Given the fact that the oral cavity is contiguous with the trachea and lower airway, it is biologically plausible that conditions within the oral cavity might influence lung function. Respiratory infections are commonly encountered among dental patients. Commonalities between chemotherapeutic options and the anatomic proximity with the oral cavity lead to much interplay between oral and respiratory infections. Recent studies have reported on oral bacteria as causative pathogens in respiratory diseases and conditions associated with significant morbidity and mortality. Furthermore, some respiratory illnesses, such as asthma, may have an effect on orofacial morphology or even on the dentition. This chapter discusses the more common respiratory illnesses and explores the relationship between these conditions and oral health.
UPPER AIRWAY DISEASES
There are several major oral health concerns for patients with upper respiratory infections. These concerns are about infectious matters; for example, the possible transmission of pathogens from patients to health care workers and reinfection with causative pathogens through fomites such as toothbrushes and removable oral acrylic appliances. Furthermore, antibiotic resistance may develop because of the use of similar types of medications for upper respiratory infections and odontogenic infections. Lastly, oral mucosal changes, such as dryness due to decongestants and mouth breathing, and increased susceptibility to oral candidiasis in patients using long‐term glucocorticoid inhalers, may be noticed.
Viral Upper Respiratory Infections
The most common cause of acute respiratory illness is viral infection, which occurs more commonly in children than in adults. Rhinoviruses account for the majority of upper respiratory infections in adults.1 These are ribonucleic acid (RNA) viruses, which preferentially infect the respiratory tree. At least 100 antigenically distinct subtypes have been isolated. Rhinoviruses are most commonly transmitted by close person‐to‐person contact and by respiratory droplets. Shedding can occur from nasopharyngeal secretions for up to 3 weeks, but 7 days or less is more typical. In addition to rhinoviruses, several other viruses, including coronavirus, influenza virus, parainfluenza virus, adenovirus, enterovirus, coxsackievirus, and respiratory syncytial virus (RSV), have also been implicated as causative agents. Infection by these viruses occurs more commonly during the winter months in temperate climates.
Viral particles can lodge in either the upper or lower respiratory tract. The particles invade the respiratory epithelium, and viral replication ensues shortly thereafter. The typical incubation period for rhinovirus is 2 days, with a symptom duration of 7 to 14 days.2 During this time, active and specific immune responses are triggered, and mechanisms for viral clearance are enhanced. The period of communicability tends to correlate with the duration of clinical symptoms.
Clinical and Laboratory Findings
Signs and symptoms of upper respiratory tract infections are somewhat variable and are dependent on the sites of inoculation.3 Common symptoms include rhinorrhea, nasal congestion, and oropharyngeal irritation. Nasal secretions can be serous or purulent. Other symptoms that may be present include cough, fever, malaise, fatigue, headache, and myalgia.2 A complete blood count (CBC) with differential may demonstrate an increase in mononuclear cells, lymphocytes, and monocytes (“right shift”). Laboratory tests are typically not required in the diagnosis of upper respiratory infections. Viruses can be isolated by culture or determined by rapid diagnostic assays. However, these tests are rarely clinically warranted.
A diagnosis is made on the basis of medical history as well as confirmatory physical findings. Diagnoses that should be excluded include acute bacterial rhinosinusitis, allergic rhinitis, and group A streptococcal pharyngitis.
The treatment of upper respiratory infections is symptomatic as most are self‐limited. Analgesics can be used for sore throat and myalgias. Antipyretics can be used in febrile patients, and anticholinergic agents may be helpful in reducing rhinorrhea. Oral or topical decongestants, such as phenylephrine and pseudoephedrine, may be effective in terms of decreasing subjective nasal congestion.4 Adequate hydration is also important in homeostasis, especially during febrile illnesses.
Antimicrobial agents have no role in the treatment of acute viral upper respiratory infections. Presumptive treatment with antibiotics to prevent bacterial superinfection is not recommended.2 Any excessive use of antibiotics can result in the development of drug‐resistant bacteria.3
Antiviral compounds have not been found to provide significant benefit for viral upper respiratory infections.5
As most patients recover in 5 to 10 days, the prognosis is excellent. However, upper respiratory infections can put patients at risk for exacerbations of asthma, acute bacterial sinusitis, and otitis media; this is especially so in predisposed patients, such as children and patients with an incompetent immune system.
Oral Health Considerations
The most common oral manifestation of upper respiratory viral infections is the presence of small round erythematous macular lesions on the soft palate. These lesions may be caused directly by the viral infection, or they may represent a response of lymphoid tissue. Individuals with excessive lingual tonsillar tissue also experience enlargement of these foci of lymphoid tissue, particularly at the lateral borders at the base of the tongue.
Treatment of upper respiratory infections with decongestants may cause decreased salivary flow, and patients may experience oral dryness (see Chapter 9 “Salivary Gland Diseases” for a discussion of the treatment of oral dryness).
Although there has been discussion in regards to a relationship between dentofacial morphology, malocclusion, and nasal obstruction, there is currently no clear causal relationship.6
Allergic Rhinitis and Conjunctivitis and Nonallergic Rhinitis
Allergic rhinitis is a chronic recurrent inflammatory disorder of the nasal mucosa. Similarly, allergic conjunctivitis is an inflammatory disorder involving the conjunctiva. When both conditions occur, the term allergic rhinoconjunctivitis is used. The basis of the inflammation is an allergic hypersensitivity (type I) to environmental triggers. Allergic rhinoconjunctivitis can be seasonal or perennial. Typical seasonal triggers include grass, tree, and weed pollens. Common perennial triggers include dust mites, cockroach, animal dander, and mold spores.
Allergic rhinitis is one of the most prevalent chronic medical conditions in the United States (US). It affects up to 58 million people in the US.7 Allergic rhinitis is associated with a significant economic burden with a total of more than $11.2 billion (US) in direct costs due to this condition in 2005.8 It is estimated that allergic rhinitis accounts for 3.5 million lost work days and 2 million missed school days each year.9
When nasal congestion, postnasal drainage and rhinorrhea are present perennially and, in the absence of significant sneezing or itching, this may be indicative of an entity called nonallergic rhinitis (NAR). NAR typically presents at a later age. The most common triggers for NAR include smoke, strong odors or fragrances, and changes in temperature or barometric pressure. When NAR occurs in conjunction with allergic rhinitis, this is termed mixed rhinitis and is the most common form of rhinitis in adults.10
Patients with allergic rhinoconjunctivitis have a genetically predetermined susceptibility to allergic hypersensitivity reactions, known as atopy. Prior to the allergic response, an initial phase of sensitization is required. This sensitization phase is dependent on exposure to a specific allergen and on recognition of the allergen by the immune system. The end result of the sensitization phase is the production of specific immunoglobulin E (IgE) antibody and the binding of this specific IgE to the surface of tissue mast cells and blood basophils. Upon re‐exposure to the allergen, an interaction between surface IgE and the allergen takes place, which results in IgE crosslinking. The crosslinking of surface IgE triggers degranulation of the mast cell and basophils causing the release of preformed mediators. This is the early‐phase allergic reaction. Histamine is the primary preformed mediator released by mast cells, and it contributes to the clinical symptoms of sneezing, pruritus, and rhinorrhea. Mast cells also release cytokines that permit amplification and feedback of the allergic response. These cytokines cause an influx of other inflammatory cells, including eosinophils, resulting in the late‐phase allergic reaction. Eosinophils produce many proinflammatory mediators that contribute to chronic allergic inflammation and to the symptom of nasal congestion.
NAR includes two main subtypes. Vasomotor rhinitis is sometimes erroneously used synonymously with NAR. It is thought that neural or glandular pathways are involved in causing symptoms of congestion and rhinorrhea in response to nonspecific environmental irritants such as temperature changes (e.g., cold or dry air) or pollutants. Another subtype of NAR termed gustatory rhinitis involves significant rhinorrhea within a few hours after eating (hot and spicy food are the most common triggers) and is thought to be due to stimulation of the vagus nerve.11
Clinical and Laboratory Findings
The symptoms of allergic rhinoconjunctivitis can vary from patient to patient and depend on the specific allergens to which the patient is sensitized. Conjunctival symptoms may include pruritus, lacrimation, crusting, and burning. Nasal symptoms may include sneezing, pruritus, clear rhinorrhea, and nasal congestion. Other symptoms can occur, such as postnasal drainage with throat irritation, pruritus of the palate and ear canals, and fatigue.
The clinical signs of allergic rhinoconjunctivitis include injection of the conjunctiva with or without cobblestoning; prominent infraorbital creases/folds (Dennie–Morgan lines), swelling, and darkening (“allergic shiners”); a transverse nasal crease; and frequent upward rubbing of the tip of the nose (the allergic “salute”). Direct examination of the nasal mucosa reveals significant edema and a pale blue coloration of the turbinates. A copious clear rhinorrhea is often present. Nasal polyps may also be visible. Postnasal drainage or oropharyngeal cobblestoning might be identified upon examination of the oropharynx. A high‐arched palate, protrusion of the tongue, and overbite may be seen.
Laboratory investigations are usually kept to a minimum. Patients with allergic rhinitis might have elevated levels of serum IgE and an elevated total eosinophil count. These findings are not, however, sensitive or specific indicators of atopy. Microscopic examination of nasal secretions often demonstrates significant numbers of eosinophils. Blood tests, such as the traditional radioallergosorbent test (RAST), is a method of testing for specific allergic sensitivities that is based on circulating levels of specific IgE. Specific IgE levels are determined by using serum samples and are quantified by using radioactive markers. Although bloodwork is somewhat less reliable than skin testing (see below), it is a useful test in certain situations, such as pregnancy or severe chronic skin disorders, including atopic dermatitis.
There is no universal classification system for allergic rhinoconjunctivitis. Many authors make the distinction between perennial and seasonal illness, with the former being caused mainly by indoor allergens (e.g., house dust mites, cockroaches, pets) and the latter being triggered primarily by outdoor allergens (e.g., trees, grasses, weeds). Perennial allergic rhinitis sufferers might benefit more from specific environmental control measures than would seasonal allergic rhinitis sufferers.
The diagnosis of allergic rhinoconjunctivitis is usually apparent, based on history and physical examination. Patients present with a history suggestive of allergic sensitivity, recurrent symptoms with specific exposures, or predictable exacerbations during certain times of the year. Symptoms that have recurred for 2 or more years during the same season are very suggestive of seasonal allergic disease. Alternatively, the history might indicate a pattern of worsening symptoms while the patient is at home, with improvement while the patient is at work or on vacation; this pattern is highly suggestive of perennial allergic disease with indoor triggers. The presence of the characteristic physical findings described above would confirm the presence of allergic rhinoconjunctivitis.
The preferred method of testing for allergic sensitivities is skin testing, which is performed with epicutaneous (prick/scratch) tests and this can be followed by intradermal testing if needed. Prick skin testing is the type most widely used. With prick testing, a small amount of purified allergen is inoculated through the epidermis only (i.e., epicutaneously) with a pricking device. Positive (histamine) and negative (saline) controls are used for comparison (Figures 13‐1A and 13‐1B). Reactions are measured at 15 minutes, and positive reactions (wheal and flare reactions) indicate prior allergen sensitization. Tests that yield negative results may be repeated intradermally to increase the sensitivity of the testing. All tests with positive results need to be interpreted carefully in the context of the patient’s history and physical findings.
NAR is a diagnosis of exclusion. Therefore, other etiologies of rhinitis such as allergic, pharmacologic, infectious, and structural, and so on, must be excluded.10
Three general treatment modalities are used in the therapy of allergic rhinoconjunctivitis: allergen avoidance, pharmacotherapy (medication), and immunotherapy (i.e., allergy injections). The best treatment is avoidance of the offending allergen. This requires the accurate identification of the allergens implicated and a thorough knowledge of effective interventions that can minimize or eliminate the exposure. Complete avoidance is rarely possible.
Pharmacotherapy is often recommended for patients with incomplete responses to allergen avoidance and for patients who are unable to avoid allergen exposures. Many treatment options are available. For patients with prominent sneezing, pruritus, or rhinorrhea, antihistamines are an excellent treatment option. Second‐generation antihistamines such as cetirizine, loratadine, and fexofenadine are now widely available. These medications deliver excellent antihistaminic activity with few side effects.12 Oral decongestants can be added to oral antihistamines to relieve nasal congestion and obstruction. Combination medications are available in once‐daily and twice‐daily dosage forms for ease of administration. Leukotriene receptor antagonists may have additional benefit as well. Some studies have demonstrated that therapy with a leukotriene receptor antagonist plus antihistamine may have a greater effect than either agent administered alone.12,13 For patients with daily nasal symptoms or severe symptoms that are not relieved with antihistamine‐decongestants, topical anti‐inflammatory agents for the nasal mucosa are available. These medications include corticosteroid, antihistamine, and cromolyn sodium nasal sprays. The benefits of topical corticosteroids include relief of the total symptom complex and once daily dosing.
Immunotherapy is an effective means of treatment for patients with allergic rhinoconjunctivitis. Numerous studies have shown the efficacy of long‐term allergen immunotherapy in inducing prolonged clinical and immunologic tolerance.14 Immunotherapy is available for a variety of airborne allergens, including grass, tree, and weed pollens; dust mites; animal dander; and mold spores. Formulations include subcutaneous injections, sublingual drops, and sublingual tablets. Excellent candidates for immunotherapy include those patients who are unable to avoid exposures, patients with suboptimal responses to pharmacotherapy, patients who prefer to avoid the long‐term use of medications, and women who are contemplating pregnancy.
First‐line treatment of NAR is either an intranasal glucocorticoid and/or an intranasal antihistamine such as azelastine. There are no head‐to‐head studies comparing these two treatment options. Combination therapy is often used if monotherapy is not sufficient. For patients with gustatory rhinitis or significant rhinorrhea, ipratropium nasal spray may be helpful. Adjunctive therapies include nasal saline sprays and nasal irrigations, oral antihistamines, and short‐term oral or nasal decongestants. Antileukotriene and intranasal chromone efficacy are less well established in NAR.15
Although allergic rhinoconjunctivitis is not a life‐threatening disorder, it does have a significant impact on the patient’s quality of life. With proper allergy care, most patients can lead normal lives, with an excellent quality of life.
Oral Health Considerations
The use of decongestants and first‐generation antihistamines may be associated with oral dryness. There may also be an increased incidence of oral candidiasis in long‐term users of topical corticosteroid‐containing sprays.
It has been reported that dental personal are at risk for allergic respiratory hypersensitivity from exposure to dental materials such as methacrylates and natural rubber latex.16 These allergenic materials, however, have been eased out of the dental workplace due to the widespread understanding of their allergic/irritant potential.
Otitis media is inflammation of the middle ear space and tissues. It is the most common illness occurring in children who are 8 years of age or younger. Approximately 70% of children experience at least one episode of otitis media by age 3 years; of these, approximately one third experience three or more episodes in this same time interval.17
Otitis media can be subdivided into acute otitis media, recurrent otitis media, otitis media with effusion, and chronic suppurative otitis media. The underlying problem in all types of otitis media is dysfunction of the Eustachian tube. A poorly functioning Eustachian tube does not ventilate the middle ear space sufficiently. This lack of proper ventilation results in pressure changes in the middle ear and subsequent fluid accumulation. The fluid frequently becomes infected, resulting in acute otitis media. The most common infectious causes are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and viruses. In chronic infections, Staphylococcus aureus and anaerobic organisms may be causative pathogens while in young infants Gram‐negative bacilli may be isolated.18
There are several factors that influence the pathogenesis of otitis media. Nasopharyngeal colonization with large numbers of bacteria such as S. pneumoniae, H. influenzae, or M. catarrhalis and pathogenic viruses can increase the risk of otitis media. The likelihood of aspiration of these nasopharyngeal pathogens can be increased by nasal congestion or obstruction, negative pressure in the middle ear space, acute viral upper respiratory infections, and exposure to tobacco smoke.19 For infants, breastfeeding can decrease the risk of otitis media, whereas impaired immune responsiveness can increase this risk.
Under normal circumstances, the Eustachian tube acts to ventilate the tympanomastoid air cell system during the act of swallowing. Any process that impairs normal Eustachian tube function can lead to negative pressure in the middle‐ear space. Transient impairments of Eustachian tube function are seen in conditions that cause nasopharyngeal mucosal edema and obstruction of the Eustachian tube orifice, such as allergic rhinitis and viral upper respiratory infections. Chronic Eustachian tube obstruction can be seen with several conditions, including cleft palate and nasopharyngeal masses, such as enlarged adenoids. Aspiration of nasopharyngeal pathogens can then occur due to negative pressure in the middle ear space, with subsequent infection by these pathogens. This leads to the clinical manifestations of otitis media.
Clinical And Laboratory Findings
The most common symptoms in acute otitis media are fever and otalgia. Other symptoms include irritability, anorexia, and vomiting. Parents may note their child pulling or tugging at one or both ears. Symptoms of a viral upper respiratory infection might also be present, preceding the development of otitis media. On physical examination, the tympanic membrane may appear erythematous and bulging, suggesting inflammation of the middle ear. Other otoscopic findings include a loss of landmarks and decreased mobility of the tympanic membrane as seen by pneumatic otoscopy.18
In otitis media with effusion, patients often complain of “clogged” ears and “popping.” Otoscopic examination reveals serous middle‐ear fluid, and air‐fluid levels may be present. The mobility of the tympanic membrane is usually diminished, and mild to moderate conductive hearing loss may be demonstrated. In chronic suppurative otitis media, otorrhea is present and can be visualized either from a tympanic membrane perforation or from surgically placed tympanostomy tubes.
Investigations that can aid in the diagnosis or management of otitis media include tympanometry and myringotomy with aspiration. Tympanometry is a technique that measures the compliance of the tympanic membrane by using an electroacoustic impedance bridge. Decreased compliance of the tympanic membrane indicates a middle‐ear effusion. Myringotomy with aspiration can be useful in situations when culture of the middle ear fluid is needed, such as with immunocompromised hosts or with patients who have persistent effusions despite medical management.
Acute otitis media is defined as middle‐ear inflammation with an infectious etiology and a rapid onset of signs and symptoms. Otitis media with effusion is defined as a middle ear effusion (often asymptomatic) that can be either residual (3 to 16 weeks following acute otitis media) or persistent (lasting more than 16 weeks). Recurrent otitis media is defined as three or more new episodes of acute otitis media in 6 months’ time or four or more new episodes in a 12‐month period. Chronic suppurative otitis media is defined as persistent otorrhea lasting longer than 6 weeks.
The diagnosis of otitis media is made on the basis of the history and physical examination. The most useful tool for diagnosing otitis media is pneumatic otoscopy, which allows the clinician not only to visualize the tympanic membrane but also to assess its mobility. As stated above, an immobile tympanic membrane probably represents the presence of middle ear fluid, and (in the context of a confirmatory medical history) the diagnosis of otitis media is made in such a case.
Recent practice guidelines in the management of otitis media without significant signs and symptoms, have suggested that observation with close follow‐up is justified.20 There is evidence that suggests that antibiotics may be more beneficial in certain children, specifically those aged less than 2 years with bilateral acute otitis media and in those with both acute otitis media and otorrhea.21,22 If antibiotics are indicated, initial antibiotic therapy is directed toward the most common middle‐ear pathogens. Common choices include amoxicillin, azithromycin, and trimethoprim‐sulfamethoxazole. In recalcitrant cases, treatment is directed toward β‐lactamase‐producing organisms and antibiotic‐resistant strains of S. pneumoniae. Common choices for this situation include high‐dose amoxicillin, amoxicillin‐clavulanate, second‐ or third‐generation cephalosporins, and clindamycin. The duration of therapy varies from 3 to 14 days.20
Multiple surgical modalities currently are used for the management of otitis media, including myringotomy with or without tympanostomy tube insertion, tympanocentesis, and adenoidectomy. Insertion of tympanostomy tubes is indicated when a patient experiences more than six acute otitis media episodes during a 6‐month period or has recurrent otitis media in addition to otitis media with effusion or persistent bilateral effusions for longer than 3 months. A trial of antibiotic prophylaxis is commonly carried out prior to surgical consultation.20
Antihistamines and decongestants are ineffective for otitis media with effusion and are not recommended for treatment.23 The management of chronic suppurative otitis media often includes parenteral antibiotics to cover infection by Pseudomonas species and anaerobic bacteria.
The prognosis for acute otitis media is excellent. Studies show that over 80% of children in the United States who were treated symptomatically for acute otitis media without antibiotics had complete resolution of otitis without suppurative complications.24 However, complications can occur, more commonly in patients younger than 1 year of age. The most common complication is conductive hearing loss related to persistent effusions. Serious complications, including mastoiditis, cholesteatoma, labyrinthitis, extradural or subdural abscesses, meningitis, brain abscess, and lateral sinus thrombosis, are uncommon.25
Oral Health Considerations
Many children with recurrent otitis media are treated frequently (and sometimes for extensive periods) with various antibiotics. Included in the antibiotic armamentarium are medications that are also used for odontogenic infections. Oral health care providers need to be aware of what type of antibiotics the patient has taken within the previous 4 to 6 months, to avoid giving the patient an antibiotic to which resistance has already developed. It has been demonstrated that antibiotic regimens used for the treatment of otitis media promote the emergence of antibiotic‐resistant bacteria.26 Furthermore, the extended use of antibiotics may result in the development of oral candidiasis.
Sinusitis is defined as an inflammation of the epithelial lining of the paranasal sinuses. The inflammation of these tissues causes mucosal edema and an increase in mucosal secretions. The most common trigger is an acute upper respiratory infection, although other causes, such as exacerbations of allergic rhinitis, dental infections or manipulations, and direct trauma can be implicated. If blockage of sinus drainage occurs, retained secretions can promote bacterial growth and subsequent acute bacterial sinusitis.
Acute sinusitis is a very common disorder, affecting about 31 million Americans per year.27 Sinusitis accounts for about $5.8 billion (US) in costs with about 73 million days of restricted activity per year.28
The paranasal sinuses are air‐filled cavities that are lined with pseudostratified columnar respiratory epithelium. The epithelium is ciliated, which facilitates the clearance of mucosal secretions. The frontal, maxillary, and ethmoid sinuses drain into an area known as the ostiomeatal complex. Rhythmic ciliary movement and the clearance of secretions can be impaired by several factors, including viral upper respiratory infections, allergic inflammation, and exposure to tobacco smoke and other irritants. In addition, foreign bodies (accidental or surgical) or a severely deviated nasal septum can cause obstruction. If blockage of the sinus ostia or obstruction of the ostiomeatal complex occurs, stasis of sinus secretions will allow pooling in the sinus cavities, which facilitates bacterial growth.
The most common organisms found in acute bacterial sinusitis are S. pneumoniae, H. influenzae, and M. catarrhalis. Organisms that are commonly associated with chronic sinusitis are Staphylococcus aureus and anaerobic bacteria such as Bacteroides spp and Fusobacterium spp. Sinusitis due to a fungal infection rarely occurs, usually in immunocompromised patients and in patients who are unresponsive to antibiotics.29
Clinical and Laboratory Findings
The symptoms of acute sinusitis include facial pain, tenderness, and headache localized to the affected region. Sinusitis affecting the sphenoid sinuses or posterior ethmoid sinuses can cause headache or pain in the occipital region. Other symptoms that are commonly described include purulent nasal discharge, fever, malaise, and postnasal drainage with fetid breath. Occasionally, there may be toothache or pain with mastication. Patients with chronic sinusitis often present with other symptoms that are often vague and poorly localized. Chronic rhinorrhea, postnasal drainage, nasal congestion, sore throat, facial “fullness,” and anosmia are common complaints.
Physical examination reveals sinus tenderness and purulent nasal drainage. On occasion, erythema and swelling of the overlying skin may be evident. The nasal mucosa can appear edematous and erythematous, and nasal polyps might also be visible.
In routine cases of suspected acute bacterial sinusitis, imaging studies are not required. When there are more persistent symptoms as in chronic sinusitis or an incomplete response to initial management, imaging studies may become appropriate. Plain‐film radiography is not helpful for establishing ostiomeatal complex disease. Computed tomography (CT) is the study of choice for documenting chronic sinusitis with underlying disease of the ostiomeatal complex and is superior to magnetic resonance imaging (MRI) for the identification of bony abnormalities. CT can also accurately assess polyps, reactive osteitis, mucosal thickening, and fungal sinusitis.29
Sinusitis is classified as either acute, subacute, or chronic, based on the duration of the inflammation and underlying infection. Acute sinusitis is defined as inflammation of less than 4 weeks, subacute as 4 to 8 weeks, and chronic as either longer than 8 to 12 weeks in duration.30
The diagnosis of acute sinusitis is made on the basis of history and physical examination. As previously noted, radiologic evaluations may be helpful in certain situations. Patients with recurrent disease need to be evaluated for underlying factors that can predispose patients to sinusitis. Allergy evaluation for allergic rhinitis is often helpful. Chronic sinusitis may be the presentation of an underlying systemic disease, such as granulomatosis with polyangiitis (formerly known as Wegener’s) or eosinophilic granulomatosis with polyangiitis (formerly Churg–Strauss). Other predisposing factors, such as tobacco smoke exposure, immunodeficiency, cystic fibrosis, primary ciliary dyskinesia, and septal deviation, should be considered.29,30
CT usually aids the diagnosis of chronic sinusitis. Evaluation of the ostiomeatal complex is crucial in the management of these patients. In addition, rhinoscopy may be helpful for direct visualization of sinus ostia.
Initial medical treatment consists of antibiotics to cover the suspected pathogens, along with topical or oral decongestants to facilitate sinus drainage. First‐line antibiotics such as amoxicillin are often effective, although second‐generation cephalosporins, azithromycin, and amoxicillin‐clavulanate can be helpful in resistant cases. Comprehensive treatment of bacterial sinusitis may also include adequate hydration, sinus rinses, steam inhalation, and pharmacologic measures intended to treat underlying disease, such as rhinitis, and to restore ostial patency. Nasal glucocorticoids are thought to be potentially effective adjuncts to antibiotic therapy, but available objective data have not unequivocally demonstrated effectiveness.31 Acute frontal or sphenoid sinusitis can be serious because of the potential for intracranial complications. Intravenous antibiotics are indicated, and surgical intervention is considered, based on the condition’s response to medical management.29
The management of chronic sinusitis involves antibiotics of a broader spectrum, and a prolonged treatment course may be required. Topical corticosteroids or short courses of oral corticosteroids may help reduce the swelling and/or obstruction of the ostiomeatal complex.29 Avoidance of exacerbating factors such as allergens or tobacco smoke should be emphasized. Patients with histories suggestive of allergy should undergo a thorough allergy evaluation. Dupilumab is currently approved for the treatment of refractory chronic rhinosinusitis with nasal polyps in adults. Several of the other biologic agents currently approved for the treatment of moderate‐to‐severe persistent asthma are actively being studied as treatment options as well (see section Asthma).32
Patients who have chronic sinusitis with evidence of disease of the ostiomeatal complex who fail medical management often require surgical intervention. Functional endoscopic sinus surgery (FESS) involves the removal of the ostiomeatal obstruction through an intranasal approach. This procedure can be performed with either local or general anesthesia and without an external incision. The recovery time from this procedure is short, and morbidity is generally low.
Patients treated for acute sinusitis usually recover without sequelae. Children with sinusitis, particularly ethmoid and maxillary sinusitis, are at risk for periorbital or orbital cellulitis. Periorbital cellulitis is most often treated on an outpatient basis with broad‐spectrum antibiotics and rarely leads to complications. Orbital cellulitis, on the other hand, requires hospital admission with broad‐spectrum intravenous antibiotics. Further treatment is tailored on a case‐by‐case basis and may entail surgical or endoscopic drainage of the infection.33
Frontal sinusitis can extend through the anterior wall and present as Pott’s puffy tumor. Sinusitis can also spread intracranially and result in abscess or meningitis. These complications, although uncommon, are more likely to occur in male adolescent patients.
Patients with chronic sinusitis are more likely to require a prolonged recovery period, with a resultant decrease in quality of life. Chronic medication use can lead to side effects or other complications, such as rhinitis medicamentosa from prolonged use of topical decongestants. Surgical intervention and underlying‐factor assessment will often reverse the chronic process, leading to an improvement in quality of life.
Oral Health Considerations
Patients with sinus infections who present with a complaint of a toothache are commonly encountered in a dental office. The oral health care professional evaluating the patient must be able to differentiate between an odontogenic infection and sinus pain. On history, sinus infections usually present with pain involving more than one tooth in the same maxillary quadrant, whereas a toothache usually involves only a single tooth. Ruling out odontogenic infections by a dental examination and appropriate periapical radiography strengthens a diagnosis. Additional testing,34 including pulp testing of teeth with large restorations as well as limited field cone beam CT of potential sources of infection may rule in an odontogenic origin of both sinus‐localized pain as well as maxillary sinusitis of endodontic origin.34,35
Chronic sinus infections are often accompanied by mouth breathing. This condition is associated with oral dryness and (in long‐time sufferers) increased susceptibility to oral conditions such as gingivitis.36
As with other conditions for which the prolonged use of antibiotics is prescribed, the potential development of bacterial resistance needs to be considered. Switching to a different class of antibiotics to treat an odontogenic infection is preferable to increasing the dosage of an antibiotic that the patient has recently taken for another condition.
The use of decongestants may be associated with oral dryness, which may need to be addressed.
Laryngitis and Laryngotracheobronchitis
The upper airway is the site of infection and inflammation during the course of a common cold, but respiratory viruses can affect any portion of the respiratory tree. Laryngitis is defined as an inflammation of the larynx, usually because of a viral infection. Laryngotracheobronchitis (also termed viral croup) involves inflammation of the larynx, trachea, and large bronchi. Although these illnesses have distinct presenting features, both result from a similar infectious process and the reactive inflammation that follows. Laryngitis can present at any age, although it is more common in the adult population.37 In contrast, laryngotracheobronchitis is an illness seen primarily in young children and has a peak incidence in the second and third years of life. These infections are most common during the fall and winter months, when respiratory viruses are more prevalent.
The viruses most commonly implicated in laryngitis are parainfluenza virus, coxsackieviruses, adenoviruses, and herpes simplex virus. The viruses most commonly associated with laryngotracheobronchitis are parainfluenza virus, RSV, influenza virus, and adenovirus.38
Acute laryngitis can also result from excessive or unusual use of the vocal cords, gastroesophageal reflux, or irritation due to tobacco smoking.
The underlying infectious process is quite similar to that seen in viral infections of the upper respiratory tract (see above). After infection of the respiratory epithelium occurs, an inflammatory response consisting of mononuclear cells and polymorphonuclear leukocytes is mounted. As a result, vascular congestion and edema develop. Denudation of areas of respiratory epithelium can result. In addition to edema, spasm of laryngeal muscles can occur. Because the inflammatory process is triggered by a viral infection, the disease processes are usually self‐limited.
Clinical and Laboratory Findings
Patients with laryngitis usually have an antecedent viral upper respiratory infection. Complaints of fever and sore throat are common. The most common manifestation of laryngitis is hoarseness, with weak or faint speech.37 Cough is somewhat variable in presentation and is more likely when the lower respiratory tract is involved.
Children presenting with viral croup commonly have an antecedent upper respiratory tract infection, which may include fever. Shortly thereafter, a barking cough and intermittent stridor develop. Stridor at rest, retractions, and cyanosis can occur in children with severe inflammation. Neck radiography will demonstrate subglottic narrowing (a finding termed “steeple sign”) on an anteroposterior view.
There is no universal classification system for these illnesses. The anatomic site most affected describes these diseases.
The diagnosis of laryngitis is based on the suggestive history. There are no specific findings on physical examination or laboratory tests, although the presence of hoarseness is suggestive. The differential diagnosis includes other causes of laryngeal edema, including obstruction of venous or lymphatic drainage from masses or other lesions, decreased plasma oncotic pressure from protein loss or malnutrition, increased capillary permeability, myxedema of hypothyroidism, and hereditary angioedema. Carcinoma of the larynx can also present with hoarseness.
The diagnosis of laryngotracheobronchitis is usually apparent and is based on a suggestive history. Radiologic evaluation may or may not aid physicians in the diagnosis. Only 50% of patients with laryngotracheobronchitis show the classic steeple sign on plain neck radiography (Figure 13‐2).38 With children, it is important to rule out other causes of stridor, including foreign‐body aspiration, acute bacterial epiglottitis, and retropharyngeal abscess.39
Most cases of laryngitis are mild and self‐limited, so only supportive care need be prescribed. The use of oral corticosteroids in severe or prolonged cases can be considered, although their routine use is controversial.39
The most important aspect in the management of laryngotracheobronchitis is airway maintenance. The standard therapy includes mist therapy, corticosteroids, and racemic epinephrine. Any child with evidence of respiratory distress should be considered a candidate for steroid treatment. Less frequently, hospitalization and intubation or tracheotomy are necessary.38
As with viral upper respiratory infections, most cases of laryngitis and laryngotracheobronchitis are self‐limited and require minimal medical intervention. Recovery within a few days to a week is expected. In some cases, laryngotracheobronchitis can recur, although the factors influencing this are not well understood.
Pharyngitis and Tonsillitis
Inflammation of the tonsils and pharynx is almost always associated with infection, either viral or bacterial. The vast majority of cases are caused by viral infections. These infections can be associated with fever, rhinorrhea, and cough. The major viral etiologies include rhinovirus, coronavirus, adenovirus, Epstein‐Barr, para‐influenza, herpes simplex virus (HSV), and influenza.40
The most common bacterial cause of acute tonsillopharyngitis is group A β‐hemolytic Streptococcus (GABHS) infection, specifically Streptococcus pyogenes infection. Proper diagnosis and treatment of this infection are extremely important in order to prevent disease sequelae, namely, acute rheumatic fever and glomerulonephritis. Less common bacterial causes include Corynebacterium diphtheriae, Neisseria gonorrhoeae, Chlamydia, and Mycoplasma pneumoniae.
Chronic mouth breathing, chronic postnasal drainage, and inflammation due to irritant exposure can also cause pharyngitis and tonsillitis.
Streptococcal infections are spread through direct contact with respiratory secretions. Transmission is often facilitated in areas where close contact occurs, such as schools and day‐care centers. The incubation period is 2 to 5 days.
Clinical and Laboratory Findings
Sore throat is the predominant symptom. Associated clinical findings are based on the infectious etiology. Patients with Epstein‐Barr virus infections develop infectious mononucleosis, a disease characterized by exudative tonsillopharyngitis, lymphadenopathy, fever, and fatigue. Physical examination can reveal hepatosplenomegaly. Common laboratory findings include leukocytosis, with more than 20% atypical lymphocytes on blood smear. Blood chemistries may reveal elevated liver enzymes.
Infection with coxsackievirus can cause several distinct illnesses, each associated with tonsillopharyngitis. Herpangina is a disease that is characterized by small ulcers that are 2 to 3 mm in size and located on the anterior tonsillar pillars and possibly the uvula and soft palate. Hand‐foot‐and‐mouth disease is characterized by ulcers on the tongue and oral mucosa, in association with vesicles found on the palms and/or soles. Small yellow‐white nodules on the anterior tonsillar pillars characterize lymphonodular pharyngitis; these nodules do not ulcerate.
Pharyngoconjunctival fever is a disorder characterized by exudative tonsillopharyngitis, conjunctivitis, and fever. Infection is due to adenovirus.
Measles is a disease with a prodromal phase that is characterized by symptoms of upper respiratory infection, tonsillopharyngitis, and small white lesions with erythematous bases on the buccal mucosa and inner aspect of the lower lip (Koplik’s spots). These lesions are pathognomonic of early measles infection.
Streptococcal pharyngitis is characterized by exudative tonsillitis and fever. Physical examination often reveals a beefy red uvula, cervical adenitis, and oral petechiae. Laboratory evaluation should include testing for group A Streptococcus.41
Pharyngotonsillitis is classified on the basis of etiology and clinical presentation (see above).
Diagnosis is based on a history of sore throat and is established by appropriate physical findings and results of testing. A rapid antigen detection test is available for diagnosing streptococcal pharyngitis. The test has a high specificity (95+%) and slightly lower sensitivity (80–90%).41 The importance of confirmatory cultures is still controversial, with some studies concluding that culture confirmation of negative rapid antigen detection tests may not be necessary in all circumstances.42
Antistreptococcal antibody titers reflect past and not present immunologic events and are of no value in the diagnosis of acute GABHS pharyngitis. They are valuable for confirmation of prior GABHS infections in patients suspected of having acute rheumatic fever or post‐streptococcal acute glomerulonephritis.
The viral causes of tonsillopharyngitis are treated symptomatically. Gargle solutions, analgesics, and antipyretics are often helpful. The course is self‐limited.
Acute streptococcal pharyngitis is treated with oral penicillin V, cephalosporins, macrolides, clindamycin, or an intramuscular injection of benzathine penicillin G. Failure rates for penicillin vary from 6 to 23%, so an additional antibiotic course may be necessary.41 GABHS carriers appear unlikely to spread the organism to close contacts and are at a low risk of developing complications. Antimicrobial therapy is generally not indicated for the majority of GABHS carriers.43
The prognosis for viral tonsillopharyngitis is very good as the infections are self‐limited. Late sequelae from group A streptococcal tonsillitis can be avoided by prompt diagnosis and treatment.43 Other complications due to streptococcal tonsillitis are uncommon but include cervical adenitis, peritonsillar abscesses, otitis media, cellulitis, and septicemia.
Oral Health Considerations
The association between GABHS infection and the development of severe complications, such as rheumatic fever and its associated heart condition, is well known. Although failure to successfully treat GABHS infections was more common in the pre‐penicillin era, there are some concerns today regarding reinfection in cases in which penicillin is unable to eradicate the organism. One study found a significant association between the persistence of GABHS on toothbrushes and removable orthodontic appliances and the recovery of GABHS in the oropharynx of symptomatic patients after 10 days of treatment with penicillin.44 Interestingly, when toothbrushes were rinsed with sterile water, organisms could not be cultured beyond 3 days, whereas nonrinsed toothbrushes harbored GABHS for up to 15 days. Thus, patients with GABHS infections should be instructed to thoroughly clean their toothbrushes and removable acrylic appliances daily. It is also advisable to change to a new toothbrush after the acute stage of any oropharyngeal infection.
LOWER AIRWAY DISEASES
The association between oral health and respiratory diseases has received renewed attention. Several articles have suggested that dental plaque may be a reservoir for respiratory pathogens involved in pneumonia and chronic obstructive pulmonary disease (COPD).45,46,47,48 Although this may not be a critical problem for ambulatory healthy individuals, deteriorating oral health may be a major factor for both morbidity and mortality among institutionalized elderly persons, as well as for patients in critical care units.
Acute bronchitis is an acute respiratory infection involving the large airways (trachea and bronchi) that is manifested predominantly by cough with or without phlegm production that lasts up to 3 weeks. In patients who are otherwise healthy and without underlying pulmonary disease, bronchitis is commonly caused by a viral infection.49 The viruses most commonly implicated are influenza, parainfluenza, and RSV. Viruses that are predominantly associated with upper respiratory tract infections, including coronavirus, rhinovirus, and adenovirus, have also been implicated as causes of acute bronchitis.50 Acute bronchitis due to bacterial infection is less common. Atypical bacteria including Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis are often important causes of bronchitis.51 Staphylococcus and Gram‐negative bacteria are common causes of bronchitis among hospitalized individuals.
The pathophysiology of acute bronchitis is similar to that of other respiratory tract infections. Following infection of the mucosal cells, congestion of the respiratory mucosa develops. Inflammation causes an increase in secretory activity, resulting in increased sputum production. Polymorphonuclear leukocytes infiltrate the bronchial walls and lumen. Desquamation of the ciliated epithelium may occur, and spasm of bronchial smooth muscle is common.
Clinical and Laboratory Findings
Acute viral bronchitis usually presents with sudden onset of cough, with or without sputum expectoration and without evidence of pneumonia, the common cold, acute asthma, or an acute exacerbation of chronic bronchitis.50 Chest discomfort may occur; this usually worsens with persistent coughing bouts.52 Other symptoms, such as dyspnea and respiratory distress, are variably present. Physical examination may reveal wheezing. The presentation may closely resemble an acute asthma exacerbation. Symptoms gradually resolve over a period of 1 to 2 weeks. Patients with underlying chronic lung disease might also experience respiratory compromise, with a significant impairment in pulmonary function.
The presentation of acute bacterial bronchitis is very similar to that of bacterial pneumonia (see below). Symptoms may include fever, dyspnea, productive cough with purulent sputum, and chest pain. Bacterial bronchitis can be differentiated from pneumonia by the lack of significant findings on chest radiography.
Although there is no universal classification scheme, acute bronchitis can be differentiated on the basis of etiology. Viral bronchitis presents differently from bacterial bronchitis, as described above.
Diagnosis of acute bronchitis is based on a suggestive history and a physical examination. Neither blood cell counts nor sputum analyses are particularly diagnostic in otherwise healthy patients. Routine testing for viruses is generally not obtained for bronchitis.53 Chest radiography may be helpful in distinguishing bacterial bronchitis from pneumonia. Patients with recurrent bouts of acute bronchitis should be evaluated for possible asthma. This evaluation should include pulmonary function testing.
Patients with persistent symptoms in the course of presumed viral bronchitis should be evaluated to determine possible underlying etiologies. Sputum cultures might prove useful in these circumstances but are not performed routinely.52
Viral bronchitis can be managed with supportive care only as most individuals who are otherwise healthy recover without specific treatment. If significant airway obstruction or hyperreactivity is present, inhaled bronchodilators, such as albuterol, may be useful. Cough suppressants, such as codeine, can also be considered for patients whose coughing interferes with sleep.
The treatment of bacterial bronchitis may include amoxicillin, amoxicillin‐clavulanate, macrolides, or cephalosporins. For suspected or confirmed pertussis infection, treatment with a macrolide or trimethoprim‐sulfamethoxazole is appropriate to decrease disease transmission. Although commonly used, inhaled β2‐agonist bronchodilators and mucokinetic agents, like expectorants, are not recommended for routine use in patients with acute bronchitis.50
Acute bronchitis carries an excellent prognosis for patients who are without underlying pulmonary disease, and recovery without sequelae is the norm. However, for patients with chronic lung disease and respiratory compromise, bronchitis can be quite serious and may often lead to hospitalization and respiratory failure. In other high‐risk individuals, such as those with human immunodeficiency virus (HIV) infection or other immunodeficiencies, acute bronchitis may lead to the development of bronchiectasis.
Oral Health Considerations
Resistance to antibiotics may develop rapidly and last for 10 to 14 days.52 Thus, patients who are taking amoxicillin for acute bronchitis should be prescribed another type of antibiotic (such as clindamycin or a cephalosporin) when an antibiotic is needed to treat an odontogenic infection.
Pneumonia is defined pathologically as an infection and a subsequent inflammation involving the lung parenchyma. Both viruses and bacteria are causes, and the presentation is dependent on the causative organism. Pneumonias can be broadly classified as either nosocomial or community‐acquired. Nosocomial infections are infections that are acquired in a hospital or health care facility and often affect debilitated or chronically ill individuals. Community‐acquired infections can affect all persons but are more commonly seen in otherwise healthy individuals. In the US, there were 52,000 deaths from community‐acquired pneumonia in 2007 with 4.2 million ambulatory care visits for this condition in 2006.54
Formerly, bacterial pneumonia was categorized into several subtypes; community‐acquired pneumonia, aspiration pneumonia, hospital‐acquired (nosocomial) pneumonia, ventilator associated pneumonia, and nursing home associated pneumonia. In all cases, connections have been made with oral health status. However, in 2005 a new category was created called health care‐associated pneumonia or HCAP.55 Health care‐associated pneumonia was defined as pneumonia occurring in a diverse group of patients, including those undergoing home‐infusion therapy or wound care, chronic dialysis, recently hospitalized patients, or nursing home residents. Patients in these settings are often at high risk for pneumonia caused by multidrug resistant organisms such as methicillin‐resistant Staphylococcus aureus or resistant Gram‐negative bacilli. Thus, treatment guidelines for HCAP include broad‐spectrum antibiotic therapy.
The most common bacterial cause of community‐acquired pneumonia is S. pneumoniae, followed by H. influenzae. The organisms responsible for HCAP include aerobic Gram‐negative bacilli, such as P. aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter species. Infections due to Gram‐positive cocci, such as S. aureus, particularly methicillin‐resistant S. aureus (MRSA), have been rapidly emerging in the United States as well.56 A related condition is aspiration pneumonia, which is typically caused by anaerobic organisms most often originating from the gingival crevice.57 Aspiration pneumonia often occurs in patients with dysphagia, depressed consciousness, or others at risk for aspiration of oral contents into the lung, including alcoholics. Aspiration pneumonia occurs both in the community and in institutional settings.
Atypical organisms commonly associated with pneumonia include M. pneumoniae, Legionella, and Chlamydia.58 The atypical organisms may cause a pneumonia that differs in clinical presentation from that caused by the aforementioned bacteria (see below). Pneumonia can be caused by viruses, such as influenza, parainfluenza, adenovirus, and RSV, as well as fungi such as Candida, Histoplasma, Cryptococcus, and Aspergillus. Pneumonia may also be caused by other organisms including Pneumocystis jiroveci (carinii), seen in immunocompromised hosts, Nocardia, and Mycobacterium tuberculosis. Infection with these organisms can often be differentiated by chest radiography.
The pathophysiology of pneumonia is dependent on the causative infectious organism. In bacterial pneumonia caused by S. pneumoniae, for example, the bacteria first enter the alveolar spaces after inhalation. Once inside the alveoli, the bacteria rapidly multiply, and extensive edema develops. The bacteria cause a vigorous inflammatory response, which includes an influx of polymorphonuclear leukocytes. In addition, capillary leakage is pronounced. As the inflammatory process continues, the polymorphonuclear leukocytes are replaced by macrophages. Subsequent deposition of fibrin ensues as the infection is controlled, and the inflammatory response resolves.58
Other infections of the lung (i.e., viral, atypical, etc.) are interstitial processes. The organisms are first inhaled into the alveolar spaces. The organisms then infect the type I pneumocytes directly. As these pneumocytes lose their structural integrity and necrosis ensues, alveolar edema begins. Type II pneumocytes proliferate and line the alveoli, and an exudative cellular debris accumulates. An interstitial inflammatory response is mounted, primarily by mononuclear leukocytes. This process can occasionally progress to interstitial fibrosis, although resolution is the norm.
Clinical and Laboratory Findings
Pneumonia due to community‐acquired bacterial infection typically presents acutely, with a rapid onset of symptoms. A prodrome similar to that seen with acute infections of the upper respiratory tract is unusual. Common symptoms include fever, pleuritic chest pain, and coughing that produces purulent sputum.52 Chills and rigors are also common. Pneumonia due to H. influenzae, which is seen more commonly in patients with COPD or alcoholism, presents with fever, cough, and malaise. Chest pain and rigors are less common.
Nosocomial pneumonia with Staphylococcus secondary to aspiration presents with fever, dyspnea, cough, and purulent sputum. In cases acquired hematogenously, signs and symptoms related to the underlying endovascular infection predominate. Otherwise, respiratory tract symptoms are mild or absent despite radiographic evidence of multiple pulmonary infiltrates. The classic clinical features of nonbacteremic Enterobacteriaceae or Pseudomonas