodontitis subjects expressed elevated levels of CXCL12. Overall, we conclude that P. gingivalis actively “commandeers” DCs by reprogramming the chemokine receptor profile, thus disrupting SLO homing, while driving migration toward inflammatory vascular sites.
Introduction: To the best of the authors’ knowledge, this is the first case report to describe the use of a perforated resorbable barrier membrane (PRBM) to enhance lateral bone augmentation for implant site development. Case Presentation: A 41‐year‐old female presented to the Advanced Specialty Education Program in Periodontics at Stony Brook University, Stony Brook, New York, for implant consultation regarding a missing maxillary right lateral incisor. The tooth had been lost as a result of trauma 10 years prior to presentation. Clinical examination and radiographs showed significant horizontal ridge deficiency (<5 mm) that supported a staged intervention. Horizontal bone augmentation was performed following guided bone regeneration principles using a mineralized mixed corticocancellous (70:30) allograft followed by a PRBM. A cone beam computed tomography scan was obtained before surgery and 8 months after treatment, from which volumetric width changes were quantified. A bone biopsy was obtained at the time of implant placement to measure new vital bone (NVB) formation, residual graft (RG) particles, and connective tissue (CT) formation. Dimensional width changes were assessed during reentry for implant placement. The lateral bone gain was 5.0 mm, clinically and radiographically. Histologically, the amount of NVB formation, RG particles, and CT infiltration was 38.1%, 38.9%, and 23.1%, respectively. Implant placement was uneventful, with no further need for bone augmentation. Conclusions: Previous studies using similar techniques and regenerative materials have shown an average of 3.5 mm of horizontal bone augmentation. The use of a PRBM appeared to significantly enhance lateral bone augmentation. An ongoing clinical trial is underway to confirm these results.
Abstract The low-grade oral infection chronic periodontitis (CP) has been implicated in coronary artery disease risk, but the mechanisms are unclear. In this study, a pathophysiological role for blood dendritic cells (DCs) in systemic dissemination of oral mucosal pathogens to atherosclerotic plaques was investigated in humans. The frequency and microbiome of CD19−BDCA-1+DC-SIGN+ blood myeloid DCs (mDCs) were analyzed in CP subjects with or without existing acute coronary syndrome and in healthy controls. FACS analysis revealed a significant increase in blood mDCs in the following order: healthy controls < CP < acute coronary syndrome/CP. Analysis of the blood mDC microbiome by 16S rDNA sequencing showed Porphyromonas gingivalis and other species, including (cultivable) Burkholderia cepacia. The mDC carriage rate with P. gingivalis correlated with oral carriage rate and with serologic exposure to P. gingivalis in CP subjects. Intervention (local debridement) to elicit a bacteremia increased the mDC carriage rate and frequency in vivo. In vitro studies established that P. gingivalis enhanced by 28% the differentiation of monocytes into immature mDCs; moreover, mDCs secreted high levels of matrix metalloproteinase-9 and upregulated C1q, heat shock protein 60, heat shock protein 70, CCR2, and CXCL16 transcripts in response to P. gingivalis in a fimbriae-dependent manner. Moreover, the survival of the anaerobe P. gingivalis under aerobic conditions was enhanced when within mDCs. Immunofluorescence analysis of oral mucosa and atherosclerotic plaques demonstrate infiltration with mDCs, colocalized with P. gingivalis. Our results suggest a role for blood mDCs in harboring and disseminating pathogens from oral mucosa to atherosclerosis plaques, which may provide key signals for mDC differentiation and atherogenic conversion.
Introduction: Asymptomatic displacement of dental implants into the maxillary sinus after a transcrestal sinus augmentation is a rare complication that can occur when there is poor bone quality and minimal residual bone height. Patient compliance with postoperative appointments and failure to comply with denture‐wearing instructions are critical contributing factors. To the best of the authors’ knowledge, no cases of implant dislodgement attributable to a removable prosthesis have been reported in the literature, although some studies have suggested that improper occlusal forces can cause a long‐standing implant to develop peri‐implantitis and subsequent displacement of an implant into the sinus cavity. Case Presentation: A 71‐year‐old female presented 6 months after undergoing transcrestal sinus lift and implant surgery that involved a modified Summers technique using mineralized solvent‐dehydrated cancellous bone allograft and placement of six maxillary implants. A displaced dental implant was retrieved from the right maxillary sinus, which had an intact Schneiderian membrane. The patient was asymptomatic and infection free. The displaced implant was accessed and retrieved via a lateral window sinus technique. No clinical signs of sinus infection were evident, and there were no additional complications during the 2‐year follow‐up period. Conclusion: This case report demonstrates a technique for the retrieval of implants that have been dislodged and migrated into the maxillary sinus cavity caused by an ill‐fitting denture and improper masticatory forces.
