IntroductionChronic Periodontitis (CP) is an inflammatory disease of bacterial origin that results in alveolar bone destruction. Porphyromonas gingivalis (Pg), one of the main periopathogens, initiates an inflammatory cascade by host immune cells thereby increasing recruitment and activity of osteoclasts, the bone resorbing cells, through enhanced production of the crucial osteoclastogenic factor, RANK-L. Antibodies directed against some cytokines (IL-1β, IL-6 and TNF-α) failed to exhibit convincing therapeutic effect in CP. It has been suggested that IL-33, could be of interest in CP.Objectivethe present study aims to analyze whether and how IL-33 and RANK-L and/or their interplay are involved in the bone destruction associated to CP.Material and MethodsmRNAs and protein expressions of IL-33 and RANK-L were analyzed in healthy and CP human gingival samples by immunohistochemistry (IHC) and RT-qPCR. Murine experimental periodontitis (EP) was induced using Pg infected ligature and Pg free ligature around the first maxillary molar. Alveolar bone loss was recorded by μCT. Mouse gingival explants were stimulated for 24 hours with IL-33 and RANK-L mRNA expression investigated by RT-qPCR. Human oral epithelial cells were infected by Pg for 6, 12; 24 hours and IL-33 and RANK-L mRNA expressions were analyzed by RT-qPCR.ResultsIL-33 is overexpressed in gingival epithelial cells in human affected by CP as in the murine EP. In human as in murine gingival cells, RANK-L was independently induced by Pg and IL-33. We also showed that the Pg-dependent RANK-L expression in gingival epithelial cells occured earlier than that of IL-33.ConclusionOur results evidence that IL-33 overexpression in gingival epithelial cells is associated with CP and may trigger RANK-L expression in addition to a direct effect of Pg. Finally, IL-33 may act as an extracellular alarmin (danger signal) showing proinflammatory properties in CP perpetuating bone resorption induced by Pg infection.

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Introduction: Central Odontogenic Fibroma (COF) is a rare benign odontogenic tumour of the jaws. Until its recent change in classification by the WHO in 2017, this entity has gone without an agreed upon definition for many years. For this reason, COF would remain largely unknown to practitioners. Corpus: The pedagogical objectives of this article are, through a systematic review of the literature using the PRISMA methodology, to list the epidemiological, aetiological, clinical, radiological, histological, therapeutic and prognostic characteristics of COF. All the data collected made it possible to establish a COF management summary for practitioners in order to optimize it. Conclusion: Based on the 135 cases listed, it appears that surgical enucleation is the treatment of choice for COF. The recurrence rate is low and malignant transformation has never been reported. However, regular clinical and radiological follow-up of patients over several years seems to be a justified precaution.

Rheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases leading to increased bone resorption. Preventing this inflammatory bone resorption is a major health challenge. Both diseases share immunopathogenic similarities and a common inflammatory environment. The autoimmune response or periodontal infection stimulates certain immune actors, leading in both cases to chronic inflammation that perpetuates bone resorption. Moreover, RA and periodontitis have a strong epidemiological association that could be explained by periodontal microbial dysbiosis. This dysbiosis is believed to be involved in the initiation of RA via three mechanisms. (i) The dissemination of periodontal pathogens triggers systemic inflammation. (ii) Periodontal pathogens can induce the generation of citrullinated neoepitopes, leading to the generation of anti-citrullinated peptide autoantibodies. (iii) Intracellular danger-associated molecular patterns accelerate local and systemic inflammation. Therefore, periodontal dysbiosis could promote or sustain bone resorption in distant inflamed joints. Interestingly, in inflammatory conditions, the existence of osteoclasts distinct from “classical osteoclasts” has recently been reported. They have proinflammatory origins and functions. Several populations of osteoclast precursors have been described in RA, such as classical monocytes, a dendritic cell subtype, and arthritis-associated osteoclastogenic macrophages. The aim of this review is to synthesize knowledge on osteoclasts and their precursors in inflammatory conditions, especially in RA and periodontitis. Special attention will be given to recent data related to RA that could be of potential value in periodontitis due to the immunopathogenic similarities between the two diseases. Improving our understanding of these pathogenic mechanisms should lead to the identification of new therapeutic targets involved in the pathological inflammatory bone resorption associated with these diseases.

Periodontitis is a prevalent chronic inflammatory disease due to the host response (IL-1β, IL-6, TNF-α and IL-17A) to oral bacteria such as Porphyromonas gingivalis. The newer members of the IL-1 family, IL-36s (IL-36α/IL-36β/IL-36γ/IL-36Ra/IL-38) are known to be involved in host defense against P. gingivalis in oral epithelial cells (OECs) and are considered as key inflammatory mediators in chronic diseases. The aim of this study was to investigate the potential role of IL-36s in periodontitis. We showed here that IL-36γ mRNA gingival expression is higher in periodontitis patients, whereas IL-36β and IL-36Ra mRNA expression are lower compared to healthy controls. Interestingly, the elevated IL-36γ expression in patients is positively correlated with the RANKL/OPG ratio, an index of bone resorption. In vitro, IL-36γ expression was induced through TLR2 activation in primary OECs infected with P. gingivalis but not in gingival fibroblasts, the most widespread cell type in gingival connective tissue. In OECs, recombinant IL-36γ enhanced the expression of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-36γ), of TLR2 and importantly, the RANKL/OPG ratio. These findings suggest that IL-36γ could be a pivotal inflammatory player in periodontitis by perpetuating gingival inflammation and its associated alveolar bone resorption and could be a relevant therapeutic target.

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Introduction: Following any oral surgery procedure, postoperative pain is an inevitable outcome and can be described as moderate to severe. The pain management is essential for the comfort and the well-being of the patients. Topical delivery and more specifically transmucosal delivery systems seem to be of great value for the development of new pain management strategies. Method: A systematic literature review was performed using PubMedCentral database. Only PubMedCentral indexed publications were selected and included if they described i) a human clinical study with pharmacokinetic and/or pain relief assessment a biomaterial for topic delivery, ii) the delivery of analgesics or NSAIDs for analgesic purpose and iii) a biomaterial for topic delivery. Results: Ten articles were selected among which 4 pharmacokinetic studies and 8 studies describing pain relief. Six of the selected articles were well defined with a good scientific level of evidence (level 2) and 4 of them with a low level of evidence. Discussion: The clinical investigations demonstrated a good analgesia, a rapid pain relief with a decrease of the administered doses compared to the oral administration. Moreover, these topic analgesics were well tolerated by the patients. Number of devices was developed for the topical delivery after oral surgery procedures. Excepting a gelatin sponge and a hydro alcoholic gel, most of the devices were made of cellulose and its derivatives. Authors reported that the materials showed a good maintenance at the site of application and the release of the analgesic was well controlled over the time. Conclusion: However, well conducted large clinical trials are still missing in order to validate the absence of side effects.