Both periodontitis and chronic obstructive pulmonary disease (COPD) are among the most common diseases associated with smoking. These conditions frequently present alongside comorbidities including diabetes, coronary heart disease, duodenal ulcer, deep vein thrombosis, pulmonary embolism, osteoporosis and muscle atrophy. Chronic inflammation contributes to the pathology of both periodontitis and COPD, and in patients suffering from both conditions treatment of periodontitis may lead to relief from COPD symptoms as well. Smoking contributes to the underlying pathophysiology by causing local inflammation, increasing the production of proinflammatory cytokines and most importantly, by locally increasing the activity of proteolytic enzymes which degrade the extracellular matrix in both periodontal and lung interstitial tissue. The increase in protease activity and extracellular matrix degradation may explain why periodontitis and COPD comorbidity is so common, a finding which also indicates that therapeutic interventions targeting protease activity and the inflammatory response may be beneficial for both conditions.
No clinical trial protocols linked to this paper
Clinical trials are automatically linked when NCT numbers are found in the paper's title or abstract.PICO Elements
No PICO elements extracted yet. Click "Extract PICO" to analyze this paper.
Paper Details
MeSH Terms
Associated Data
No associated datasets or code repositories found for this paper.
Related Papers
Related paper suggestions will be available in future updates.