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26
WHO Classification of Tumours: An Overview
Muhammed Yakin and Richard Logan
Adelaide Dental School, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, Australia
26.1 Introduction
The terms neoplasia and tumour are sometimes used interchangeably and can cause some
confusion to learners, particularly in their undergraduate training. It is, therefore, essential to
understand the meaning of these terms so they are used accurately and in the correct context.
The term ‘neoplasia’ is originally Greek and means new (neo) tissue (- plasia). Neoplasia is an
abnormal, internally driven, uncontrolled growth of tissue or cells that does not depend on external factors. On the other hand, the term ‘tumour’, Latin (tumour), denotes an abnormal swelling
or mass and can be of various pathogenesis.
The word tumour has two meanings: the first is any abnormal swelling of neoplastic or nonneoplastic origin. In other words, any clinically detectable swelling can be termed a tumour. Most
of the tumours of the oral and maxillofacial regions are of reactive and infective origin. The second
meaning of the word tumour is a neoplasm, which refers to benign or malignant space- occupying
neoplasms.
Knowledge of and distinction between the two terms is clinically relevant because many of the
lesions that should be in the differential diagnosis of oral and maxillofacial tumours are nonneoplastic but have overlapping clinical presentations.
Neoplasms of the oral and maxillofacial regions arise from a wide range of sites and tissues. In
the latest WHO classification of Head and Neck tumours, the more common neoplasms are
covered in Chapter6– oral cavity and mobile tongue tumours(1), Chapter8– odontogenic and
maxillofacial bone tumours(2) and Chapter5– salivary gland tumours(3). The generally less common neoplasms, including melanocytic tumours, soft tissue tumours and haematolymphoid
proliferations, are covered in Chapters12,10 and11, respectively(4– 6). Chapter13 covers tumours
and tumour- like head and neck lesions and includes common and relevant lesions for the practising dentist and oral pathologist(7). The last 17th Chapter covers genetic tumour syndromes of the
head and neck(8).
This chapter aims to provide an overview of the oral and maxillofacial tumours described in the
most recent WHO classification of Head and Neck Tumours. The WHO classification includes
most lesions that should be considered in the differential diagnosis of oral and maxillofacial
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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26.2 Developmental Tumours
disease. However, due to length or space restrictions, it does not include some common lesions
which would normally be included in the differential diagnosis of these tumours. In terms of
pathological mechanisms of disease, the oral and maxillofacial tumours covered in the WHO
Classification of Head and Neck Tumours encompass the following categories:
Developmental
● Inflammatory/Infective
● Immune- mediated
● Neoplastic
● Metabolic/hormonal
● Idiopathic
The above categories also form a surgical sieve, which is helpful in clinical practice to work
through possible diagnoses and determine investigative and treatment pathways. Regarding relative frequency, reactive/inflammatory tumours are most common, followed by developmental and
then neoplastic tumours. A small number of tumours result from immune- mediated, metabolic or
hormonal processes, and an even smaller number are idiopathic, with some evidence indicating a
reactive or neoplastic pathogenesis, which is why they are included under the other four headings
in the discussion below.
26.2 Developmental Tumours
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Developmental lesions are the second most commonly biopsied group(9) and include inherited
and acquired lesions that may be present at birth (congenital) or develop later in life. Genetic
abnormalities drive the pathogenesis of these lesions. The presentation of these lesions varies in
terms of symptoms, size and patient profile, depending on their natural history and histogenesis.
This group of lesions’ management depends on the symptoms they cause. Many need to be excised,
but some can be left without treatment as they pose little to no risk to the patient. An essential
distinction between developmental and neoplastic tumours is that the latter include mutations
that lead to uncontrolled cell proliferation. Moreover, inherited tumour syndromes are not developmental but neoplastic, resulting from inherited mutations that put the offspring at a higher risk
of developing neoplasia.
Tumours with developmental aetiology comprise the bulk of the odontogenic cysts and are covered in the chapter on odontogenic and maxillofacial bone tumours. Developmental lesions of the
salivary glands are rare and do not usually present as tumours. Some of the common developmental lesions of the oral cavity, such as lymphoepithelial cyst, thyroglossal cysts and dermoid and
teratoid cysts, are covered in Chapter13 of the WHO book on tumours and tumour- like lesions of
the neck and lymph nodes, and lymphangioma is covered in Chapter10 on soft tissue tumours.
The most common examples of intraosseous developmental tumours in the oral regions are
odontomas and hamartomas rather than neoplastic lesions. Hamartomas refer to masses of haphazardly arranged tissue in an appropriate location. In this context, an odontoma comprises a
disorganised mass of enamel, dentine, cementum and pulp, which are local to the site from which
they arise. The pathogenesis remains elusive, but the activation of the WNT/B- catenin pathway
involved in embryonic development has been shown to drive its formation(10, 11).
Other examples of developmental jaw tumours include developmental odontogenic cysts such
as dentigerous cysts and odontogenic keratocysts (OKC), the second and third most common
odontogenic cysts of the jaws, respectively. Dentigerous cysts are developmental cysts arising from
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26 WHO Classification of Tumours: An Overview
442
fluid accumulation between the reduced enamel epithelium and the tooth enamel it usually covers.
Local fluid and venous drainage disturbances have been suggested as possible mechanisms of cyst
expansion, driven by increasing hydrostatic pressure in the cyst cavity. OKC was classified as a
cystic neoplasm in the 2005WHO classification. It was termed a keratocystic odontogenic tumour
(KCOT) due to its aggressive behaviour and higher recurrence compared to most other odontogenic cysts. One point of confusion is between cysts and cystic neoplasms. For any lesion to be
categorised as neoplastic, there must be inherent potential for growth and expansion, irrespective
of any external stimuli. The classification as a neoplasm was driven by several factors, such as the
presence of patched gene (PTCH) mutations and a different growth pattern that depends on epithelial proliferation and secretion of matrix metalloproteinases to break down connective tissue
that aid the expansion of OKC. In addition, the presence of daughter or satellite cysts and fragility
of the cyst epithelium meant that enucleation resulted in higher recurrence rates. However, with
further clinical and molecular evidence of its cystic rather than neoplastic nature, including
decompression by marsupialisation, the lesion was reclassified to a cyst in the 2017WHO classification and has remained the same, i.e. a cyst in the 2022WHO classification. Nevertheless, the
2022WHO classification lists KCOT as an acceptable alternative term to OKC(2).
Among fibro- osseous and giant cell lesions of the jaws, fibrous dysplasia and cherubism are
inherited disorders characterised by distinct molecular signatures of GNAS and SH3BP2 mutations, respectively. Both are self- limiting lesions that cease to grow after skeletal maturation,
though some surgical intervention may be required for aesthetic and functional reasons(2).
Soft tissue developmental lesions such as lymphoepithelial cysts and dermoid cysts have unclear
aetiopathogenesis, although epithelial inclusions trapped following embryonic tissue fusions are
likely pathogenic mechanisms. In contrast, failure of fusion of branchial arches is the mechanism
for developing branchial cleft cysts. A thyroglossal duct cyst results from cystic degeneration rather
than complete disintegration of the epithelial remnants along the path of migration of the thyroid
gland(7). As for developmental oropharyngeal tumours, covered in Chapter7 of the WHO book,
hamartomatous polyps may be seen, although they only comprise approximately 2% of tumours of
the tonsil(12).
26.3 Reactive Inflammatory andInfective Tumours
Although the bulk of the WHO book comprises neoplastic tumours, reactive lesions comprise the
bulk of biopsies submitted to diagnostic services(9, 13). Reactive inflammatory tumours are the
most common of all tumours of the oral and maxillofacial regions and can arise in both soft and
hard tissues.
26.3.1 Mucosal Reactive Tumours
The oral mucosa’s most common reactive inflammatory mucosal tumours are fibroepithelial
hyperplasias, which are not included in the WHO classification(9, 13). Some of these are also
referred to as fibromas despite their non- neoplastic nature. The lesions in the chapter on the
oral cavity and mobile tongue tumours include haemangioma and peripheral giant cell granuloma. Haemangioma, or lobular capillary haemangioma, is a reactive vascular tumour– covered
in Chapter10 of the WHO book under soft tissue tumours. Peripheral giant cell granuloma is
covered in Chapter8, Odontogenic and maxillofacial bone tumours. Multifocal epithelial hyperplasia is also a reactive lesion to infection and is covered under non- neoplastic lesions in
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Chapter6 of the WHO book(1). While ranulas are reactive salivary gland tumours, they are
covered in Chapter13 under tumours and tumour- like lesions of the neck and lymph nodes.
Only two other reactive salivary gland lesions are covered in the book in Chapter5 salivary
gland tumours: nodular oncocytic hyperplasia and lymphoepithelial sialadenitis(3). Necrotising
sialometaplasia, the reactive salivary gland lesion which is less common but clinically important as a mimicker of oral squamous cells, is covered in Chapter6 under the tumours of the oral
cavity and mobile tongue(1).
Lobular capillary haemangiomas, also referred to as pyogenic granuloma– which is a misnomer,
as the lesion is neither pus forming nor a true granuloma, are common in sites subject to mechanical trauma and irritation from sharp edges of calculus, cavities, restorations and appliances, or
biting, including the buccal and labial mucosae, lateral borders of the tongue and the gingiva. The
response is modified by hormonal factors resulting in exuberant growth, particularly in pregnant
women, which is termed pregnancy epulis when arising from the gingiva. The traumatised tissue,
initially by high- grade trauma, forms granulation tissue comprised of budding capillaries, fibroblasts, myofibroblasts and macrophages. This is healing tissue, which then usually goes on to
mature into more fibrous tissue akin to a scar. However, continuous irritation leads to further
granulation tissue formation and growth of the lesion, which is clinically red, soft, ulcerated and
often bleeds. Some lobular capillary haemangiomas show rapid and florid growth, which may be
alarming to the patient and clinician and, therefore, be biopsied along with removing the causative
factors. Peripheral giant cell granuloma, commonly presenting as an epulis, is a reactive lesion
with a reactive rather than neoplastic aetiopathogenesis. Trauma and irritation are likely causative
factors of this growth(5).
Oral melanoacanthoma is a reactive mucosal lesion which presents as a rapidly growing brownpigmented patch in the oral mucosa. Oral melanoacanthoma does not present as a tumour and has
a benign course(1). However, because it mimics malignant melanoma, this lesion is discussed in
the chapter on the oral cavity and mobile tongue tumours of the WHO classification. In contrast,
oral mucosal melanoma is covered separately in Chapter12 on melanocytic tumours(4).
Ranulas develop from trauma to the sublingual gland, leading to the extravasation of saliva to
the submucosal tissues of the floor of the mouth and an inflammatory reaction involving the production of granulation tissue by the body to contain the mucus. The lesion causes pressure symptoms and can affect speech, eating and swallowing, so it needs to be excised(7). Necrotising
sialometaplasia is an alarming salivary gland disease usually presenting in the palatal mucosa due
to ischaemia or hypoxia resulting from trauma. The deep ulceration mimics OSCC but has an
uneventful outcome following biopsy to exclude OSCC(3).
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26.3.2 Intraosseous Reactive Lesions
Several reactive and inflammatory lesions of the jaws are included under odontogenic maxillofacial bone tumours in Chapter8, most notably inflammatory radicular cysts, which are the most
Radicular cysts are inflammatory cysts associated with the roots of non- vital teeth. The pathogenesis of radicular cysts involves the proliferation of the odontogenic epithelial rests of Malassez
as a result of the influx of bacterial toxins from the pulp and periapical areas and the associated
inflammatory response. Once these cellular proliferations reach a certain size, they break down in
the middle, forming a cystic cavity. Tissue death and an increase in the osmotic pressure lead to the
influx of more water into the area, leading to the secreting of E2 and E3 prostaglandins, which
promote bone resorption and expansion of the lesion(2).
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26 WHO Classification of Tumours: An Overview
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The other collateral inflammatory cysts, such as mandibular buccal bifurcation (MBBC) and
paradental cysts, have a different pathogenesis. These cysts are characterised by communication with
the oral cavity through a gingival pocket, leading to the accumulation of debris leading to inflammation and then bone resorption, or in the case of the MBBC, bone expansion, as the cyst size increases(2).
26.4 Tumours withImmune- mediated Pathogenesis
There are only a few tumours which have immune- mediated pathogenesis.
The most significant are oral lichen planus (OLP) and related lesions, although these do not
present as tumours, they are epithelial precursor lesions which may precede the development of
OSCC(14). Although OLP does not have a dedicated section in the chapter on the oral cavity and
mobile tongue tumours, it is discussed among the oral potentially malignant disorders (OPMD)(1).
The disease pathogenesis is through immune- mediated destruction of the basal cells by cytotoxic
CD8+ T- cells. Despite being described as an auto- immune process by some authors, the exact antigen remains unknown(15, 16).
In the salivary glands, lymphoepithelial sialadenitis develops due to an autoimmune disease,
usually Sjogren syndrome and rheumatoid arthritis, and is characterised by swelling and pain of
salivary glands(3, 17). IgG4- related disease involving mainly the submandibular glands and cervical lymph nodes also has an immunologically mediated pathogenesis. Repeated stimulation of the
immune system by specific antigens leads to activation of CD4+ T- cells and M2 macrophages,
which in turn promote the proliferation and activation of fibroblasts that produce collagen and
lead to fibrosis and hence the now not recommended name: IgG4- related sclerosing disease. As a
result of its pathogenic mechanism, this non- neoplastic disease is covered in Chapter 11 on
haematolymphoid proliferation and neoplasia(6).
26.5 Neoplastic Tumours
The title of this section is deliberately worded as such to emphasise the earlier points about the
terminology around neoplasms as opposed to tumours. The vast majority of the entities described
in the WHO classification are neoplasms. They have variable clinical presentation and histogenesis. Regarding frequency, malignant lesions account for approximately 2– 5% of biopsies submitted
for histopathological examination in adults(9, 13) compared with 0.13– 0.7% of children(18, 19).
Benign neoplasms have a lower relative frequency of 1.2– 2%(9, 13) of adult accessions if squamous cell papilloma is excluded (infra vide). The pathogenesis of neoplasia is described in detail
elsewhere in this book. Briefly, genetic mutations result in a combination of loss of function of
tumour suppressor genes, gain of function of protooncogenes, and cellular immortalisation, leading to uncontrolled cell proliferation.
Salivary gland neoplasms are categorised according to their histogenesis and behaviour under
three main categories: benign epithelial tumours, of which pleomorphic adenoma is most common; malignant epithelial tumours, and mesenchymal tumours specific to the salivary glands; the
latter of which covers only sialolipoma(3).
Similarly, oral cavity and mobile tongue tumours are addressed under the three subsections of nonneoplastic lesions, epithelial tumours and tumours of uncertain histogenesis. The section on
non- neoplastic lesions was highlighted previously in the section on reactive inflammatory and
infective tumours(1).
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The second section of the WHO book covers epithelial tumours under three subsections. The first
subsection is papillomas and includes only squamous papillomas. Squamous papilloma, or squamous cell papilloma, is one of the most common benign tumours of the oral mucosa and is included
in the WHO Chapter: Tumours of the Oral Cavity and Mobile Tongue under Epithelial Tumours.
The pathogenesis of this lesion is through viral entry into the epithelium through trauma, followed
by entry of the viral DNA into the nucleus. The infection clears in most individuals over time. Most
pathologists regard squamous papilloma as a non- neoplastic but a rather reactive proliferation of
tissue to viral infection by low- risk human papillomavirus subtypes in the form of a pedunculated
mass of fibrovascular fronds covered by hyperplastic epithelium that shows some degree of viral
changes such a koilocytosis and nuclear indentation or halos. The lesion has no potential for
malignant transformation. However, squamous papillomas of the oral cavity have a much more
innocuous course than sinonasal and laryngeal papillomas, which is one of the reasons for
including them under neoplastic disease(20). The second subsection, under epithelial tumours,
covers OPMD. OPMD do not present as tumours but are included due to their clinical significance
and the higher risk of progression to or development of malignancy in individuals with OPMD. The
third subsection is on malignant neoplasms of the oral cavity, 90% of which are squamous cell
carcinomas, with the rest being other malignancies such as verrucous carcinomas(1).
The third section covers a range of tumours of uncertain histogenesis. The first three, congenital
granular cell epulis– which is considered developmental, granular cell tumour and ectomesenchymal chondromyxoid tumour– behave non- aggressively. The fourth one, the melanotic neuroectodermal tumour of infancy, shows aggressive and even malignant behaviour(1).
Neoplastic mesenchymal lesions are uncommon in the oral cavity and are covered in Chapter10
on soft tissue tumours(5) and Chapter11 on haematolymphoid proliferation and neoplasia(6).
Most of the lesions described in these two chapters are neoplastic, apart from a few exceptions,
such as haemangioma and fibroblastic and myofibroblastic tumours. Lipoma is the most common
true mesenchymal neoplasm of the oral cavity.
Neoplasms of the jawbones are covered comprehensively in Chapter8 on odontogenic and maxillofacial bone tumours and include a range of odontogenic lesions, which are histopathologically
intriguing(2). Apart from the lesions covered in the section on odontogenic cysts, which are either
inflammatory or developmental, the vast majority of these tumours are neoplastic and are divided
into odontogenic tumours, giant cell lesions and bone cysts and bone and cartilage tumours.
Odontogenic tumours are mostly benign, originating from odontogenic epithelium, a combination
of odontogenic epithelium and mesenchyme, or odontogenic mesenchyme only. Except for odontomas, the rest of the tumours are neoplastic, with ameloblastoma being the most common lesion.
Giant cell lesions and bone cysts are mostly reactive. The only possible exception is central giant cell
granuloma, which is most likely neoplastic based on its aggressive clinical behaviour and increasing
molecular evidence and association with several tumour syndromes(2, 8). All the bone and cartilage tumours covered in the WHO classification are neoplastic with the notable exception of the
first three fibro- osseous lesions, which are cemento- osseous dysplasia, which is most likely reactive,
segmental maxillary odontodysplasia and fibrous dysplasia, both of which are developmental(2).
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26.6 Tumours withMetabolic andHormonal Pathogenesis
Brown tumour of hyperparathyroidism is the most prominent of these lesions and is associated
with hyperparathyroidism jaw tumour syndrome. In primary hyperparathyroidism, which may be
related to tumour syndromes, there is a consistent increase in the production of parathyroid
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26 WHO Classification of Tumours: An Overview
446
hormone, usually from an adenoma, whereas in secondary hyperparathyroidism, the increase in
the production of parathyroid hormone results from low serum calcium levels. Decreasing serum
calcium concentrations leads to bone resorption, increasing serum calcium. This results in multilocular radiolucencies in the jaws and other bones. An earlier radiographic sign is the change in
the trabecular pattern of the alveolar bone, resulting in the loss of lamina dura and a ground glass
appearance of the bone(8).
Congenital granular cell epulis seen in newborns is one of the few examples of oral soft tissue
lesions with possible degenerative aetiopathogenesis. The lesion is benign and can be managed
conservatively(1).
Phosphaturic mesenchymal tumour is another example of a tumour with known pathogenesis but
unknown aetiology and uncertain histogenesis. This tumour induces osteomalacia through the production of fibroblast growth factor- 23. This growth factor’s effect blocks the renal phosphate uptake,
leading to phosphaturia, hypophosphatasia, and ultimately tumour- induced osteomalacia(2).
26.7 Summary
The WHO classification of tumours includes a range of common and essential pathology that
present as swellings or space- occupying lesions in the oral and maxillofacial regions. The terms
neoplasia and tumour are sometimes used interchangeably but can have different pathologic
basis. Neoplasia means new tissue growth and refers to an abnormal internally driven uncontrolled growth of tissue or cells that does not depend on external factors. On the other hand, the
term tumour denotes an abnormal swelling or mass and can be of various pathogenesis.
The most common tumours of the oral and maxillofacial regions are inflammatory, while some
are developmental, neoplastic, or other. Understanding the pathological basis of these tumours is
important as it determines the course of treatment of the lesions if required.
The WHO classification includes most lesions that should be considered in the differential diagnosis of oral and maxillofacial disease. However, due to length or space restrictions, it does not
have some common lesions which would normally be included in the differential diagnosis of
these tumours.
Clinicians and pathologists need to understand the pathological basis, clinicopathologic correlation, and differential diagnosis of oral and maxillofacial pathology to provide the best care for
patients.
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