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Periodontal Disease, Association with Systemic Conditions and Periodontal Pathogens: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 25 September 2025 | Viewed by 1783

Special Issue Editor

Dr. Evangelos Papathanasiou

E-Mail Website
Guest Editor
Department of Periodontology, Tufts University School of Dental Medicine, Boston, MA 02111, USA
Interests: periodontitis; gingivitis; inflammation; antibodies; cytokines; immune response; antigens; bacteria
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Periodontitis is a chronic prevalent non-communicable disease (NCD) characterized by complex dynamic interactions among specific bacterial pathogens and the inflammatory destruction of the tooth-supporting tissues. In recent decades, a significant body of evidence supports independent associations between severe periodontitis and various systemic conditions, such as diabetes mellitus, cardiovascular disease, obesity, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis and adverse pregnancy outcomes. Consequently, the field of “periodontal medicine” has evolved, to study how periodontal infection/inflammation may impact extraoral health. While the field has significantly progressed, there is a need for continued extensive research on the associations between systemic conditions and the infectious, immune, inflammatory and systemic characteristics of periodontitis. Therefore, the aim of this Special Issue of the International Journal of Molecular Sciences is to provide an update on the current knowledge in the research field of “Periodontal Disease, Association with Systemic Conditions and Periodontal Pathogens”, and this Special Issue welcomes both original research articles and review papers that encompasses molecular biology studies on the etiology, diagnosis, prognosis and treatment of periodontitis and periodontal–systemic interactions.

Dr. Evangelos Papathanasiou
Guest Editor

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Keywords

  • periodontal disease
  • periodontitis
  • periodontal medicine
  • periodontal–systemic interactions
  • immune response
  • periodontal pathogens

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Published Papers (2 papers)

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Research

20 pages, 4100 KiB  
Article
Inhibition of CD38 by 78c Enhanced NAD+, Alleviated Inflammation, and Decreased Oxidative Stress in Old Murine Macrophages Induced by Oral Pathogens
by Kimberly Cao, Nityananda Chowdhury, Bridgette Wellslager, William D. Hill, Özlem Yilmaz and Hong Yu
Int. J. Mol. Sci. 2025, 26(13), 6180; https://doi.org/10.3390/ijms26136180 - 26 Jun 2025
Abstract
CD38, a nicotinamide adenine dinucleotide (NAD+) glycohydrolase, increases in old murine macrophages after infection compared to young controls. We aimed to determine whether the increase in CD38 in old murine macrophages after infection is directly associated with enhanced inflammation induced by [...] Read more.
CD38, a nicotinamide adenine dinucleotide (NAD+) glycohydrolase, increases in old murine macrophages after infection compared to young controls. We aimed to determine whether the increase in CD38 in old murine macrophages after infection is directly associated with enhanced inflammation induced by the oral pathogens Aggregatibacter actinomycetemcomitans (Aa) or Porphyromonas gingivalis (Pg) when compared to young controls. Additionally, we determined the effects of a specific CD38 inhibitor (78c) on CD38, NAD+, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α expressions, and anti-oxidative responses in old murine macrophages induced by oral pathogens. Old and young murine macrophages were either uninfected or infected with the oral pathogens Aa or Pg for 1 to 24 h. Protein levels of CD38 and protein kinases, including nuclear factor kappa-B (NF-κB), phosphoinositide 3-kinase (PI3K), and mitogen-activated protein kinases (MAPKs), NAD+, and inflammatory cytokine (IL-1β, IL-6, TNF-α) levels were evaluated. Additionally, old murine macrophages were treated with a vehicle or a CD38 inhibitor (78c) and cells were either uninfected or infected with Aa or Pg. CD38, NAD+, cytokine (IL-1β, IL-6, TNF-α) levels, reactive oxygen species (ROS), NAPDH oxidase 1 (Nox1), and anti-oxidative enzymes, including superoxide dismutase1 (Sod1), glutathione peroxidase 4 (Gpx4), Peroxiredoxin 1 (Prdx1), thioredoxin reductase 1 (Txnrd1), and catalase (Cat), were evaluated. The results showed that old murine macrophages significantly enhanced CD38 and reduced NAD+ levels 24 h after Aa or Pg infection compared to young controls. This enhanced CD38 in old murine macrophages was not directly correlated with the activation of protein kinases (NF-κB, PI3K, and MAPKs), nor the (IL-1β, IL-6, TNF-α) levels in macrophages. The inhibition of CD38 by 78c reduced CD38, enhanced NAD+ levels, attenuated IL-1β, IL-6 and TNF-α pro-inflammatory cytokine levels, reduced ROS and Nox1 expressions, and enhanced expressions of Sod1, Gpx4, Prdx1, Txnrd1, and Cat in old murine macrophages infected with Aa or Pg. These results suggest that the inhibition of CD38 by 78c is a promising therapeutic strategy to treat aging-associated periodontitis. Full article
(This article belongs to the Special Issue Periodontal Disease, Association with Systemic Conditions and Periodontal Pathogens: 2nd Edition)
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14 pages, 3266 KiB  
Article
Anti-Inflammatory Activity of No-Ozone Cold Plasma in Porphyromonas gingivalis Lipopolysaccharide-Induced Periodontitis Rats
by Kwang-Ha Park, Yoon-Seo Jang, Ji-Young Joo, Gyoo-Cheon Kim and Jeong-Hae Choi
Int. J. Mol. Sci. 2024, 25(11), 6161; https://doi.org/10.3390/ijms25116161 - 3 Jun 2024
Cited by 2 | Viewed by 1302
Abstract
Periodontitis is an inflammatory disease caused by Porphyromonas gingivalis (P. gingivalis) in the oral cavity. This periodontal disease causes damage to the periodontal ligament and alveolar bone and can cause tooth loss, but there is no definite treatment yet. In this [...] Read more.
Periodontitis is an inflammatory disease caused by Porphyromonas gingivalis (P. gingivalis) in the oral cavity. This periodontal disease causes damage to the periodontal ligament and alveolar bone and can cause tooth loss, but there is no definite treatment yet. In this study, we investigated the possibility of using no-ozone cold plasma to safely treat periodontitis in the oral cavity. First, human gingival fibroblasts (HGFs) were treated with P. gingivalis-derived lipopolysaccharide (PG-LPS) to induce an inflammatory response, and then the anti-inflammatory effect of NCP was examined, and a study was conducted to identify the mechanism of action. Additionally, the anti-inflammatory effect of NCP was verified in rats that developed an inflammatory response similar to periodontitis. When NCP was applied to PG-LPS-treated HGFs, the activities of inflammatory proteins and cytokines were effectively inhibited. It was confirmed that the process of denaturing the medium by charged particles of NCP is essential for the anti-inflammatory effect of NCP. Also, it was confirmed that repeated treatment of periodontitis rats with NCP effectively reduced the inflammatory cells and osteoclast activity. As a result, this study suggests that NCP can be directly helpful in the treatment of periodontitis in the future. Full article
(This article belongs to the Special Issue Periodontal Disease, Association with Systemic Conditions and Periodontal Pathogens: 2nd Edition)
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