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AimThe aim of the study is to assess the long-term effect of active periodontal therapy on serum inflammatory parameters in patients with aggressive (AgP) and chronic (ChP) periodontitis in a non-randomised clinical study.MethodsTwenty-five ChP and 17 AgP were examined clinically prior to (baseline), 12 weeks and 60 months after subgingival debridement of all pockets within 2 days. Systemic antibiotics were prescribed if Aggregatibacter actinomycetemcomitans was detected (10 AgP, 8 ChP), flap surgery was rendered if required. Neutrophil elastase (NE), C-reactive protein (CRP), lipopolysaccharide binding protein, interleukin 6, 8, and leukocyte counts were assessed at baseline, 12 weeks and 60 months.ResultsClinical parameters improved significantly in both groups from 12 weeks to 60 months. Eleven AgP and 18 ChP patients received surgical treatment after the 12 weeks examination. Only 3 patients in each group attended ≥ 2 supportive maintenance visits per year. NE and CRP were significantly higher in AgP than ChP at baseline and 60 months (p < 0.01). For leukocyte counts in ChP, significant changes were observed (baseline: 6.11 ± 1.44 nl−1; 12 weeks: 5.34 ± 1.40 nl−1; 60 months: 7.73 ± 2.89 nl−1; p < 0.05). Multiple regression analysis identified African origin, surgical treatment and female sex to correlate with better clinical improvement.ConclusionDespite comprehensive periodontal treatment, AgP patients exhibit higher NE and CRP levels than ChP patients up to 5 years after therapy.Clinical relevanceSystemic inflammatory burden in AgP patients is higher than in ChP patients even 5 years after periodontal treatment.

Background: the establishment of periodontitis is regulated by the primary etiological factor and several individual conditions including the immune response mechanism of the host and individual genetic factors. It results when the oral homeostasis is interrupted, and biological reactions favor the development and progression of periodontal tissues damage. Different strategies have been explored for reinforcing the therapeutic effect of non-surgical periodontal treatment of periodontal tissue damage. Gaseous ozone therapy has been recognized as a promising antiseptic adjuvant, because of its immunostimulating, antimicrobial, antihypoxic, and biosynthetic effects. Then, we hypothesized that the adjunct of gaseous ozone therapy to standard periodontal treatment may be leveraged to promote the tissue healing response. Methods: to test this hypothesis, we conducted a prospective randomized study comparing non-surgical periodontal treatment plus gaseous ozone therapy to standard therapy. A total of 90 healthy individuals with moderate or severe generalized periodontitis were involved in the study. The trial was conducted from September 2019 to October 2020. Forty-five patients were randomized to receive scaling and root-planning (SRP) used as conventional non-surgical periodontal therapy plus gaseous ozone therapy (GROUP A); forty-five were allocated to standard treatment (GROUP B). The endpoint was defined as the periodontal response rate after the application of the ozone therapy at 3 months and 6 months, defined as no longer meeting the criteria for active periodontitis. Statistical analysis was performed employing SPSS v.18 Chicago: SPSS Inc. Results: periodontal parameters differed significantly between patients treated with the two distinct procedures at 3 months (p ≤ 0.005); a statistically significant difference between groups was observed from baseline in the CAL (p ≤ 0.0001), PPD (p ≤ 0.0001) and BOP (p ≤ 0.0001) scores. Conclusions: The present study suggests that SRP combined with ozone therapy in the treatment of periodontitis revealed an improved outcome than SRP alone.

Periodontitis causes the destruction of tooth-supporting tissues, and current therapies for periodontal regeneration are invasive. In this study, a human dental pulp stem cell (DPSC; hDP-MSC) injection was developed to promote periodontal regeneration through a non-invasive procedure. A total of 132 patients with chronic periodontitis (158 teeth) from two centers in China were included. Thirty-six were randomly assigned to different DPSC dose groups (ranging from 1 × 10 6 to 1 × 10 7 DPSCs per tooth, with nine injected with saline only), and 96 were randomly assigned to a single-injection group (1 × 10 7 /0.6 mL DPSCs), a double-injection group (1 × 10 7 /0.6 mL DPSCs × 2), or a saline group, in a 1:1:1 ratio. At 6 months post-therapy, attachment loss (AL), periodontal probing depth (PD), gingival recession (GR), tooth mobility (TM), and bone defect depth (BDD) were examined. The primary outcome was AL. DPSC injection resulted in greater improvement in BDD (0.30 ± 0.484 mm) compared to saline injection (0.04 ± 0.315 mm). Post hoc analysis showed that DPSC injection had significantly better outcomes in patients with stage III periodontitis (AL ≥ 5 mm): 54 patients received DPSCs, and 40 received saline. AL improved by 1.67 ± 1.508 mm in the DPSC group (26.81% improvement) and by 1.03 ± 1.310 mm in the saline group (17.43% improvement). The therapeutic effects encompassed improvements in both soft and hard tissues. In summary, DPSC injection was safe and improved clinical outcomes compared to saline injection in patients with stage III periodontitis. Larger trials are warranted to validate these findings (ClinicalTrials.gov registration: NCT05924373).

Tooth-related inflammatory disorders, including caries, pulpitis, apical periodontitis (AP), and periodontitis (PD), are primarily caused by resident oral microorganisms. Although these dental inflammatory conditions are typically not life-threatening, neglecting them can result in significant complications and greatly reduce an individual’s quality of life. Nuclear factor κB (NF-κB), a family formed by various combinations of Rel proteins, is extensively involved in inflammatory diseases and even cancer. This study reviews recent data on NF-κB signaling and its role in dental pulp stem cells (DPSCs), dental pulp fibroblasts (DPFs), odontoblasts, human periodontal ligament cells (hPDLCs), and various experimental animal models. The findings indicate that NF-κB signaling is abnormally activated in caries, pulpitis, AP, and PD, leading to changes in related cellular differentiation. Under specific conditions, NF-κB signaling occasionally interacts with other signaling pathways, affecting inflammation, bone metabolism, and tissue regeneration processes. In summary, data collected over recent years confirm the central role of NF-κB in dental inflammatory diseases, potentially providing new insights for drug development targeting NF-κB signaling pathways in the treatment of these conditions. Keywords: NF-κB, dental caries, pulpitis, apical periodontitis, periodontitis.

Innate immunity represents the semi-specific first line of defense and provides the initial host response to tissue injury, trauma, and pathogens. Innate immunity activates the adaptive immunity, and both act highly regulated together to establish and maintain tissue homeostasis. Any dysregulation of this interaction can result in chronic inflammation and autoimmunity and is thought to be a major underlying cause in the initiation and progression of highly prevalent immune-mediated inflammatory diseases (IMIDs) such as psoriasis, rheumatoid arthritis, inflammatory bowel diseases among others, and periodontitis. Th1 and Th2 cells of the adaptive immune system are the major players in the pathogenesis of IMIDs. In addition, Th17 cells, their key cytokine IL-17, and IL-23 seem to play pivotal roles. This review aims to provide an overview of the current knowledge about the differentiation of Th17 cells and the role of the IL-17/IL-23 axis in the pathogenesis of IMIDs. Moreover, it aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL-17/IL-23 axis.

This study aims to evaluate the efficacy of photodynamic therapy as an adjunct to conventional endodontic treatment in patients with apical periodontitis and fistulas. In this study, a fistula is characterized as a pathological conduit originating from the infected region at the root apex of the tooth, traversing the oral mucosa, and extending to the external surface of the gingiva. This pathological condition frequently complicates the management of endodontic infections, thereby necessitating the evaluation of supplementary therapeutic interventions. The standard treatment for endodontic infections involves thorough disinfection of the root canal system to remove microbial contamination from the canal and surrounding tissues. To potentially augment the efficacy of conventional treatment, aPDT is proposed as a supplementary, non-invasive technique. This innovative technique uses a photosensitizer, which is a light-sensitive dye, in combination with a light source to produce reactive oxygen species. Reactive oxygen species can effectively target and eliminate bacteria in the root canal system, potentially enhancing treatment outcomes. The study will involve 140 teeth with apical periodontitis and fistulas. The teeth will be randomly assigned to one of two treatment groups. Group I will receive only the conventional endodontic treatment, which includes root canal cleaning, shaping, and obturation. Group II will undergo the same conventional endodontic treatment, but with an additional step of aPDT. The aPDT procedure involves applying a photosensitizer to the root canal and irradiating it with light to produce reactive oxygen species. Each group will consist of 70 teeth to ensure adequate statistical power. The primary outcome is fistula resolution, assessed clinically at 15 and 30 days post-treatment. The secondary outcome is the comparison of apical radiolucency from periapical radiographs to evaluate healing and reduction of periapical pathology. The study aims to determine if adding aPDT significantly improves the management of apical periodontitis and overall success rates of endodontic treatment. The results will provide insights into the effectiveness of aPDT as an adjunctive treatment and its potential benefits in clinical practice.

The immune system evolved to efficiently eradicate invading bacteria and terminate inflammation through balancing inflammatory and regulatory T-cell responses. In autoimmune arthritis, pathogenic T H 17 cells induce bone destruction and autoimmune inflammation. However, whether a beneficial function of T-cell-induced bone damage exists is unclear. Here, we show that bone-damaging T cells have a critical function in the eradication of bacteria in a mouse model of periodontitis, which is the most common infectious disease. Bacterial invasion leads to the generation of specialized T H 17 cells that protect against bacteria by evoking mucosal immune responses as well as inducing bone damage, the latter of which also inhibits infection by removing the tooth. Thus, bone-damaging T cells, which may have developed to stop local infection by inducing tooth loss, function as a double-edged sword by protecting against pathogens while also inducing skeletal tissue degradation. IL-17-producing T cells are protective against infection, but the authors of this article previously showed that these cells also contribute to inflammatory bone destruction. Here they show in the context of periodontitis that microbiota-driven Th17-mediated bone destruction may actually be a physiological rather than a pathological process, as associated tooth loss prevents dissemination of oral bacteria.