We present this critical review with the aim of highlighting the current status of periodontal diseases, focusing on the relevance of host modulating agents and immune pathways, in addition to new complementary therapeutic approaches for the treatment of these pathologies. Periodontal diseases are prevalent pathologies worldwide and the main cause of edentulism in the adult population. Their pathogenesis seems to be based on a dysbiosis of the oral microbiota that interacts with the host's immune defenses and is responsible for the inflammatory/immune response, which would be modified by a number of conditions such as individual susceptibility, environmental and sociodemographic factors, certain systemic pathologies and the individual's genetic condition, among others. Numerous studies have reported on the complex web of inflammatory mediators in periodontal disease and their role in tissue destruction as well as in homeostatic imbalance. Precisely, the role of epigenetics as a modifier of the host genetic condition has captured research attention in recent years. Therefore, this mini-review first discusses an updated etiological hypothesis of periodontal disease and the roles of certain cytokines in the immune response. In addition, the latest therapeutic trends with new developments and future perspectives are summarized.
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http://dx.doi.org/10.3389/fcimb.2024.1493818 | DOI Listing |
Cureus
December 2024
Faculty of Dentistry, Pharos University, Alexandria, EGY.
Background Odontogenic maxillary sinusitis arises mainly from dental origins, emphasizing the connection between dental health and sinus issues. Understanding these relationships is crucial for implant planning, sinus augmentation procedures, and managing post-extraction complications. This knowledge can help clinicians make informed decisions about treatment timing and approach.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Odontology, Section for Molecular Periodontology, Umeå University, Umeå, Sweden.
Introduction: Periodontitis is associated with rheumatoid arthritis (RA). One hypothesis posits that this connection arises from the formation of autoantibodies against citrullinated proteins (ACPA) in inflamed gums, possibly triggered by . We previously demonstrated an increased antibody response to arginine gingipains (anti-Rgp IgG), not only in individuals with severe periodontitis compared to controls, but in RA versus controls, with an association to ACPA.
View Article and Find Full Text PDFJ Dent Res
January 2025
MICORALIS, Faculté de Chirurgie Dentaire, Université Côte d'Azur, Nice, France.
Periodontitis, a prevalent and costly oral disease, remains incompletely understood in its etiopathogenesis. The conventional model attributes it to pathogenic bacteria, but emerging evidence suggests dysbiosis involving bacteria, herpesviruses, and an exaggerated host immune response. Among herpesviruses, Epstein-Barr virus (EBV) closely links to severe periodontitis, yet the mechanisms underlying EBV-related pathogenesis remain elusive.
View Article and Find Full Text PDFClin Implant Dent Relat Res
February 2025
Department of Dental Medicine, Division of Pediatric Dentistry, Karolinska Institutet, Huddinge, Sweden.
Objective: This cross-sectional study aimed to investigate the salivary profile of inflammatory mediators in individuals with periodontal and peri-implant disease as compared to individuals with periodontal and peri-implant health.
Materials And Methods: Saliva samples were collected from 155 participants (mean age 63.3 ± 11.
Clin Implant Dent Relat Res
February 2025
Unit of Basic Oral Investigation-UIBO, School of Dentistry, Universidad El Bosque, Bogotá, Colombia.
Background: This cross-sectional study aimed to compare the composition of the submucosal microbiome of peri-implantitis with paired and unpaired healthy implant samples.
Methods: We evaluated submucosal plaque samples obtained in 39 cases, including 13 cases of peri-implantitis, 13 cases involving healthy implants from the same patient (paired samples), and 13 cases involving healthy implants from different individuals (unpaired samples). The patients were evaluated using next-generation genomic sequencing (Illumina) based on 16S rRNA gene amplification.
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