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COPD is a chronic inflammatory disease with various comorbidities. Pulmonary emphysema and airway remodeling are two major pathological abnormalities in COPD, and these components can be quantified with imaging techniques such as chest computer assisted tomography (CT). Using CT images, we can evaluate local and regional information in the lung that cannot be obtained by other clinical indices such as pulmonary function tests. Furthermore, the alteration in pulmonary vasculature and chest wall including skeletal muscles and bones can be also evaluated in chest CT images. Recently, regional lung volume assessment using nonrigid image registration techniques or oxygenated oxygen-enhanced MR imaging are developed as functional imaging techniques to evaluate regional oxygenation or ventilation.

Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow limitation caused by a loss of elastic recoil of the lung and/or small airway remodeling. Emphysema is the major pathological lesion in COPD, defined as the abnormal and permanent enlargement of distal airspaces and destruction of alveolar walls. Emphysema correlates most closely with a loss of elastic recoil of the lung and is associated with both airflow limitation and loss of diffusion capacity, while the airway component contributes mainly to airflow limitation. Pulmonary functions reflect these pathological changes and are standard indices for "lung physiological abilities", so that these seem to be appropriate to evaluate the general lung status in vivo. In CT, emphysema is identified as low attenuation and airway wall thickening, and airway lumen narrowing can also be quantified. These CT indices shows the morphological changes/abnormalities that correspond to pathological changes. Thus, CT indices reflect pathological abnormality more precisely and have several advantages over pulmonary functions because those can give us regional information that pulmonary function tests cannot offer. Through the rigorous investigation of COPD pathophysiology using these CT indices, some aspects of the COPD course, such as emphysema progression, and the relationship between COPD pathophysiology and systemic manifestations are becoming clear. (Review).

Chronic obstructive pulmonary disease (COPD) is a progressing lung disorder mainly caused by cigarette smoking. The central pathogeneses are inflammation, oxidative stress, apoptosis and excessive proteases which lead to matrix degradation and loss of lung cells. The inflammation is somehow perpetuated even after quit smoking and is generally refractory to glucocorticoid therapy. It is thus hoped to develop novel anti-inflammatory agents for prevention of disease progression. As molecular mechanisms of COPD are gradually clarified, numerous numbers of molecular targeted agents have been developed for therapeutics. In this section, novel agents for COPD targeted at signal transduction molecules, cytokines, chemokines and those receptors, adhesion molecules, oxidative stress and proteases are discussed.

Cigarette smoking is the most important causal factor for developing chronic obstructive pulmonary disease(COPD). On the other hand, a substantial proportion of COPD cases suffer from obstructive disorder by other causes than smoking, especially among younger persons, females, and residents of developing countries. There are evidences that several rare genetic syndromes(such as alpha 1-antitrypsin deficiency) and occupational exposures as causes of COPD. Environmental tobacco smoke, biomass smoke, and dietary factors are likely causes of COPD, although their contribution is much less compared to active smoking. Smoking during pregnancy may also pose a risk for the fetus, by affecting lung growth and development in uterus. The quicker the smoking cessation is achieved, the more improvements in the lung functions the COPD patients can obtain. Smoking should be avoided as soon as possible in all the COPD subjects and those who are at risk for developing COPD.

COPD is characterized by chronic and persistent inflammation in the small airways and lung parenchyma, which lead to airway remodeling and parenchymal destruction. This inflammation is mediated by the increased expression of multiple inflammatory genes. For the initiation of the transcription of inflammatory genes, the acetylation of core histones is necessary to open up the chromatin structure, that allow transcription factors and RNA polymerase to bind to DNA. Conversely, deacetylation of these histones switches off for the gene transcription. In the COPD lung, the reduced expression of histone deacetylases (HDACs), particularly HDAC-2 is thought to be a key mechanism for the persistence of airway inflammation and corticosteroid resistance.