Host modulation by therapeutic agents

Elavarasu, Sugumari; Sekar, Santhosh; Thamaraiselvan, Murugan

doi:10.4103/0975-7406.100244

Cited by 23 publications

(8 citation statements)

References 12 publications

(13 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gingival inflammation that accompanies periodontal disease can damage supporting connective tissues and disrupt tooth anchoring to the jawbone. Several modulating agents have been investigated as potential therapies for periodontal disease, including antiproteinases, anti-inflammatory drugs, and bone-sparing drugs [1] .…”

Section: Introductionmentioning

confidence: 99%

Azilsartan Increases Levels of IL-10, Down-Regulates MMP-2, MMP-9, RANKL/RANK, Cathepsin K and Up-Regulates OPG in an Experimental Periodontitis Model

Araújo

Varela

Brito³

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

AimsThe aim of this study was to evaluate the effects of azilsartan (AZT) on bone loss, inflammation, and the expression of matrix metallo proteinases (MMPs), receptor activator of nuclear factor κB ligand (RANKL), receptor activator of nuclear factor κB (RANK), osteoprotegerin (OPG), cyclooxygenase-2 (COX-2), and cathepsin K in periodontal tissue in a rat model of ligature-induced periodontitis.Materials and MethodsMale Wistar albino rats were randomly divided into 5 groups of 10 rats each: (1) nonligated, water; (2) ligated, water; (3) ligated, 1 mg/kg AZT; (4) ligated, 5 mg/kg AZT; and (5) ligated, 10 mg/kg AZT. All groups were treated with saline or AZT for 10 days. Periodontal tissues were analyzed by histopathology and immunohistochemical detection of MMP-2, MMP-9, COX-2, RANKL, RANK, OPG, and cathepsin K. Levels of IL-1β, IL-10, TNF-α, myeloperoxidase (MPO), and glutathione (GSH) were determined by ELISA.ResultsTreatment with 5 mg/kg AZT resulted in reduced MPO (p<0.05) and IL-1β (p<0.05), increased levels of IL-10 (p<0.05), and reduced expression of MMP-2, MMP-9, COX-2, RANK, RANKL, cathepsin K, and increased expression of OPG.ConclusionsThese findings reveal that AZT increases anti-inflammatory cytokines and GSH and decreases bone loss in ligature-induced periodontitis in rats.

show abstract

Section: Introductionmentioning

confidence: 99%

Azilsartan Increases Levels of IL-10, Down-Regulates MMP-2, MMP-9, RANKL/RANK, Cathepsin K and Up-Regulates OPG in an Experimental Periodontitis Model

Araújo

Varela

Brito³

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…Bacteria are essential for the development of periodontitis but not sufficient to cause disease alone. For periodontitis to develop, a susceptible host is required [ 28 , 29 ]. Page et al in 1999 reported that periodontal disease was characterized by high concentrations of matrix metalloproteinases (MMPs), cytokines, and prostaglandins in the periodontal tissue.23 Certain cytokines, including IL-1β and TNF-α, play a critical role in the pathogenesis of periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Preventive effects of the novel antimicrobial peptide Nal-P-113 in a rat Periodontitis model by limiting the growth of Porphyromonas gingivalis and modulating IL-1β and TNF-α production

Wang

et al. 2017

BMC Complement Altern Med

View full text Add to dashboard Cite

BackgroundP-113 (AKRHHGYKRKFH-NH2) is a 12-amino-acid histidine-rich peptide derived from histatin 5 that is highly degradable in high salt concentrations and biological fluids such as serum, plasma and saliva. Nal-P-113, a novel antimicrobial peptide whose histidine residues are replaced by the bulky amino acids β-naphthylalanine, causes the antimicrobial peptide to retain its bactericidal activity even in physiological environments. This study evaluated the effect of the novel antimicrobial peptide Nal-P-113 in a rat periodontitis model and the mechanisms of action of Nal-P-113 for suppressing periodontitis.MethodsPeriodontitis was induced in mandibular first molars in rats receiving a ligature and infected with Porphyromonas gingivalis. Animals were randomly divided into six groups: a, P. gingivalis W83 alone; b, P. gingivalis W83 with 6.25 μg/mL of Nal-P-113; c, P. gingivalis W83 with 25 μg/mL of Nal-P-113; d, P. gingivalis W83 with 100 μg/mL of Nal-P-113; e, P. gingivalis W83 with 400 μg/mL of Nal-P-113; and f, control without P. gingivalis W83 or Nal-P-113. Morphometric analysis was used to evaluate alveolar bone loss. Microbiological assessment of the presence of Porphyromonas gingivalis and total bacteria was performed using absolute quantitative real-time PCR and scanning electron microscopy. Gingival tissue was collected for western blot and immunohistochemical assays of IL-1β and TNF-α levels.ResultsAlveolar bone loss was inhibited by 100 μg/mL or 400 μg/mL of Nal-P-113 compared to the control group (P < 0.05). Lower amounts of P. gingivalis and total bacteria were found in groups d and e compared with group a (P < 0.05). A decrease in the levels of IL-1β and TNF-α was detected in group d and group e compared to the control group (P < 0.05). The amount of P. gingivalis was positively correlated with IL-1β and TNF-α expression in periodontal tissue (P < 0.05).ConclusionsNal-P-113 exhibited protective effects on Porphyromonas gingivalis-induced periodontitis in rats by limiting the amount of bacteria and modulating IL-1β and TNF-α production. The use of Nal-P-113 in vivo might serve as a beneficial preventive or therapeutic approach for periodontitis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-017-1931-9) contains supplementary material, which is available to authorized users.

show abstract

“…Bacteria is an essential key to periodontitis, but it is not sufficient to cause the disease alone. Inflammatory mediators have been recorded to play a key role in periodontal tissue damage, as it is a double-edged sword [ 12 ]. Host modulation therapy is a treatment concept that aims to modify the host’s response towards the inflammatory process of a disease, reducing its damage ( Fig.…”

Section: Host Modulation Therapymentioning

confidence: 99%

“…Host modulation therapy (HMT), a term developed almost three decades ago, is an adjunct treatment strategy that aims to promote periodontal regeneration and restore the balance of pro-inflammatory mediators, as seen in healthy individuals [ 12 ]. While the use of sub antimicrobial-dose doxycycline (SDD) has been approved as an adjunct to conventional periodontitis treatment, studies have shown that non steroid anti-inflammatory drugs (NSAIDs) and bisphosphonate as HMT have raised some concerns.…”

Section: Introductionmentioning

confidence: 99%

Probiotics and metabolites regulate the oral and gut microbiome composition as host modulation agents in periodontitis: A narrative review

Deandra

Ketherin²,

Rachmasari³

et al. 2023

Heliyon

View full text Add to dashboard Cite

Host modulation by therapeutic agents

Cited by 23 publications

References 12 publications

Azilsartan Increases Levels of IL-10, Down-Regulates MMP-2, MMP-9, RANKL/RANK, Cathepsin K and Up-Regulates OPG in an Experimental Periodontitis Model

Azilsartan Increases Levels of IL-10, Down-Regulates MMP-2, MMP-9, RANKL/RANK, Cathepsin K and Up-Regulates OPG in an Experimental Periodontitis Model

Preventive effects of the novel antimicrobial peptide Nal-P-113 in a rat Periodontitis model by limiting the growth of Porphyromonas gingivalis and modulating IL-1β and TNF-α production

Probiotics and metabolites regulate the oral and gut microbiome composition as host modulation agents in periodontitis: A narrative review

Contact Info

Product

Resources

About