Abstract:A large amount of information is available, in the medical literature, on the molecular and immunological mechanisms in which T- and B-cells are involved in the pathogenesis of inflammatory diseases. This review attempts to describe the most important features of the T-cell subsets and their cytokine networks in periodontitis, including the interaction of pathogens with different cell subsets and their gene-expression profiles. Additionally, the known interactions of T- and B-cell subsets in periodontitis are … Show more
“…Periodontitis is an inflammatory disease with an important microbial component in which the immuno‐inflammatory response against dysbiotic subgingival biofilm leads to alveolar bone resorption, resulting in tooth loss. Although bacterial dysbiosis is the principal cause of periodontitis initiation, periodontal tissue breakdown is mainly determined by the host's immuno‐inflammatory response, where the T‐lymphocyte subpopulations play an important role in tooth‐supporting alveolar bone resorption …”
Section: Introductionmentioning
confidence: 99%
“…Regulatory T lymphocytes (Tregs) play a key role in the homeostatic control of the host's immuno‐inflammatory response by suppressing the proliferation and cytokine production of effector T cells, mainly T helper (Th)1 and Th17 lymphocytes . Nonetheless, their role during the pathogenesis of periodontitis has not been fully clarified.…”
Section: Introductionmentioning
confidence: 99%
“…Nonetheless, their role during the pathogenesis of periodontitis has not been fully clarified. In fact, the scarcity of human evidence, as well as the heterogeneity among different animal models assessing the role of Tregs during the pathogenesis of periodontitis, prevents the precise interpretation of their function and their potential to suppress immuno‐inflammatory‐driven alveolar bone resorption . Furthermore, it is unclear the level of risk of bias (RoB) and the comprehensiveness of reporting in many animal experiments .…”
This systematic review aimed to: (a) generate a descriptive synthesis of preclinical studies assessing the therapeutic potential of regulatory T lymphocytes (Tregs) to arrest periodontitis, (b) evaluate the methodological heterogeneity of the reviewed animal studies and (c) assess the risk of bias (RoB) of the included studies. The electronic search for animal studies included the MEDLINE, EMBASE, Web of Science and LILACS databases. In addition, a manual search assessed the high‐ranked scientific journals in “periodontics/immunology” and the references listed in the included studies. There were no language, year or publication status restrictions. Two independent reviewers selected and extracted the data, and Cohen's Kappa coefficient was calculated to determine the inter‐examiner agreement. The Systematic Review Center for Laboratory Animal Experimentation's (SYRCLE) tool was used to assess the RoB. A total of 21 of the 425 studies obtained from the database search were included. Treg function was mainly described in Porphyromonas gingivalis‐induced periodontitis (57.1%) in mice (76.2%), where Treg suppression was strongly related to disease progression and Treg induction was strongly related to immuno‐inflammatory response reduction. Of those 21 studies, eight included eight animal experiments using three distinct therapeutic approaches, including: P. gingivalis‐driven immunization (n = 3), retinoic acid inoculation (n = 2) and anti‐inflammatory molecules in polymeric carriers (n = 3), which could modulate the Treg activity through cytokine production (interleukin‐10 and transforming growth factor‐β1), CC‐chemokine‐ and CC‐chemokine receptor‐mediated chemoattraction (CCL22 and CCR4) or Th17‐associated receptor activator of nuclear factor κB ligand (RANKL) downregulation. However, the studies with animal experiments did not specify the randomization sequences and housing conditions that were used, and therefore, 42.11% of the entries were rated as unclear RoB. Distinct therapeutic strategies involving Tregs could potentially suppress the immuno‐inflammatory response and restore alveolar bone homeostasis during periodontitis. Nevertheless, important methodological variability, poor reporting of treatment effect estimates and unclear RoB suggest using caution when assessing the results of these studies.
“…Periodontitis is an inflammatory disease with an important microbial component in which the immuno‐inflammatory response against dysbiotic subgingival biofilm leads to alveolar bone resorption, resulting in tooth loss. Although bacterial dysbiosis is the principal cause of periodontitis initiation, periodontal tissue breakdown is mainly determined by the host's immuno‐inflammatory response, where the T‐lymphocyte subpopulations play an important role in tooth‐supporting alveolar bone resorption …”
Section: Introductionmentioning
confidence: 99%
“…Regulatory T lymphocytes (Tregs) play a key role in the homeostatic control of the host's immuno‐inflammatory response by suppressing the proliferation and cytokine production of effector T cells, mainly T helper (Th)1 and Th17 lymphocytes . Nonetheless, their role during the pathogenesis of periodontitis has not been fully clarified.…”
Section: Introductionmentioning
confidence: 99%
“…Nonetheless, their role during the pathogenesis of periodontitis has not been fully clarified. In fact, the scarcity of human evidence, as well as the heterogeneity among different animal models assessing the role of Tregs during the pathogenesis of periodontitis, prevents the precise interpretation of their function and their potential to suppress immuno‐inflammatory‐driven alveolar bone resorption . Furthermore, it is unclear the level of risk of bias (RoB) and the comprehensiveness of reporting in many animal experiments .…”
This systematic review aimed to: (a) generate a descriptive synthesis of preclinical studies assessing the therapeutic potential of regulatory T lymphocytes (Tregs) to arrest periodontitis, (b) evaluate the methodological heterogeneity of the reviewed animal studies and (c) assess the risk of bias (RoB) of the included studies. The electronic search for animal studies included the MEDLINE, EMBASE, Web of Science and LILACS databases. In addition, a manual search assessed the high‐ranked scientific journals in “periodontics/immunology” and the references listed in the included studies. There were no language, year or publication status restrictions. Two independent reviewers selected and extracted the data, and Cohen's Kappa coefficient was calculated to determine the inter‐examiner agreement. The Systematic Review Center for Laboratory Animal Experimentation's (SYRCLE) tool was used to assess the RoB. A total of 21 of the 425 studies obtained from the database search were included. Treg function was mainly described in Porphyromonas gingivalis‐induced periodontitis (57.1%) in mice (76.2%), where Treg suppression was strongly related to disease progression and Treg induction was strongly related to immuno‐inflammatory response reduction. Of those 21 studies, eight included eight animal experiments using three distinct therapeutic approaches, including: P. gingivalis‐driven immunization (n = 3), retinoic acid inoculation (n = 2) and anti‐inflammatory molecules in polymeric carriers (n = 3), which could modulate the Treg activity through cytokine production (interleukin‐10 and transforming growth factor‐β1), CC‐chemokine‐ and CC‐chemokine receptor‐mediated chemoattraction (CCL22 and CCR4) or Th17‐associated receptor activator of nuclear factor κB ligand (RANKL) downregulation. However, the studies with animal experiments did not specify the randomization sequences and housing conditions that were used, and therefore, 42.11% of the entries were rated as unclear RoB. Distinct therapeutic strategies involving Tregs could potentially suppress the immuno‐inflammatory response and restore alveolar bone homeostasis during periodontitis. Nevertheless, important methodological variability, poor reporting of treatment effect estimates and unclear RoB suggest using caution when assessing the results of these studies.
“…Microorganisms and their components present in the dental biofilm stimulate inflammation during injury in the periodontal tissues. In an attempt to resist this process, inflammatory cells migrate to the affected area to prevent the action of aggressive agent . In addition to cell migration, vascular changes occur at the site of injury in the cases of periodontal disease owing to the presence of the dental biofilm.…”
Section: Discussionmentioning
confidence: 99%
“…Angiogenesis and lymphangiogenesis are vascular events that occur during gingival inflammation owing to the release of by‐products by the microorganisms present in the dental biofilm as well as the migration of defense cells and secretion of inflammatory mediators at the site of aggression …”
Background and objective
The aim of this study was to evaluate the angiogenesis and lymphangiogenesis in gingival tissue biopsy specimens of individuals with clinically healthy gingiva, chronic gingivitis, and chronic periodontitis (n = 30 per clinical condition).
Material and methods
Histological sections were stained using hematoxylin and eosin as well as immunohistochemically with hematopoietic progenitor cell antigen CD34 and podoplanin (PDPN) antibodies to evaluate the microvascular count, area, and perimeter of blood and lymphatic vessels, respectively.
Results
The results revealed a correlation between the microvascular count of blood and lymphatic vessels (P = 0.03; however, in individuals with chronic periodontitis, fewer lymphatic vessels were present than in the clinically healthy gingival tissue (P = 0.01), which was not observed in the case of microvascular area and perimeter. Podoplanin labeling was present in the epithelium, and the intensity of labeling was positively correlated to the intensity of the inflammatory infiltrate (P = 0.03).
Conclusion
In this study, we concluded that an increase in the number of blood and lymphatic vessels was not observed in bouth gingivitis and periodontitis samples. Podoplanin expression is highly associated with an increased inflammatory infiltration suggesting that PDPN might play an additional role in periodontal disease, other than solely as a lymphangiogenesis marker.
Periodontitis and hypertension often occur as comorbidities, which need to be treated at the same time. To resolve this issue, a controlled‐release composite hydrogel approach is proposed with dual antibacterial and anti‐inflammatory activities as a resolution to achieve the goal of co‐treatment of comorbidities. Specifically, chitosan (CS) with inherent antibacterial properties is cross‐linked with antimicrobial peptide (AMP)‐modified polyethylene glycol (PEG) to form a dual antibacterial hydrogel (CS‐PA). Subsequently, curcumin loaded into biodegradable nanoparticles (CNP) are embedded in the hydrogel exhibiting high encapsulation efficiency and sustained release to achieve long‐term anti‐inflammatory activities. In a mouse model of periodontitis complicated with hypertension, CS‐PA/CNP is applied to gingival sulcus and produced an optimal therapeutic effect on periodontitis and hypertension simultaneously. The therapeutic mechanisms are deeply studied and indicated that CS‐PA/CNP exerted excellent immunoregulatory effects by suppressing the accumulation of lymphocytes and myeloid cells and enhanced the antioxidant capacity and thus the anti‐inflammatory capacity of macrophages through the glutathione metabolism pathway. In conclusion, CS‐PA/CNP has demonstrated its superior therapeutic effects and potential clinical translational value in the co‐treatment of periodontitis and hypertension, and also serves as a drug delivery platform to provide combinatorial therapeutic options for periodontitis with complicated pathogenesis.
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