354 ■ Burket’s Oral Medicine

inhibiting the activity of trypsin and other proteases in the serum and tissues. The
characteristic p anlobular emphysematous changes that are seen in α1-antitrypsin
deficiency are related to the loss of alveolar walls. More commonly, risk factors for the
disease include environmental exposure to tobacco smoke, heavy exposure to
occupational dusts and chemicals (vapors, irritants, fumes), and indoor/outdoor
pollution.146 The clinical course of patients with COPD is quite varied. Most patients
display some degree of progressive dyspnea, exercise intolerance, and fatigue. In
addition, patients are susceptible to frequent exacerbations, usually caused by
infections of the upper or lower respiratory tract. Most patients with COPD have little
respiratory reserve. Therefore, any process that causes airway inflammation can lead to
clinical deterioration.

Pathophysiology Three processes are thought to be important in the pathogenesis of

COPD: chronic inflammation throughout the airways, parenchyma, and pulmonary
vasculature; oxidative stress; and an imbalance of proteases and antiproteases in the
lung. These pathologic changes lead to the physiologic changes characteristic of the
disease, including mucus hypersecretion, ciliary dysfunction, airflow limitation,
pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, and
cor pulmonale.146 Expiratory airflow limitation is the primary physiologic change in
COPD. Airflow limitation results from fixed airway obstruction mainly. Patients with
COPD may also have airway hyperresponsiveness overlapping with asthma.147 Mucus
hypersecretion and ciliary dysfunction lead to chronic cough and sputum production. In
advanced COPD, peripheral airway obstruction, parenchymal destruction, and
pulmonary vascular abnormalities reduce the lung’s capacity for gas exchange, leading
to hypoxemia and hypercapnia.146 Many toxins in tobacco smoke can cause a vigorous
inflammatory response. In humans, chronic exposure to tobacco smoke results in an
increase in the number of goblet cells because of hyperplasia and metaplasia. Acrolein,
for example, causes both impairment of both ciliary and macrophage activities, as well
as increases mucin hypersecretion.148 Nitrogen dioxide causes direct toxic damage to
the respiratory epithelium. Hydrogen cyanide is responsible for the functional
impairment of enzymes that are required for respiratory metabolism. Carbon monoxide
causes a decrease in the oxygen-carrying capacity of red blood cells by associating with
hemoglobin to form carboxyhemoglobin. Lastly, polycyclic hydrocarbons have been
implicated as carcinogens. Hypoxemia is the result of the ventilation-perfusion
mismatch that accompanies airway obstruction and emphysema. Portions of the lung
that are not aerated due to obstruction cannot oxygenate the blood. This causes a
decrease in overall oxygen concentrations. In addition, emphysema causes a decreased
diffusion capacity because of a loss of air-space capillary units. Hypercarbia also
develops and is often progressive
and asymptomatic. Pulmonary hypertension can result from chronic hypoxia due to
vasoconstriction of pulmonary vessels. Patients with emphysema alone have less
ventilation- perfusion mismatching early in the course of the disease; this is due to the
loss of both air space and supplying blood vessels. Severe hypoxia, pulmonary
hypertension, and cor pulmonale are generally not seen until late in the disease process.
Emphysema manifests as loss of the elastic recoil of the lungs, making the lungs more
compliant. The work of breathing is therefore not significantly increased. However, the
decrease in recoil allows the easy collapse of the peripheral airways, leading to further
airway obstruction and airflow limitation.149 Clinical and Laboratory Findings Patients
with COPD have symptoms of dyspnea, cough, and sputum production. An increase in
the production of purulent sputum is a sign of exacerbation due to respiratory infection.
Physical findings include diffuse wheezing, possibly associated with signs of respiratory
distress, including the use of accessory muscles of respiration (retractions) and
tachypnea.150 Liver enlargement due to congestion, ascites, and peripheral edema can
develop as the disease progresses to pulmonary hypertension and cor pulmonale. This
leads to the characteristic clinical patient presentation termed the blue bloater. Patients
with emphysema present primarily with dyspnea. Patients can be adequately
oxygenated in the early stages of the disease and thus can have fewer signs of hypoxia;
the term pink puffer has been used to describe these patients. Physical findings include
an increase in chest wall size. Wheezing is present to varying degrees. Chest radiography
may show evidence of an increase in lung compliance, with flattened diaphragms,
hyperexpansion, and an increase in anteroposterior diameter (Figure 14-6). Spirometry
will show evidence of airflow limitation. A post bronchodilator FEV1/FVC ratio of <0.7
confirms the presence of airflow limitation that is not fully reversible, complete
pulmonary function studies will also indicate an increase in residual volume and total
lung capacity.150 Pulmonary d iffusion capacity will be decreased due to a loss of gas-e
xchanging units. Classification COPD is now classified into five stages: at risk, mild,
moderate, severe, and very severe. The at-risk stage is defined by normal spirometry,
but patients have chronic symptoms of cough and sputum production. Mild, moderate,
and severe COPD has evidence of increasing airway obstruction on spirometry in each
progressive stage. Finally, very severe COPD is defined by severe airway obstruction with
chronic respiratory failure. Patients with severe COPD are at more risk for other
systemic diseases including cardiovascular disease, osteoporosis, lung cancer, and
depression.152 Diagnosis The diagnosis is suggested by the history and physical findings.
Patients often have cough, dyspnea, and sputum production and/or a history of
exposure to risk factors. Alternative diagnoses, such as asthma, CF, and congestive heart
failure, should be considered. Complete pulmonary function tests are a valuable means
of assessing airflow limitation and any reversibility. For patients with more severe
disease, assessment of oxygen status with pulse oximetry is a valuable office procedure.
A determination of arterial blood gases is important for patients who are clinically
deteriorating and for the management of hospitalized patients.153 Chest radiography
can be helpful to exclude alternative diagnoses but is rarely diagnostic in COPD.
Management There are no curative treatments for chronic bronchitis and emphysema.
Smoking cessation is the single most important intervention to stop the progression of
COPD. Reduction of exposures to occupational dusts and chemicals and indoor/outdoor
pollution can also decrease the p rogression of disease.146 Influenza and pneumococcal
vaccines are recommended. Management focuses on reducing symptoms and
exacerbations. The most recent Global Initiative for Obstructive Disease guidelines gives
management recommendations after patients have been assessed combining symptom
scores, airflow limitations, and exacerbations (Figure 14-7).146 Maintenance therapy
includes trials of inhaled bronchodilators such as β-agonists and ipratropium bromide.
Long-acting bronchodilators, such as formoterol or salmeterol, may be added as well as
mucolytics. Theophylline products have also been used with some efficacy as well as
phosphodiesterase-4 inhibitors. Long-term monotherapy with oral or inhaled
corticosteroids is not recommended146 as inhaled steroids with long acting β-agonists
are more effective. Chest physiotherapy has not been proven to be of value in the
management of COPD. The long-term administration of oxygen therapy to patients with
chronic respiratory failure increases survival. Additionally, during exacerbations, oxygen
therapy is often required. Caution must be used when administering oxygen

to patients with COPD as their ventilatory drive will often be diminished. This is the
result of chronic retention of carbon dioxide and subsequent insensitivity to
hypercarbia. As a result, patients with COPD are sensitive to increases in oxygen tension,
which provides the major stimulus for respiratory drive. Oxygen therapy during sleep
can also be a useful means of limiting hypoxemia and subsequent pulmonary
hypertension. An option for some patients involves lung-volume reduction which
removes severely emphysematous tissue from the both upper lobes allowing the
remaining tissue to expand and function more effectively.152 Antibiotics are often used
during exacerbations of COPD. The presence of purulent sputum during an exacerbation
generally requires treatment with 7–10 days of an oral antibiotic chosen based on local
bacterial resistant patterns. The primary pathogens in COPD exacerbations include
S. pneumoniae, H. influenzae, and M. catarrhalis. Prognosis The prognosis is poor for
patients who are frequently symptomatic due to COPD. The need for hospital admission
for an exacerbation, especially if intensive care is required, is an ominous prognostic sign
in COPD as about half of such patients admitted to the intensive care unit do not survive
a year after admission.154 Oral Health Considerations The association, if any, between
oral disease and lung disease was analyzed by the National Health and Nutrition
Examination Survey I (NHANES I).155 Of 23,808 individuals, 386 reported a suspected
respiratory condition (as assessed by a physician) categorized as a confirmed chronic
respiratory disease (chronic bronchitis or emphysema) or acute respiratory disease
(influenza, pneumonia, acute bronchitis), or not to have a respiratory disease. Significant
differences were noted between subjects having no disease and those having a chronic
respiratory disease confirmed by a physician. Individuals with a confirmed chronic
respiratory disease had a significantly greater oral hygiene index (OHI) than subjects
without a respiratory disease. Logistic regression analysis was performed to
simultaneously control for multiple variables, including gender, age, race, OHI, and
smoking status. The results of this analysis suggest that for patients having the highest
OHI values, the odds ratio for chronic respiratory disease was 4.5. Another study of
elderly subjects (aged 70–79) found that, after controlling for smoking status, age, race,
and gender, there was a significant association between periodontal health and airway
obstruction in former smokers.156 A more recent study, however, suggested that
cigarette smoking may be a cofactor in the relationship between periodontal disease
and COPD.157 Further longitudinal epidemiologic studies and clinical trials are necessary
to determine the role of oral health status in COPD. These results were supported by a
subsequent study that measured associations between poor oral health and chronic