-
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