Severe COVID-19 Lung Infection in Older People and Periodontitis

Aquino-Martínez, Rubén; Hernández-Vigueras, Scarlette

doi:10.3390/jcm10020279

Cited by 44 publications

(53 citation statements)

References 186 publications

(215 reference statements)

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“…Moreover, increased salivary IL-1b levels may have applications as a biomarker for evaluation of periodontal health in patients with type 2 diabetes and coronary heart disease (217,218). Severe acute respiratory syndrome coronavirus may also aggravate periodontal pocket formation by enhancing the expression of pro-inflammatory cytokines, including IL-1b, and the dissemination of periodontal pathogens, and increased IL-1b release may exacerbate coronavirus disease 2019 lung infection (219,220). Likewise, IL18 polymorphisms are associated with susceptibility to periodontitis, and increased IL-18 levels in chronic periodontitis may positively correlate with periodontal destruction (153,(221)(222)(223).…”

Section: Inflammasomes In Periodontitismentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

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Section: Inflammasomes In Periodontitismentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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“…The latest review by Aquino-Martinez (2021) [ 142 ] highlights how the dissemination of periodontal bacteria into lung tissues may cause lipopolysaccharide-induced senescence, which facilitates SARS-CoV-2 cell attachment, entry and replication. The authors explain that LPS interacts with the SARS-CoV-2 spike protein, which potentiates the NF-kB activation, and referred to recent publications where a connection between periodontitis and COVID-19 is suggested by a common proinflammatory cytokine expression profile.…”

Section: Polymicrobial Oral Synergy and Endotoxinsmentioning

confidence: 99%

“…Patients with SARS-CoV-2 might present progressive respiratory failure, the most common cause to require intensive care assistance. The intubation and invasive ventilation necessary in some of the cases is a high-risk procedure with potential complications as the ventilator-associated pneumonia (VAP) described by Aquino-Martinez et al (2021) [ 142 ]. The disease is a polymicrobial infection, but the major group of pathogens isolated from samples of patients with VAP is Gram-negative bacteria like periodontal pathogens and bacteria from the dorsal surface of the tongue or those contaminated present in upper air-way secretions.…”

Section: Polymicrobial Oral Synergy and Endotoxinsmentioning

confidence: 99%

Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease

Marcano

Córdoba-Díaz

et al. 2021

Toxins

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It is widely recognized that periodontal disease is an inflammatory entity of infectious origin, in which the immune activation of the host leads to the destruction of the supporting tissues of the tooth. Periodontal pathogenic bacteria like Porphyromonas gingivalis, that belongs to the complex net of oral microflora, exhibits a toxicogenic potential by releasing endotoxins, which are the lipopolysaccharide component (LPS) available in the outer cell wall of Gram-negative bacteria. Endotoxins are released into the tissues causing damage after the cell is lysed. There are three well-defined regions in the LPS: one of them, the lipid A, has a lipidic nature, and the other two, the Core and the O-antigen, have a glycosidic nature, all of them with independent and synergistic functions. Lipid A is the “bioactive center” of LPS, responsible for its toxicity, and shows great variability along bacteria. In general, endotoxins have specific receptors at the cells, causing a wide immunoinflammatory response by inducing the release of pro-inflammatory cytokines and the production of matrix metalloproteinases. This response is not coordinated, favoring the dissemination of LPS through blood vessels, as well as binding mainly to Toll-like receptor 4 (TLR4) expressed in the host cells, leading to the destruction of the tissues and the detrimental effect in some systemic pathologies. Lipid A can also act as a TLRs antagonist eliciting immune deregulation. Although bacterial endotoxins have been extensively studied clinically and in a laboratory, their effects on the oral cavity and particularly on periodontium deserve special attention since they affect the connective tissue that supports the tooth, and can be linked to advanced medical conditions. This review addresses the distribution of endotoxins associated with periodontal pathogenic bacteria and its relationship with systemic diseases, as well as the effect of some therapeutic alternatives.

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“…Therefore, the presence of periodontitis in patients who are infected with SARS-CoV-2 could represent an as yet unrecognized comorbidity that could contribute to more severe symptoms of COVID-19. While there are now emerging scientific publications that align with this suggestion (70,71), it still stands in the grounds of scientific inference. Two plausible mechanisms may explain this association: one being related to the periodontitis-induced inflammatory response; a pre-existing pro-inflammatory state.…”

Section: Periodontal Disease-induced Immunopathology and Covid-19mentioning

confidence: 96%

The Advent of COVID-19; Periodontal Research Has Identified Therapeutic Targets for Severe Respiratory Disease; an Example of Parallel Biomedical Research Agendas

et al. 2021

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The pathophysiology of SARS-CoV-2 infection is characterized by rapid virus replication and aggressive inflammatory responses that can lead to acute respiratory distress syndrome (ARDS) only a few days after the onset of symptoms. It is suspected that a dysfunctional immune response is the main cause of SARS-CoV-2 infection-induced lung destruction and mortality due to massive infiltration of hyperfunctional neutrophils in these organs. Similarly, neutrophils are recruited constantly to the oral cavity to combat microorganisms in the dental biofilm and hyperfunctional neutrophil phenotypes cause destruction of periodontal tissues when periodontitis develops. Both disease models arise because of elevated host defenses against invading organisms, while concurrently causing host damage/disease when the immune cells become hyperfunctional. This represents a clear nexus between periodontal and medical research. As researchers begin to understand the link between oral and systemic diseases and their potential synergistic impact on general health, we argue that translational research from studies in periodontology must be recognized as an important source of information that might lead to different therapeutic options which can be effective for the management of both oral and non-oral diseases. In this article we connect concepts from periodontal research on oral inflammation while exploring host modulation therapy used for periodontitis as a potential strategy for the prevention of ARDS a deadly outcome of COVID-19. We suggest that host modulation therapy, although developed initially for management of periodontitis, and which inhibits proteases, cytokines, and the oxidative stress that underlie ARDS, will provide an effective and safe treatment for COVID-19.

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Severe COVID-19 Lung Infection in Older People and Periodontitis

Cited by 44 publications

References 186 publications

Inflammasomes in Alveolar Bone Loss

Inflammasomes in Alveolar Bone Loss

Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease

The Advent of COVID-19; Periodontal Research Has Identified Therapeutic Targets for Severe Respiratory Disease; an Example of Parallel Biomedical Research Agendas

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