Download Chronic Inflammatory Diseases of the Nasal Cavity and Paranasal

Chronic Inflammatory Diseases
Chronic Inflammatory Diseases
Abstract
Chapter 1
Chronic Inflammatory Diseases of the
Nasal Cavity and Paranasal Sinuses
Hanadi A Fatani1*
1
King Fahad Medical City, KSA
Corresponding Author: Hanadi A Fatani, King Fahad
Medical City, Riyadh, 59046, KSA. Email: h.fatani@
kfmc.med.sa
*
First Published March 10, 2016
Copyright: © 2016 Hanadi A Fatani.
This article is distributed under the terms of the Creative
Commons Attribution 4.0 International License
(http://creativecommons.org/licenses/by/4.0/), which
permits unrestricted use, distribution, and reproduction
in any medium, provided you give appropriate credit to
the original author(s) and the source.
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In this chapter, we examine the chronic inflammatory
diseases of the nasal cavity and paranasal sinuses. First, we
examine the basic characteristics of the various chronic
inflammatory diseases of the nasal cavity and paranasal
sinuses and chronic inflammatory diseases of the oral
cavity. Further, we discuss the etiopathogenesis, diagnosis, differential diagnosis, and treatment options for the
various conditions. The chapter is aimed at helping gain
some insight into the current views regarding chronic inflammatory conditions of the nasal cavity and paranasal
sinuses as well as the oral cavity.
Chronic Inflammatory Disease of Nasal Cavity and Paranasal Sinuses
Currently, the prevalence of chronic inflammatory
diseases of the nasal cavity and paranasal sinuses is high.
It has been reported that every 10th European has chronic
inflammation of the nose and paranasal sinuses [1]. A basic understanding of the various nasal and paranasal diseases is paramount to approaching them clinically. Below
is a short description of various chronic inflammatory diseases affecting the nasal cavity and the paranasal sinuses.
Rhinosinusitis
Sinusitis, or rhinosinusitis, is defined as the inflammation of the paranasal sinuses and nasal cavity [2]. Rhinosinusitis is the more preferred term because it encompasses
the inflammation of both the nasal cavity and the inflamwww.avidscience.com
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mation of the paranasal sinuses. Rhinosinusitis may present in the acute or chronic form, and chronic rhinosinusitis (CRS) may present with or without nasal polyps. The
most common symptoms of CRS are nasal obstruction,
nasal congestion, discharge, fatigue, headache, facial pressure, and dysosmia, which may also show worsening in
certain seasons, such as winter [3]. CRS frequently occurs
in conjunction with nasal polyps and asthma, presenting
as a complex allergic entity. Thus, CRS tends to compromise the patient’s quality of life and daily functioning. The
diagnostic modalities commonly used for the diagnosis of
this condition are paranasal sinus computed tomography
(CT), fiberoptic endoscopy, and anterior rhinoscopy [3].
The mainstay in the treatment of CRS is nasal corticosteroids, both in the presence and absence of nasal polyps
[3]. Other predominant treatment options in the absence
of nasal polyps are nasal wash, nasal decongestants, and
systemic corticosteroids [3].
Sinonasal Inflammatory Polyp
In 20–40% of the cases of CRS, nasal polyps are detected [3]. Inflammatory nasal polyps are inflammatory,
polypoidalsinonasal mucous tissues that arise in response
to inflammatory stimuli, such as allergy and infections, or
as a component of a systemic process such as aspirin intolerance or cystic fibrosis [4]. The diagnosis of sinonasal
polyps is generally established by CT or MRI. Sinonasal
polyps are generally considered benign, and the condition is generally treated symptomatically, unless severe. In
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20-35% of the cases, surgery is required [3]. The mainstay
in the medical treatment of sinonasal polyps is nasal corticosteroids [3]. The treatment of chronic rhinosinusitis
with polyps is discussed in subsequent sections in detail.
Paranasal Nasal Sinus Mucocele
Mucoceles are defined as benign cystic lesions limited
by the mucosa of the paranasal sinus itself and occurring
most frequently in the paransal sinus[5]. The condition
generally does not give rise to any specific group of symptoms and is most often manifested by pressure symptoms
giving rise to ophthalmic or intracranial complications
[6]. In fact, studies have shown that even in the presence
of large lesions with significant erosion of involved tissue,
the condition may remain asymptomatic [7]. A long-term
study showed that a very high percentage of patients with
paransal sinus mucoceles develop opthalomologic complications [8]. Surgical excision is the standard treatment
for these lesions, with the endoscopic approach being the
gold standard [6].
Infections
Fungal sinusitis may occur as allergic fungal sinusitis,
mycetoma andacute or chronic invasive fungal sinusitis
[9].
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Allergic Fungal Sinusitis
Allergic fungal sinusitis affects atopic immunocompetent individuals with fungal colonization of the sinuses.
The fungus acts as an allergen triggering inflammatory
reactions and thereby leading to sinus obstruction and
stasis, which further promotes fungal proliferation [9].
The diagnostic criteria for this condition are detection of
allergic mucin; detection of fungal specific IgE; absence
of fungal invasion of the submucosa, blood, or bone; absence of immunosuppression; and radiologic evidence of
opacity of the involved sinua. Typical CT findings of airfluid level seen in bacterial sinusitis are rare in fungal sinusitis, and in fact, the absence of air-fluid levels may be
considered diagnostic for this condition [10,11]. Allergic
fungal sinusitis has been often linked with socioeconomic
conditions, and it has been observed to affect low income
groups [12,13].
Mycetoma
Mycetoma, sometimes referred to as “fungal ball”
typically occurs in immunocompetentnonatopicindividuals[9]. In this condition, the fungus remains in the
secretion, without invading the mucosa. Mycetomas are
masses of fungal hyphae that elicit a low-grade chronic
noninvasive inflammation of the sinuses. Most commonly, only one sinus, often the maxillary sinus, is affected
[9].The condition may lead to sclerosis or calcification of
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the sinus walls, which may be evident radiologically [9].
Clinically,the condition is mildly symptomatic or may be
asymptomatic [9].
Invasive fungal sinusitis
Chronic invasive fungal sinusitis extending to the orbits or the brain may occur in patients who are immunocompetent[9]. Fungal pathogens in this condition proligerate in the sinuses, eventually invading the mucosa [9].
Sinonasalmucormycosis
Sinonasalmucomycosis is a rare fulminant disease affecting immunocompromised individuals. In the pediatric population, it is rare but potentially fatal [14].
Rhinosporidiosis
Rhinosporidosis is an infectious disease predominantly reported from India and Sri Lanka [15] . It is caused
by Rhinosporidiumseeberi. The nasal form of the disease
presents with chronic mucoid discharge with painless
unilateral obstruction and possible involvement of paranasal sinuses. It is also likely to affect other tissues such as
conjunctiva, orapharyngeolaryngeal mucosa, and urethra
[15].
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Bacterial Infection
Rhinoscleroma
Rhinoscleroma is a chronic granulomatous disease
of the nasal cavity, nasopharynx, and paranasal sinuses
caused by Klebsiellarhinoscleromatis. The clinical disease
progresses through the catarrhal/rhinitic stage to the
granulomatous/florid and sclerotic/cicatricial stages. Initial presentation involves non-specific rhinitis, followed
by chronic foul purulent discharge, frequent epistaxis,
nasal obstruction, crustation, and granulation, eventually
resulting in permanent nasal and oral deformities [16].
Leprosy
Leprosy is caused by Mycobacterium leprae and is
characterized by involvement of the skin and peripheral
nerves.Depression of the nasal bridge is a characteristic
feature of leprosy. The nasal mucosa is the main point of
entry and exit of the bacteria [17].
Tuberculosis
Tuberculosis is caused by Mycobacterium tuberculosis. It is clinically characterized by prolonged cough, night
sweats, and weight loss, often presenting as a prolonged
low-grade fever of unknown origin. The diagnosis is confirmed by detection of acid-fast bacilli in pathological examination of sputum and radiological evidence. Vacancies
are now administered in countries where the condition is
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endemic, and the treatment involves administration of
isoniazid, rifampicin, and pyrazinamide for six months
[18].
Protozoal
Mucocutaneousleishmaniasis
Mucocutaneousleishmaniasis is caused by Leishmaniabrasiliensis. Almost 40% of patients develop mucocutaneous involvement, with the typical early symptoms being nasal obstruction associated with a nodule or polyp at
the inferior turbinate. The disease eventually progresses to
destroy the nasal septum and destroy the nose and mouth
if not controlled [19].
Viral Infection
Herpes
Herpes simplex is caused by herpes simplex virus (HSV) type I or II and manifests as painful blisters
or ulcers around the nose and mouth [20]. Oral lesions
are generally caused by HSV type I. Tingling, itching, or
burning may be experienced before the appearance of the
blisters [20].
CMV
Cytomegalovirus infection (CMV) is a self-limiting
disease caused by human herpes simplex virus 5. CMV is
clinically similar to CMV and characterized by fever, gen-
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eralized lymphadenopathy and hepatosplenomegaly [21].
Infectious mononucleosis
Infectious mononucleosis is caused by Epstein-Barr
virus and manifests as fever, pharyngitis, and lymphadenopathy. The condition is self-limiting and generally occurs in immunocompetent individuals [22].
Chronic Inflammatory Diseases of
the Oral Cavity
Drug-Related Gingival Hyperplasia
Some anticonvulsants such as phenytoins, calciumchannel blockers such as nifedipine, and immunosuppresants such as cyclosporine cause clinically and histologically similar gingival enlargement in susceptible patients
[26].
Gingival Fibromatosis
Periodontal Disease
Periodontal diseases are diseases affecting the gingiva
and alveolar bone. It is a growing public health concern,
with many risk factors, including poor oral hygiene; tobacco use or smoking; psychological factors such as stress;
related systemic conditions such as diabetes mellitus, obesity, and cardiovascular disease; use of drugs influencing
salivary flow; being the main risk factors for periodontal
diseases [23].
Gingivits
Chronic gingivitis is the chronic inflammation of the
gingiva.
Plasma Cell Gingivitis
Plasma cell gingivitis is a rare condition that is characterized by the diffuse and extensive infiltration of plasma
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cells into the sub-epithelial tissue [24]. It may be caused by
allergens, be neoplastic in origin, or idiopathic [25] and is
manifested by hypersensitivity [24].
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Gingival fibramatosis is defined as the overgrowth of
the collagenous portion of the non-epithelial gingival tissue [27]. It may be hereditary, idiopathic, or drug-induced.
Bacterial Infection
Streptococcal tonsillitis with pharyngitis
Streptococcal tonsillitis generally presents with highgrade fever (above 100°F), pharyngitis, tonsillar exudates,
and cervical lymphadenopathy. The diagnostic standard is
detection of the bacteria in throat culture.
Tuberculosis
Although TB usually affects the lungs, it can also have
extra-pulmonary manifestations. The oral lesions are typically asymptomatic appearing in the oral buccal mucosa
and may be either primary or secondary [28]. They generwww.avidscience.com
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ally affect the oral mucosa, especially the tongue, or the
gingival tissue and appear as chronic ulcers, nodules, or
granulomas. Diagnostic confirmation by pathology and
proper treatment are necessary.
Leprosy
Oral manifestations of leprosy range from non-specific lesions such as enanthema of palate to specific lesions
such as nodules or ulcers that may show positivity for the
pathogenic bacteria (Mycobacterium leparae).The lesions
are insidious and may be aymptomatic [29].
Actinomycosis
Actinomycoses is a rare chronic bacterial infection
caused by anaerobic bacteria of Actinomyces spp., which
colonize in the mouth and the digestive and genital tracts.
Typical microscopic findings include necrosis with yellowish sulfur granules and filamentous gram–positive
fungal pathogens [30]. Apart from the common respiratory tract presentation, the disease can also manifest in a
cervicofacial form, which is acquired via a mucosal breach
and presents as an slow-growing indurated mass with subsequent abscess formation and appearance of yellowish
exudates containing sulfur granules.
Cat scratch disease
Cat scratch disease is a bacterial zoonotic disease generally presented as lympadenopathynear the site of cat
scratch or bite, fever, and fatigue. It is caused by Bartonellahenselae.
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Fungal and Protozoal Disease
Candidiasis
Oropharyngeal candidiasis is caused by Candidia spp.,
most often Candidiaalbicans. The infection is generally regarded as an opportunistic infection, mainly affecting immunocompromised individuals. Clinically, the lesions are
characterized by pseudomembranous, erythematous, or
hyperplastic appearance. Chronic atrophic candiasis is a
form of the disase that is associated with denture use. [31].
Zygomycosis
Zygomycosis or mucormycosis is a fungal disease
caused by fungi of the order Mucorales. The disease is
characterized by a high mortality rate and genrally affects
immunocompromised lesions. Oral lesions such as ulcers
serve as point of entry for the organism, which evades the
hard palate, maxillary bone,paranasal sinuses, and the orbital and intracranial cavities [32].
Aspergillosis
Aspergillosis of the sinonasal tract is caused by Aspergillus sp. Predisposing factors are immunosuppression
and obstructive nasal lesions [33].
Viral Disease
Herpes simplex virus
Oral lesions of herpes simplex are generally caused by
HSV I. The lesions typically occur as localized clusters of
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painful blisters or ulcers occurring around the mouth.
Cytomegalovirus infection
Cytomegalovirus infection is caused by CMV.Although similar in clinical presentation to infectious mononucleosis, CMV infection rarely includes pharyngitis.
Clinical Feature Site
Etiology
Lam et al discussed the current understanding on the
etiopathogenesis of CRS intheir review [34]. These hypotheses suggest the notion that CRS occurs due to an interplay between individual host characteristics and exogenous factors. They grouped the current concepts on CRS
etiology and pathogenesis into the following categories:
(1) the “fungal hypothesis,” (2) the “superantigen hypothesis,” (3) the “biofilm hypothesis,” and (4) the “microbiome hypothesis,” all of which emphasize key environmental factors, and (5) the “eicosanoid hypothesis” and (6) the
“immune barrier hypothesis,” which describe specific host
factors [34].
Some of the common bacterial infections are caused
by the pathogenic transformation of bacteria that are normally present in the nasal and oral mucosa, e.g., actinomycosis and candidiasis.Certain viral infections such as
cytomegalovirus occur in those immunocompromised.
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Risk
With regard to CRS and allergic fungal rhinosinustis, a recent cohort study of patients from North Carolina
showed that patients with CRS have higher income, more
access to primary care, and lower markers of disease severity than those with allergic fungal rhinosinusitis [13].
The role of socioeconomic factors in the occurrence of
allergic fungal rhinosinusitis has also been reported by
others [12]. Miller et al [35] have shown that markers of
disease severity (namely, bone erosion and orbitocranial
involvement) in AFRS were associated with low income,
rural residence, poor housing quality, and less health care
access.Several diseases of the oral cavity such as tuberculosis also spread because of overcrowding, poor oral hygiene, and denture use.
Gender and Age
Diseases such as infectious mononucleosis are common in adolescents and young adults, while CSR is mostly
seen in middle aged adults. No particular gender predilection is seen for these diseases.
Histology
The main histological characteristics of chronic rhinosinusitis with nasal polyps are proliferation of pseudostratified respiratory epithelium, thickening of the
basement membrane, focal fibrosis and eosinophilic and
lymphocytic infiltration of the lamina propria [36].Alwww.avidscience.com
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though the exact etiopathogenesis of nasal polyps remains
elusive, currently two hypotheses are predominantly implcated: “hypothesis of staphylococcal superantigens” and
“hypothesis of immune barrier dysfunction” [36]. Further,
more recent findings indicate that HMG B1 may play a
crucial role in the pathogenesis of CRS with nasal polyps
[37].
Differential Diagnosis
The diagnosis of CRS on the basis of the symptom
presentation alone is difficult.
Bhattacharya [38] conducted a study on the correlation between reported symptoms and radiographic
evidence of chronic sinusitis and found that there is little correlation between the two, thereby suggesting that
the diagnosis of CRS based on symptom criteria alone is
difficult because most symptoms (other than dysosmia)
do not distinguish between radiographically normal and
diseased patients. The presence of a polyp and dysosmia
were found to be the only criteria that successfully distinguished between radiographically diseased and normal
individuals. Similarly, Lange et al investigated the value
of questionnaire-based and clinical-based diagnosis and
evaluation of CRS and found only moderate agreement
self-reported questioannaire scores and clinical-based assessment.As stated above, the absence of air-fluid levels
may be suggestive of the diagnosis of allergic fungal sinusitis. [10,11]. In cases of allergic fungal sinusitis, CT scans
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may show opacity in the affected sinus, and the absence
of the typical air-fluid levels in the case of acute bacterial
sinusitis. In cases of mycetoma, sclerosis or calcification of
the sinus wall may be seen in later stages [9].
Most diseases of the oral cavity, such as herpes, present
with typical lesions. Isolation of the pathogenic bacteria,
such as acid-fast bacilli, from oral mucosa or secretions is
generally necessary to establish the diagnosis. Others such
as tuberculosis, which may present with non-specific lesions need to be investigated by histopathological studies
to confirm the diagnosis. Diseases with systemic manifestations such as leprosy may be distinguished by their typical clinical presentation and diagnostic features.
Treatment
The mainstay in the treatment of CRS is nasal corticosteroids, nasal washes, and decongestants [3]. About
20–35% of the patients require surgery [3]. For CRS with
nasal polps, evidence for short-term use of systemic corticosteroids has been shown to be favorable, but not as
much in CRS without nasal polyps [39]. Topical corticosteroids improve symptom scores in both CRS subgroups.
The role of microbes in CRS is still controversial. Culturedirected antibiotics are recommended for CRSsNP with
exacerbation. Long-term use of low dosage antibiotics is
recommended for CRSsNP for their anti-inflammatory
effects [39].
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With respect to allergic fungal rhinosinusitis, the
treatmentmainly relies upon the surgical removal of fungal hyphae in eosinophilicmucin [40]. A recent review
[40] suggested that although several uncontrolled studies
support the beneficial effect of antifungal agents in AFRS,
but randomized trials of topical and systemic antifungal
therapies have not shown beneficial results in CRS. Antifungal treatment within the sinonasal cavities does not appear to be an effective approach for most chronic sinusitis,
and antifungal therapy for AFRS is unproven [40].
Recent studies [41] have shown that refractory
CRS that significantly affect the patient’s quality of life
does not respond to continued medical therapy. A recent
meta-analysis showed that current trend is to recommend
endoscopic sinus surgery after failure of 8-week course
of topical intranasal corticosteroids and 3-week course
of oral antibiotics, and in some cases the use of systemic
corticosteroids [42]. On the other hand, studies have also
indicated that no clear evidence is available to prove the
superiority of surgical treatment over medical treatment
for chronic sinusitis with polyp, in terms of symptom
scores or quality of life scores; therefore, further investigations are necessary to determine the most suitable forms
of treatment for this condition [43].
Watt and Petersen [23] highlighted the importance of
shifting from individual focus to developing effective public health measures to combat periodontal disease. Infective diseases such as tuberculosis and leprosy need to be
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tackled by widespread, effective public health measures,
particular in countries where the conditions are endemic.
Further, awareness regarding the maintenance of oral hygiene and the effects of tobacco use, which are causes for
several types of oral lesions, need to be generated in the
public. This will help reduce the incidence of diseases such
as chronic gingivitis.
Figure 1: Paranasal sinuses (From Mosby’s Medical Diction-
ary, 8th edition. S.v. “Paranasal sinus diseases.” Retrieved on January 09, 2016 from http://medical-dictionary.thefreedictionary.com/
Paranasal+sinus+diseases)
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Figure 2 and Figure 3: Treatment for chronic rhinosinusitis. (From Piromchai P, Kasemsiri P, Laohasiriwong S, Thanavirata-
nanich S. Chronic rhinosinusitis and emerging treatment options. Int
J Gen Med. 2013 Jun 7;6: 453-464. doi: 10.2147/IJGM.S29977. Print
2013.)
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Figure 4: Chronic gingivitis. (a) Histopathologic characteristics in a biopsy section of the epithelial and connective tissues of mild non-specific chronic gingivitis: Epithewww.avidscience.com
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lial hyperplasia, mild inflammatory lymphocyte infiltrate.
HE. Original magnification ×100. (b) Histopathologic
characteristics in a biopsy section of the epithelial and
connective tissues of moderate non-specific chronic gingivitis: Proliferation of epithelial crests, moderate inflammatory lymphocyte infiltrate, congestion. HE. Original
magnification ×100. (c) Histopathologic characteristics in
a biopsy section of the epithelial and connective tissues of
severe non-specific chronic gingivitis: Epithelial atrophy,
spongiosis, severelymphoplasmocytic infiltration. HE.
Original magnification ×200. (From Myriam A. Koss, Cecilia
E. Castro,1 Silvia Carino,2 and Maria E. LópezHistopathologic and
histomorphometric studies and determination of IL-8 in patients
with periodontal disease J Indian SocPeriodontol. 2014 Mar-Apr;
18(2): 145–149.)
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