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Pathogenesis
Overall, sinonasal papilloma accounts for 16% of
all unilateral nasal polypoid lesions [1]. Inverted
papilloma (IP) accounts for 0.4–7% of sinonasal
cavity tumors [3]. The incidence is uncommon
and ranges between 0.6 and 1.5/100,000 per year;
the gender ratio is 5 men to 1 women; the peak
incidence is 55years [4]. Inverted papilloma typically originates along the lateral nasal wall or
maxillary sinus and has a propensity to recur.
The estimated prevalence of each of the three
main histological subtypes is inverted (62%),
exophytic (32%), and oncocytic papilloma (6%).
Inverted Sinonasal Papilloma (IP)
(Fig.30.1a)
Histologically, an inverted papilloma appears as
thickened respiratory epithelium that protrudes
into the underlying stroma. The protrusions do
not invade the underlying basement membrane
and give the characteristic “inverted” description
[1]. The respiratory epithelium may be accompanied by squamous cells or have a transitional cell
appearance, but it is strictly not transitional cell
epithelium as occurs typically within the bladder.
The microscopic appearance of ISP can be combined with exophytic histological features.
Intraepithelial neutrophilic inammation is a
characteristic feature.
In contrast to inammatory nasal polyps,
eosinophils are sparse throughout the stroma of
the papilloma.
Oncocytic Sinonasal Papilloma
(Fig.30.1c)
The oncocytic tumor displays columns of cylindrical cells that may have endophytic and exophytic features. The oncocytic papilloma has a
characteristic histological appearance; clinically,
it behaves in a similar way to inverted papilloma,
and the recurrence rate and malignant tendency
are about the same for both tumor types. This
subtype accounts for 3–5% of sinonasal papilloma. It has been referred to as a microcystic papillary adenoma and may be misdiagnosed as a
low-grade adenocarcinoma.
For the purpose of simplicity, the oncocytic
papilloma will not be differentiated from the IP
within the various sections of this chapter.
Etiology
The etiology of sinonasal papilloma is unknown.
However, most research is focused on inverted
papilloma.
A viral etiology has been considered, but the
evidence for Epstein–Barr virus (EBV) is inconclusive [5]. Evidence for human papillomavirus
(HPV) being associated with sinonasal papilloma
has been reported but is inconsistent and variable
[6]. Recent reports do not support HPV as having
an etiological role in the pathogenesis of inverted
papilloma, nor in tumor recurrence [7, 8].
Malignant Transformation
Exophytic Papilloma (Fig.30.1b)
The exophytic papilloma has a characteristic histological exophytic growth pattern and is difcult
to differentiate from a warty growth, both microscopically and macroscopically.
The transformation rate of inverted papilloma to
malignancy is estimated to be about 7.6% with
malignant change being either synchronous
(7.1%) or metachronous (3.6%) [9]. However,
one substantial review found only 1.9% malignant transformation (740 patients over 10years),
with no specic identiable risk factors. Most
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malignant transformations arose within an existing inverted papilloma, and metachronous tumors
were always preceded by recurrence [10].
The most likely malignancy to arise from cell
transformation in inverted papilloma is transitional cell carcinoma. Squamous cell carcinoma
(SCC) is sometimes associated with coexisting
inverted papilloma. However, such tumors are
often well advanced at presentation and the coexistence of tumor types may just be a pathological
phenomenon due to abnormal development of
cell lines rather than malignant transformation
from inverted papilloma.
Diagnosis of malignant transformation: The
endoscopic appearance of malignant transformation may not be obvious, and biopsies will only
be diagnostic if taken from an affected area.
Conrmation of the histological diagnosis
may be challenging and is dependent on the specialist expertise of the histopathologist and consideration of tumor behavior. Low-grade
malignant cells are not easily identied in the
early stages of tumor formation. With time, this
leads to an underdiagnosis of squamous cell carcinoma, and once clinically apparent, it is later
reported as malignant transformation.
Reasons for transformation: Why transformation occurs is not fully understood. Research into
the etiology and risk of malignant change by
exploring the whole human genome seems logical but would be extremely challenging and
expensive.
Factors that have been considered include the
cell cycle, angiogenic factors, environmental and
occupational exposure, chronic inammation,
and viruses [11]. Whilst the viral theory for
malignant transformation is very topical and
seems logical, there is no denite proof that this
is the case. However, inverted papilloma is
uncommon, and malignant transformation even
more uncommon. In order to address this particular dilemma, large meaningful standardized multicenter studies with robust methodology are
required. However, a recent meta-analysis does
report an increased risk of malignancy in patients
infected with HPV 16, 18, 11/16, and 16/18 compared to those with HPV 6, 11, and 6/11 [12].
Biomarkers ofMalignant
Transformation
There is currently no agreement about the principal biomarkers that will either predict the risk of
transformation or identify malignancy (IP-SCC)
(see Table30.1).
Tumors with concomitant positive HPV are
often accompanied with biomarkers associated
with early carcinogenesis such as elevated epidermoid growth factor receptor (EGFR) and
transforming growth factor-alfa (TGF-a).
Mutation of the p53 tumor suppressor gene
and increased expression of p21 and p53 have
been described in associated malignancy [22,
23]. However, the degree of atypia or dysplasia
is not closely associated with malignant
change.
Table 30.1 Biomarkers, inverted sinonasal papilloma,
and malignancy (references listed in a separate list)
Biomarker Description References
P53 Opinion remains
inconclusive
P21
Cyclin-dependent
kinase inhibitor
Muscle segment
homeobox gene
MSX2
Tumor suppressor
gene PDCD4
Serum squamous
cell carcinoma
antigen
Fascin protein Levels increased in
Survivin Apoptosis inhibitor
COX-2 Possible association
Osteopontinvascular
endothelial
growth factor
(VEGF)
Ki-67 Marker of cell
Evidence
inconclusive
Elevation linked with
progression, growth,
and recurrence of ISP
severe dysplasia
higher in malignancy
with malignancy
Affects tumor growth
and angiogenesis.
Increased in higher
stage IP
proliferation.
Possible predictor of
prognosis and
malignancy
[13]
[14]
[15, 16]
[17]
[18]
[19]
[20]
[21]
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Clinical Features
A sinonasal papilloma typically presents as a unilateral nasal lesion with nonspecic features.
Exophytic Sinonasal Papilloma (ESP)
The exophytic sinonasal papilloma typically
presents as a warty growth within the anterior
part of the nasal cavity (Fig.30.2). These lesions
typically occur on the anterior nasal septum in a
younger age group. Exophytic papilloma may
extend superiorly and inferiorly to the nasal oor.
They may be multiple and spread to the posterior
nasal cavity. Recurrence is likely, but there is
typically no risk of malignant change. Rarely, the
tumour may change character to become an
inverted sinonasal papilloma, supporting the
view that all excised tissue should be sent for histopathological review.
Inverted andOncocytic Sinonasal
Papilloma (ISP, OSP)
Presenting symptoms: Symptoms include nasal
obstruction, anterior and/or posterior rhinorrhea,
headache, hyposmia or anosmia, epistaxis, and
facial pain. Inverted papilloma may mimic any
sinonasal disease. Epiphora may occur should
the nasolacrimal duct be involved. Isolated sphenoid lesions may present with nonspecic symp-
toms such as headache, diplopia, and visual
anomalies [24]. Sinonasal papilloma can present
as an unexpected nding in patients with other
pathologies [25].
The duration of symptoms is reported to range
from 5months to 20years with a mean duration
of 3.9years [26].
Endoscopic appearance: The inverted papilloma typically appears as a polypoid pale gray
mass with a grapelike irregular, convoluted, papillary surface with multiple digitations. The
endoscopic appearance is variable and can be difcult to differentiate from a “simple” inammatory nasal polyp; it can also present as an inamed
vascular polypoid lesion (Fig. 30.3a–d). The
indistinct appearance makes it even more important to submit all surgically removed polypoid
tissue to histological review.
Tumor site: ISP typically arises from the lateral nasal wall adjacent to the middle turbinate
(Fig.30.3a–c).
Tumors can arise from various sites within the
sinonasal cavity: ethmoid 48%; maxillary sinus
28%; sphenoid sinus 7.5%; frontal sinus 2.5%; inferior turbinate 2.5%; and nasal septum 2.5% [27].
Sinonasal papilloma may extend beyond the
ethmoid to the frontal or sphenoid sinuses [28].
Isolated lesions of the sphenoid sinus are unusual.
There are occasional instances of inverted papilloma affecting the nasal vestibule, lacrimal sac,
and nasal oor (Fig.30.3d).
Bilateral sinonasal papillomata are unusual:
the incidence of bilateral disease is <1–9%.
Malignancy should always be excluded in such
cases [29, 30].
Intracranial spread is infrequent but more
likely in recurrent tumors that transgress the cribriform plate or ethmoid roof [31].
Intraorbital extension may occur in lesions
with extensive ethmoid involvement and typically pushes orbital contents laterally, without
invading the periorbita [32].
Differential Diagnosis: An isolated unilateral
nasal polyp or mass should raise the suspicion of
an inverted papilloma. Unilateral lesions may
present as a single small polyp, numerous polyps
(Fig. 30.3b), or a single large polyp that looks
similar to an antrochoanal polyp.Fig. 30.2 Exophytic papilloma
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ab
Fig. 30.3 (a–d) Various endoscopic appearances of
inverted papilloma. (a) Multiple smooth polypoid lesions.
(b) Single hemorrhagic polyp. (c) Inverted papilloma
A rare polypoid lesion that can cause histologi-
cal dispute or confusion is the respiratory epithe-
emanating from middle meatus. (d) Endoscopic view of
IP arising on nasal oor.
dental keratocyst, bro-osseous lesions, and
fungal disease
lial adenomatoid hamartoma (REAH). This is an
epithelial proliferation of columnar epithelium in
a setting of chronic rhinosinusitis. There is con-
Association withNasal Polyps
troversy amongst pathologists as to whether this
is neoplastic, nonneoplastic, or premalignant.
Other rare lesions to exclude are:
Inverted papilloma may coexist with chronic rhinosinusitis with nasal polyps (CRSwNP), but the
reported incidence is <1%. This reinforces the
– Malignant tumors such as squamous cell car-
cinoma, adenocarcinoma, lymphoma, and
esthesioblastoma/olfactory neuroblastoma
– Other benign lesions that may be associated
with polyp formation, such as mucoceles,
importance of subjecting all resected polyps to
histological review, noting especially the side
that the tissue was taken from.
The low reported incidence of ISP with nasal
polyps may be due to various factors: many may
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go unreported, sampling may be incomplete
during surgery and histological analysis, and
histological expertise may vary. Histology of
polyps is not a precise science; it has been suggested that 17% of papillomas are initially diagnosed as inammatory polyps [33]. It is also
important to appreciate that hyperplastic polyps
may be misdiagnosed histologically as inverted
papilloma.
Imaging
The combination of CT and MRI scans is complementary to each other and helps to establish a
diagnosis and evaluate the extent of the tumor.
High-resolution CT sinus scan: CT is sensitive but nonspecic. The scan typically shows a
unilateral lobulated heterogeneous mass with
characteristic increased ‘calcied’ densities in
20% of cases (Fig.30.4) [34]. The opacity often
originates from the middle meatus and extends to
the maxillary antrum, nasal cavity, and/or frontal
sinus.
CT does not differentiate between trapped
mucus and tumor extension, especially in an
opaque frontal or sphenoid sinus. CT scans show
excellent bone denition that may demonstrate
diffuse sclerotic bony thickening or bone dehiscence. Hyperostosis can appear as a central platelike lesion (or as a “cone-shaped” prominence)
[35]. Localized hyperostosis or irregular sclerosis
along the sinus wall often correlates with tumor
origin and attachment (positive predictive value
(PPV) of 89–95%) [36].
Bone remodeling and resorption showing
localized bony sinus dehiscence suggest bone
destruction from malignant transformation and,
whilst not diagnostic, require urgent management and exploration (Fig.30.5a) [37].
MRI scan of sinuses (see Table30.2): MRI is
particularly helpful in differentiating the tumor
interface from retained mucus and inammatory
sinonasal mucosa from tumor (Fig. 30.6) [38].
An MRI scan has a 93–100% positive predictive
value of diagnosing inverted papilloma and may
also accurately identify tumor attachment.
a
b
Fig. 30.4 CT sinus scan showing calcied densities
Fig. 30.5 CT and MRI sinus images of malignant trans-
formation to transitional cell carcinoma invading the anterior skull base: (a) Coronal CT scan of sinuses. (b) MR
scan of sinuses/head
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Table 30.2 Characteristic features of inverted sinonasal
papilloma on MRI scans
T1-weighted MRI
sequence
T1-weighted IP is hypointense but
hyperintense post-gadolinium
Hyperostosis appears
hypodense
T1 and T2
sequences
T2-weighted MRI
sequence
T2-weighted
sequences
T2-weighted
images
Post-gadolinium
sequences
T1-weighted
images
Key features
MRI and CT
combined
images
Diffuse convoluted cerebriform
pattern (CCP)
Tumor iso- or hypointense
compared to the normal mucosa
Interchanging hypointense and
hyperintense bands
Interchanging hypointense and
hyperintense bands
Diffuse convoluted cerebriform
pattern (CCP) and bone
remodeling on CT scan
MRI may also demonstrate features of malignancy, and transformation should be considered
if there is localized disruption of the convoluted
cerebriform pattern and bone destruction [39]
(Fig.30.5b).
PET-CT scan: PET-CT studies show a higher
maximum standard uptake value (SUVmax) of
FDG uptake by inverted papilloma lesions that is
even greater with malignant transformation (IPSCC) [40].
PET-CT is useful in evaluating patients with
IP-SCC but is not a dependable diagnostic modality in those patients without cancer and may erroneously diagnose malignancy should the SUV be
high.
Classication
Several staging systems have been described
for inverted papilloma, according to radiological signs, tumor site, extent, and origin [4,
41–45].
The Krouse staging system is based on a
radiological evaluation of tumor extent and is
popular, simple, reproducible, and comprehensive (Table 30.3) [41]. The classication correlates with outcome but does not guide therapeutic
management [46].
Fig. 30.6 MRI sinus scan showing inverted sinonasal
papilloma of left ethmoid and mucus collection trapped in
maxillary sinus
Table 30.3 Krouse staging system for inverted
papilloma
T1Tumor conned to nasal cavity
T2Tumor involving the ostiomeatal complex,
ethmoid sinuses, and/or medial portion of
maxillary sinus±involvement of nasal
cavity
T3Tumor involving the lateral, inferior, superior,
anterior, or posterior walls of maxillary sinus,
the sphenoid sinus, and/or the frontal sinus
with or without involvement of the nasal
cavity
T4All malignant tumors and those tumors with
extranasal and extrasinus extension
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Management
Surgical resection is key in the management of
sinonasal papilloma.
Exophytic Sinonasal Papilloma
Exophytic papilloma lesions should be completely excised, leaving the underlying cartilage
exposed. The denuded area of mucosa will normally heal over a period of weeks, but extensive
resection may risk brosis that may later obstruct
the nasal valve.
Inverted Sinonasal Papilloma
Surgery to resect inverted papilloma ranges from
limited removal of an intranasal polypoid mass to
extensive resection with associated potential
risks. The primary aim of surgery should ideally
be to achieve complete resection of the tumor to
prevent recurrence and eliminate the risk of
malignant transformation.
Occasionally, complete resection may not be
possible during a single operation. Circumstances
include the operative conditions, bleeding, anesthesia, instruments, or equipment failure. However,
staged resection is perfectly acceptable in such
instances.
Widespread eld change within the nasal cavity may cause a dilemma regarding the completeness of clearance. Radical resection of nasal
mucosa that creates a large, denuded area within
the nose may cause long-term crusting. Inadequate
clearance will lead to increased risk of recurrence.
Such situations are best managed by considered
denitive planned treatment following histological conrmation and further clinical evaluation.
Radiotherapy might be occasionally recommended as an alternative modality for patients
with medical conditions that preclude surgical
intervention.
Whilst malignant change has been reported
in 5–15% of cases of inverted papilloma, these
estimates are often from large tertiary referral
centers that will attract the more challenging
tumors, especially if malignant. Most ENT surgeons will mostly see benign sinonasal papillomata and very little malignancy. A balance must
be struck, and whilst patients should not be
overly alarmed by quoting a relatively high risk
of malignancy, there must be a degree of caution
and vigilance.
The clinical features that may suggest an
increased risk of malignancy include aggressive
tumor behavior, rapid recurrence after resection,
bone remodeling and erosion, and invasion
beyond the sinuses into adjacent vital structures.
External Surgical Approach Vs.
Endoscopic Resection
Prior to the development of endoscopic techniques, lateral rhinotomy and medial maxillectomy became the preferred operation of choice
many years ago, enabling complete removal of
lesions arising from the lateral nasal wall.
Midfacial degloving offered an alternative
approach for extensive tumors. Extension to the
frontal sinus was typically resected via an osteoplastic ap.
Lateral rhinotomy reduced the high incidence
of tumor recurrence compared to previous surgical methods but carried a risk of complications
such as epiphora, chronic dacryocystitis, transient diplopia, Eustachian tube dysfunction,
facial scars, scar contraction, as well as a longer
hospital stay.
However, with the advent of minimally invasive
endonasal endoscopic techniques, excellent tumor
resection with minimal morbidity and outcomes
became feasible. Endoscopic resection is now
accepted as the preferred gold standard of care.
Whilst the old concept of radical oncological
resection with wide tumor margins is no longer
justied for benign sinonasal papilloma, resection must still be complete and performed with
precision to decrease the likelihood of later tumor
recurrence.
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Combined Approach Surgery
Tumors that extend across several sinuses may be
best addressed by a combined approach. Selecting
the precise approach is at times a difcult surgical judgement and will depend on personal expertise, location and size of the tumor, risk of
complications, and medical factors that may
inuence the type of surgery.
Whilst most inverted papillomas can be
removed endoscopically, the endoscope can be
combined with external surgery to enhance the
exposure and access to the tumor.
Endoscopic surgical images enable a magnied
view of the tumor and its attachment, thus facilitating precise resection but minimizing unnecessary
removal of healthy tissues (Video 30.1).
Endoscopic surgery will also facilitate the early
recovery and return of normal mucociliary ow.
Management options must be explained to the
patient during the consent process, and patient
choice may then determine the type of procedure.
Adjuvant therapy should also be considered in
difcult situations.
Attachment-Oriented Endoscopic
Resection andFrozen Section
(Video 30.2). Precise mucosal clearance from the
attachment site with small pediatric micro-instruments is most important should the tumor base be
inaccessible to accurate drilling. Frozen section
should be considered in difcult situations but
relies on local availability and services.
Categorization ofTumor
andSurgery
Attempts have been made to categorize the tumor
and its treatment to standardize management and
interpretation of outcomes (Tables 30.4 and 30.5)
[48, 49].
Table 30.4 Categorization by tumor characteristics and
treatment
Denition of
tumor Description of tumor
Primary tumor No preceding surgery
Diagnosis conrmed by biopsy
Residual
tumor
Recurrent
tumor
Preceding endoscopic surgery for
polyps
Histology unexpectedly reported as
inverted papilloma
Previous surgery for inverted
papilloma
Tumor recurrence necessitating
revision surgery
The concept of attachment-oriented endoscopic
resection for inverted papilloma was described in
2008 [47]. The key surgical steps include:
1. Tumor debulking
2. Precise identication of the tumor’s mucosal
attachment site
3. Dissection of the subperiosteal attachment
site
4. Excision of the tumor attachment site and its
surrounding normal mucosa with frozen section control if available and considered
necessary
5. Resection or drilling underlying bone at the
tumor attachment site
Gentle drilling of the bone surface by a diamond
burr with irrigation/suction channel at the tumor
attachment site ensures removal of microscopic
disease, thus reducing the likelihood of recurrence
Table 30.5 Classication of tumor extent and surgery
Extent of tumor Extent of surgery
Type 1:
Fig.30.7a
Type 2:
Fig.30.7b
Type 3:
Fig.30.7c
Conned to middle
meatus
Extends beyond
frontal recess
Involves alveolar
recess mucosa;
posterolateral,
anterior, or inferior
walls of maxillary
sinus
Endonasal
endoscopic
ethmoidectomy
Wide maxillary
antrostomy
Sphenoidotomy
Radical
ethmoidectomy
Medial
maxillectomy
Resection of
middle turbinate
Widening of
frontal recess by
Draf II–III
Endonasal
modied Denker
procedure
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a
b
c
Fig. 30.7 (a) Type 1 tumor resection. Extent of inverted
papilloma shown in green. Endoscopic ethmoidectomy
with wide antrostomy and sphenoidotomy shown in blue.
(b) Type 2 tumor resection. Extent of inverted papilloma
shown in black. Medial maxillectomy with ethmoidectomy and sphenoidotomy for IP partially invading the
Maxillary Sinus Surgery
Inverted papillomas arising from the lateral,
inferior, or anterior maxillary sinus wall involvement may require extended endoscopic medial
maxillectomy (Video 30.3), transnasal endoscopic partial maxillectomy/modied Denker
approach, or endoscopic prelacrimal recess maxillary window [50].
maxillary sinus shown in red. (c) Type 3 tumor resection.
Maxillary sinus lesions of lateral and/or anterior wall
shown in green/red. Bony window entrance shown in yellow. Extended endoscopic medial maxillectomy, with
extension to anterior maxillary wall, shown in blue
Transnasal Endoscopic Partial
Maxillectomy (TEPM): This procedure requires
removal of the lateral nasal wall facilitating wide
access into the maxillary sinus. The bony resection may extend to include the adjacent piriform
aperture and anterior wall of the maxillary sinus
but preserving the infraorbital wall (modied
Denker procedure: Fig. 30.8; Videos 30.3 and
30.4) [51].
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Transection of the nasolacrimal duct may be
required, but nasolacrimal drainage normally
remains unaffected, and stents are not required.
Combined approaches such as transnasal
endoscopic surgery with a Caldwell-Luc procedure offer a good alternative for surgeons who are
not trained in advanced endoscopic techniques.
Endoscopic Prelacrimal Recess Approach: A
relatively recently described approach is the prelacrimal recess operation, which preserves the integrity of the inferior turbinate and the nasolacrimal
duct (Fig.30.9; Video 30.5). An intranasal mucosal
ap is raised on the lateral nasal wall in the anterior
nasal cavity. The inferior turbinate concha is sepa-
Fig. 30.8 Endoscopic modied Denker procedure. The anterior bony section of the left piriform aperture is removed
and extended to include the anterior maxillary sinus wall
Fig. 30.9 The prelacrimal recess approach to the maxillary sinus. The bony window is created anterior to the nasolacrimal duct
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