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cancer(3). It has been attributed to microcytic hypochromic anaemia(3). Anaemia is known to
cause epithelial atrophy; however, what role (if any) it plays in OPMDs remains to be
determined(3).
Bloom syndrome (congenital telangiectatic erythema) is a rare autosomal recessive disorder of
DNA helicase function(39). Sun sensitivity, telangiectatic erythema of the face and stunted
growth are characteristic(39). Affected individuals are at high risk of developing cancer, including lymphomas, leukaemia, adenocarcinoma of the colon and oral and oesophageal squamous
cell carcinoma(39).
Despite several genetic diseases being associated with an increased risk of OSCC, except dyskeratosis congenita, it is difficult to determine whether an OPMD precedes the disease(3, 9). This
also holds for immunosuppression. Although renal transplant patients and those with HIV- related
immunosuppression are at increased risk of developing OSCC, data regarding OPMDs is scarce(9).
Very few studies or case reports have been published. While an increased risk of developing OSCC
has been reported, the cases are more likely to appear de novo(9). Only a handful of papers have
reported a link between immunosuppression and leukoplakia(41, 42).
27.15 Role ofNutrition
Haematinics are essential to the maintenance of general health(43). Vitamin B12, folic acid and
iron are fundamental to maintaining oral epithelial integrity(43). Folic acid and vitamin B12 are
involved in DNA synthesis and cell division, and iron is essential to the normal functioning of
epithelial cells(43). Haematinic deficiencies have been implicated in malignancies, including of
the aerodigestive tract (e.g. Plummer– Vinson syndrome)(39, 43).
Higher frequencies of anaemia, serum vitamin B12 and folic acid deficiencies, and hyperhomocysteinemia have been demonstrated in patients with OPMDs compared to healthy controls(43).
Suggested reasons for folate deficiency include elevated folate turnover in response to rapid tissue
proliferation or repair; inactivation or alteration of its function by external agents such as tobacco,
alcohol or drugs; or altered metabolism or tissue uptake caused by an inborn error(43). It is currently unknown if supplementation may delay the progression and malignant transformation of
OPMDs to cancer(43). Nonetheless, at least in the case of vitamin B12, epithelial changes associated with deficiency (disordered keratinocyte maturation, basal cell hyperplasia, nuclear atypia,
hyperchromatism, increased mitosis and abnormal mitosis) are reversible upon correction of the
deficiency(44).
Deficiencies of other micronutrients, such as vitamins A and C, have also been implicated as
possible risk factors for OSCC(9). However, data regarding their role in OPMDs is lacking(9).
469
27.16 Prediction ofMalignant Transformation
The natural history of OPMDs is variable and remains unpredictable(45). Thus, the foresight of
progression, regression or stability is challenging. Despite numerous limitations, the presence and
grade of OED are still the most important prognostic factors for malignant transformation, with
the overall risk determined by the highest grade of dysplasia in any sample, irrespective of when
in the timeline of biopsies that sample was obtained(6, 46). Clinicians and pathologists contribute
to the limitations surrounding dysplasia, which are centred around inter- and intra- observer
t.me/Dr_Mouayyad_AlbtousH
470
variations in reporting dysplasia and its gardening and sampling errors when choosing biopsy
sites(46). One study has shown that in 35% of cases, biopsies had underdiagnosed the extent of the
disease(47). Studies of biomarkers, aneuploidy and LOH have shown promise; however, none can
be relied upon for accurate prognostication in routine clinical practice. Nonetheless, risk assessment does not lie entirely with the tissue sample. Patient factors (e.g. gender, exposure to risk factors, medical comorbidities, personal and family cancer history), clinical history and lesion
characteristics (e.g. site, size, multifocality, red, white, speckled, nodular or verrucous appearance)
also aid risk stratification(48).
Management of OPMDs ranges from observation to medical treatments to surgical intervention
and is governed by the perceived risk of malignant transformation(6, 9, 48). Management of OED,
in particular, is complicated by the lack of universally accepted, evidence- based protocols(49).
Irrespective of risk perception and treatment protocols implemented in individual patients, modification of the known and modifiable risk factors is also paramount(48). Thus far, risk modification and its impacts have received little attention in the literature. Until difficulties associated with
diagnosis, risk assessments and management protocols are overcome, all patients with OPMDs
should undergo regular and lifelong surveillance.
27.17 Summary
In summary, OED is a premalignant condition characterised by abnormal changes in the cells lining the oral cavity. These changes involve the mucosal lining of the mouth, including the lips,
tongue and gums. OED is often associated with chronic irritants such as tobacco and alcohol use,
as well as viral infections like HPV. Clinically, OED may present as white or red patches in the oral
mucosa, typically identified through a biopsy and microscopic examination of the tissue. The
degree of dysplasia can vary, ranging from mild to severe, and it serves as an essential indicator of
the risk for progression to oral cancer. Regular monitoring and appropriate management of OED
are crucial to detect any malignant transformation early on. Patients with OED often require close
follow- up, cessation of risk factors like smoking and excessive alcohol consumption, and in some
cases, surgical intervention to remove the affected tissue. Early detection and intervention play a
key role in preventing the development of oral cancer in individuals with OED.
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8 Mahmood H, Bradburn M, Rajpoot N, Islam NM, Kujan O, Khurram SA. Prediction of malignant
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9 Tilakaratne WM, Jayasooriya PR, Jayasuriya NS, De Silva RK. Oral epithelial dysplasia: causes,
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10 Woo SB. Oral epithelial dysplasia and premalignancy. Head Neck Pathol. 2019;13(3):423– 39.
11 Iocca O, Sollecito TP, Alawi F, Weinstein GS, Newman JG, De Virgilio A, etal. Potentially
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12 Nag R, Kumar DR. Analysis of images for detection of oral epithelial dysplasia: a review. Oral
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13 Warnakulasuriya S. Histological grading of oral epithelial dysplasia: revisited. J Pathol.
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14 Yuwanati M, Gadbail A, Gondivkar S, Sarode SC, Dande R, Mhaske S, etal. A systematic scoping
review on utility of cytomorphometry in the detection of dysplasia in oral potentially malignant
disorders. J Oral Biol Craniofac Res. 2020;10(4):321– 8.
15 Kim E, Chung M, Jeong HS, Baek CH, Cho J. Histological features of differentiated dysplasia in the
oral mucosa: a review of oral invasive squamous cell carcinoma cases diagnosed with benign or
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16 Lerman MA, Almazrooa S, Lindeman N, Hall D, Villa A, Woo SB. HPV- 16in a distinct subset of
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17 Abdulmajeed AA, Farah CS. Can immunohistochemistry be an alternative to subjective
histopathological diagnosis of oral epithelial dysplasia? Biomark Cancer. 2013;5:49– 60.
18 Nankivell P, Williams H, Matthews P, Suortamo S, Snead D, McConkey C, etal. The binary oral
dysplasia grading system: validity testing and suggested improvement. Oral Surg Oral Med Oral
Pathol Oral Radiol. 2013;115(1):87– 94.
19 Al- Hashimi I, Schifter M, Lockhart PB, Wray D, Brennan M, Migliorati CA, etal. Oral lichen
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20 Odell EW. Aneuploidy and loss of heterozygosity as risk markers for malignant transformation in
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21 Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000;100(1):57– 70.
22 Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646– 74.
23 Pitiyage G, Tilakaratne WM, Tavassoli M, Warnakulasuriya S. Molecular markers in oral epithelial
dysplasia: review. J Oral Pathol Med. 2009;38(10):737– 52.
24 Kujan O, Huang G, Ravindran A, Vijayan M, Farah CS. Cyclin- dependent kinases’ role in
potentially malignant oral disorders and oral squamous cell carcinoma. J Oral Pathol Med.
2019;48(7):560– 5.
25 Kujan O, Idrees M, Anand N, Soh B, Wong E, Farah CS. Efficacy of oral brush cytology cell block
immunocytochemistry in diagnosing oral leukoplakia and oral squamous cell carcinoma. J Oral
Pathol Med. 2021;50(5):451– 8.
26 Kujan O, Shearston K, Farah CS. The role of hypoxia in oral cancer and potentially malignant
disorders: a review. J Oral Pathol Med. 2017;46(4):246– 52.
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27 Smith J, Rattay T, McConkey C, Helliwell T, Mehanna H. Biomarkers in dysplasia of the oral
cavity: a systematic review. Oral Oncol. 2009;45(8):647– 53.
28 Kujan O, van Schaijik B, Farah CS. Immune checkpoint inhibitors in oral cavity squamous cell
carcinoma and oral potentially malignant disorders: a systematic review. Cancers (Basel).
2020;12(7):1937.
29 Kaunein N, Ramani RS, Koo K, Moore C, Celentano A, McCullough M, etal. A systematic review
of MicroRNA signatures associated with the progression of leukoplakia with and without
epithelial dysplasia. Biomolecules. 2021;11(12):1879.
30 El- Sakka H, Kujan O, Farah CS. We are assessing miRNAs profile expression as a risk stratification
biomarker in oral potentially malignant disorders: a systematic review. Oral Oncol. 2018;77:57– 82.
31 Kujan O, Siddiqui I, Lee C, Idrees M, Shearston K, Farah CS. Automated immunohistochemical
quantification of hypoxia biomarkers shows a correlation with dysplastic epithelial changes. J Oral
Pathol Med. 2023;52:504– 13.
32 Bradley G, Odell EW, Raphael S, Ho J, Le LW, Benchimol S, etal. Abnormal DNA content in oral
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33 Alaizari NA, Sperandio M, Odell EW, Peruzzo D, Al- Maweri SA. Meta- analysis of the predictive
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papillomavirus in oral epithelial dysplasia: systematic review and meta- analysis. Head Neck.
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35 Khanal S, Trainor PJ, Zahin M, Ghim SJ, Joh J, Rai SN, etal. Histologic variation in high- grade oral
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36 McCord C, Xu J, Xu W, Qiu X, McComb RJ, Perez- Ordonez B, etal. Association of high- risk
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Oral Radiol. 2013;115(4):541– 9.
37 Theofilou VI, Alfaifi A, Montelongo- Jauregui D, Pettas E, Georgaki M, Nikitakis NG, etal. The oral
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39 Porter S, Gueiros LA, Leao JC, Fedele S. Risk factors and etiopathogenesis of potentially
premalignant oral epithelial lesions. Oral Surg Oral Med Oral Pathol Oral Radiol.
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40 Bongiorno M, Rivard S, Hammer D, Kentosh J. Malignant transformation of oral leukoplakia in a
patient with dyskeratosis congenita. Oral Surg Oral Med Oral Pathol Oral Radiol. 2017;124(4):e239– e42.
41 King GN, Healy CM, Glover MT, Kwan JT, Williams DM, Leigh IM, etal. Increased prevalence of
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42 Hernandez G, Arriba L, Jimenez C, Bagan JV, Rivera B, Lucas M, etal. Rapid progression from oral
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44 Theaker JM, Porter SR, Fleming KA. Oral epithelial dysplasia in vitamin B12 deficiency. Oral Surg
Oral Med Oral Pathol. 1989;67(1):81– 3.
45 Edwards PC. The natural history of oral epithelial dysplasia: perspective on Dost etal. Oral Surg
Oral Med Oral Pathol Oral Radiol. 2014;117(3):263– 6.
46 Speight PM, Khurram SA, Kujan O. Oral potentially malignant disorders: risk of progression to
malignancy. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018;125(6):612– 27.
47 Holmstrup P, Vedtofte P, Reibel J, Stoltze K. Oral premalignant lesions: is a biopsy reliable? J Oral
Pathol Med. 2007;36(5):262– 6.
48 Kerr AR, Lodi G. Management of oral potentially malignant disorders. Oral Dis.
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49 Min Ang X, Chi Khang Au P, Kwok K, Yeon Park K, Kujan O, Frydrych AM, etal. Quality of life in
patients with oral leukoplakia. J Oral Pathol Med. 2019;48(7):574– 80.
473
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Section 7
Neoplastic Diseases ofthe Oral Mucosa andSalivary Glands
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28
Global Burden, Risk factors andPathobiology ofMalignant
Neoplasms ofthe Oral Mucosa andthe Oropharynx
Paul Hankinson and Syed Ali Khurram
Unit of Oral and Maxillofacial Pathology, School of Dentistry, University of Sheffield, Sheffield, UK
28.1 Introduction
Many malignant neoplasms may affect the oral cavity and oropharynx with a wide range of origins.
This can include sarcomas, lymphomas, mucosal melanomas or adenocarcinomas. However, all of
these neoplasms are uncommon when compared with squamous cell carcinomas (SCCs), which
arise from the epithelial lining of the oral cavity (oral SCC [OSCC]) and oropharynx (oropharynx
SCC [OPSCC]). These are often described collectively with cancers of the sinonasal tract and larynx as head and neck squamous cell carcinomas (HNSCCs). SCCs are thought to account for 90%
of malignant neoplasms of the oral cavity and oropharynx(1). There are many subtypes of OSCC
and OPSCC(2). The subtypes of OSCC are generally histological, with similar aetiologies and
limited clinical importance and will not be discussed here. OPSCC, however, has two distinct subtypes: human papillomavirus (HPV) associated OPSCC (HPV+veOPSCC) and HPV- independent
OPSCC (HPV−veOPSCC)(2). These two subtypes have distinct aetiological factors, clinical features and outcomes, and so both subtypes will be discussed. The global burden, risk factors and
pathobiology of OSCC and OPSCC will be the focus of this chapter. Though there is some overlap
between these diseases, there are also contrasting trends in incidence and survival, divergent
aetiology and differing pathogenesis. These differences will be highlighted throughout this chapter.
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28.2 Epidemiology
Studying the prevalence, incidence and mortality of cancers across different populations can give
insights into aetiology, prevention, optimisation of management and prioritisation of resources(3).
Interpretation of epidemiological data for OSCC and OPSCC is often hampered by the quality of
reporting in cancer registries, leading to over- representation of Western populations(4– 6). This is
a major factor in discrepancies between cancer data reported by different global organisations(7).
Variable coding of head and neck sites by cancer registries and how studies assign HPV status also
lead to difficulty in interpreting these studies(4). Despite these difficulties, several trends can be
identified.
Pathological Basis of Oral and Maxillofacial Diseases, First Edition. Edited by S. R. Prabhu, Syed Ali Khurram,
Omar Kujan and Merva Soluk Tekkesin.
© 2025 John Wiley & Sons Ltd. Published 2025 by John Wiley & Sons Ltd.
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28 Global Burden, Risk factors andPathobiology ofMalignant Neoplasms ofthe Oral Mucosa andthe Oropharynx
Estimated age-standardised incidence rates (World) in 2020, lip, oral cavity, both sexes, all ages
No data
478
28.2.1 Global Prevalence, Incidence, Regional Variations ofOral
andOropharyngeal Cancers
Prevalence describes the number of cases present in a population, whereas incidence describes the
number of new cases in a population over a set period of time. An estimated global prevalence of
959,248 cases for OSCC and 258,543 cases for OPSCC was reported in 2020(8). When OSCC and
OPSCC are combined, there are 476,125 new cases each year (8). This has increased since
2012when there was an estimated total of 302,500new cases(9). Alongside crude cancer rates, it
can be helpful to look at age- standardised rates (ASRs) which account for variable age distributions across different populations. The global ASR for OSCC is 4.1 per 100,000 and 1.1 per 100,000
for OPSCC(8). These have increased over time for OSCC(10). In 2012, OSCC had an ASR of 2.7
per 100,000 for OSCC, though, the International Agency for Research on Cancer (IARC) gave a
similar incidence for OPSCC in 2012 as in 2020(9).
These trends vary globally (Figures28.1 and28.2)(4, 5, 8, 10) with regional differences seen
between subsites associated with HPV and subsites which are not(4). The majority of new OSCC
ASR (World) per 100 000
≥ 4.0
2.6–4.0
1.7–2.6
1.3–1.7
< 1.3
Not applicable
No data
Estimated age-standardised mortality rates (World) in 2020, lip, oral cavity, both sexes, all ages
ASR (World) per 100 000
≥ 1.6
1.2–1.6
0.87–1.2
0.63–0.87
< 0.63
Not applicable
Figure28.1 A heat map of global incidence and mortality rates for OSCC. Top global incidence rates.
Bottom global mortality rates. Source: Adapted from(8).
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Estimated age-standardised incidence rates (World) in 2020, oropharynx, both sexes, all ages
ASR (World) per 100000
No data
≥ 1.7
0.80–1.7
0.41–0.80
0.20–0.41
< 0.20
Not applicable
No data
Estimated age-standardised mortality rates (World) in 2020, oropharynx, both sexes, all ages
28.2 pidemiology
479
ASR (World) per 100000
≥ 0.75
0.40–0.75
0.23–0.40
0.11–0.23
< 0.11
Not applicable
Figure28.2 A heat map of global incidence and mortality rates for OPSCC. Top global incidence rates.
Bottom global mortality rates. Source: Adapted from(8).
cases occur in Asia (8, 11), followed by Europe and North America (8). This trend reverses for
OPSCC with more new cases occurring in Europe and North America than in Asia(8). This is similar to 2012when OPSCC had a higher incidence rate in countries with a higher human development index (9). Differences in exposure to risk factors may account for these trends. There is
a much higher portion of HPV+veOPSCC in Europe and North America compared with
Asia (12,13). However, smokeless tobacco (SLT) and other similar products which are more
commonly consumed in Asia, drive a higher incidence of OSCC(14).
There is a worrying trend of increasing incidence of OSCC and OPSCC in younger patients
(<45 years) over the past 60 years (5). This trend is especially true in Asia and Africa with
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28 Global Burden, Risk factors andPathobiology ofMalignant Neoplasms ofthe Oral Mucosa andthe Oropharynx
480
Pakistan and Nigeria being the worst countries affected(5). Both OSCC and OPSCC are more
common in men than women(8– 10), though the gap in incidence is narrowing. Although there
have been increases in OSCC(11) and HNSCC at other subsites in women over the past few
decades(4), limited increase in OPSCC has been seen(4). Conversely, rates of OSCC though
rising have begun to stabilise in men(11), whereas OPSCC have seen large increases in men over
the past 60 years(4). Despite this, some studies, though limited to Western populations, show
similar rates of HPV in OPSCC between men and women, even though men account for more
cases of OPSCC overall (15, 16). Rates of HPV+veOPSCC have increased in both men and
women(15, 16).
28.2.2 Mortality Rates andTrends ofOral andOropharyngeal Cancers
There were thought to be 177,757 deaths from OSCC and 48,143 deaths from OPSCC in the
year 2020 (8). There is significant geographical variation in mortality associated with both
OSCC and OPSCC (Figures28.1 and 28.2). Most deaths for both diseases occur in Asia,
accounting for 74% of global deaths(8). Clear differences are seen in OSCC outcomes between
developed and low- and middle- income countries, and this likely plays a role in the regional
variation seen(10). Differences in regional mortality may also be due to distinct aetiologies for
OPSCC in different regions. HPV+veOPSCC, which has a better prognosis compared with
HPV−veOPSCC(17, 18), is much more common in the Western world and more developed
countries(12, 13).
The number of OSCC- related global deaths has doubled since the 1990s, though the agestandardised mortality rates accounting for population growth have remained steady over this
period(10). This stable mortality rate is due to improvements in survival in developed countries
despite worsening mortality rates in developing regions(10). Approximately twice as many men
than women die of OSCC each year(8), while four times as many men die from OPSCC(6, 8, 19).
This is partially explained by greater incidence of both diseases in men(8), though some studies
link improved survival with gender, while others do not(19– 21).
28.3 Risk Factors forCancers ofthe Oral Mucosa
Cancer is caused by an accumulation of mutations that lead to changes in cell behaviour. These
mutations may occur due to ‘intrinsic risk’ (random chance and failure of normal cell processes)(22). However, most cancers are caused by ‘non- intrinsic’ risk factors defined as carcinogens or promoters(22). For example, chemical carcinogens or radiation cause direct damage to the
DNA structure leading to mutations, though not all carcinogens are genotoxic and some lead to
cancer without damaging DNA(22, 23). Alternatively, promoters are not carcinogens, do not cause
DNA damage but may increase malignant transformation risk in other ways, for example, by driving cell proliferation(22, 23). Cancer risk factors are also often categorised in different ways, for
example, into exogenous risk factors such as tobacco smoke compared to endogenous factors such
as ageing(22). They may also be classified as modifiable or non- modifiable(22, 24), though the
degree to which different risk factors are modifiable is debated(22).
The predominant risk factors for OPSCC and OSCC vary, mainly due to the significant role of
HPV in OPSCC(25), whereas HPV plays a more limited role in OSCC(2). However, there is an
overlap in the aetiological factors of OSCC and HPV−veOPSCC(26). The risk factors for OSCC will
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