Periodontitis and Chronic Obstructive Pulmonary Disease

Chronic periodontitis and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases in which neutrophilic inflammation plays a major role. There are a few studies showing that these two entities share various predisposing factors and pathogenetic mechanisms; however, a direct connection between them has not yet been achieved. Epidemiology data may also show a connection between the two conditions. Neutrophilic inflammation in periodontitis and COPD is orchestrated by CD8+ lymphocytes and macrophages, leading to the aggregation of neutrophils and causing an imbalance to the proteases and antiproteases equilibrium. Finally, further research is needed to clarify the common pathogenesis of the two diseases to optimize their therapeutic management

Early Career Members at the Lung Science Conference and the Sleep and Breathing Conference 2019.

The Lung Science Conference and the Sleep and Breathing Conference 2019 brought together leading experts in the field to discuss the latest cutting-edge science, as well as various career development opportunities for early career members http://bit.ly/2XNX6V6

Metabolic disturbances in patients with sleep disordered breathing

Introduction: Obstructive Sleep Apnoea Syndrome (OSA) is a respiratory disorder characterized by recurrent airflow obstruction caused by total or partial collapse of the upper airway. It is estimated that 4% of men and 2% of women aged 30–60 years suffer from OSA. OSA is an established independent factor of cardiovascular risk together with other risk factors such as smoking and elevated lipids. Moreover, it is supposed to play an important role in arterial hypertension, although the relating mechanisms still remain unclear. The aim of our study was to measure serum levels of aldosterone and renin in OSA patients, and compare them to matched healthy subjects in order to reveal the impact of chronic intermittent hypoxia and Autonomic Nervous System (ANS) activation on the Renin-Angiotensin-Aldosterone System (RAAS).Materials and methods: The subjects that enrolled in this study were 19 OSA patients who had undergone overnight polysomnography and had an Apnoea Hypopnoea Index (AHI) greater than 10 events/hour. They were compared to 20 healthy non-OSA controls. Sleep apnea patients were closely matched to the controls regarding their age, gender and Body Mass Index (BMI). An overnight full polysomnography was performed in all participants to determine the presence and severity of OSA. Blood samples for the measurement of renin and aldosterone were obtained at 6 AM, when the patient was awakened in the sleep laboratory, in a supine position before any physical activity. Routine laboratory measurements were performed in the biochemistry laboratory. Serum renin and aldosterone concentrations were measured by radioactive immunoassay.Results: Aldosterone concentration follows a diurnal variation, therefore all blood samples were obtained at the same time from all the subjects (6 AM), before initiation of any kind of physical activity. There were no significant differences in serum aldosterone levels between the two studied groups of OSA patients and the healthy subjects group (140.6 pg/ml ± 25.2 vs 133.2 pg/ml ± 18.5 with p = 0.223). Similar were the results for the renin levels (25.0 ± 6.9 vs 24.9 ± 4.4 with p = 0.360).Discussion: Our study shows that patients with OSA have aldosterone and renin levels similar to healthy subjects. According to our findings, it does not seem to exist a direct connection between OSA and the development of arterial hypertension through RAAS.Εισαγωγή: Το Σύνδρομο Άπνοιας κατά τον Ύπνο (ΣΑΥ) είναι ένα σύνδρομο που χαρακτηρίζεται από διαλείπουσα διακοπή της ροής του αέρα που προκαλείται από πλήρη ή μερική σύμπτωση των ανωτέρων αεραγωγών και γι’ αυτό απασχολεί πολύ συχνά τους πνευμονολόγους. Υπολογίζεται ότι το 4% των ανδρών και το 2% των γυναικών ηλικίας 30–60 ετών πάσχουν από ΣΑΥ. Το ΣΑΥ θεωρείται πλέον ως ανεξάρτητος παράγοντας καρδιαγγειακού κινδύνου, μαζί με άλλους παράγοντες όπως το κάπνισμα και τα αυξημένα λιπίδια. Επιπλέον, πιστεύεται ότι παίζει σημαντικό ρόλο στην εμφάνιση αρτηριακή υπέρτασης, ωστόσο οι παθογενετικοί μηχανισμοί δεν είναι ακόμη σαφείς. Σκοπός της μελέτης μας ήταν να μετρηθούν τα επίπεδα αλδοστερόνης και ρενίνης σε ασθενείς με ΣΑΥ, και να συγκριθούν με υγιή άτομα, με στόχο την ανάδειξη της επίδρασης της χρόνιας διαλείπουσας υποξίας στην ενεργοποίηση του αυτονόμου νευρικού συστήματος και του άξονα ρενίνης-αγγειοτενσίνης-αλδοστερόνης.Υλικό και μέθοδος: Τα άτομα που συμμετείχαν στη μελέτη αυτοί ήταν 19 ασθενείς με ΣΑΥ , που είχαν κάνει πλήρη πολυσωματοκαταγραφική μελέτη ύπνου και είχαν Δείκτη Άπνοιας/Υπόπνοιας (Apnoea Hypopnoea Index – AHI) μεγαλύτερο από 10 επεισόδια/ώρα. Αυτοί συγκρίθηκαν με 20 υγιή άτομα που δεν έπασχαν από ΣΑΥ και χρησιμοποιήθηκαν ως μάρτυρες. Οι ασθενείς με ΣΑΥ εμφάνιζαν παραπλήσια χαρακτηριστικά με τους μάρτυρες σε σχέση με την ηλικία, το φύλο και το Δείκτη Μάζας Σώματος (Body Mass Index – BMI). Πλήρης πολυσωματοκαταγραφική μελέτη ύπνου έγινε σε όλους τους συμμετέχοντες. Τα δείγματα αίματος για τη μέτρηση της ρενίνης και της αλδοστερόνης ελήφθησαν στις 6 π.μ., αμέσως μετά την αφύπνιση στο εργαστήριο ύπνου, σε ύπτια θέση και πριν την έναρξη φυσικής δραστηριότητας. Οι συνήθεις εργαστηριακές μετρήσεις έγιναν στα εργαστήρια του νοσοκομείου. Οι προσδιορισμοί της ρενίνης και αλδοστερόνης στον ορό έγιναν με ραδιενεργά αντισώματα.Αποτελέσματα: Η συγκέντρωση της αλδοστερόνης εμφανίζει ημερήσια διακύμανση, επομένως όλα τα δείγματα ελήφθησαν την ίδια ώρα (6 π.μ.), πριν από την έναρξη φυσικής δραστηριότητας. Δεν υπήρξαν στατιστικά σημαντικές διαφορές στα επίπεδα αλδοστερόνης μεταξύ των δύο ομάδων των ασθενών με ΣΑΥ και των υγιών ατόμων (140,6 pg/ml ± 25,2 vs 133,2 pg/ml ± 18,5 με p = 0,223). Παρόμοια ήταν τα αποτελέσματα και για τα επίπεδα της ρενίνης (25,0 ± 6,9 vs 24,9 ± 4,4 με p = 0,360).Συμπεράσματα: Η μελέτη μας αποδεικνύει ότι οι ασθενείς με ΣΑΥ έχουν επίπεδα ρενίνης και αλδοστερόνης παρόμοια με τα υγιή άτομα. Επομένως, δε φαίνεται να υπάρχει άμεση σχέση ανάμεσα στο ΣΑΥ και την ανάπτυξη αρτηριακή υπέρτασης μέσω του συστήματος ρενίνης-αγγειοτενσίνης-αλδοστερόνης

DNA sequence variations of metalloproteinases: their role in asthma and COPD

Asthma and chronic obstructive pulmonary disease (COPD) are complex genetic diseases that cause considerable morbidity and mortality worldwide. Genetic variability interacting with environmental and ethnic factors is presumed to cause tobacco smoke susceptibility and to influence asthma severity. A disintegrin and metalloproteinase 33 (ADAM33) and matrix metalloproteinase‐9 (MMP9) appear to have important roles in asthma and COPD pathogenesis. ADAM33 and MMP9 genetic alterations could possibly contribute to the establishment and progression of these multifactorial diseases, although their association with the clinical phenotypes has not yet been elucidated. However, the occurrence of these alterations does not always result in clear disease, implying that either they are an epiphenomenon or they are in proximity to the true causative alteration. This review summarises the most recent literature dealing with the genetic variations of metalloproteinases and outlines their potential pathogenetic outcome

The impact of osteoporosis and vertebral compression fractures on mortality and association with pulmonary function in COPD: A meta-analysis

Objective: Osteoporosis is highly prevalent among patients with chronic obstructive pulmonary disease (COPD) and most commonly presents as a vertebral compression fracture (VCF). Our objective was to quantify the effect of osteoporosis and VCFs on the mortality and pulmonary function tests (PFTs), such as forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), of patients with COPD. Methods: A PubMed/Medline search was conducted using the search terms “chronic obstructive pulmonary disease”, “osteoporosis” and “vertebral compression fracture”. Meta-analyses were conducted to evaluate the differences in mortality and PFTs between patients with COPD with and without osteoporosis or VCFs, according to PRISMA guidelines. PROSPERO registration: CRD42019120335. Results: Of the 896 abstracts identified, 27 studies describing 7662 patients with COPD of which 1883 (24.6%) had osteoporosis or VCFs, were included. Random effects model analysis demonstrated that patients with COPD and osteoporosis or VCFs had an increased OR for mortality of 2.40 (95% CI: 1.24; 4.64, I2 = 89%, P < 0.01), decreased FEV1/FVC with a mean difference of −4.80% (95% CI: −6.69; −2.90, I2 = 83%, P < 0.01) and decreased FEV1, with a mean difference of −4.91% (95% CI: −6.51; −3.31, I2 = 95%, P < 0.01) and −0.41 L (95% CI: −0.59; −0.24, I2 = 97%, P < 0.01), compared to control subjects. Apart from FEV1 (liters) in subgroup 1 (P = 0.06), all subgroup analyses found significant differences between groups, as did sensitivity analysis of low risk of bias studies. Conclusion: Osteoporosis and VCFs are associated with a significant reduction in survival and pulmonary function among patients with COPD