42

The respiratory system includes the nasal and oral cav-ities: the sinuses and larynx as the upper airway, and thetrachea, bronchi, bronchioles, and alveoli as the lowerairway. Many of the diseases that occur in the oral cav-ity are also found in the upper airway regions. Inflam-matory lesions, both infectious and allergic are found inthe nose, sinuses, nasopharynx, oropharynx, and lar-ynx. Tumors of the upper air passages are similar to oralneoplasms, with a few lesions being unique to thesinonasal region. The respiratory mucosal lining over-lies mucinous glands, and these glands can give rise tosalivary type tumors. Since these tissues are in closeproximity to the oral cavity, the dentist should be famil-iar with the basic disease processes that are diagnosedand treated by the otolaryngologist.

Diseases of the lower tract are typically referred to aspulmonary diseases. Acute and chronic pulmonary infec-tions are of concern to the dental team since some ofthese infections are transmissible in the dental office.Pulmonary infections can compromise respiratory func-tion and pose a risk during inhalation anesthesia. Aller-gic reactions of the airway, particularly anaphylacticshock, can be induced by a variety of drugs and mayconstitute a medical emergency. Asthma is also animmunopathologic condition that is characterized byairway constriction and can become an emergency whena severe attack develops. A group of chronic pulmonarydiseases progressively lead to a loss of pulmonary func-tion, a condition known as chronic obstructive pul-monary disease (COPD). Patients with COPD have dif-ficulty breathing, particularly when reclined, and theyalso pose a risk during inhalation anesthesia. Chronicobstructive pulmonary disease is one of the major causesof death each year in the United States.

Pathophysiology

The upper air passages are lined by either stratified squa-mous or respiratory pseudostratified columnar epithelia.Respiratory epithelium is found throughout thesinonasal tract, whereas stratified squamous epitheliumis found throughout the oral cavity, in certain regions ofthe oropharynx, and covering the vocal apparatus in thelarynx. In all regions, minor mucus-secreting glands arefound, and these glands transmit their secretionsthrough ducts that empty onto the surface of the airwayepithelium to form the moist mucosal surface.

Anatomically, the paranasal sinuses are locatedaround the nasal cavity, and all of these sinuses have exitsites, or ostia, that allow mucous secretions to drain intothe nasal cavity. The sinuses, being hollow cavities withinthe skull, reduce the bony mass and weight of the headwhile serving to moderate the temperature of inspired air.The connective tissues of the lateral nasal walls are tra-versed by a rich supply of blood vessels. Inflammatorydiseases of the sinonasal region are common and are usu-ally of an allergic nature, although bacterial and viralmucosal infections are also common in these regions.

Most of the sinonasal allergies are IgE-mediatedimmediate hypersensitivity reactions. Inspired allergens,such as pollens, dander, and various other particles, canstimulate a specific IgE response (Figure 5–1). These IgEantibodies (reagins) are bound to mast cell membranes bya specific receptor that binds to a ligand on the Fc region.When allergen passes into the mucous membrane and dif-fuses into the submucosa, binding to the IgE-mast cellcomplex causes bridging of two contiguous immunoglob-ulins, a conformational event that triggers internal sig-naling pathways that initiate degranulation and release of

Pathophysiology, 42

Clinical features, 47

Oral manifestations, 50

Dental management, 51

Suggested reading, 53

5 Respiratory DiseasesL. Roy Eversole, DDS, MSD, MA

R E S P I R A T O R Y D I S E A S E S 43

Neoplastic processes of the nose and sinuses are ofboth the benign and malignant varieties. There are threehistologic variants of papillomas that occur in the nose,usually arising on the lateral wall and also extendinginto the antrum. Fungiform papillomas are innocuous,whereas inverting type papillomas are aggressive, caus-ing osseous destruction. Inverting papillomas are asso-ciated with human papillomavirus (HPV), usually types6, 11, and 16, although Epstein-Barr virus DNA hasalso been identified in the papilloma tissues. It is moreprobable that the HPVs are causative. About 5% ofinverting papillomas undergo carcinomatous transfor-mation. The cylindric cell papilloma is histologicallyunique and is rare.

histamine. Histamine induces vasodilation and increasedcapillary permeability with leakage of proteins fromserum, including kinins and other mediators that causepruritus and sneezing. Protein leaks increase tissueosmotic pressure, culminating in edema and swelling ofthe mucous membranes. Prolonged exposure to allergensover many years may stimulate proliferation of the softtissues, the result of which is the formation of nasal andantral polyps. Mucosal edema that develops in eitherinfectious or allergic inflammations can lead to swellingand occlusion of the sinus ostea, with resulting pain andfluid retention. These changes are readily visualized oncomputed tomography (CT) scans and magnetic reso-nance imaging (MRI) of the sinus regions.

Bronchiolarconstriction

Histamine

Histamine

Mast cell

IgE

Ag

Edema

HypotensionVessel

Bronchiole

Figure 5–1 IgE-mediated reactionsin allergic pulmonary inflammatorydiseases. Allergens react with reagin(IgE) antibodies that are bound toreceptors on mast cells. Histamineand leukotrienes are released andexert pharmacologic effects onendothelial cells, mucus-secretingepithelial cells, and smooth muscle. Inanaphylactic shock, acute and severevasodilation with bronchospasmsoccur following systemic introductionof allergen. In asthma, hypotensivereaction is lacking, since the allergenis introduced via the airway and onlyaffects bronchiolar smooth muscle.

44 C H A P T E R 5

Squamous cell carcinoma is the most common can-cer to arise in the sinuses. Adenocarcinomas are seen inthe nasal cavity; hardwood saw dust is considered a riskfactor for these adenocarcinomas, many of whichmicroscopically have the appearance of intestinalepithelium. As stated previously, the presence of numer-ous salivary type glands accounts for the occurrence ofsalivary gland tumors in the airway. Certain neoplasmsare unique to the sinonasal region. The olfactory neuro-blastoma derives from neuroblasts in the olfactory bulb.Craniopharyngiomas arise in the pituitary gland andmay invade the upper nasopharynx. A unique vasculartumor that arises in young boys is located in the poste-rior nasal cavity and apparently arises from the vascu-lar tissues that are so plentiful in the lateral nasal wall.Carcinomas that are poorly differentiated or undiffer-entiated are also found in this region. The sinonasalundifferentiated carcinoma is a neoplasm with a poorprognosis that is encountered in the adult. Nonkera-tinizing squamous cell carcinoma is a nasopharyngealmalignancy of teenage males that is often first detectedas a neck metastasis.

The larynx is also a site of inflammatory disease.Both allergies and infections can cause laryngitis. Severeinfections with marked edema can compromise the air-way and even lead to death. Laryngospasm or bron-chospasm secondary to anaphylactic shock can also bea fatal event. The same mechanisms described earlierare operational in anaphylactic shock. Allergen IgEreponses with histamine release can be systemic or localwith profound hypotension and loss of consciousness.The effect of histamine release on bronchiolar smoothmuscle is constriction, with airway stricture. A similarreaction is encountered in asthma. Leukoplakia of thelarynx is relatively common, and squamous cell carci-nomas of the larynx account for more than 1200 malig-nancies each year in the United States.

Inflammatory diseases of the lungs include allergies,as well as bacterial, viral, and fungal infections. Theseinfections involve the bronchioles and the alveolar airsacs (Figure 5–2). Pneumonia is a wide-spread infectionof the lung parenchyma in which a lobe or an entirelung becomes infected with either bacteria or virus,resulting in purulent exudate accumulation in the alve-olar air sacs (Figure 5–3). Gaseous exchange canbecome severely compromised, leading to death. Whenthe infection is multifocal throughout the lungs, thecondition is referred to as bronchopneumonia. Whenthe infection localizes to an entire lobe, the term lobarpneumonia is used.

Foreign bodies may be aspirated into the airway fromthe oral cavity. Endodontic files and reamers coated withpathogenic microorganisms can cause lung abscess.There are instances where crown castings and even par-tial dentures have been aspirated. Because the right main

stem bronchus courses vertically, whereas the leftbronchus is angled to the left, most foreign bodies lodgein the right lung. Many can be visualized radiographi-cally; the majority can be retrieved during bronchoscopy.

There are a group of microorganisms that causechronic granulomatous infections of the lung; tuberculo-sis is the most common. Certain fungi, including histo-plasmosis, blastomycosis, and coccidioidomycosis causechronic lung infections with granuloma formation. Asthese granulomas enlarge over time, they may erode ves-sels, causing hemoptysis, coalesce, and compromise pul-monary function. Organisms are subsequently seededinto other alveolar air sacs, thus disseminating the infec-tion throughout both lungs. The granulomas are readilyvisualized radiographically if sufficiently large.

Tuberculosis (TB) is contracted by aerosol spread inclose contact with an infected subject. The primaryinfection occurs at the periphery of the lung tissue, theGhon focus, and via lymphatics, a hilar lymph nodebecomes infected and subsequently enlarged with gran-ulomas, the Ghon complex (see Figure 5–3). This pri-mary infection usually becomes quiescent. Reinfectionor reactivation of the tubercle bacillus results in sec-ondary TB. The secondary infection occurs in the faceof an intact T-cell response and a positive tuberculin

Bronchiole Interstitialcapillaries

TerminalalveoliProximal

alveoli

Type IIepithelium

Figure 5–2 Normal histology of the lung parenchyma.

R E S P I R A T O R Y D I S E A S E S 45

of septation. When the terminal alveoli along thepleural margin are dilated as blister-like sacuoles, thecondition is referred to as bullous emphysema. In bron-chitis, irritants cause mucinous secretions to accumulatein the bronchioles, with resulting chronic productivecough. Long-standing COPD shows classic clinical fea-tures, and affected patients are at risk for serious pul-monary infections and cor pulmonale (pulmonaryartery hypertension).

Bronchiectasis is a lesion that occurs in the bronchi-oles after repeated bouts of influenza or other pul-monary infections. The bronchiolar walls become thinand aneurysmal. These focal dilatations accumulatemucins, leading to chronic productive cough andCOPD. Brochiectasis is particularly problematic in cys-tic fibrosis. This childhood illness is an autosomal reces-sive disease that results from a mutation on chromo-some 7, involving a gene that encodes a transmembranechloride channel. In sweat ducts, excessive chloride issecreted, whereas in lung tissues chloride does not pass

skin test. Granulomas develop as a response to theorganism, enlarge within the lungs, cavitate, and thencan be disseminated systemically, a condition referred toas miliary TB. Tuberculosis is a major global cause ofdeath, but is under control in the United States. Anti-biotic-resistant mycobacterium is a considerable prob-lem in controlling TB.

When the alveolar surface area available for gaseousexchange is damaged and reduced, pulmonary functionis hampered. The diseases that result in this damage arecollectively referred to as chronic obstructive pul-monary disease (COPD). The primary etiologic factor istobacco smoke, and the two chief diseases are emphy-sema and bronchitis (Figure 5–4). In most instances ofCOPD, the patient suffers from both emphysema andbronchitis. In centrilobular emphysema the terminalbronchioles leading into the alveolar air sacs becomedilatated and lose septation; in panacinar emphysemaboth terminal bronchioles and alveolar air sacs are dam-aged by chemical toxins, resulting in dilatation and loss

Bronchopneumonia Lobar pneumonia

Secondary tuberculosis Primary tuberculosis

Figure 5–3 Bronchopneumonia is a multifocalinfection of the entire lung; lobar pneumonia is aconsolidated infection affecting an entire lobe. Inprimary tuberculosis, the Ghon complex is char-acterized by peripheral granulomas and hilarlymph node granulomas. Multiple granulomasare seen within one or both lungs in reactivatedor secondary tuberculosis.

46 C H A P T E R 5

from the epithelial lining cells into the lumen, andsodium is retained as well. The result is a dry airwaywith compensatory hyperplasia of the epithelial lining.This airway loses its mucinous wet layer, and ciliaryaction is impaired, leading to repeated pulmonary infec-tions that progress to bronchiectasis.

Asthma is also considered a form of COPD. Unlikebronchitis, emphysema, and bronchiectasis, asthmabegins at a young age and is an allergic disorder with apsychosomatic element and a genetic predisposition.The condition is equivalent to anaphylactic shock inthat allergen binding in conjunction with emotional

stress leads to airway constriction. Severe attacks areknown as status asthmaticus, an emergency situation inwhich the airway shuts down.

Restrictive pulmonary disease is a condition thatevolves as a consequence of environmental exposure totoxic chemicals or to certain infections. Common to allof these diseases is interstitial fibrosis. The tissuesbetween the alveoli and bronchioles are loose, areolar,and fibrovascular. In the restrictive lung diseases, thisinterstitial tissue becomes progressively scarified, and asit does, the alveolar air spaces become compressed. Inpneumoconiosis, a group of fibrosing lesions evolvefrom prolonged exposure to inspired chemicals, such ascoal dust (anthracosis), beryllium, asbestos, and silica.Certain infections with viruses and bacteria lead tointerstitial pneumonitis, whereby the interstitial spacesare edematous and inflamed and heal by fibrosis.

Cancer of the lungs can arise from the bronchiolarepithelium, mucous glands, or the pleural cells. The mostcommon form of lung cancer is bronchogenic carci-noma; 80% of cases are related to smoking tobacco. Thebronchiolar epithelium undergoes squamous metaplasiaand dysplasia and, ultimately, transforms into squamouscell carcinoma. Interestingly, in laboratory animals,forced smoking does not cause lung tumors. Neverthe-less, a variety of potential carcinogens exist in tobaccosmoke. Prolonged heavy exposure to asbestos alsoincreases the risk for bronchogenic carcinoma, and whentobacco and asbestos exposure are combined, the rela-tive risk for lung cancer is 90-fold. Adenocarcinomas arerare, as is mesothelioma, a cancer of the lung pleura thatis typically encountered in asbestos mine workers.

The diseases that compromise pulmonary function,particularly COPD and restrictive lung disease, affectrespiratory physiology. Pulmonary function tests can beused to assess various parameters that are diagnosticallyuseful. The spirometer is an instrument that measuresvarious inspiratory and expiratory volumes. In a normalindividual without lung disease, the total lung capacity isover 5500 mL of air (Figure 5–5). Regular breathinginvolves a volume of about 500 mL of air with eachinspiration and expiration, a measure referred to as thetidal volume. The amount of air that is able to beinspired maximally, in excess of inspired tidal volumelevel is called the inspiratory reserve volume. This repre-sents the maximum amount of air that can possibly enterthe lungs, about 3000 mL. After a normal exhalationduring the tidal cycle, more air can be forcefully exhaled;this is the excretory reserve volume. Even after this max-imal exhalation there is still residual air in the alveoli(the residual volume) that is not available for respiratoryfunction. In pulmonary diseases, in which alveolar sur-face area is decreased, or in lesions that restrict gaseousexchange, perturbations in these volumes can be identi-fied when testing with the spirometer (Figure 5–6).

Normal

Centrilobularemphysema

Panacinaremphysema

Bronchitis Bronchiectasis

Figure 5–4 In centrilobular emphysema the terminal bronchiole-proximal alveoli are dilatated, whereas in panlobular emphysema, bothproximal and distal regions of the alveoli are dilatated with loss of sep-tation. Mucus plugs accumulate in bronchitis and are retained within thelumens of aneurysmal-like dilatations of the airway in bronchiectasis.

R E S P I R A T O R Y D I S E A S E S 47

the knees while seated. Transillumination of the sinusesin a dark room shows clouding. Radiography may dis-close soft-tissue thickening of the sinus membranes oran air:fluid level may be seen on an anterior posteriorskull radiogram, Waters’ sinus projection, or computedtomography (CT) scan. When the patient is febrile, aninfectious process is probable and may be of viral orbacterial origin. Acute pain symptoms in the sinus aremost indicative of bacterial sinusitis, and culture of thenasal discharge is in order.

Sinonasal symptoms indicative of neoplasias includepersistant nasal obstruction, nasal speech, dysosmia, andswelling in the lateral nasal wall or the palate. Infraorbitalparesthesia or hypesthesia are suspicious signs for malig-nancy within the maxillary sinus, and epistaxis may occurwith sinonasal malignancies. Imaging studies disclosessoft-tissue, space-occupying lesions, bony wall expansionand osseous perforation or destruction (Figure 5–7).Biopsy is then required to derive a definitive diagnosis.

Nasopharyngeal carcinoma is characterized by pain,stuffiness, unilateral hearing loss, epistaxis, and cervicallymph node enlargement. It is not uncommon for anenlarged indurated node to be the first sign of nasopha-ryngeal carcinoma. Benign vascular tumors (juvenilenasopharyngeal angiofibroma) also cause nasal stuffi-ness and obstruction.

Pharyngeal symptoms most commonly centeraround irritation and pain. Laryngitis is characterizedby hoarseness, throat pain, and dysphonia. Examina-tion of the larynx shows edematous swelling of the bothtrue and false vocal cords along with erythema. Laryn-gitis may be caused by vocal cord trauma (eg, yelling,loud forced singing), allergy, or infection with eithervirus or bacteria. Neoplastic disease of the vocal struc-tures is similar to that seen in the oral cavity. Laryngealpapillomatosis is encountered primarily in children andteenagers. On laryngoscopy polypoid masses are seenon the true and false cords. These HPV-induced lesionsare difficult to eradicate; recurrence after excision orlaser ablation may occur.

Clinical features

Upper airway diseases present with sinonasal symp-toms. The inflammatory diseases typically manifestnasal stuffiness, sneezing, rhinorrhea, dysosmia,mucosal itchyness, nasal obstruction, or pain. The tem-perature should be taken in these situations; if elevated,infection is favored over allergy. Allergic rhinitis andsinusitis are typically seasonal. Some patients have hadallergy testing and, therefore, are aware of the environ-mental allergens that trigger an immediate hypersensi-tivity response. Physical examination discloses a nasaldischarge along with erythema of the mucous mem-branes. Long-standing allergic disease may result inpolyp formation. Nasal polyps are a common cause ofloss of smell. With a nasal speculum, the polyps appearas pink fleshy masses high in the nasal cavity, usuallyabove the middle turbinate.

When the ostia become obstructed, sinus pain maydevelop and can mimic toothache. The sinuses may betender to palpation over the malar eminence and theentire maxillary quadrant may manifest a chronic dullaching pressure sensation. All teeth in the quadrant areoften percussion sensitive. The pain and pressure areexacerbated if the patient places his or her head below

Inspiratoryreserve volume

Expiratoryreservevolume Residual

volume

Funtionalresidualcapacity

Vitalcapacity

Tidal volume

Inspiratoryreserve volume

Expiratoryreserve volume

Residualvolume

Vitalcapacity

No change

Delayedexpiration

Functionalresidualcapacity

Tidal Volume

Inspiratoryreservevolume

Vitalcapacity

Expiratoryreserve volume

Residualvolume

Functionalresidualcapacity

No change

Tidal Volume

Figure 5–5 Normal spirometer tracing showing gas volume parame-ters. Upward deflections on the graph represent inspirations; down-ward deflections are expirations.

Figure 5–6 Spirometer patterns in obstructed and restricted lung. A, In COPD from emphysema, there is an increase in residual volume, a reductionin expiratory reserve volume, and a delay in expiration after maximal inhalation, owing to air trapped in dilatated alveoli. B, In restrictive lung dis-ease attributable to pneumoconiosis, the inspiratory reserve volume and vital capacity are decreased because of loss of airway space. COPD = chronicobstructive pulmonary disease.

A B

48 C H A P T E R 5

Carcinoma of the laryngeal mucosa is typically associ-ated with smoking. These tumors are squamous cell carci-nomas. The signs are hoarseness and dysphonia; symp-toms include a scratchy feeling and pain. Occasionally,blood-tinged saliva is found from tumor bleeding. Clini-cally, early lesions are white, red, or mixed red and whitelesions with focal ulcerations. Tumefaction is seen, andwhen the tumor invades the adjacent cartilages, ausculta-tion discloses a loss of normal crepitus, since the carti-lagenous structures become invaded and fixed. Invasion ofcontiguous structures may also cause true cord paralysis.

The primary clinical manifestations of pulmonarydisease include dyspnea, cough (productive or nonpro-ductive), hemoptysis, and respiratory distress. The accu-mulation of viscous mucin within bronchioles andbronchi, as well as constriction of the airway because ofsmooth muscle contraction act as impediments to airflow. These obstructive changes may be detectable withthe stethoscope placed over the lung fields on thepatient’s back. A constricted airway causes wheezing onboth inspiration and expiration. Mucus accumulationproduces crackling and gurgling sounds termed rales andrhonchi. Orthopnea, shortness of breath while supine, isanother sign of pulmonary disease. The signs and symp-toms may be associated with a variety of pulmonary dis-eases, and alone are not diagnostic of any one disorder.

The most common infectious diseases to affect thelungs are the common cold and respiratory flu, both ofwhich are viral in origin. These common infections arecharacterized by productive cough, fever, and malaise,with a 7- to 10-day course. Serious infections of the lungsare the pneumonias. Pneumonia is a widely disseminatedlung disease that may be caused by either viruses or bac-teria. The more common organisms to cause pneumoniaare the bacteria Streptococcus pneumoniae, staphylococci,Haemophilus influenzae, Pseudomonas aeruginosa, andcoliform rods. When the infection is widely disseminatedwithin the parenchyma as multiple foci, the disease istermed bronchopneumonia. When the infection diffuselyinvolves an entire lobe it is referred to as lobar pneumo-nia. In response to infection, the air passages secrete exces-sive mucins and the fibrovascular septae show vesselengorgement and congestion with exudative fluid accu-mulation in the airway. This leads to dyspnea along withdeep cough that is productive in the beginning, yet as theinfection consolidates, a dry cough follows. The patient isfebrile. Percussion and auscultation of the chest discloseevidence of fluid accumulation, and radiographs showpatchy opacification in bronchopneumonia and diffuseopacification in lobar pneumonia. Patients with pneumo-nia require hospitalization and selection of appropriateantibiotics when bacteria are causative. In debilitatedpatients, death is a common outcome. Pneumonia and fluare leading causes of death in the United States. Dissemi-nated malignant neoplasms and immunodeficiencies ofvarious types are often complicated by pneumonia.

Infections of the lung parenchyma may extend to thepleural lining where inflammatory foci develop and fib-rin may be deposited, a lesion known as pleuritis. As thelungs expand and contract, these inflammatory focimay scrape across adjacent regions of the parietalpleura lining the internal chest wall. These movementscan be painful and upon chest auscultation the scrapingsounds often are detectable as a friction rub.

Influenza virus, respiratory syncytial virus, and adeno-virus among others cause interstitial pneumonia.Mycoplasma pneumoniae, a bacterium, also causes infec-tion, with inflammatory lesions involving the interstitialfibrovascular tissues that constitute the lung septae.Patients complain of headache, extremity muscle pain,fever, and cough. Elevated serum cold agglutinin titers areencountered in M. pneumoniae infection, yet are absentin most other viral forms of interstitial pneumonia. Mostof these infections run their course without complication;however, fatal outbreaks have been encountered.

Pulmonary infections are commonly seen in cysticfibrosis along with other exocrine lesions, such as bowelobstruction, malabsorption, and xerostomia. Onlyhomozygotes are affected. Children develop bronchiec-tasis with dyspnea and chronic cough due to a lack ofairway wetting. The mucins are thick and ropey (muco-

Figure 5–7 Computed tomography scan showing a maxillary sinusmalignancy in a patient who complained of nasal obstruction and peri-odic epistaxis. The lesion perforated the buccal plate, presenting as amaxillary vestibular mass (arrow).

R E S P I R A T O R Y D I S E A S E S 49

viscidosis) and obstruct the airway. These problems leadto pneumonia or cor pulmonale and eventuate in deathfor many of the affected children.

Chronic granulomatous infections of the lungs, TBbeing the most prevalent, begin with coughing in theabsence of fever, or there may be a low-grade elevationin temperature. Weight loss and fatigue are frequentlyassociated. As more and more lung parenchymabecomes involved and as granulomas enlarge, they maycavitate in the zones of caseous necrosis. A productivecough ensues and hemoptysis is commonly encountered.These individuals are infectious and can transmit TBorganisms. Sputum specimens can be cultured orsmeared to identify tubercle baccilus organisms. Recallthat deep invasive fungi, such as histoplasmosis, blasto-mycosis, and coccidioidomycosis, can cause similargranulomatous infections. Chest auscultation and per-cussion are abnormal in late disease. Radiographs dis-close the presence of granulomas and hilar lymph nodeenlargement. Long-term antibiotic treatment is requiredfor active tuberculosis, and most patients are hospital-ized until the infection is controlled. In contrast to theglobal epidemic, TB in the United States is under control.The main TB problem in industrialized countries residesin poverty areas of large cities, in immunocompromisedpatients, and with antibiotic-resistant mycobacteria.

Dyspnea is a common sign in congestive heart fail-ure (see Chapter 3). Recall that left-sided failure resultsin passive congestion of the lungs with accumulation ofedema fluid and inflammation in the alveolar spaces.Physical examination, cardiac auscultation, electrocar-diography, echocardiography, and radiographic studiesidentify the nature of the cardiopathy.

Patients suffering from the various forms of COPDmanifest dyspnea as the chief complaint. In emphysemaand bronchitis, the signs and symptoms begin in midlifeand become severe in the elderly. Cigarette smoking isthe primary causative factor for both of these condi-tions. Bronchitis is characterized by chronic productivecough as tobacco irritants stimulate inflammation andmucus secretion in the bronchi and bronchioles (bron-chiolitis). Emphysema is characterized by dyspnea. Asthe terminal airway loses septal surface area for gaseousexchange, expirations must be forced. Affected patientsare slender and barrel chested. In most cases, bronchi-tis, bronchiolitis, and emphysema occur together.Spirometer readings disclose normal tidal volume and

inspiration reserve volume with a significantlydecreased expiratory reserve and an increased residualvolume (see Figure 5–6). After forced inhalation, thereis a delay in the duration of exhalation as air is forcedby contraction of the intercostal muscles. Chronicobstructive pulmonary disease in this setting is irre-versible. Cessation of smoking is essential to prevent thecomplications and death that may ultimately occur.

Two common appellations applied to COPD patientsdefine their clinical appearance. The euphoniously so-called Red Puffer suffers from emphysema. The facialskin is flushed from over-inspiration and oxygenation,and the lips are puckered as the affected person forces airfrom the lungs on expiration. These patients have nor-mal blood gas values. The second descriptive term isapplied to the patient with chronic severe bronchitis: theBlue Bloater is cyanotic with facial palor and a bluishcast to the skin as a result of poor oxygenation withhypercapnia. The neck is full from being distended as aconsequence of constant coughing.

Asthma is a complex disease that is divided into twomajor subtypes: extrinsic and intrinsic (Table 5–1). Inboth forms, the condition usually evolves in early child-hood. Extrinsic asthma secondary to airway-introducedallergens is frequently worsened during episodes ofstress and anxiety. As the airway becomes constrictedand accumulates mucous plugs, the chief clinical sign iswheezing and coughing, without fever. When the asth-matic attack is severe and prolonged over many days,bronchospasm may occur and can be fatal, a conditionreferred to as status asthmaticus. Asthmatics are treatedwith orally administered bronchodilator drugs, corti-costeroids, and inhalation bronchodilators. In someforms of childhood allergic asthma, the conditionimproves with ensuing age. Occupational asthma hassimilar signs and symptoms and represents and idiosyn-cratic reaction among select individuals upon exposureto certain chemicals found in the workplace. Epoxyresins, formaldehyde, toluene, cotton fibers, and wooddust are common precipitating elements that can initiatean IgG or IgE response. Intrinsic asthma is caused byhyper-reactivity of the airway to infectious agents,aspirin, or vigorous physical activity.

The restrictive lung diseases are uncommon. As theinterstitium becomes scarified, the total lung volume isdecreased. The spirometer patterns show decreasedinspiratory reserve and vital capacity volumes (see Figure

Table 5–1 Classification of Asthmatic Disease

Extrinsic Intrinsic

Allergen-induced (IgE response) Nonreaginic respiratory infectionsOccupational chemical exposure (IgE and IgG response) Sports asthma (high physical activity)Aspergillosis allergy Aspirin sensitivity

50 C H A P T E R 5

5–6). Patients may also have a chronic cough secondaryto bronchiolitis from toxic irritants. Dyspnea is also amajor sign. Pneumoconiosis is a group of lung diseasescaused by inhalation of irritant chemicals. Anthracosis(coal minor’s black lung disease) results in severe inter-stitial fibrosis with marked restriction in airway volume.Asbestosis is usually only seen in asbestos miners whohave been breathing asbestos dust for many years. Asmentioned earlier, these individuals are at increased riskfor development of bronchogenic carcinoma andmesothelioma. Other forms of restrictive lung diseaseinclude the following: sarcoidosis, a granulomatousinflammatory disease of unknown etiology (see Chapter24); hypersensitivity to allergens that find their way intothe terminal bronchioles; hemorrhagic lung syndromessuch as Goodpasture syndrome (a condition that alsoaffects the kidneys; Wegener granulomatosis (see Chap-ter 24); and lupus erythematosus (see Chapter 21).

Bronchogenic carcinoma is a leading cancer amongmales and is increasing in females. Morbidity and mor-tality are high. Most cases are associated with smokingcigarettes. Chronic cough is a sign of pulmonary irrita-tion from inhaled smoke, with COPD developing aftermany years of use. When these signs are accompaniedby hemoptysis, carcinoma should be suspected, andchest films must be secured. If a cough is productive,sputum cytology may show malignant cells. In fact, lungcancer can be a silent killer and is often discovered afterroutine chest radiographs disclose a mass. In some casesafter metastasis has occurred at another site, a biopsyindicates malignant cells primary in the lung. Small-cellcancer of the lung is not smoking-related. Some of thesesmall “oat” cell carcinomas secrete hormones, and thefirst manifestation of disease is clinical endocrinopathy,with hyperparathyroidism being common, owing tosecretion of a parathormone-like peptide by the malig-nant cells (see Chapter 10).

Oral manifestations

Patients with sinonasal diseases often show oral signsand symptoms. Halitosis can be a common sign ofchronic allergic sinusitis and rhinitis whereby postnasalsecretions fall upon the base of the tongue and maycause malodor (see Chapter 27 on special senses). Casesof antral cancer are seen in which the tumor erodes thepalatal bone and presents as an ulceration or fistula (seeFigure 5–7; Figure 5–8). Invasive fungal infections ofthe sinonasal region can also erode into the palate ascan nasal midline necrotizing diseases such as Wegenergranulomatosis (Figure 5–9) and malignant reticulosis,a form of angiocentric T-cell lymphoma (Figure 5–10).Infraorbital paresthesia is a sign of antral carcinoma,and when present, appropriate imaging studies must be

ordered. Cranial base malignancies may cause neuro-logic deficits of the cranial nerves including paresthesiasand motor deficits of cranial nerves III, IV, V, and VI.

Oral signs are rare in pulmonary diseases. Patientswith lung cancer often develop metastases to bone, andthe mandible may become a focus of distant spread. Typ-ically, the patient complains of an insidious onset of pares-thesia of the lower lip on the affected side as tumor cellsinvade the inferior alveolar nerve. A dental radiographdiscloses a poorly marginated radiolucency, which usuallyis confined to the posterior body and ramus of themandible yet may also occur as a soft-tissue mass (Figure5–11). Biopsy discloses the presence of metastatic malig-nant cells with morphology consistent with lung carci-noma. As mentioned previously, uncovering a metastaticfocus may be the first indication that the patient has aprimary cancer in the lung; but it also indicates advanceddisease with essentially no chance for cure.

Figure 5–9 Gingival masses in Wegener granulomatosis. Lung involve-ment is often seen as well.

Figure 5–8 Antral carcinoma perforating the palate and presenting asan ulcerated mass.

R E S P I R A T O R Y D I S E A S E S 51

Tuberculosis and invasive fungi may also spread tothe oral cavity from the primary infection in the lung. Theorganisms gain access to the oral regions by hematoge-nous spread, and when they adhere to oral tissues, a siteof granulomatous inflammation develops. These granu-lomas may be red and granular or ulcerated with rolledmargins, thus resembling a primary carcinoma (Figure5–12). Tuberculous lymphadenitis occurs in individualswho have ingested nonpasturized milk contaminated withmycobacteria. The nodes are firm to palpation, movable,and often bilateral (Figure 5–13). Tuberculosis and histo-plasmosis are the more common granulomatous infec-tions seen in the oral mucosa. Biopsy is required to makethe diagnosis, and the pathologist usually needs to applyspecial stains to identify the microorganisms. Acid-fastZiehl-Neelsen staining is used to identify mycobacteria;periodic acid-Schiff (PAS) or gram methenamine silveridentifies histoplasma and other fungal organisms, all ofwhich have distinct morphologic features. Histoplasmo-sis in the oral cavity can be an opportunistic infection

among human immunodeficiency virus (HIV)-infectedsubjects and may or may not be associated with pul-monary disease (see Chapter 14).

In cystic fibrosis, all secretions of exocrine origin areaffected, including those of the major and minor sali-vary glands. Affected children complain of xerostomiaand may require artificial saliva preparations to keepthe mucosa moist and comfortable.

Dental management

Patients with pulmonary diseases usually do not pose asignificant problem for dental care unless general anes-thesia is to be performed. It must be realized that thecommon respiratory infections are transmissible in thedental operatory, necessitating adherence to infectioncontrol procedures (see Chapter 19). Currently, in mostdental practices, patients are placed in a supine position,and in the patient with a compromised airway, orthop-

Figure 5–11 A, Ill-defined radiolucency of the posterior mandible in a patient with mental nerve paresthesia. Biopsy disclosed metastatic bron-chogenic carcinoma. B, Soft-tissue metastasis of bronchogenic carcinoma.

A B

Figure 5–10 Midline destructive lymphoma sometimes referred to as midline lethal granulomas: A, prior to therapy; B, after radiation therapy.

A B

52 C H A P T E R 5

unaware if they were exposed once before and were nevergiven another prescription after the initial dosing. Foodallergens can also induce anaphylactic reactions. At theonset of an anaphylactic event, the patient notices diffi-culty breathing, and wheezing may be detected. Severerespiratory distress ensues rapidly as histamine andleukotrienes are released in the airway mucosa and sub-mucosa. The blood pressure also drops, and the patientmay lose consciousness, owing to hypoperfusion of cere-bral vessels. Death may ensue if this medical emergency isnot treated. A call to 911 should be undertaken, oxygenshould be administered and 1:1000 epinephrine shouldbe injected sublingually, because vascular collapse makesintravenous injection difficult if not impossible. To beeffective, diphenhydramine as an intravenous emergencydrug can be administered only in the early stages, prior toairway closure and hypotensive shock. Because this anti-histamine is a histamine-receptor blocker, its use in late-stage anaphylaxis is of no benefit, since the receptors arealready occupied by the IgE-mediated release of hista-mine; alternatively, epinephrine exerts a direct dilatingeffect on bronchiolar smooth muscle, opening up the air-way within seconds to minutes.

Patients with asthma are at increased risk for anasthmatic attack while undergoing any dental care thatmay elevate stress levels. Pain and anxiety are commonprecipitating factors for both allergic and nonallergic

nea may become a significant problem. When patientshave a full stomach and are placed in supine positionfor prolonged periods, there is always the risk for regur-gitation with subsequent aspiration of acidic contentsinto the lungs. Aspiration of dental instruments, materi-als, tooth fragments, and prostheses that may be conta-minated with oral microorganisms may initiate a lungabscess. The use of the rubber dam helps to eliminatethe chance for introduction of such foreign bodies.

Recognition of the patient’s pulmonary disease sta-tus with regard to severity of dyspnea and orthopnea isan important consideration when long periods of dentaltherapy are contemplated and the patient is placed in areclined position. It is advisable to seat the patientupright or to stop all procedures on a regular basis andreturn them to an upright position periodically. Oxygenshould be readily available and equipment should be inplace in case assisted breathing is required. It should benoted, however, that forcing air into the lungs of apatient with emphysema, particularly the bullous vari-ant, can burst the pleural lining resulting in pneumo-thorax, a condition that leads to respiratory arrest,owing to collapse of the lungs.

It is axiomatic that patients with upper respiratoryinfections with nasal congestion or blockage are unableto receive rountine dental care when a rubber dam is tobe used, because the oral airway will be blocked. If thenasal mucus can be expelled by blowing the nose, treat-ment can be implemented; if not, the patient should berescheduled.

The most severe respiratory emergency is anaphylac-tic shock. Such an event in the dental office setting isextremely rare, yet can occur if the patient is introducedto a provoking antigen just prior to or during an officevisit. Recall that a variety of pharmacologic agents cancause anaphylaxis, particularly penicillins. Most patientsare aware of an allergy to penicillin, yet others may be Figure 5–13 Scrofuloderma. Enlarged cervical nodes are evident.

Figure 5–12 Tuberculous ulcer in a patient with concomitant pul-monary tuberculosis.

R E S P I R A T O R Y D I S E A S E S 53

forms of asthma. Sedative drugs with anticholinergiceffects are to be avoided. Narcotics and barbiturates areknown to trigger an attack. Local anesthetics used indentistry contain sodium metabisulfite, an antioxidantthat prevents oxidation of epinephrine. Twenty percentof asthmatics are allergic to sulfur compounds, andtherefore, administration of local anesthetics should beundertaken with caution, always questioning patients asto whether they have experienced any adverse reactionsto local anesthetics. The severity and periodicity of asth-matic attacks is highly variable from one affectedpatient to another. Before engaging in extensive dentalprocedures, particularly surgical interventions, the his-tory should be explored in detail. If attacks are mild andinfrequent, treatment can be initiated with caution. It isalways prudent to be certain that patients maintain theirbronchodilator daily drug regimen prior to dental treat-ment and any inhaler devices should be placed withineasy reach. Severe asthmatics may also be taking corti-costeroids. In these individuals there may be anincreased risk for infection. Patients with a history ofsevere and frequent bronchospasms should be hospital-ized for extensive and invasive dental care. Consultationwith the physician must be undertaken, and an anesthe-siologist should be included on the treatment team.

In rare instances, patients develop asthma afteradministration of aspirin. Any patient who gives a his-tory of asthma should be questioned about the role ofaspirin in the causation of their disease, and obviously,aspirin-containing drugs should be eliminated as anal-gesic medications. Acetaminophen or propoxypheneshould be considered as substitute analgesics for atten-uation of dental pain. Oxycodone and hydrocodoneshould be administered with care since codeine-relateddrugs and opiates may aggrevate asthmatic attacks.Some asthmatic patients have coincidental complaintsof xerostomia. Sialagogues (parasympathomimetics) arecontraindicated, because they cause airway congestion.

Children with cystic fibrosis have dry airways, andadministration of inhalation sedation can be danger-ous when the gases are not humidified. General anes-

thesia is also problematic because concurrent adminis-tration of anticholinergic drugs further aggravates air-way dryness. If anesthesia is required for dental care,the patient should be hospitalized and managed by ananesthesiologist.

General anesthetics for adult patients with pul-monary disease must also be used with caution. MildCOPD or restrictive lung disease is generally not prob-lematic. Moderate to severe pulmonary disease can beaggravated and degenerate to severe respiratory distresswhen inhalation anesthetics are used. This is particu-larly so in conjunction with intravenous drugs thatdepress the respiratory center of the central nervous sys-tem, and with anticholinergic drugs that may be admin-istered during intubation. When general anesthesia isnecessary for patients in this category, they should behospitalized and managed by an anesthesiologist. Inaddition, the dentist should consult with the patient’sphysician prior to rendering treatment.

Suggested reading

Becker DE. Management of respiratory complications in clin-ical dental practice. Pathophysiological and technical con-siderations. Anesth Prog 1990;37:169–75.

Hatch CL, Canaan T, Anderson G. Pharmacology of the pul-monary diseases. Dent Clin North Am 1996;40:521–41.

Hoffman MJ, Haug RH, Shepard LS, Indresano AT. Care ofthe asthmatic and maxillofacial surgery patients. J OralMaxillofac Surg 1991;49:69–75.

Lapointe HJ, Armstrong JE, Larocque B. A clinical decisionmaking framework for the medically compromised patient:ischemic heart disease and chronic obstructive pulmonarydisease. J Can Dent Assoc 1997;63:510–2, 515–6.

Levin JA, Glick M. Dental management of patients with asthma.Compend Cont Educ Dent 1996;17:284, 287–8, 290.

Scannapieco FA. Role of oral bacteria in respiratory infection.J Periodontol 1999;70:793–802.

Zhu JF, Hidalgo HA, Holmgreen WC, et al. Dental managementof children with asthma. Pediatr Dent 1996;18:363–70.

Ch1: Procurement of the HistoryCh2: Physical Diagnosis of the Head and NeckCh3: Cardiovascular DiseasesCh4: Renal Diseases and HypertensionCh5: Respiratory DiseasesCh6: Diseases of the Liver and Gastrointestinal TractCh7: Bleeding DisordersCh8: Blood DyscrasiasCh9: Endocrine DiseasesCh10: Parathyroid Disease and Calcium MetabolismCh11: Adverse Drug ReactionsCh12: Mechanisms of Infection and Host DefenseCh13: Herpesviruses and EnterovirusesCh14: Human Immunodeficiency Virus DiseaseCh15: Human Papillomaviruses and Papillary Oral LesionsCh16: Hepatitis B and Hepatitis C Virus InfectionsCh17: Bacterial InfectionsCh18: Oral Fungal InfectionsCh19: Infection ControlCh20: Oral Premalignancies and Squamous Cell CarcinomaCh21: Immunopathologic Mucosal LesionsCh22: Pigmentations of the Oral Mucosa and Facial SkinCh23: Swellings and Tumors of the Oral Cavity and FaceCh24: Orofacial Granulomatosis and Other Inflammatory LesionsCh25: Developmental Mucosal ConditionsCh26: Diseases of the Salivary GlandsCh27: Special Senses: Disorders of Taste and SmellCh28: Pain MechanismsCh29: Pain and BehaviorCh30: Temporomandibular DisordersCh31: HeadacheCh32: Orofacial Neuralgias and Neuropathic PainCh33: Atypical Facial PainCh34: Burning Mouth SyndromeCh35: Regional and Referred Orofacial PainCh36: Orofacial Pain in Patients with CancerIndexExit