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Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) are Gram-negative anaerobic bacteria possessing several virulence factors that make them potential pathogens associated with periodontal disease. Periodontal diseases are chronic inflammatory diseases of the oral cavity, including gingivitis and periodontitis. Periodontitis can lead to tooth loss and is considered one of the most prevalent diseases worldwide. P. gingivalis and F. nucleatum possess virulence factors that allow them to survive in hostile environments by selectively modulating the host’s immune-inflammatory response, thereby creating major challenges to host cell survival. Studies have demonstrated that bacterial infection and the host immune responses are involved in the induction of periodontitis. The NLRP3 inflammasome and its effector molecules (IL-1β and caspase-1) play roles in the development of periodontitis. We and others have reported that the purinergic P2X7 receptor plays a role in the modulation of periodontal disease and intracellular pathogen control. Caspase-4/5 (in humans) and caspase-11 (in mice) are important effectors for combating bacterial pathogens via mediation of cell death and IL-1β release. The exact molecular events of the host’s response to these bacteria are not fully understood. Here, we review innate and adaptive immune responses induced by P. gingivalis and F. nucleatum infections and discuss the possibility of manipulations of the immune response as therapeutic strategies. Given the global burden of periodontitis, it is important to develop therapeutic targets for the prophylaxis of periodontopathogen infections.

Introduction: The presently used impulse echo ultrasound examination is not suitable to provide relevant and reliable information about the jawbone, because ultrasound (US) almost completely reflects from the hard cortical jawbone. At the same time, “focal osteoporotic bone marrow defects” (BoneMarrowDefects = BMD) in jawbone are the subject of scientific presentations and discussions.

Purpose: Can a newly developed trans-alveolar ultrasonic sonography (TAU-n) device locate and ascertain BMD?

Patients and methods: TAU-n consists of a two-part handpiece with an extraoral ultrasound transmitter and an intraoral ultrasound receiver. The TAU-n computer display shows the different jawbone densities with corresponding colour coding. The changes in jawbone density are also displayed numerically. The validation of TAU-n readings: A usual orthopantomogram (2D-OPG) on its own is not suitable for unequivocally determining jawbone density and has to be excluded from this validation. For validation, a 3D-digital volume tomogram@/cone beam computer tomogram (DVT@/CBCT) with the capacity to measure Hounsfield units (HU) and a TAU-n are used to determine the presence of preoperative BMD in 82 patient cases. Postoperatively, histology samples and multiplex analysis of RANTES@/CCL5 (R@/C) expression derived from surgically cleaned BMD areas are evaluated.

Results: In all 82 bone samples, DVT-HU, TAU-n values and R/C expressions show the presence of BMD with chronic inflammatory character. However, five histology samples showed no evidence of BMD. All four evaluation criteria (DVT-HU, TAU-n, R/C, histology) confirm the presence of BMD in each of the 82 samples.

Conclusion: The TAU-n method almost completely matches the diagnostic reliability of the other methods. The newly developed TAU-n scanner is a reliable and radiation-free option to detect BMD.

For more than 25 years, I have been, as a gastroenterologist, interested in inflammatory bowel disease—Crohn’s disease and ulcerative colitis—and the gut-brain connection, particularly in childhood autism. In addition, I am concerned with the environmental factors that are driving the current epidemics of both autism and inflammatory bowel disease. The issue is contentious, and one’s view depends greatly on perspective. This article provides one perspective on the delicate and often misunderstood ecological balance between man and microbe, a misunderstanding fraught with assumptions and wishful thinking.

Temporomandibular disorders (TMD) are a common stomatognathic disease affecting all age groups. Patients with internal derangement (ID) or osteoarthritis (OA) of temporomandibular joint (TMJ) often have TMJ synovitis. When TMJ synovial membrane is damaged, many inflammatory cytokines are produced and secreted from TMJ synoviocytes to synovial fluid of TMJ. It has been widely reported that many kinds of biologic factors are produced from TMJ synoviocytes stimulated with interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha. One of the major symptoms of TMD is pain of the TMJ. Many study groups have studied relations between the development of TMJ pain and biologic factors secreted into synovial fluid of TMJ. Here, we summarize previous reports trying to elucidate this correlation. On the other hand, it has been reported that a new molecular mechanism of IL-1beta secretion called inflammasome is involved in several diseases with sterile inflammation. Because TMJ synovitis with ID and OA of TMJ is also sterile inflammation, inflammasome may be involved in the development of TMJ synovial inflammation. This review describes some molecular mechanisms underlying inflammation in TMJ, especially in TMJ synovitis, which may be useful for the development of new therapies against TMD.

This paper reports on the conclusions of two workshops held in Copenhagen in September 2017 and November 2018 focused on medication-related osteonecrosis of the jaws (MRONJ). The workshops were organized and attended by a European task force on MRONJ, i.e. a multidisciplinary group of European clinical investigators with a special interest in the diagnosis and management of MRONJ and a track record of relevant research and publications. The aim of the workshops were to (i) highlight some of the most controversial aspects of current knowledge on MRONJ, including definition and classification, risk factors and management, and (ii) provide an expert opinion-based consensus with a view to inform clinicians and advise researchers, as a first step of reaching solutions. It should be pointed out that all results and comments presented are the authors (the workshop group members) personal views and the present form of this publication is based on genuine consensus of all authors

Prevention of dental caries (tooth decay), one of the most common chronic diseases globally,1 requires the global implementation of WHO’s guideline on sugars intake.2,3 WHO recommends that individuals consume less than 10% of total energy intake from free sugars and that intake below 5% would be beneficial.3 The global dental research community, as the Lancet oral health Series1,2argues, has an important role in the implementation
of the WHO guideline by promoting research on public health and dietary interventions, among other actions. However, dental research activities have not focused on sugars for many years. To remedy this, the European Organisation for Caries Research (ORCA) and the European Association of Dental Public Health (EADPH) organised a joint symposium on sugars in 2015 to stimulate new research.4 The same year, the American Dental Association urged the US National Institute of Dental and Craniofacial Research (NIDCR) to increase research on sugars and oral health.5

Background: Rheumatoid arthritis (RA) and periodontal disease are inter-related conditions. However, factors predictive of periodontal disease progression in patients with early rheumatoid arthritis (eRA) are lacking. The aim of this study was to identify factors associated with the progression of clinical attachment loss (CAL) in interproximal dental sites of eRA patients.

Methods: Twenty-eight eRA patients were evaluated for the progression of CAL at 280 interproximal dental sites at 1 year of follow-up. Markers of RA activity (rheumatoid factor, erythrocyte sedimentation rate, and C-reactive protein), a marker of bone resorption (Dickkopf-related protein 1), Disease Activity Score 28 and Simple Disease Activity Index were included as potential systemic predictive factors. Plaque index, gingival index, pocket depth, clinical attachment level and Dickkopf-related protein 1 in crevicular fluid at baseline were included as potential local predictive factors. Data were analysed in a hierarchical structure using generalised linear mixed models for progression at each site (> 2 mm) during follow-up.

Results: C-reactive protein level was the most important predictive systemic factor for the progression of CAL. The mean CAL and a high degree of gingival inflammation in interproximal sites at baseline were important predictive local factors (p < 0.0001). Patients who received combined treatment with disease-modifying antirheumatic drugs and corticosteroids exhibited less CAL (p < 0.0001). The predictive value of the generalised linear mixed model for progression was 85%.

Conclusions: Systemic factors, including RA disease activity and baseline periodontal condition, were associated with periodontal progression. Pharmacological treatment may affect periodontal progression in patients with early RA.