BackgroundThe possible relationship between chronic inflammatory diseases and their co-morbidities has become an increasing focus of research. Both chronic periodontitis and chronic obstructive pulmonary disease are neutrophilic, inflammatory conditions characterized by the loss of local connective tissue. Evidence suggests an association and perhaps a causal link between the two diseases. However, the nature of any relationship between them is unclear, but if pathophysiologically established may have wide-reaching implications for targeted treatments to improve outcomes and prognosis.DiscussionThere have been a number of epidemiological studies undertaken demonstrating an independent association between chronic periodontitis and chronic obstructive pulmonary disease. However, many of them have significant limitations, and drawing firm conclusions regarding causality may be premature. Although the pathology of both these diseases is complex and involves many cell types, such as CD8 positive cells and macrophages, both conditions are predominantly characterized by neutrophilic inflammation. Increasingly, there is evidence that the two conditions are underpinned by similar pathophysiological processes, especially centered on the functions of the neutrophil. These include a disturbance in protease/anti-protease and redox state balance. The association demonstrated by epidemiological studies, as well as emerging similarities in pathogenesis at the level of the neutrophil, suggest a basis for testing the effects of treatment for one condition upon the severity of the other.SummaryAlthough the evidence of an independent association between chronic periodontitis and chronic obstructive pulmonary disease grows stronger, there remains a lack of definitive studies designed to establish causality and treatment effects. There is a need for future research to be focused on answering these questions.

AimTo 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.MethodsThe 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.ResultsCOPD 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.ConclusionThe 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.

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IntroductionChronic obstructive pulmonary disease (COPD) is an inflammatory disease associated with comorbidities including periodontitis.1–2 Periodontitis is characterised by plaque build-up, anaerobic bacterial overgrowth and gingival inflammation which promotes recruitment and activation of neutrophils leading to alveolar bone destruction and tooth loss. However, the characterisation of periodontitis varies between studies causing some uncertainty of any association.AimTo determine whether clinical indices of periodontitis affects its prevalence in COPD patients with and without Alpha-1-antitrypsin deficiency (AATD) and any association with lung function.Methods108 COPD and 63 PiZ AATD patients underwent dental examinations and lung function testing as part of an EU FP7 cross sectional study.Varying definitions of periodontitis used in previous publications were applied; including criteria from the Centres for Disease Control and Prevention in collaboration with the American Academy of Periodontology CDC-AAP (CDC-AAP) and 5th European Workshop in Periodontology.Periodontal indices of probing depth (PD – depth from gingival margin to the base of periodontal pocket) and clinical attachment level (CAL – distance from the cemento-enamel junction to the gingival margin plus probing depth) were then compared to lung function parameters.ResultsThe prevalence of periodontitis varied depending on the definition used.Prevalence ranged from 0.7–98.6% for the whole cohort, with the lowest prevalence for average probing depth >4 mm, but CDC-AAP criteria gave a prevalence of 84.2% and 98.6% with the 5th European workshop criteria.Lung function was significantly correlated with indices of periodontitis for AATD patients; see Table.ConclusionsThe prevalence of periodontitis depends on the definition used. PD is a marker of current status, whilst CAL represents cumulative disease activity, rather like current lung function parameters.Periodontal indices are correlated with lung function parameters in AATD patients which could reflect the inflammatory and predominantly neutrophilic pathophysiology leading to excessive tissue destruction in both diseases.ReferencesShen TC, et al. Risk of Periodontal Diseases in Patients With Chronic Obstructive Pulmonary Disease: A Nationwide Population-based Cohort Study. Medicine (Baltimore) 2015;94(46):e2047.Chung JH, et al. J Periodontol2016:1–11.Abstract P52 Table 1Relationships between clinical indices of periodontitis and lung function in COPD and AATDSpearman’s Rho and p-valueAverage Probing Depth (PD)Average Clinical Attachment Level (CAL)COPDAATDCOPDAATD% predicted FEV10.085p = NS−0.42p < 0.01−0.03p = NS−0.52p < 0.001% predicted TLCO−0.06p = NS−0.34p < 0.010.01p = NS−0.51p < 0.001% predicted KCO−0.10p = NS−0.30p < 0.05−0.04p = NS−0.42p < 0.01