Periodontal Diseases: Major Exacerbators of Pulmonary Diseases?

Periodontal diseases are a range of polymicrobial infectious disorders, such as gingivitis and periodontitis, which affect tooth-supporting tissues and are linked to playing a role in the exacerbation of several pulmonary diseases. Pulmonary diseases, such as pneumonia, chronic obstructive pulmonary disease (COPD), asthma, tuberculosis, COVID-19, and bronchiectasis, significantly contribute to poor quality of life and mortality. The association between periodontal disease and pulmonary outcomes is an important topic and requires further attention. Numerous resident microorganisms coexist in the oral cavity and lungs. However, changes in the normal microflora due to oral disease, old age, lifestyle habits, or dental intervention may contribute to altered aspiration of oral periodontopathic bacteria into the lungs and changing inflammatory responses. Equally, periodontal diseases are associated with the longitudinal decline in spirometry lung volume. Several studies suggest a possible beneficial effect of periodontal therapy in improving lung function with a decreased frequency of exacerbations and reduced risk of adverse respiratory events and morbidity. Here, we review the current literature outlining the link between the oral cavity and pulmonary outcomes and focus on the microflora of the oral cavity, environmental and genetic factors, and preexisting conditions that can impact oral and pulmonary outcomes.

Download Full-text

The Buccale Puzzle: The Symbiotic Nature of Endogenous Infections of the Oral Cavity

Canadian Journal of Infectious Diseases ◽

10.1155/2002/492656 ◽

2002 ◽

Vol 13 (1) ◽

pp. 34-41 ◽

Cited By ~ 23

Author(s):

John Ruby ◽

Jean Barbeau

Keyword(s):

Oral Health ◽

Dental Caries ◽

Oral Cavity ◽

Periodontal Diseases ◽

Oral Disease ◽

Continuous Change ◽

Mutualistic Symbiosis ◽

Normal Microflora ◽

Caries Progression ◽

Indigenous Microflora

The indigenous, 'normal' microflora cause the majority of localized infectious diseases of the oral cavity (eg, dental caries, alveolar abscesses, periodontal diseases and candidiasis). The same microflora also protect the host from exogenous pathogens by stimulating a vigorous immune response and providing colonization resistance. How can a microflora that support health also cause endogenous oral disease? This paradoxical host-symbiont relationship will be discussed within the dynamic of symbiosis.Symbiosis means 'life together' - it is capable of continuous change as determined by selective pressures of the oral milieu. Mutualistic symbiosis, where both the host and the indigenous microflora benefit from the association, may shift to a parasitic symbiosis, where the host is damaged and the indigenous microflora benefit. Importantly, these are reversible relationships. This microbial dynamism, called amphibiosis, is the essential adaptive process that determines the causation of endogenous oral disease by a parasitic microflora or the maintenance of oral health by a mutualistic microflora.Complex microbial consortiums, existing as a biofilm, usually provide the interfaces that initiate and perpetuate the infectious assault on host tissue. The ecology of the various oral microhabitats is critical for the development of the appropriate selecting milieux for pathogens. The microbiota associated with dental caries progression are primarily influenced by the prevailing pH, whereas periodontal diseases and pulpal infection appear to be more dependent on redox potential. Candidiasis results from host factors that favour yeast overgrowth or bacterial suppression caused by antibiotics. Oral health or disease is an adventitious event that results from microbial adaptation to prevailing conditions; prevention of endogenous oral disease can occur only when we realize that ecology is the heart of these host-symbiont relationships.

Download Full-text

Oral and Oropharyngeal Sensory Function in Adults With Chronic Obstructive Pulmonary Disease

American Journal of Speech-Language Pathology ◽

10.1044/2019_ajslp-19-00095 ◽

2020 ◽

Vol 29 (2) ◽

pp. 864-872

Author(s):

Fernanda Borowsky da Rosa ◽

Adriane Schmidt Pasqualoto ◽

Catriona M. Steele ◽

Renata Mancopes

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Oral Cavity ◽

Pulmonary Disease ◽

Thermal Sensation ◽

Sensory Function ◽

Control Group ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Age Related ◽

Copd Patients

Introduction The oral cavity and pharynx have a rich sensory system composed of specialized receptors. The integrity of oropharyngeal sensation is thought to be fundamental for safe and efficient swallowing. Chronic obstructive pulmonary disease (COPD) patients are at risk for oropharyngeal sensory impairment due to frequent use of inhaled medications and comorbidities including gastroesophageal reflux disease. Objective This study aimed to describe and compare oral and oropharyngeal sensory function measured using noninstrumental clinical methods in adults with COPD and healthy controls. Method Participants included 27 adults (18 men, nine women) with a diagnosis of COPD and a mean age of 66.56 years ( SD = 8.68). The control group comprised 11 healthy adults (five men, six women) with a mean age of 60.09 years ( SD = 11.57). Spirometry measures confirmed reduced functional expiratory volumes (% predicted) in the COPD patients compared to the control participants. All participants completed a case history interview and underwent clinical evaluation of oral and oropharyngeal sensation by a speech-language pathologist. The sensory evaluation explored the detection of tactile and temperature stimuli delivered by cotton swab to six locations in the oral cavity and two in the oropharynx as well as identification of the taste of stimuli administered in 5-ml boluses to the mouth. Analyses explored the frequencies of accurate responses regarding stimulus location, temperature and taste between groups, and between age groups (“≤ 65 years” and “> 65 years”) within the COPD cohort. Results We found significantly higher frequencies of reported use of inhaled medications ( p < .001) and xerostomia ( p = .003) in the COPD cohort. Oral cavity thermal sensation ( p = .009) was reduced in the COPD participants, and a significant age-related decline in gustatory sensation was found in the COPD group ( p = .018). Conclusion This study found that most of the measures of oral and oropharyngeal sensation remained intact in the COPD group. Oral thermal sensation was impaired in individuals with COPD, and reduced gustatory sensation was observed in the older COPD participants. Possible links between these results and the use of inhaled medication by individuals with COPD are discussed.

Download Full-text

Understanding racial differences of COPD patients with an ecological model: two large cohort studies in the US and Korea

Therapeutic Advances in Chronic Disease ◽

10.1177/2040622320982455 ◽

2021 ◽

Vol 12 ◽

pp. 204062232098245

Author(s):

Hye Yun Park ◽

Hyun Lee ◽

Danbee Kang ◽

Hye Sook Choi ◽

Yeong Ha Ryu ◽

...

Keyword(s):

Racial Differences ◽

Large Scale ◽

Ecological Model ◽

Prevalence Ratio ◽

Poor Quality ◽

Smoking History ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Copd Patients ◽

The Us

Background: There are limited data about the racial difference in the characteristics of chronic obstructive pulmonary disease (COPD) patients who are treated at clinics. We aimed to compare sociodemographic and clinical characteristics between US and Korean COPD patients using large-scale nationwide COPD cohorts. Methods: We used the baseline demographic and clinical data of COPD patients aged 45 years or older with at least a 10 pack-per year smoking history from the Korean COPD Subtype Study (KOCOSS, n = 1686) cohort (2012–2018) and phase I (2008–2011) of the US Genetic Epidemiology of COPD (COPDGene) study ( n = 4477, 3461 were non-Hispanic whites [NHW], and 1016 were African Americans [AA]). Results: Compared to NHW, AA had a significantly lower adjusted prevalence ratio (aPR) of cough >3 months (aPR: 0.67; 95% CI [confidence interval]: 0.60–0.75) and phlegm >3 months (aPR: 0.78, 95% CI: 0.70–0.86), but higher aPR of dyspnea (modified Medical Round Council scale ⩾2) (aPR: 1.22; 95% CI: 1.15–1.29), short six-minute walk distance (<350 m) (aPR: 1.98; 95% CI: 1.81–2.14), and poor quality of life (aPR: 1.10; 95% CI: 1.05–1.15). Compared to NHW, Koreans had a significantly lower aPR of cough >3 months (aPR: 0.53; 95% CI: 0.47–0.59), phlegm >3 months (aPR: 0.75; 95% CI: 0.67–0.82), dyspnea (aPR: 0.72; 95% CI: 0.66–0.79), and moderate-to-severe acute exacerbation in the previous year (aPR: 0.73; 95% CI: 0.65–0.82). NHW had the highest burden related to chronic bronchitis symptoms and cardiovascular diseases related to comorbidities. Conclusion: There are substantial differences in sociodemographic characteristics, clinical presentation, and comorbidities between COPD patients from the KOCOSS and COPDGene, which might be caused by interactions between various intrapersonal, interpersonal, and environmental factors of the ecological model. Thus, a broader and more comprehensive approach would be necessary to understand the racial differences of COPD patients.

Download Full-text

The Effects of Corticosteroids on the Respiratory Microbiome: A Systematic Review

Frontiers in Medicine ◽

10.3389/fmed.2021.588584 ◽

2021 ◽

Vol 8 ◽

Author(s):

Julia E. Hartmann ◽

Werner C. Albrich ◽

Marija Dmitrijeva ◽

Christian R. Kahlert

Keyword(s):

Systematic Review ◽

Research Question ◽

Corticosteroid Treatment ◽

Pulmonary Diseases ◽

Chronic Obstructive ◽

Cochrane Central Register ◽

Obstructive Pulmonary Disease ◽

Randomized Controlled Studies ◽

Culture Independent ◽

Respiratory Microbiome

Background: Since its discovery, the respiratory microbiome has been implicated in the pathogenesis of multiple pulmonary diseases. Even though corticosteroid treatments are widely prescribed for pulmonary diseases, their effects on the respiratory microbiome are still poorly understood. This systematic review summarizes the current understanding of the effects of corticosteroids on the microbiome of the airways.Research Question: How does treatment with corticosteroids impact the respiratory microbiome?Study Design and Methods: According to the PRISMA guidelines, Embase, Medline, and the Cochrane Central Register of Controlled Trials (CENTRAL) databases were systematically searched for all observational or randomized-controlled studies comparing the microbiome parameters of patients receiving corticosteroids to those of controls. The primary outcomes of interest were changes in the diversity, composition and total burden of the respiratory microbiome as assessed by culture-independent molecular methods.Results: Out of 1,943 identified reports, five studies could be included: two on patients with asthma, two on patients with chronic obstructive pulmonary disease and one on patients with chronic rhinosinusitis. The studies were highly heterogeneous with regards to the methods used and the populations investigated. Microbiome diversity increased with corticosteroids at least transiently in three studies and decreased in one study. The effects of corticosteroids on the composition of the respiratory microbiome were significant but without a clear shared direction. A significant increase in microbial burden after corticosteroids was seen in one study.Interpretation: Data on the effect of corticosteroids on the respiratory microbiome are still limited, with considerable heterogeneity between studies. However, available data suggest that corticosteroid treatment may have significant effects on the composition and possibly the diversity of the respiratory microbiome. Further research is needed to better understand the influence of corticosteroids on the respiratory microbiome and thus better target its widespread therapeutic use.

Download Full-text

Research Advances in COPD Drugs and Novel Targets

Nano LIFE ◽

10.1142/s1793984421400080 ◽

2021 ◽

Vol 11 (03) ◽

pp. 2140008

Author(s):

Lveli Wang ◽

Chuang Xiao ◽

Yaping Liang ◽

Zhiying Weng ◽

Weimin Yang

Keyword(s):

Inflammatory Responses ◽

Treatment Strategies ◽

New Drugs ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Phosphodiesterase 4 Inhibitors ◽

Novel Targets ◽

Anti Inflammatory ◽

To Come ◽

Exacerbation Of Copd

Chronic obstructive pulmonary disease (COPD) is the third-most deadly disease in the world and will be a major healthcare problem for decades to come. Its etiology is mainly related to the exposure to cigarette smoke and poisonous gases, and the infections of viruses including COVID-19 induce acute exacerbation of COPD, which may cause death in patients. Few advances have been made in COPD pathological mechanism, and the current clinical treatment strategies focus on both bronchodilator and anti-inflammatory interventions; but with limited clinical therapeutic agents, COPD therapies still lack more drugs especially those that antagonize COPD-specific inflammatory responses. We review the COPD clinically applied drugs, and the progress of research on new drugs and related novel targets, including [Formula: see text] agonists and anti-muscarinic drugs for airway diastole, glucocorticoids and phosphodiesterase-4 inhibitors for anti-inflammatory, protease inhibitors, emerging antioxidants, adhesion factor inhibitors, growth factor antagonists, adenylate cyclase agonists, chemokine antagonists, etc. We thus provide insights on the COPD new drugs research and development.

Download Full-text

Asthma and COPD Patients’ Perception of Appropriate Metered-Dose Inhaler Technique

Dose-Response ◽

10.1177/1559325820917832 ◽

2020 ◽

Vol 18 (2) ◽

pp. 155932582091783 ◽

Cited By ~ 1

Author(s):

Wijdan H. Ramadan ◽

Aline Sarkis ◽

Sandrine Sarine Aderian ◽

Aline Milane

Keyword(s):

Pulmonary Disease ◽

Reliability And Validity ◽

Pulmonary Diseases ◽

Dose Inhaler ◽

Chronic Obstructive ◽

Community Pharmacies ◽

Obstructive Pulmonary Disease ◽

Survey Tool ◽

Metered Dose ◽

The Mean

Objectives: Asthma and chronic obstructive pulmonary disease (COPD) are chronic illnesses of the airways affecting a good number of people in Lebanon and the Middle East. Pressurized metered-dose inhalers (pMDIs) are important drug delivery systems used to treat such pulmonary diseases. Drugs proven to be valuable and effective may fail to act effectively if such inhalers are used incorrectly. The purpose of this study was to assess the technical use of pMDIs by patients with pulmonary diseases presenting to the community pharmacies in Lebanon. Methods: A structured questionnaire was developed to collect data. A total of 601 patients using drugs delivered through pMDIs and presenting to 12 Lebanese community pharmacies were recruited to participate in the research project. The questionnaire items were divided into 3 subscales: subscale 1—assessing the device preparation; subscale 2—investigating the device use; and subscale 3—examining the knowledge and use of spacers. After confirming the reliability and validity of the survey tool, patients’ responses were analyzed and compared according to many variables. Results: Many patients answered inaccurately to questions assessing both the device preparation and use. Around 40% of patients said they do not coordinate the inhalation with pressing the canister down. The mean scores were 1.72 (± 0.73) over 6 and 5.67 (± 1.44) over 7 for subscales 1 and 2, respectively. The mean total score on all questions was 7.39 over 13, with a standard deviation of 1.75. While patients’ age did not impact the results, asthmatic, well-educated, male patients had fewer wrong answers when it comes to preparing and using the device ( P < .01). Conclusions: Our study showed that many patients with asthma and COPD might not be properly using their pMDIs. Appropriate inhaler use is crucial for successful pulmonary disease management. As pMDIs are one of the most difficult devices to use, proper and tailored instructions should be given to patients.

Download Full-text

Eosinophil-derived IL-13 promotes emphysema

European Respiratory Journal ◽

10.1183/13993003.01291-2018 ◽

2019 ◽

Vol 53 (5) ◽

pp. 1801291 ◽

Cited By ~ 10

Author(s):

Alfred D. Doyle ◽

Manali Mukherjee ◽

William E. LeSuer ◽

Tyler B. Bittner ◽

Saif M. Pasha ◽

...

Keyword(s):

Mouse Model ◽

Inflammatory Responses ◽

Pulmonary Inflammation ◽

Forced Expiratory Volume ◽

Chronic Obstructive ◽

Chronic Type ◽

Obstructive Pulmonary Disease ◽

Lung Eosinophilia

The inflammatory responses in chronic airway diseases leading to emphysema are not fully defined. We hypothesised that lung eosinophilia contributes to airspace enlargement in a mouse model and to emphysema in patients with chronic obstructive pulmonary disease (COPD).A transgenic mouse model of chronic type 2 pulmonary inflammation (I5/hE2) was used to examine eosinophil-dependent mechanisms leading to airspace enlargement. Human sputum samples were collected for translational studies examining eosinophilia and matrix metalloprotease (MMP)-12 levels in patients with chronic airways disease.Airspace enlargement was identified in I5/hE2 mice and was dependent on eosinophils. Examination of I5/hE2 bronchoalveolar lavage identified elevated MMP-12, a mediator of emphysema. We showed, in vitro, that eosinophil-derived interleukin (IL)-13 promoted alveolar macrophage MMP-12 production. Airspace enlargement in I5/hE2 mice was dependent on MMP-12 and eosinophil-derived IL-4/13. Consistent with this, MMP-12 was elevated in patients with sputum eosinophilia and computed tomography evidence of emphysema, and also negatively correlated with forced expiratory volume in 1 s.A mouse model of chronic type 2 pulmonary inflammation exhibited airspace enlargement dependent on MMP-12 and eosinophil-derived IL-4/13. In chronic airways disease patients, lung eosinophilia was associated with elevated MMP-12 levels, which was a predictor of emphysema. These findings suggest an underappreciated mechanism by which eosinophils contribute to the pathologies associated with asthma and COPD.

Download Full-text

Integrative Analysis Reveals Common and Unique Roles of Tetraspanins in Fibrosis and Emphysema

Frontiers in Genetics ◽

10.3389/fgene.2020.585998 ◽

2020 ◽

Vol 11 ◽

Author(s):

Lokesh P. Tripathi ◽

Mari N. Itoh ◽

Yoshito Takeda ◽

Kazuyuki Tsujino ◽

Yasushi Kondo ◽

...

Keyword(s):

Pulmonary Fibrosis ◽

Molecular Mechanisms ◽

Inflammatory Responses ◽

Enrichment Analysis ◽

Functional Enrichment Analysis ◽

Functional Enrichment ◽

Integrative Approach ◽

Chronic Obstructive ◽

Lung Pathology ◽

Obstructive Pulmonary Disease

While both chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are multifactorial disorders characterized by distinct clinical and pathological features, their commonalities and differences have not been fully elucidated. We sought to investigate the preventive roles of tetraspanins Cd151 and Cd9 -that are involved in diverse cellular processes in lung pathophysiology- in pulmonary fibrosis and emphysema, respectively, and to obtain a deeper understanding of their underlying molecular mechanisms toward facilitating improved therapeutic outcomes. Using an integrative approach, we examined the transcriptomic changes in the lungs of Cd151- and Cd9-deficient mice using functional-enrichment-analysis, pathway-perturbation-analysis and protein-protein-interaction (PPI) network analysis. Circadian-rhythm, extracellular-matrix (ECM), cell-adhesion and inflammatory responses and associated factors were prominently influenced by Cd151-deletion. Conversely, cellular-junctions, focal-adhesion, vascular-remodeling, and TNF-signaling were deeply impacted by Cd9-deletion. We also highlighted a “common core” of factors and signaling cascades that underlie the functions of both Cd151 and Cd9 in lung pathology. Circadian dysregulation following Cd151-deletion seemingly facilitated progressive fibrotic lung phenotype. Conversely, TGF-β signaling attenuation and TNF-signaling activation emerged as potentially novel functionaries of Cd9-deletion-induced emphysema. Our findings offer promising avenues for developing novel therapeutic treatments for pulmonary fibrosis and emphysema.

Download Full-text

Protective Features of Autophagy in Pulmonary Infection and Inflammatory Diseases

Cells ◽

10.3390/cells8020123 ◽

2019 ◽

Vol 8 (2) ◽

pp. 123 ◽

Cited By ~ 12

Author(s):

Kui Wang ◽

Yi Chen ◽

Pengju Zhang ◽

Ping Lin ◽

Na Xie ◽

...

Keyword(s):

Pulmonary Infection ◽

Inflammatory Responses ◽

Inflammatory Diseases ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Autophagy Pathway ◽

Pulmonary Arterial ◽

Cellular Components ◽

Cellular Stressors

Autophagy is a highly conserved catabolic process involving autolysosomal degradation of cellular components, including protein aggregates, damaged organelles (such as mitochondria, endoplasmic reticulum, and others), as well as various pathogens. Thus, the autophagy pathway represents a major adaptive response for the maintenance of cellular and tissue homeostasis in response to numerous cellular stressors. A growing body of evidence suggests that autophagy is closely associated with diverse human diseases. Specifically, acute lung injury (ALI) and inflammatory responses caused by bacterial infection or xenobiotic inhalation (e.g., chlorine and cigarette smoke) have been reported to involve a spectrum of alterations in autophagy phenotypes. The role of autophagy in pulmonary infection and inflammatory diseases could be protective or harmful dependent on the conditions. In this review, we describe recent advances regarding the protective features of autophagy in pulmonary diseases, with a focus on ALI, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), tuberculosis, pulmonary arterial hypertension (PAH) and cystic fibrosis.

Download Full-text

Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease

Journal of Innate Immunity ◽

10.1159/000441299 ◽

2015 ◽

Vol 8 (2) ◽

pp. 121-128 ◽

Cited By ~ 7

Author(s):

Chang Min Yoon ◽

Milang Nam ◽

Yeon-Mok Oh ◽

Charles S. Dela Cruz ◽

Min-Jong Kang

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Pulmonary Disease ◽

Inflammatory Responses ◽

Pulmonary Inflammation ◽

Innate Immune ◽

Western Society ◽

Future Research ◽

Chronic Obstructive ◽

Inflammasome Activation ◽

Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is characterized by enhanced chronic airway and lung inflammatory responses to noxious particles or gases. It is a major unmet medical need worldwide, and in Western society is strongly associated with exposure to cigarette smoke (CS). CS-induced inflammation is believed to be a key immune driver in the pathogenesis of COPD. Since the concept of inflammasomes was first introduced nearly a decade ago, these have been increasingly recognized as a central player in innate immune and inflammatory responses. In addition, studies have emerged demonstrating that mitochondrial innate immune signaling plays an important role in CS-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. Here, recent discoveries about inflammasome activation and mitochondrial biology and their role in COPD pathogenesis are reviewed. In addition, the current limitations of our understanding of this theme and future research directions are discussed.

Download Full-text