Background: Periodontitis (P) is a chronic inflammatory disease characterized by the destruction of periodontium support tissue generated by different immuno-inflammatory mechanisms, including the RANK/RANKL/OPG and the IL-23/IL-17 axis. Methods: The study was performed with healthy subjects (HS) and patients with periodontitis. Plasma samples were obtained from peripheral blood and the gingival tissue (GT) during periodontal surgery. The ELISA technique was used to evaluate the levels of IL-23, IL-17A, IL-23R, and IL-17RA. Results: In the plasma, a significant decrease in IL-17A was observed in patients with periodontitis than HS. In the GT, IL-23, IL-17A, and IL-17RA levels were increased in periodontitis patients; on the contrary, IL-23R levels were decreased in periodontitis patients when compared with HS. Finally, several positive correlations were found: soluble IL-17RA (sIL-17RA) levels in plasma between the percentage of radiographic bone loss (RBL%), and IL-23 with IL-17A in gingival tissue. Conclusions: The detection of the IL-23/IL-17A axis in gingival tissue and plasma provides us with more information on the behavior of this axis in a localized way in the periodontal microenvironment, in contrast to the systemic levels evaluated according to the new classification of periodontitis.

Background: Chronic periodontitis (CP) is a prevalent inflammatory disease worldwide, characterized by the destruction of periodontal tissue due to an immune response triggered by periodontopathogenic bacteria and the prolonged release of reactive oxygen species (ROS). Excess ROS leads to tissue damage through mechanisms such as lipid peroxidation and DNA damage. The aim of this study was to evaluate oxidative and genotoxic damage by quantifying 8-hydroxy-2-deoxiguanosine (8-OHdG), malondialdehyde (MDA), and nuclear abnormalities (NAs) in individuals with CP. Methods: The participants were divided into a CP group (n = 30) and a control group without CP (n = 30). Saliva was collected to quantify 8-OHdG (via ELISA) and MDA (via spectrophotometry). Buccal mucosa samples were collected to assess NAs. Periodontal parameters, probing depth (PD), clinical attachment level (CAL), plaque index (PI), and bleeding on probing (BOP), were recorded. Results: The levels of 8-OHdG and MDA were significantly higher in the CP group. NAs were also significantly increased. Positive correlations were observed between 8-OHdG, MDA levels and NAs with clinical parameters. Conclusions: The elevated levels of 8-OHdG, MDA and NAs reflect oxidative and genotoxic damage correlated with CP severity. These biomarkers could complement diagnosis, monitor progression, and assess treatment efficacy. Their elevation may also indicate increased systemic disease risk.

Background: Patients usually present pain due to the release of different inflammatory mediators such as prostaglandin E2 and RANK-L. Analgesics such as acetaminophen and ketorolac can inhibit RANK-L expression and this can affect orthodontic treatment by decreasing bone remodeling and slowing orthodontic dental movement. Several studies have reported a decrease in dental movement after administering some non-steroidal anti-inflammatory drugs. Proposal: The objective was to evaluate the RANK-L levels and a possible modulation by administering acetaminophen and ketorolac in patients starting orthodontic treatment. Methodology: A double-blind, randomized clinical trial was carried out with 24 subjects divided into three study groups: calcined magnesia as a placebo, acetaminophen, and ketorolac. Gingival crevicular fluid was obtained at four time points: before pharmacological intervention, at 24 h, at 48 h, and on the 5th day. RANK-L concentrations were evaluated through ELISA analysis. Also, interproximal space generated by the elastic separator at the end of the study was recorded in the different study groups using the visual analog scale. Results: An increase in RANK-L at 24 h was observed in the placebo group compared to the ketorolac and acetaminophen groups. However, no significant differences were observed in the interproximal space at day 5 in the three study groups. Conclusion: Patients who do not take analgesics at the start of orthodontic treatment have higher levels of RANK-L. Therefore, the use of ketorolac or acetaminophen could decrease bone remodeling and interfere with orthodontic dental movement.

Background: Periodontitis is a chronic immunoinflammatory disease involving various components that affect the tissues surrounding the tooth. The host immune response to the presence of periodontopathogenic microorganisms activates several cytokine systems involved in alveolar bone resorption in periodontitis; among them is the receptor activator of nuclear factor‐κB (RANK)/receptor activator of nuclear factor‐κB ligand (RANKL) system, which depends on the interleukin (IL)‐23/IL‐17 axis. There is a tendency toward increased IL‐23, IL‐17, and IL‐17 receptor (IL‐17RA) and a discrepancy in IL‐23 receptor (IL‐23R) in gingival tissue (GT) of patients with periodontitis. Therefore, the aim of this study was to quantify the expression of the IL‐23/IL‐17A axis using the western blotting (WB) technique in GT samples from patients with periodontitis. Materials and Methods: This cross‐sectional study included 49 subjects: 25 healthy subjects and 24 subjects with periodontitis. GT samples were collected during periodontal surgery. WB was used to evaluate the levels of IL‐23, IL‐17A, IL‐23R, and IL‐17RA. Results: We found a significant increase in IL‐23, IL‐17A, IL‐23R, and IL‐17RA protein levels in the periodontitis group compared with the healthy group; we also detected bands with unexpected molecular weights for both receptors. Moreover, we found a significant positive correlation between IL‐23 and IL‐17A with both receptors, while IL‐23, IL‐17A, IL‐23R, and IL‐17RA correlated positively with two periodontal clinical parameters, namely the clinical attachment level and the percentage of radiographic bone loss (%RBL). Conclusion: In this study, we detected overexpression of IL‐23, IL‐17A, and their receptors in GT of patients with periodontitis, confirming that the IL‐23/IL‐17A axis is involved in periodontal disease.

Candida species can shift from commensal organisms to opportunistic pathogens. Both Candida albicans and non-albicans Candida (NAC) species colonize oral biofilms and periodontal pockets, where they may contribute to inflammation and the progression of periodontal disease. This study aimed to determine the prevalence and antifungal susceptibility profiles of Candida species in individuals with different stages of periodontal disease. A cross-sectional study was conducted in 100 participants whose periodontal status was clinically evaluated. Saliva samples were cultured on chromogenic agar for yeast isolation, species identification was confirmed by MALDI-TOF MS, and antifungal susceptibility to fluconazole, clotrimazole, nystatin, and amphotericin B was assessed. Candida spp. was detected in 35% of participants, where C. albicans was the most prevalent species, followed by Nakaseomyces glabratus (formerly Candida glabrata), Candida parapsilosis, Candida dubliniensis, and Candida tropicalis. Species distribution varied according to periodontal status, with N. glabratus predominating in early periodontitis and C. albicans appeared more frequently in higher severe stages of periodontitis. Susceptibility testing showed resistance of C. albicans to clotrimazole (63.6%) and nystatin (22.7%), whereas amphotericin B and fluconazole remained effective. NAC species, particularly N. glabratus, exhibited resistance to nystatin and variable resistance to clotrimazole but remained susceptible to amphotericin B. These findings underscore the importance of early detection and personalized antifungal strategies for managing periodontal disease complicated by Candida colonization.