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The clinical and inflammatory relationships between periodontitis and chronic obstructive pulmonary disease
Author(s) -
Sapey Elizabeth,
Yonel Zehra,
Edgar Ross,
Parmar Sabrina,
Hobbins Stephanie,
Newby Paul,
Crossley Diana,
Usher Adam,
Johnson Sarah,
Walton Georgia M.,
McGuinness Adam,
Chapple Iain,
Stockley Robert
Publication year - 2020
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.13334
Subject(s) - periodontitis , copd , medicine , alpha 1 antitrypsin deficiency , exacerbation , disease , immunology
Aim To investigate associations between periodontitis and chronic obstructive pulmonary disease (COPD) with and without alpha‐1 antitrypsin deficiency (AATD), including neutrophil functions implicated in tissue damage. Methods The presence and severity of periodontitis (using two international criteria) and lung disease were assessed in 156 COPD patients with and without AATD accounting for common confounding factors. Saliva and systemic inflammatory markers were measured by ELISA together with neutrophil migration. Results COPD and AATD patients exhibited higher prevalence of periodontitis (COPD 95%; AATD 88%) than reported in unselected community‐dwelling populations even when risk factors (age, smoking history, socio‐economic status and dental habits) were considered. Periodontitis severity associated with lung disease severity (AATD, periodontitis versus no periodontitis; FEV1 = 56% versus 99% predicted; TLCO = 59% versus 81% predicted, p < .0001 for both). Neutrophil migratory accuracy declined in stage II–IV periodontitis patients with COPD or AATD compared to COPD or AATD with no or stage I periodontitis. Improved dental habits appeared to be associated with a reduction in exacerbation frequency in COPD. Conclusion The results support shared pathophysiology between periodontitis and COPD, especially when associated with AATD. This may reflect an amplification of neutrophilic inflammation and altered neutrophil functions, already described in periodontitis, COPD and AATD.