Efficacy of Antibiotics Used as an Adjunct in the Treatment of Peri-implant Mucositis and Peri-implantitis: A Systematic Review and Meta-analysis.

PURPOSE: This systematic review aimed to assess the clinical efficacy of antibiotics when used as an adjunct in treating peri-implant diseases. MATERIALS AND METHODS: A systematic search of papers published between January 1980 and March 2020 was conducted. Randomized clinical trials with at least 10 patients who had peri-implant diseases, treated with or without adjunctive antibiotics in combination with surgical or nonsurgical therapies, and with a minimum of at least 3 months of follow-up were included. Meta-analyses were conducted to analyze weighted mean differences in probing depth reduction, radiographic bone level gain, and odds ratio of treatment success. RESULTS: From the 856 articles identified, 10 articles met the inclusion criteria and were selected. Of these, 7 articles were used for the meta-analysis. The adjunctive use of antibiotics in the treatment of peri-implant diseases yielded significantly greater probing depth reduction (weighted mean differences = 0.56 mm at 3 months, P = .001; 0.77 mm at 6 months, P < .00001; 0.92 mm at 12 months, P < .00001), radiographic bone level gain (weighted mean differences = 0.64 mm, P = .03), and treatment success (odds ratio = 1.74, P = .04) compared to the same treatment without antibiotics. CONCLUSION: Based on the existing evidence, the use of adjunctive antibiotics to treat peri-implant diseases, especially peri-implantitis, provided potential benefits in clinical outcomes for up to 12 months posttherapy.

CAD/CAM and 3D-Printing Applications for Alveolar Ridge Augmentation.

PURPOSE OF REVIEW: CAD/CAM and 3D-printing are emerging manufacturing technologies in dentistry. In the field of alveolar ridge augmentation, graft customization utilizing these technologies can result in significant reduction of surgical time. A review of the literature on materials, techniques and applications of CAD/CAM and 3D-printing available for alveolar ridge augmentation was performed. RECENT FINDINGS: CAD/CAM applications for milling of customized block grafts of allogeneic, xenogeneic, and alloplastic origins have been reported, and currently only limited products are commercially available. 3D-printing applications are limited to alloplastic graft materials and containment shells, and have been mostly used in animal studies for optimizing biomaterials' properties. SUMMARY: While current data support the potential use of CAD/CAM and 3D-printing for graft customization for alveolar ridge augmentation procedures, additional research is needed on predictability and long-term stability of the grafted sites.

Effects of Conventional Synthetic Disease-Modifying Antirheumatic Drugs on Response to Periodontal Treatment in Patients with Rheumatoid Arthritis.

Rheumatoid arthritis (RA) and periodontitis are common chronic inflammatory diseases and periodontitis is known to be more common and more severe in patients with RA. Based on a paucity of studies about the relationship between common conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) and periodontitis, this prospective study aimed to evaluate the adjunctive effect of csDMARDs on response to nonsurgical periodontal treatment in patients with RA. Thirty-two patients with RA (RA group) and 32 systemically healthy patients (control group) with periodontitis were included in this study. The RA group patients were treated with csDMARDs, such as methotrexate, hydroxychloroquine, and sulfasalazine. Conventional nonsurgical periodontal treatment with scaling and root planing was performed in both groups. The extent and severity of periodontitis were evaluated by plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP) at baseline and 4 weeks after periodontal treatment. There was no statistically significant difference of periodontal parameters between the RA and control groups at baseline. Four weeks after scaling and root planing, PD reduction, and CAL gain were higher in the RA group treated with csDMARDs compared to the control group, and the difference was statistically significant (P = 0.006 and 0.003, respectively). A post hoc analysis of the RA group showed no statistically significant difference on the response to nonsurgical periodontal treatment in multiple csDMARDs therapy and addition of NSAIDs and/or steroids to csDMARDs. In patients with RA, csDMARDs showed beneficial effect on periodontal clinical parameters following the nonsurgical periodontal treatment.

Periodontal diseases.

Periodontal diseases comprise a wide range of inflammatory conditions that affect the supporting structures of the teeth (the gingiva, bone and periodontal ligament), which could lead to tooth loss and contribute to systemic inflammation. Chronic periodontitis predominantly affects adults, but aggressive periodontitis may occasionally occur in children. Periodontal disease initiation and propagation is through a dysbiosis of the commensal oral microbiota (dental plaque), which then interacts with the immune defences of the host, leading to inflammation and disease. This pathophysiological situation persists through bouts of activity and quiescence, until the affected tooth is extracted or the microbial biofilm is therapeutically removed and the inflammation subsides. The severity of the periodontal disease depends on environmental and host risk factors, both modifiable (for example, smoking) and non-modifiable (for example, genetic susceptibility). Prevention is achieved with daily self-performed oral hygiene and professional removal of the microbial biofilm on a quarterly or bi-annual basis. New treatment modalities that are actively explored include antimicrobial therapy, host modulation therapy, laser therapy and tissue engineering for tissue repair and regeneration.

Epithelial cell pro-inflammatory cytokine response differs across dental plaque bacterial species.

AIM: The dental plaque is comprised of numerous bacterial species, which may or may not be pathogenic. Human gingival epithelial cells (HGECs) respond to perturbation by various bacteria of the dental plaque by production of different levels of inflammatory cytokines, which is a putative reflection of their virulence. The aim of the current study was to determine responses in terms of interleukin (IL)-1beta, IL-6, IL-8 and IL-10 secretion induced by Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum and Streptococcus gordonii in order to gauge their virulence potential. MATERIALS AND METHODS: HGECs were challenged with the four bacterial species, live or heat killed, at various multiplicity of infections and the elicited IL-1beta, IL-6, IL-8 and IL-10 responses were assayed by enzyme-linked immunosorbent assay. RESULTS: Primary HGECs challenged with live P. gingivalis produced high levels of IL-1beta, while challenge with live A. actinomycetemcomitans gave high levels of IL-8. The opportunistic pathogen F. nucleatum induces the highest levels of pro-inflammatory cytokines, while the commensal S. gordonii is the least stimulatory. CONCLUSION: We conclude that various dental plaque biofilm bacteria induce different cytokine response profiles in primary HGECs that may reflect their individual virulence or commensal status.

Porphyromonas gingivalis induce apoptosis in human gingival epithelial cells through a gingipain-dependent mechanism.

BACKGROUND: The oral pathogen Porphyromonas gingivalis has been shown to modulate apoptosis in different cell types, but its effect on epithelial cells remains unclear. RESULTS: We demonstrate that primary human gingival epithelial cells (HGECs) challenged with live P. gingivalis for 24 hours exhibit apoptosis, and we characterize this by M30 epitope detection, caspase-3 activity, DNA fragmentation and Annexin-V staining. Live bacteria strongly upregulated intrinsic and extrinsic apoptotic pathways. Pro-apoptotic molecules such as caspase-3, -8, -9, Bid and Bax were upregulated after 24 hours. The anti-apoptotic Bcl-2 was also upregulated, but this was not sufficient to ensure cell survival. The main P. gingivalis proteases arginine and lysine gingipains are necessary and sufficient to induce host cell apoptosis. Thus, live P. gingivalis can invoke gingival epithelial cell apoptosis in a time and dose dependent manner with significant apoptosis occurring between 12 and 24 hours of challenge via a gingipain-dependent mechanism. CONCLUSION: The present study provides evidence that live, but not heat-killed, P. gingivalis can induce apoptosis after 24 hours of challenge in primary human gingival epithelial cells. Either arginine or lysine gingipains are necessary and sufficient factors in P. gingivalis elicited apoptosis.

Neutrophils rescue gingival epithelial cells from bacterial-induced apoptosis.

In the pathogenesis of chronic inflammatory periodontal disease, neutrophils are recognized as a major cellular component from the histopathology of the periodontal lesion around teeth and from clinical cases where absence or dysfunction of neutrophils results in major periodontal destruction. Neutrophils are recruited in vast numbers into the gingival crevice during periodontal inflammation, attracted by microbial plaque chemoattractants and chemokines released following microbial perturbation of gingival epithelial cells. Porphyromonas gingivalis, a major periodontopathogen, triggers a vast array of cellular responses in gingival epithelial cells but also induces apoptosis. We demonstrate here that neutrophils, when combined in a P. gingivalis challenge assay of epithelial cells, prevent epithelial cell apoptosis by phagocytosing P. gingivalis and later undergoing apoptosis themselves. By removing P. gingivalis by phagocytosis, neutrophils also protect the host from the harmful effects of its microbial proteases, which degrade inflammatory cytokines and other host molecules.

In vitro modeling of host-parasite interactions: the 'subgingival' biofilm challenge of primary human epithelial cells.

BACKGROUND: Microbial biofilms are known to cause an increasing number of chronic inflammatory and infectious conditions. A classical example is chronic periodontal disease, a condition initiated by the subgingival dental plaque biofilm on gingival epithelial tissues. We describe here a new model that permits the examination of interactions between the bacterial biofilm and host cells in general. We use primary human gingival epithelial cells (HGEC) and an in vitro grown biofilm, comprising nine frequently studied and representative subgingival plaque bacteria. RESULTS: We describe the growth of a mature 'subgingival' in vitro biofilm, its composition during development, its ability to adapt to aerobic conditions and how we expose in vitro a HGEC monolayer to this biofilm. Challenging the host derived HGEC with the biofilm invoked apoptosis in the epithelial cells, triggered release of pro-inflammatory cytokines and in parallel induced rapid degradation of the cytokines by biofilm-generated enzymes. CONCLUSION: We developed an experimental in vitro model to study processes taking place in the gingival crevice during the initiation of inflammation. The new model takes into account that the microbial challenge derives from a biofilm community and not from planktonically cultured bacterial strains. It will facilitate easily the introduction of additional host cells such as neutrophils for future biofilm:host cell challenge studies. Our methodology may generate particular interest, as it should be widely applicable to other biofilm-related chronic inflammatory diseases.