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6 Advancements andInnovations inSleep Surgery
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49. Liu SYC, Huon LK, Ruoff C, Riley RW, Strohl KP, Peng Z.Restoration of sleep architecture
after maxillomandibular advancement: success beyond the apnea-hypopnea index. Int J Oral
Maxillofac Surg. 2017;46(12):1533–8.
50. Boyd SB, Chigurupati R, Cillo JE, Eskes G, Goodday R, Meisami T, etal. Maxillomandibular
advancement improves multiple health-related and functional outcomes in patients with
obstructive sleep apnea: a multicenter study. J Oral Maxillofac Surg. 2019;77(2):352–70.
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Chapter 7
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Oral Dysplasia
LiorAljadeff andAnthonyB.Morlandt
Terminology
The term “precancer” was initially introduced in 1805 when a panel of physicians
in Europe suggested that some benign disease can progress to invasive malignancy
if given enough time [1]. Over time, the terms “precancer,” “premalignancy,” and
“precursor lesion” have become synonymous with oral dysplasia. However, during
the 2005 WHO workshop (published in 2007), a panel of experts proposed replacing these terms with the more precise term “oral potentially malignant disorder”
(OPMD) [2]. This term is dened as any “clinical presentations that carry a risk of
cancer development in the oral cavity, whether in a clinically denable precursors
lesion or in clinically normal oral mucosa.” [3]. The reasons for this shift were multifold. For one, the phrase “potentially malignant” highlights the fact that not all
patients diagnosed with an OPMD will develop an oral malignancy. The new term
implies that there is an unknown potential for carcinogenesis, rather than framing it
as inevitable given enough time. Additionally, the term “disorder” highlights the
fact that patients diagnosed with an OPMD have an increased risk of developing
carcinoma anywhere in their mouth over their lifetime. Data show that patients can
develop oral squamous cell carcinoma in sites that are separate from the mucosal
changes of their OPMD [2]. This reinforces the importance of shifting our view of
OPMDs from “precancerous lesions” to disorders that represent a eld of molecular
mucosal changes in which cancer is more likely to develop [4, 5]. Recently, a newer
term, “potentially premalignant oral epithelial lesion (PPOEL),” has emerged in the
literature to replace OPMDs. However, the 2020 WHO working group rejected this
terminology because the term OPMD is now well-established in the literature since
L. Aljadeff · A. B. Morlandt (*)
Department of Oral and Maxillofacial Surgery, Section of Oral Oncology, University of
Alabama at Birmingham, Birmingham, AL, USA
e-mail: laljadeff@uabmc.edu; amorlandt@uabmc.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
J. C. Melville et al. (eds.), Advancements and Innovations in OMFS, ENT, and
Facial Plastic Surgery, https://doi.org/10.1007/978-3-031-32099-6_7
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its introduction in 2007, and they felt PPOEL neither added nor changed anything
signicant [6, 7].
Fundamentally speaking, OPMD is a broad term that encompasses anything that
has a risk of progressing to oral cancer, including clinically normal oral mucosa.
OPMD includes both strictly clinical conditions (e.g., leukoplakia, erythroplakia,
and erythroleukoplakia) and a variety of diagnoses that have well-established clinical and histologic characteristics (e.g., submucous brosis, dyskeratosis congentia,
smokeless tobacco keratosis, chronic candidiasis lichen planus, discoid lupus erythematosus, syphilitic glossitis, and actinic keratosis). In contrast, dysplasia is a
histological diagnosis that describes “abnormal growth” at the cellular level, as its
name implies. The WHO denes oral epithelial dysplasia (OED) as “a spectrum of
architectural and cytological epithelial changes caused by an accumulation of
genetic changes, associated with an increased risk of progression to squamous cell
carcinoma” [3]. The distinction between these two is important.
OPMDs carry a risk of malignant transformation; however, they may or may not
contain histological evidence of the epithelial dysplasia. In fact, although OED is a
common nding in erythroplakia and erythroleukoplakia, it is only present in a
minority of leukoplakias, despite the malignant potential of many leukoplakic
lesions. The presence of dysplasia is important because it has been shown to carry
prognostic signicance in predicting malignant transformation, even in clinically
normal appearing mucosa. Thus, any lesion with dysplasia is, by denition, an
OPMD (although the converse is not true). However, OPMDs can progress to oral
squamous cell carcinoma (OSCC) without any previous histological evidence of
dysplasia. Chaturvedi etal. demonstrated that a substantial proportion of cancers
(39.6%) arose from lesions histologically classied as nondysplastic [8].
The diagnostic criteria for epithelial dysplasia includes both architectural and
cytological epithelial changes that serve as evidence of the cellular misbehavior that
is thought to progress to oral squamous cell carcinoma (OSCC). However, although
a plethora of grading scales, models, and biomarkers exist, no one has been able to
reliably predict if and when epithelial dysplasia will traverse the basement membrane and invade the underlying connective tissue to progress to OSCC.This leaves
clinicians with a difcult conundrum in the management and surveillance of these
historically controversial conditions. Before surgeons can intelligently use the most
recent data and technology to personalize treatment plan for a patient with OPMD
or OED, they must have a clear understanding of the terminology described above.
L. Aljadeff and A. B. Morlandt
Oral Potentially Malignant Disorders
It is outside the scope of this chapter to discuss all OPMDs; however, leukoplakia,
erythroplakia, and erythroleuoplakia are the most common, controversial, and confusing OPMDs and are thus included herein.
First, it is important to understand that leukoplakia, erythroplakia, and erythroleukoplakia are clinical terms that simply describe a lesion as “white plaque,” “red
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patch,” or a predominantly white plaque with red areas, respectively. To be clear,
these are not histologic diagnoses. In fact, there is a broad range of conditions that
can present as a white plaque in the oral cavity, many of which have wellcharacterized clinicohistopatholgic ndings that allow for a formal diagnosis. These
include frictional keratosis, lichen planus, oral candidiasis, and white sponge nevus,
to name a few. Thus, the term leukoplakia can rst be used as a provisional diagnosis at the time of detection if nothing else on the list of differential diagnoses appears
more likely. However, a biopsy is indicated to rule out the many other wellestablished diagnoses that present as white plaques of the oral cavity in order to
establish oral leukoplakia as the diagnosis of exclusion [9, 10]. The same is true for
erythroplakia and erythroleukoplakia.
Oral leukoplakia is the most common OPMD with a prevalence of 1–4% [10].
The published malignant transformation rate of oral leukoplakia is highly variable,
ranging from 0 to 36%, largely due to differences in geographic region, population
risk proles, denitions, and study design [8]. Iocca etal. recently published the
most thorough systematic review and meta-analysis on OPMDs to date, and they
calculated a malignant transformation rate of 9.5% with an annual transformation
rate of 1.5% [11]. Waldron and Shafer studied 3256 cases of oral leukoplakia and
reported that 19.9% had some degree of epithelial dysplasia [12]. Risk factors for
malignant transformation of oral leukoplakia include: (1) female patients, (2) nonsmokers, (3) longstanding lesions, (4) oor-of-mouth and tongue subsites (5) nonhomogeneous leukoplakia, (6) presence of Candida albicans within the lesion, and
(7) presence of epithelial dysplasia in the lesion [13]. Proliferative verrucous leukoplakia (PVL) is an aggressive and problematic subtype of leukoplakia that is most
common in elderly women with a malignant transformation rate of approximately
50% and an annual malignant transformation rate of 9.3% [11, 14].
In 1911, Vincent Jules Louis Queyrat, a French dermatologist, described a brightred precancerous lesion of the glans penis, which he termed “erythroplasie,” and is
known today as Erythroplasia of Queryat [15]. The term was subsequently adapted
to “erythroplakia” and used to describe potentially premalignant red patches of the
oral cavity that were thought to be analogous to the already well-described potentially premalignant white plaques of the oral cavity, leukoplakia. Years later, the
term “erythroplakia” was recognized to be a misnomer because, in contrast to leukoplakia, erythroplakia does not typically form plaques at all but are more erosive
or atrophic-appearing lesions that are continuous with or even depressed below the
surrounding mucosa [13, 16]. Over the years, the denition of oral erythroplakia has
changed; however, the most widely accepted denition today was proposed by
Pindborg and colleagues in 1997: “a ery red patch that cannot be characterized
clinically or pathologically as any other denable lesion” [17]. An array of lesions
with overlapping clinical appearances have since been described, and terms such as
erythroleukoplakia, erosive leukoplakia, leukoerythroplakia, and speckled erythroplakia were coined, which further complicated the literature.
Shafer etal. has shown that 51% of homogenous erythroplakia had evidence of
invasive carcinoma at the time of biopsy, and 40% showed carcinoma in situ [18].
Furthermore, Iocca etal. have shown that the rate of malignant transformation of
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oral erythroplakia, even without any prior evidence of dysplasia, was still as high as
33.1% [11]. Although poorly understood at the molecular level, clinical evidence of
erythroplakia represents an ominous disease process that should be managed more
aggressively than its more common and benign counterpart, leukoplakia.
L. Aljadeff and A. B. Morlandt
Oral Dysplasia: Grading andClassication
In 1957, Slaughter popularized the principle of “eld cancerization,” which stated
that if carcinogens caused clinically detectable premalignant or malignant changes
in one part of the oral cavity, there is equal risk of it causing those changes in other
parts of the oral cavity that were exposed to those carcinogens as well [19]. This
concept helped reconcile the rising number of synchronous and metachronous
tumors that were being observed and reported in the literature. Ultimately, it shed
light on the existence of subclinical lesions that made the entire oral cavity, especially high-risk sites such as the tongue and the oor of the mouth, susceptible to
malignancy. Years later, in 1996, Califano and colleagues published their landmark
description of the genetic progression model for head and neck cancer. This model
proposed a “genetic pathway to malignancy.” They proposed that mutations begin in
clinically and histologically normal mucosa and accumulate to cause phenotypic
changes at the microscopic and/or clinical level that eventually culminate in the
development of dysplasia and cancer [20]. This model lay the foundation for our
current understanding of oral epithelial dysplasia as a continuum of cytological and
architectural changes in epithelium that may progress to oral squamous cell carcinoma. Califano’s model also provided a molecular explanation for the “eld cancerization” that Slaughter carefully observed and described [19].
The challenge that continues to plague clinicians, scientists, and ultimately
patients is predicting which dysplastic lesions will progress to carcinoma and when.
Over the years, many methods have been proposed and tested to predict the progression from dysplasia to carcinoma; the most well-known of which is histological
grading.
Smith and Pindborg were the rst to describe a classication system for grading
epithelial dysplasia of oral mucosa in 1969 [21]. They evaluated 13 histologic features, which were standardized by a set of photographs. After comparing the slides
with the photographic standard, each feature was graded as absent, slight, or marked
and given a score. The scores were then added to produce an epithelial atypia index
(EAI) (which could range from 0 to 75). A score of 10 or less was considered nondysplastic, a score between 11 and 25 was considered mild dysplasia, a score of
26–45 was considered moderate dysplasia, and a score above 45 was considered
severe dysplasia.
Currently, the most widely used grading system for dysplasia is the one rst
proposed by the WHO in 1997 and revised in 2005 and then again in 2017 [22]. In
1967, the WHO established a Collaborating Center for Oral Precancerous Lesions
in Copenhagen, Denmark that set out to characterize and dene oral lesions that
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Table 7.1 1978 WHO criteria for oral epithelial dysplasia
1. Loss of polarity of basal cells
2. Basaloid appearance in more than one layer of cells
3. An increased nuclear-cytoplasmic ratio
4. Drop-shaped rete pegs
5. Irregular epithelial stratication
6. Increased number of mitotic gures
7. Mitotic gures in the supercial half of the epithelium
8. Cellular polymorphism
9. Nuclear hyperchromatism
10. Enlarged nucleoli
11. Reduction of cellular cohesion
12. Keratinization of single cells or cell groups in the prickle cell layer
Data taken from: WHO (1978). Collaborating Centre for Oral Precancerous Lesions. Denition of
leukoplakia and related lesions: an aid to studies on oral precancer. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 46:518–539
125
should be considered “precancer” and to determine their relative risk of becoming
malignant. They published their rst report in 1978, which dened 12 characteristics of epithelial dysplasia (Table7.1), and graded it as mild, moderate, or severe
based on whether dysplastic features were restricted to the lower third of epithelium, involved the middle third as well, or went all the way to the upper third,
respectively [23]. In 2005, the classication was expanded to ve stages based on
the level of architectural and cytological alterations that were present. Briey, these
were squamous hyperplasia, mild dysplasia, moderate dysplasia, severe dysplasia
and carcinoma in situ (CIS) [2]. In 2017, the WHO dropped the terms “squamous
hyperplasia” and “carcinoma in situ” from their classication system (Table7.2)
and made minor changes to the diagnostic criteria [3].
Unfortunately, data have shown that the inter- and even intra-observer reproducibility of this classication system is poor [24–26]. A study by Brothwell etal.
showed that when three oral pathologists were asked to simply identify the presence
or absence of oral epithelial dysplasia in 64 slides, the inter-observer agreement was
only moderate with a kappa score of 0.51 [24]. The intra-observer agreement was
extremely variable; one pathologist had a kappa score of only 0.22, which means he
had only mild agreement with himself. Other studies have shown equally poor inter and intra-observer agreement using the WHO classication with one reporting a
kappa agreement scores as low as 0.15 between six pathologists reviewing 150
slides [25]. This lack of consistency in the diagnosis and grading of oral epithelial
dysplasia signicantly confounds the data on the prognostic implications of dysplasia and makes it highly controversial [26].
In 2006, Warnakulasuriya etal. sought to address this problem by proposing a
two-tier classication for lesions: low risk (no dysplasia, questionable dysplasia, or
mild dysplasia) versus high risk (moderate or severe dysplasia) for undergoing
malignant transformation [27]. They felt this would have better reproducibility and
clinical utility. Kujan et al. argued that the binary system has superior
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Table 7.2 Comparison of the evolving WHO classication for oral epithelial dysplasia
1978 classication 2005 classication 2017 classication
Mild dysplasia Squamous hyperplasia Mild dysplasia
Mild dysplasia
Moderate dysplasia Moderate dysplasia Moderate dysplasia
Severe dysplasia Severe dysplasia Severe dysplasia
Carcinoma in situ
1978 WHO Classication taken from: WHO (1978). Collaborating Centre for Oral Precancerous
Lesions. Denition of leukoplakia and related lesions: an aid to studies on oral precancer. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 46:518–539
2005 WHO Classication taken from: Warnakulasuriya S, Johnson NW, van der Waal
I.Nomenclature and classication of potentially malignant disorders of the oral mucosa. J Oral
Pathol Med. 2007;36:575–580
2017 WHO Classication taken from: Reibel J, Gale N, Hille J, etal. Oral potentially malignant
disorders and oral epithelial dysplasia. In: El-Naggar AK, Chan JKC, Grandis JR, Takata T,
Slootweg PPJ, eds. WHO Classication of Head and Neck Tumours. 4th ed. Lyon, France: IARC;
2017: 112–115.
L. Aljadeff and A. B. Morlandt
reproducibility and a similar prognostic ability when compared to the three-tier
WHO system; however, when they tested this binary system with four architectural
and ve cytological criteria for dysplasia, they still only demonstrated a moderate
inter-observer agreement (κ of 0.5) [28]. Nankivell etal. tested the binary system
with four architectural and four cytological features and had a slightly higher interobserver kappa of 0.59 [29].
Oral Dysplasia: Detection andDiagnosis
As mentioned early, oral epithelial dysplasia is a histological diagnosis and thus
requires tissue biopsy. Furthermore, current guidelines suggest that a biopsy is also
indicated to make the provisional diagnosis of leukoplakia or erythroplakia a denitive one by excluding other conditions. However, there has a been a strong practical
and nancial incentive to identify minimally invasive adjunctive tests that can be
used to either screen for dysplasia or further characterize lesions with a suspicious
clinical appearance. Additionally, they can help guide clinicians in selecting a specic location to obtain their tissue biopsy.
Although it is outside the scope of this chapter to review the ever-evolving landscape of chairside adjuncts developed for oral epithelial dysplasia and OSCC, we
will briey review some important principles about using them and a few of the
most common types.
First, it is important to understand that adjuncts are not intended to replace tissue
biopsy when a lesion appears frankly invasive or even highly concerning for dysplasia [30]. Second, it is important to understand that there are two main ways to use
these technologies: as a screening test or a “case-nding” test [30]. Lingen and colleagues, citing the WHO Public Health Papers from 1968, say that a screening test
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is dened as a test used for “people who are apparently free from the disease in
question in order to sort out those who probably have the disease from those who
probably do not. The important factor is that screening involves checking for the
presence of disease in a person who is symptom free.” Meanwhile, they dene a
case-nding test as a test that is “applied to a patient who has abnormal signs or
symptoms in order to establish a diagnosis and bring the patient to treatment.” These
distinctly different applications of a technology have signicant implications for the
test’s sensitivity, specicity, positive predictive value, and negative predictive value.
Unfortunately, there is a lot of literature that confuses these terms and even uses
them interchangeably, which confounds epidemiologic data and emphasizes the
importance of critically evaluating the literature supporting an adjunct before incorporating it into a practice [30].
A conventional oral examination with special attention to high-risk subsites has
long been the standard of care method to screen for oral cancer and dysplasia. A
large meta-analysis done by Downer etal. calculated a sensitivity of 85% and a
specicity of 97% [31]. Furthermore, Kerala etal. conducted a randomized controlled trial that was initiated in 1995 and involved over 130,000 individuals randomized into two groups (screening or control) with results presented at 3, 6, and
9years. At 9years, although there was no increase in survival observed for the
overall population, they found a decreased mortality among males who were using
tobacco and alcohol and received oral cancer screening.
Light-based detection systems have been studied as both screening tests and
case-nding tests. There are two main categories of light-based detection tests: tests
that assess tissue reectance (e.g., ViziLite Plus and MicroLux DL) and tests that
assess tissue autouorescence (e.g., VELscope). Tissue reectance was being used
as an adjunct in cervical mucosa long before it was used in the oral cavity. In the oral
cavity, these tests begin with a 1% acetic acid solution pre-rinse that is thought to
remove surface cellular debris and cause mild dehydration of epithelial cells to
increase visibility of their nuclei. A blue-white LED light is then applied to the oral
mucosa, and normal tissue absorbs it, causing it to appear dark, whereas abnormal
tissue reects it, causing it to appear white. However, there is no data to demonstrate
that this technology can identify mucosal abnormalities not already detected by
visual examination. Furthermore, there is no data to show it can reliably predict
histopathological abnormalities in clinically suspicious lesions identied by visual
exam [30].
Tissue autouorescence is based on the principle that cellular alterations in dysplasia and carcinoma change the concentration of uorophores in tissue, which
affect the way abnormal tissue scatters and absorbs certain wavelengths of light.
Tissue autouorescence technology does not require the use of a pre-rinse. The
VELscope uses a blue light (with a wavelength of 400–460nm) to excite the tissue.
Normal oral mucosa emits a pale green autouoresence when viewed through a
narrow-band lter in the handpiece. In contrast, abnormal tissue has less autouoresence and appears dark in comparison to the bright surrounding normal mucosa.
When used as a case-nding test (on suspicious lesions that were detected by visual
exam under incandescent light), one study showed a high sensitivity (98%) and high
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specicity (100%) in discriminating mucosa with histologic evidence of carcinoma
or dysplasia from mucosa that is histologically normal [32]. However, the data is
mixed with one systematic review reporting sensitives as low as 15.3% and specicities as low as 30% [33]. Furthermore, there is no good evidence to show tissue
autouorescence can reliably identify histopathologically abnormal mucosa that is
not detectable by clinical oral exam, which limits its use as a screening test [30].
Another popular adjunct is brush biopsy. This technology is used as a casending test and works by allows clinicians to collect exfoliated cells in a clinically
suspicious lesion. The cells are then xed on a histology slide and undergo specialized computer-aided analysis. Because the test evaluates individual cells, its assessment is based solely on cellular atypia. Thus, it cannot evaluate epithelial architecture
and cannot differentiate dysplasia from invasive carcinoma. It was introduced in
1999 and marketed as a minimally invasive adjunct that could further characterize
innocuous appearing lesions that clinicians would not normally biopsy. If the test
resulted as “abnormal” or “positive,” clinicians are encouraged to follow up with a
formal scalpel biopsy for denitive diagnosis. The data on this has been mixed as
well with sensitivities and specicities ranging from 71% to 100% and 32% to
100%, respectively [30]. However, Lingen and colleagues argue that this adjunct
may be helpful in patients with multiple lesions throughout the oral cavity who are
not willing to undergo scalpel biopsy for all of them.
A third main category of adjuncts is dyes, most commonly toluidine blue, which
have a high afnity for nucleic acids and thus presumably stain dysplastic and
malignant tissue because of their high DNA content. Toluidine blue has been used
for decades in other countries as both a screening test and case-nding test for oral
cavity dysplasia and cancer [34]. Surgeons have also used toluidine blue to decide
on margins for excision of a lesion [35]. Although a lot of data exist on toluidine
blue, there is none that supports its use as a screening test. Overall, its sensitivity
and specicity for detecting oral cancer ranges from 78% to 100% and 31% to
100%, respectively [30].
In summary, these adjuncts may have a role in the detection and diagnosis of
dysplasia, but only in the hands of informed clinicians who understand their indications and use them appropriately.
L. Aljadeff and A. B. Morlandt
Oral Dysplasia: Management (Treatment andSurveillance)
Treating dysplasia before it progresses to oral cancer can be lifesaving; however,
there is still no way to accurately predict which dysplastic lesions will progress and
when. Furthermore, because dysplasia is a disease that is restricted to the epithelium, there are many different management options including observation, topical
therapy (retinoids and vitamin A), cryotherapy, laser vaporization, and surgical
excision. Each of these have different levels of morbidity, rely on different amounts
of patient compliance, have different costs, and require different expertise and
equipment from clinicians. Additionally, unlike oral squamous cell carcinoma, there
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is no consensus or data-drive guidelines to follow. Thus, the management of dysplasia has become a matter of surgeon preference and a source of signicant
controversy.
For purposes of this chapter, we will review a few algorithms that help provide a
framework for managing patients with oral epithelial dysplasia. In 2015, the
University of Liverpool published an algorithm that divides epithelial dysplasia into
two main categories: mild or moderate/severe/CIS [36]. This is based on strong data
that lesions with a higher degree of dysplasia have a higher tendency to undergo
malignant transformation [37]. Specically, a meta-analysis conducted by Iocca
etal. showed that the “the odds of malignant transformation in moderate/severe
dysplasia are much higher than mild dysplasia (OR 2.37, 99% CI 1.47–3.79)” [11].
They calculated an annual malignant transformation rate of 1.7% for mild dysplasia
and 3.57% for severe dysplasia. Furthermore, Speight has shown that while less
than 5% of mild dysplasia will undergo malignant transformation, up to 50% of
severe dysplasia will [37]. In the Liverpool algorithm, mild dysplasia gets monitored for 5years by a specialist and then discharged to their primary care for surveillance, whereas moderate and severe dysplasia gets treated, re-biopsied, or closely
observed long term by a specialist. The only exception to this is that mild dysplasia
that has a concerning clinical appearance or exists in a patient with signicant risk
factors gets managed more vigilantly along the moderate/severe dysplasia pathway
of the treatment algorithm.
In 2018, Awadallah and colleagues published their own algorithm for managing
dysplasia [38]. Similar to the Liverpool algorithm, their algorithm was based on risk
stratication; however, they proposed a unique treatment for moderate dysplasia
rather than grouping it with severe dysplasia and CIS.Interestingly, they excise
severe dysplasia and CIS with 5mm margins and moderate dysplasia with 2 mm
margins and combine excision with laser ablation. Although there is no strong data
to support their selection of margins, it reects their concern that lesions with severe
dysplasia and CIS identied on biopsy are more likely to have a focus of Squamous
cell carcinoma (SCCa) that may be identied after complete excision. Additionally,
the surveillance is different for moderate dysplasia versus severe dysplasia/CIS.The
surveillance for severe dysplasia/CIS closely mimics the regimen outlined by the
National Comprehensive Cancer Network (NCCN) for head and neck cancer, again,
reecting the concern that severe dysplasia and CIS are most likely to undergo malignant transformation. Meanwhile, mild dysplasia in patients with clinically innocuous
lesions and no risk factors undergo “conservative management,” whereas higher-risk
patient undergo excision with or without laser ablation. The long-term follow-up
they propose for mild dysplasia is similar to their follow up for moderate dysplasia.
Ultimately, both the Liverpool and Awadallah algorithms focus on two main
modalities of treatment: surgical excision or CO2 laser ablation. The main advantage of surgical excision over CO2 laser ablation is that it provides a specimen for
histopathological analysis that may affect treatment (for example, if a focus of carcinoma was found in the specimen). However, laser ablation is often less morbid
that surgical excision and can be used in lesions that are not amenable to excision
either because of location or distribution.
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