Background Rheumatoid arthritis (RA) and periodontitis (P) are chronic inflammatory diseases characterized by joint and radiographic bone loss, respectively. IL‐23 and IL‐17 have an essential role in the immunopathogenesis of RA, and P. IL‐23 stimulates Th17 cells through which produces IL‐17, IL‐21, and RANKL. IL‐17 stimulates fibroblasts to produce RANKL, which initiates bone loss in the joints in RA and the periodontal tissue in periodontitis. The aim of this study was to determine the expression pattern of IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA of patients with RA presenting P (RAP). Material and methods Healthy subjects (HS) (n = 42), patients with P (n = 40), RA (n = 20), and patients with RAP (n = 40) were included. Plasma samples were obtained to evaluate the IL‐23, IL‐17A, sIL‐23R, and sIL‐17RA by ELISA technique. A nonparametric Mann‐Whitney U test was used to compare the differences between groups. A Chi‐square was used to compare gender, grade and stage of periodontitis, and DAS28‐ESR between the groups. Spearman's rank correlation coefficient was used to study the association between the molecules and clinical parameters. Results IL‐23 levels were increased in the RAP group, and lower sIL‐23R levels were found in the RAP groups. However, IL‐17A was lower in the P and RAP group but not in RA patients. RAP group showed a decrease IL‐17A levels in advanced stages of the periodontal disease. Conclusion These results suggest that IL‐23 and IL‐17A tend to downregulate their expression patterns when patients present both rheumatoid arthritis and periodontitis.
ObjectiveTo determine the efficacy of clindamycin compared with amoxicillin-metronidazole after a 7-day regimen during nonsurgical treatment of periodontitis in patients with type 2 diabetes mellitus.Research design and methodsIn this double-blind, randomized clinical trial, a total of 42 patients with chronic periodontitis and type 2 diabetes were included. Patients were randomly assigned to treatment with either clindamycin or amoxicillin-metronidazole three times a day during 7 days. Clinical determinations (probing depth, bleeding on probe, and plaque index) were performed to determine the extent and severity of periodontitis before and after the pharmacological treatment.ResultsAfter 7 days of administration of clindamycin or amoxicillin-metronidazole, no differences were observed between the clinical determinations, probing depth (0.44 vs 0.50 mm, p=0.624), plaque index (17.62 vs 15.88%, p=0.910), and bleeding on probing (16.12 vs 22.17%, p=0.163), respectively. There were no adverse events in either group.ConclusionThe administration during 7 days of clindamycin or amoxicillin/metronidazole showed the same efficacy for the reduction of probing depth, plaque index, and bleeding on probing in patients with periodontitis and type 2 diabetes.
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.
Revisión bibliogRáfica RESUMEN La artritis reumatoide (AR) y la periodontitis (P) son enfermedades inflamatorias crónicas. De manera reciente, se ha descrito que 90% de los pacientes con AR presentan P. Ambas patologías se caracterizan por la destrucción de la articulación y el hueso alveolar, respectivamente. Se sabe que 1% de la población mundial presenta artilugios y en México es el 1.6%. Sobre la periodontitis, su prevalencia es de 15 a 20% de la población mundial y en México es de 60%. La etiología de ambas enfermedades es similar, ya que son multifactoriales y comparten varios factores de riesgo que pueden desencadenarlas, como lo son factores genéticos, biológicos o ambientales, dentro de los cuales uno de los que mantiene más cercana la relación de estas enfermedades es el factor biológico, donde una disbiosis a nivel bucal o intestinal puede comenzar con inflamación local y a su vez sistemática. Las citocinas proinflamatorias IL-23 e IL-17 y sus receptores juegan un papel muy importante en la inmunopatología de estas enfermedades. IL-23 activa y expande los clones Th17 a través de IL-23R y promueve la producción de IL-17 y RANKL; sin embargo, la IL-23R soluble puede bloquear el receptor de IL-23 al inhibir su señalización. IL-17 a través de IL-17RA puede activar fibroblastos y macrófagos que expresan RANKL que activa los precursores de osteoclastos e inicia la erosión ósea en las articulaciones y el hueso alveolar. Al igual que el receptor soluble de IL-23R, el ser soluble de IL-17RA puede bloquear a IL-17A e inhibir su señalización.
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