Periodontitis: Molecular Mechanisms of Pathogenesis and New Approaches to Therapy
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 2362
Special Issue Editors
Interests: Genetics, connective tissues, hereditary connective tissue diseases, infectious diseases, periodontium, molecular mechanisms, aetiopathogenesis, virulence, cell therapy, genetic engineering
Special Issues, Collections and Topics in MDPI journals
2. Department of Periodontology, Preventive Dentistry and Oral Medicine, Jagiellonian University, Krakow, Poland
Interests: periodontal diseases; pathomechanisms of the periodontal diseases; links between periodontitis and general health; immune system; biofilm; treatments of the periodontal diseases
Special Issue Information
Dear Colleagues,
This Special Issue is supervised by Dr. Marta Cześnikiewicz-Guzik and Dr. Katarzyna Gawron, and assisted by our Topical Advisory Panel Member Dr. Pawel Plakwicz (Medical University of Warsaw).
Periodontitis (PD) affects over 30% of adults worldwide and is the most common chronic inflammatory disease of tooth-supporting tissues caused by bacterial infection. It is manifested by gingival bleeding, periodontal ligament degradation, attachment loss and alveolar bone resorption which result in the formation of periodontal pocket(s) and tooth mobility; if left untreated, the disease may lead to tooth exfoliation. PD is initiated by the spreading of subgingival biofilm and enhanced colonization of periodontal gingival pockets by bacterial species of the red complex, i.e., Porphyromonas gingivalis (P. gingivalis), Tannerella forsythia and Treponema denticola. The interaction of bacterial biofilm with the host immune system leads to development of chronic inflammation in periodontal tissues which is stimulated constantly by the virulence factors of the bacteria, has no resolution and consequently causes the periodontal tissue’s damage.
Among red complex species, P. gingivalis, a Gram-negative, anaerobic bacterium equipped with lipopolysaccharide, cysteine proteases (gingipains), fimbriae, hemolysins and peptidylarginine deiminase, has been proposed as an important causative agent of PD. Using the same process of citrullination as mammalian peptidylarginine deiminases, the bacterial enzyme deiminates the guanidino group of carboxy-terminal arginine and free L-arginine residue to yield a citrulline residue. The conversion of positively charged arginine into neutral citrulline may affect the folding and stability of proteins and peptides, alter their susceptibility to proteolysis and abrogate their biological activity. For example, citrullination of C-terminal arginine of epidermal growth factor (EGF) impairs its biological activity, which may at least partially contribute to the periodontal tissue damage and delayed healing. PPAD activity has been also shown to contribute to P. gingivalis’s adherence, invasion and activation of the PGE2-dependent pathway in gingival fibroblasts, contributing to the inflammation of gingival tissue and PGE2-dependent bone resorption. In addition to polypeptide citrullination, ammonia released during catalysis enhances the survival of P. gingivalis within the periodontal pocket by increasing acid tolerance and is associated with pathogenic effects on host cell function. Additionally, the cooperative effects of gingipains with bacterial peptidylarginine deiminase have been proposed as a mechanism responsible for the inactivation of several plasma constituents, increased gingival crevicular fluid flow and P. gingivalis persistence in gingival pockets.
The main goal of PD therapy is to stop the progression of the disease and regeneration of injured periodontal tissues. Surgical therapies, such as mechanical scaling, root planing and surgery in combination with antimicrobials, result in a reduction in supragingival plaque and gingival inflammation and in most cases are sufficient to stop periodontal destruction. Complete periodontal regeneration includes the complex composed of bone, cementum and periodontal ligament. Although it is still challenging, potentially promising strategies include the use of endogenous oral stem cells, e.g., dental pulp stem cells (DPSCs); stem cells from human exfoliated deciduous teeth (SHED); periodontal ligament stem cells (PDLSC); dental follicle stem cells (DFSC); engineered stem cells, e.g., induced pluripotent stem cells (iPSCs); or recombinant growth factors, e.g., fibroblast growth factor-2 (FGF-2) and platelet-derived growth factor (PDGF).
In this Special Issue, we will publish high-quality original papers and comprehensive reviews demonstrating/discussing important aspects of pathogenetic processes, including molecular mechanisms of PD and experimental studies on novel promising approaches to PD therapy.
Dr. Katarzyna Gawron
Dr. Marta Cześnikiewicz-Guzik
Guest Editors
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