Peri-implant diseases: Consensus Report of the Sixth European Workshop on Periodontology

Issues related to peri-implant disease were discussed. It was observed that the most common lesions that occur, i.e. peri-implant mucositis and peri-implantitis are caused by bacteria. While the lesion of peri-implant mucositis resides in the soft tissues, peri-implantitis also affects the supporting bone. Peri-implant mucositis occurs in about 80% of subjects (50% of sites) restored with implants, and peri-implantitis in between 28% and 56% of subjects (12-40% of sites). A number of risk indicators were identified including (i) poor oral hygiene, (ii) a history of periodontitis, (iii) diabetes and (iv) smoking. It was concluded that the treatment of peri-implant disease must include anti-infective measures. With respect to peri-implant mucositis, it appeared that non-surgical mechanical therapy caused the reduction in inflammation (bleeding on probing) but also that the adjunctive use of antimicrobial mouthrinses had a positive effect. It was agreed that the outcome of non-surgical treatment of peri-implantitis was unpredictable. The primary objective of surgical treatment in peri-implantitis is to get access to the implant surface for debridement and decontamination in order to achieve resolution of the inflammatory lesion. There was limited evidence that such treatment with the adjunctive use of systemic antibiotics could resolve a number of peri-implantitis lesions. There was no evidence that so-called regenerative procedures had additional beneficial effects on treatment outcome

Gingival tissue human beta-defensin levels in relation to infection and inflammation.

Aim To profile gingival tissue levels of human beta-defensin (hBD)-2 and hBD-3 in relation to gingival inflammation, Th17-related cytokine concentrations, Porphyromonas gingivalis counts, and gingipain and total protease activities. Materials and Methods Gingival tissue and subgingival plaque samples were collected from 21 periodontitis patients including 48 periodontal pocket sites with marginal, mild, or moderate to severe inflammation. hBD levels were determined by immunodetection, P. gingivalis counts with real-time polymerase chain reaction, protease activities with fluorogenic substrates, and cytokine concentrations with Luminex technique. Data were statistically analysed using Kruskal-Wallis and Mann-Whitney U tests and Spearman correlation coefficients. Results Subgingival plaque counts of P. gingivalis (p = .001) and gingipain activity (p <.001), as well as interleukin (IL)-1 beta (p = .012), IL-10 (p = .024), IL-17A (p = .002), IL-17F (p = .006), and IL-23 (p = .036) concentrations were elevated in severely inflamed sites, whereas no change was observed in hBD-2 and hBD-3 levels. Negative correlations were found between protease activity and hBD-2 (p = .033) and hBD-3(p = .003) levels. Conclusions Shift in gingival inflammation from marginal to mild stage is related to elevations in subgingival plaque P. gingivalis counts and gingipain activity, but not to tissue hBD levels. Negative correlations between hBDs and total protease activity suggest the degradation of these antimicrobial peptides in progressed inflammation.Peer reviewe

Gingival Tissue Human Beta-Defensin Levels in Relation to Infection and Inflammation

AimTo profile gingival tissue levels of human beta‐defensin (hBD)‐2 and hBD‐3 in relation to gingival inflammation, Th17‐related cytokine concentrations, Porphyromonas gingivalis counts, and gingipain and total protease activities.Materials and MethodsGingival tissue and subgingival plaque samples were collected from 21 periodontitis patients including 48 periodontal pocket sites with marginal, mild, or moderate to severe inflammation. hBD levels were determined by immunodetection, P. gingivalis counts with real‐time polymerase chain reaction, protease activities with fluorogenic substrates, and cytokine concentrations with Luminex technique. Data were statistically analysed using Kruskal–Wallis and Mann–Whitney U tests and Spearman correlation coefficients.ResultsSubgingival plaque counts of P. gingivalis (p = .001) and gingipain activity (p p = .012), IL‐10 (p = .024), IL‐17A (p = .002), IL‐17F (p = .006), and IL‐23 (p = .036) concentrations were elevated in severely inflamed sites, whereas no change was observed in hBD‐2 and hBD‐3 levels. Negative correlations were found between protease activity and hBD‐2 (p = .033) and hBD‐3(p = .003) levels.ConclusionsShift in gingival inflammation from marginal to mild stage is related to elevations in subgingival plaque P. gingivalis counts and gingipain activity, but not to tissue hBD levels. Negative correlations between hBDs and total protease activity suggest the degradation of these antimicrobial peptides in progressed inflammation.</p

Increased Risk of Temporomandibular Joint Closed Lock: A Case-Control Study of ANKH Polymorphisms

Objectives: This study aimed to carry out a histological examination of the temporomandibular joint (TMJ) in ank mutant mice and to identify polymorphisms of the human ANKH gene in order to establish the relationship between the type of temporomandibular disorders (TMD) and ANKH polymorphisms.\ud \ud Materials and Methods: Specimens from the TMJ of ank mutant and wild-type mice were inspected with a haematoxylin and eosin staining method. A sample of 55 TMD patients were selected. Each was examined with standard clinical procedures and genotyping techniques.\ud \ud Results: The major histological finding in ank mutant mice was joint space narrowing. Within TMD patients, closed lock was more prevalent among ANKH-OR homozygotes (p = 0.011, OR = 7.7, 95% CI 1.6–36.5) and the elder (p = 0.005, OR = 2.4, 95% CI 1.3–4.3).\ud \ud Conclusions: Fibrous ankylosis was identified in the TMJ of ank mutant mice. In the human sample, ANKH-OR polymorphism was found to be a genetic marker associated with TMJ closed lock. Future investigations correlating genetic polymorphism to TMD are indicated

Bacterial Diversity in Oral Samples of Children in Niger with Acute Noma, Acute Necrotizing Gingivitis, and Healthy Controls

Noma is a devastating gangrenous disease that leads to severe facial disfigurement, but its cause remains unknown. It is associated with high morbidity and mortality and affects almost exclusively young children living in remote areas of developing countries, particularly in Africa. Several factors have been linked to the disease, including malnutrition, immune dysfunction, lack of oral hygiene, and lesions of the mucosal gingival barrier, particularly the presence of acute necrotizing gingivitis, and a potentially non-identified bacterial factor acting as a trigger for the disease. This study assessed the total bacterial diversity present in 69 oral samples of 55 children in Niger with or without acute noma or acute necrotizing gingivitis using culture-independent molecular methods. Analysis of bacterial composition and frequency showed that diseased and healthy site bacterial communities are composed of similar bacteria, but differ in the prevalence of a limited group of phylotypes. We failed to identify a causative infectious agent for noma or acute necrotizing gingivitis as the most plausible pathogens for both conditions were present also in sizeable numbers in healthy subjects. Most likely, the disease is initiated by a synergistic combination of several bacterial species, and not a single agent

New Insights into Alzheimer's Disease Progression: A Combined TMS and Structural MRI Study

BACKGROUND: Combination of structural and functional data of the human brain can provide detailed information of neurodegenerative diseases and the influence of the disease on various local cortical areas. METHODOLOGY AND PRINCIPAL FINDINGS: To examine the relationship between structure and function of the brain the cortical thickness based on structural magnetic resonance images and motor cortex excitability assessed with transcranial magnetic stimulation were correlated in Alzheimer's disease (AD) and mild cognitive impairment (MCI) patients as well as in age-matched healthy controls. Motor cortex excitability correlated negatively with cortical thickness on the sensorimotor cortex, the precuneus and the cuneus but the strength of the correlation varied between the study groups. On the sensorimotor cortex the correlation was significant only in MCI subjects. On the precuneus and cuneus the correlation was significant both in AD and MCI subjects. In healthy controls the motor cortex excitability did not correlate with the cortical thickness. CONCLUSIONS: In healthy subjects the motor cortex excitability is not dependent on the cortical thickness, whereas in neurodegenerative diseases the cortical thinning is related to weaker cortical excitability, especially on the precuneus and cuneus. However, in AD subjects there seems to be a protective mechanism of hyperexcitability on the sensorimotor cortex counteracting the prominent loss of cortical volume since the motor cortex excitability did not correlate with the cortical thickness. Such protective mechanism was not found on the precuneus or cuneus nor in the MCI subjects. Therefore, our results indicate that the progression of the disease proceeds with different dynamics in the structure and function of neuronal circuits from normal conditions via MCI to AD

Understanding the roles of gingival beta-defensins

Gingival epithelium produces β-defensins, small cationic peptides, as part of its contribution to the innate host defense against the bacterial challenge that is constantly present in the oral cavity. Besides their functions in healthy gingival tissues, β-defensins are involved in the initiation and progression, as well as restriction of periodontal tissue destruction, by acting as antimicrobial, chemotactic, and anti-inflammatory agents. In this article, we review the common knowledge about β-defensins, coming from in vivo and in vitro monolayer studies, and present new aspects, based on the experience on three-dimensional organotypic culture models, to the important role of gingival β-defensins in homeostasis of the periodontium

dispersal and reception in northern italy comparing systems along the brenner route

In the last decades, policy restrictions and practices at national and local levels have curtailed the rights of seekers and holders of international protection, thus impacting on their lives and on the territories they transit through. This is particularly evident in border contexts. Various border areas have gradually transformed into internal hotspots, with increasing border enforcement. This includes Brenner, situated at the border between Italy and Austria. In the wider Brenner route area, particularly in the nearby Italian cities of Verona, Trento and Bolzano, "spaces of transit" have emerged and both public and humanitarian actors have been "forced" to deal with it. This chapter draws upon the work of the multilevel governance of migration (Caponio and Borkert 2010), and on the proliferation of borders (Mezzadra and Neilson 2016), to present a comparative analysis of the reception scenario in these three cities. By building on qualitative data analysis (legal analysis of policy documents, content analysis of interviews and newspaper articles), it discusses to what extent and how the respective local systems of reception have managed to cater for migrants that transit through them. Similarities and differences are pointed out, as well as the relevance of factors such as geographical proximity in influencing the respective approaches