Received: 5 June 2019 | Accepted: 5 June 2019

DOI: 10.1111/jop.12899

SPECIAL ISSUE ARTICLE

Malignant transformation rate of oral leukoplakia in an

Australian population

Kate Shearston1 | Behrooz Fateh1 | Shixiong Tai1 | Dzikamai Hove1 |

Camile S. Farah1,2

1
UWA Dental School, University of Western
Australia, Nedlands, Western Australia,
Australia
2
Australian Centre for Oral Oncology
Research & Education, Nedlands, Western
Australia, Australia
Correspondence
Camile S. Farah, Australian Centre for Oral
Oncology Research & Education, Nedlands,
WA, 6009, Australia.
Email: camile@oralmedpath.com.au
Abstract
Objectives: Oral leukoplakia (OLK) is one of the most common oral potentially ma‐
lignant lesions (OPMD) and is reported to undergo malignant transformation (MT)
to oral squamous cell carcinoma (OSCC) at rates of between 0.13% and 34%. This
study seeks to determine the proportion of OLK lesions that develop into OSCC in an
Australian population and assess the risk factors associated with this transformation.
Methods: The study is a retrospective audit of patients from a private oral medicine
clinic, diagnosed with OLK using clinical and histopathological data between 2006
and 2014. Patients were cross‐matched with Cancer Registry data for OSCC, and the
rate and time to malignant transformation were determined.
Results: Oral leukoplakia patients with histopathological confirmation of their lesions
underwent MT at a rate of 1.49% (3/202), with an average time to MT (TMT) of
5.2 years. When patients without histopathological confirmation were assessed, the
MT rate was slightly less (1.30%; 4.9 years TMT). Patients who transformed were
more likely to be older females with a history of smoking and alcohol use, with OLK
present on the tongue or floor of mouth. The rate of oral epithelial dysplasia (OED) in
the transformed group was surprisingly low (one third).
Conclusions: Oral leukoplakia is at a moderate risk of malignant transformation which
can be reduced by careful management. Current tools for identifying high‐risk OLK,
including histopathological assessment of OED, may not capture all lesions that un‐
dergo MT and should be supplemented by unbiased molecular biomarkers.

KEYWORDS
Australia, malignant transformation, oral epithelial dysplasia, oral leukoplakia, oral squamous
cell carcinoma

1 | I NTRO D U C TI O N
Oral cancer, of which the most common type is oral squamous cell
carcinoma (OSCC), is a serious disease with more than 5000 new
1
cases diagnosed in Australia every year. The overall 5‐year sur‐
vival rate of oral cancer in Australia is 58.8%, and it is frequently
diagnosed at a late stage, which significantly compromises patient
outcomes.1 Early diagnosis and treatment of OSCC have the poten‐
tial to improve patient quality of life and lift a substantial burden
from the Australian healthcare system.
Oral squamous cell carcinoma is commonly preceded by oral po‐
tentially malignant disorders (OPMDs), which include a variety of mu‐
cosal lesions such as oral leukoplakia (OLK), oral lichen planus (OLP),
oral lichenoid lesions (OLL) and oral lichenoid dysplasia (OLD). In the

J Oral Pathol Med. 2019;00:1–8. wileyonlinelibrary.com/journal/jop © 2019 John Wiley & Sons A/S. | 1
Published by John Wiley & Sons Ltd
2 | SHEARSTON et al.

literature, OPMDs are reported to undergo malignant transforma‐

tion (MT) at rates of between 0% and 34%; however, this varies sub‐

Mean time
to MT (y)

5.9 ± 0.8
stantially between OPMD type, lesion site, the cohort studied and a
range of risk factors.2 Leukoplakia is a clinical diagnosis defined by the

6.4
World Health Organization (WHO) as “a white patch or plaque that

Rate of MT
cannot be characterised clinically or pathologically as any other de‐
finable lesion”.3,4 A 2005 update added that it should exclude “known

0.70
0.8
(%)
diseases or disorders that carry no increased risk for cancer”.5

Patients with >5 y of follow‐up

A recent systematic review indicated the worldwide prevalence

No. patients
undergoing
of OPMD was 4.47% and that OLK was one of the most common at
4.11%.6 Leukoplakia is more common in males and smokers and usually

MT
presents in the 4th decade of life. Common sites of leukoplakia include

2
1
the tongue and buccal mucosa.5 Leukoplakia is a clinical diagnosis, and

patients (%)
there are a number of clinical features that can be used to assess the

142 (70)
251 (65)
risk of OLK undergoing MT. These include lesion size, site and homo‐

No. of
geneity, as well as patient risk factors such as smoking, alcohol use
and age.7,8 Adjunctive techniques such as tissue autofluorescence can

4.6 ± 0.2
4.2 ± 0.7
also provide additional information about the malignant potential of

time to
MT (y)
Mean
specific lesions.9,10 Typically however, lesions must be biopsied and
submitted for histopathological assessment and the presence and
grade of oral epithelial dysplasia (OED) used to assess the risk of MT.11

Rate of MT
Higher risk OLK includes those that are larger, non‐homogeneous,

2.22
3.33
exhibit a loss of autofluorescence on imaging and display features of

Patients with <5 y of follow‐up

(%)
OED, with the risk increasing with the grade.8,9 Proliferative verrucous

No. patients
leukoplakia (PVL) is a particularly aggressive variant of OLK charac‐

undergoing
terised by multifocal lesions and a corrugated clinical appearance, and
displays a particularly high MT rate of between 40% and 70%.12

MT

3
2
Leukoplakia can be managed by excision of lesions or by review,

patients

135 (35)
and there is variable evidence for the effectiveness of these two main

60 (30)
No. of

approaches. Typically, leukoplakia not displaying OED, or in some (%)

cases mild OED on biopsy, is relegated to the “watch and wait” ap‐
proach, whilst those with OED, particularly higher grades, are excised.
5.2 ± 1.1
4.9 ± 1.1
time to

The goal of this study was to assess the rate of malignant trans‐
MT (y)
Mean

formation of oral leukoplakia in an Australian population and to as‐

sess the impact of various risk factors and management strategies
on the risk of MT in this cohort. This has the potential to shape the
Rate of MT
Patient cohort and malignant transformation rates

management of OLK by providing a greater understanding of the risk

1.30
1.49

of MT in Australian patients.
(%)
No. patients
undergoing

2 | M E TH O DS
mt

5
3

The study is a retrospective audit of patients from a private oral

medicine clinic, diagnosed with OLK between 2006 and 2014.
All Patients

The study was conducted in accordance with human ethics guide‐

patients
No. of

lines approved by the University of Western Australia's Human

386
202

Ethics Committee (RA/4/20/4028). Public Health Act approval

was obtained from the Queensland Government to access Cancer
Clinical leukoplakia

Registry data (RD007425). Patient records were searched to

identify cases of OLK and then cross‐matched with oral cancer
leukoplakia
TA B L E 1

records from the Queensland Cancer Registry data up until the

Biopsied

end of 2015. Time to malignant transformation (TMT) was calcu‐

lated from the biopsy date of the original lesion till development
SHEARSTON et al.
of malignancy. Patients were divided into two groups: those with
follow‐up <5 years and those with follow‐up >5 years.
Clinical MT, which may or may not have histological confirmation,
was calculated from the first clinical assessment by an oral medicine
specialist (CSF) to the date of OSCC diagnosis. WHO MT (biopsy‐
proven OLK) includes only those cases of OLK that have had their
diagnosis confirmed by both clinical examination/photographs and
histological assessment. OLK was further sub‐classified into those
with a histopathological diagnosis of oral epithelial dysplasia (OED)
and those displaying an absence of OED.
3 | R E S U LT S
A total of 386 clinical OLK cases were identified, and of these, five
individuals underwent malignant transformation generating an MT
F I G U R E 1 Patient characteristics and
risk factors of the biopsy‐proven cohort
| 3
rate of 1.30%. The mean time to malignant transformation (TMT)
was 4.9 years ± 1.1 SD (Table 1). The clinical cohort was predomi‐
nantly male (53%), with a mean age of 57 (56.6 ± 13.4), and the ma‐
jority of patients were in the 50‐ to 60‐year age range.
A total of 202 biopsy‐proven OLK were identified, and within
this group, 60 cases had <5‐year follow‐up and 142 had >5‐year
follow‐up. Three patients underwent MT at the same site as their
original lesion, two to OSCC and one to carcinoma in situ (CIS). TMT
was 5.2 years (±1.1 SD), which generated an MT rate of 3.33% in the
<5‐year group and an MT of 1.49% overall.
Males predominated in the biopsy‐proven cohort, compris‐
ing 55% of the patients (Figure 1). The mean age was 56 years
(56.5 ± 12.1) with the majority of patients in the 50‐ to 70‐year
age range. The tongue was the most common site for OLK,
followed by the buccal mucosa, alveolar ridge and floor of
mouth. More than half the cohort (59%) were past or current
 4 | SHEARSTON et al.

smokers, 25% reported regular alcohol consumption and 7%

SCC, NOS

SCC, NOS

SCC, NOS
SCC, NOS
diagnosis
were diabetic.
Tumour Patients who underwent MT ranged in age from 40 to 79 years at

CIS
the time of cancer diagnosis with a mean age of 64 (63.9 ± 14.9 SD;
Ventral tongue Table 2). With the exception of Patient 1, who developed OSCC at

Lower gingiva
Anterior floor
the comparatively young age of 40, the patients in this group were
Tumour site

Oral cavity,

of mouth
older than the overall OLK cohort (which averaged 56 years). In con‐

Tongue
NOS trast to the overall cohort, 60% of the MT group were female (cf.
45% in the overall cohort). Rates of smoking and alcohol intake were
higher than the overall cohort, with 80% reporting past or present
Treatment of
initial lesion

smoking, and 80% reporting regular alcohol consumption compared

Wait and

Wait and

Wait and
Wait and

Excision
Watch

Watch

Watch
Watch

with 59% and 25%, respectively, in the overall cohort. The tongue
(40%) was the most common site for OSCC development, with the
remainder evenly divided between floor of mouth, alveolar ridge and
determined

determined

gingiva (20% each). The homogeneity of lesions was not reported in

Biopsy type

Incisional

Incisional

Incisional

all cases; with 29% of lesions described as non‐homogeneous, 12%

described as homogeneous, and 59% not specified.
Not

Not

Details obtained from clinical notes and chart review. Clinical photographs and histopathological slides were not available for assessment.

Excisional and incisional biopsies were made at similar rates

(50.7% and 48.3%, respectively), with 3.5% of biopsies initially inci‐
OLK histopatho‐
logical diagnosis

hyperkeratosis

Not determined

Not determined
hyperkeratosis

sional then referred for excision and 1% unknown (Table 3). Lesions
Hyperplasia/

Hyperplasia/

Severe OED

were predominantly non‐dysplastic, with 75.5% exhibiting no OED.

Of the lesions that were diagnosed as dysplastic, the majority were
mild OED (15%) and a minority were moderate or severe (4.0% and
2.5%, respectively). In 3.0% of cases, the lesion was characterised as
Non‐homogene‐

Non‐homogene‐
Non‐homogene‐

Homogeneous
Homogeneous

dysplastic without stating a grade.

presentation

The excisional biopsy group displayed a higher rate of OED than

Clinical

the incisional biopsy group (27.5% OED vs 21.4% OED) and a trend
ous

ous
ous

towards higher grades of dysplasia, with comparable proportions

of mild dysplasia (14.7% vs 15.3%, respectively) but higher rates of
Floor of mouth
alveolar ridge

Lateral border

moderate (4.9% vs 3.1%) and severe (3.9% vs 1.0%). These data in‐
Right ventral

of tongue
Lesion site

Lower left

clude patients who received surgical excision of their lesion as de‐

Details of patients and lesions undergoing malignant transformation

tongue

Gingiva

finitive treatment following an incisional biopsy. Despite this, two

patients who underwent MT had incisional biopsies which did not
display OED (Table 2; Figure 2).
Alcohol

Yes

Yes
Yes

Yes
Yes

4 | D I S CU S S I O N
Smoker

Yes

Yes

Yes
Yes
No

This study assessed the malignant transformation rate of a cohort of

Australian patients from a single oral medicine clinic, suffering from
Time to
MT (y)

oral leukoplakia. We observed the MT rate in 386 patients with clini‐

3.5
6.3

5.3
4.8
4.4

Abbreviations: NOS, not otherwise specified.

cal correlation only and 202 patients who had both clinical and histo‐
pathological assessment, allowing us to apply WHO criteria for OLK
diagnosis

and exclude other OPMDs such as OLP or clinically similar benign

cancer
Age at

40.4

66.9
79.1

73.1
60.1

conditions such as reactive/frictional keratoses.13

The rates of MT in our study were fairly consistent between clin‐
initial lesion

ical MT and WHO MT with rates of 1.30% and 1.49%, respectively.

diagnosis

This is at the lower end reported in the literature (range 0.13%‐34%)

Age at

34.2

55.3
74.6

61.6

69.6

and substantially less than the mean of 14.9% reported in a recent

meta‐analysis incorporating 24 studies auditing OPMDs,14 and still
Patient 4 a

Patient 5a
TA B L E 2

Patient 1

Patient 2

Patient 3

lower than the estimated rate of 3.54% for the total population
studied.14 An earlier meta‐analysis focused on OPMD with dysplasia
found a mean MT rate of 12.1%.15 Studies vary considerably in size,
a
SHEARSTON et al. | 5

patient cohort and follow‐up time, but in general our MT rates were
more similar to studies performed in India, Croatia, Denmark and

dergoing MT (%)
No. patients un‐
Sweden (range 0.13%‐2.7%) rather than those in the UK, USA, China,
the Netherlands and Norway (range 8.9%‐34%).14 Some of these

2 (2.60)
2 (2.04)
studies included only patients with OED which was unsurprisingly
associated with higher MT rates.16,17 The timeframe to MT in our

0
0
0
0
% of patients cohort was also quite consistent with the literature, with TMT values
of approximately 5 years.14,15 The follow‐up times in our cohort vary
from 1.5 to 14 years, with 42% of the biopsy‐proven OLK group with
<5‐year follow‐up, which suggests that the current MT rates in our
48.3
78.6
15.3

2.0
1.0
3.1
study may slightly underestimate the true rate. As a comparison, in a
Incisional biopsies

landmark early study from Sweden, the MT rate increased from 1.3%
No. of patients

at 3 years to 2.4% at 10 years and finally 4% after 20 years.18

Our cohort of biopsy‐confirmed OLK patients was fairly typical
of that in the literature, with a preponderance of older males with a
77
15
98

high proportion of smoking and alcohol use reported. The majority of

2
3
1

OLK lesions biopsied (74.9%) were non‐dysplastic, with 14.8% show‐

No. patients under‐

ing mild OED, 3.9% moderate OED and 2.5% severe OED which is
similar to other studies that have performed stratification based on
going MT (%)

OED grade.19 However, patients who underwent MT in our study

1 (0.98)

were more likely to be older females most of whom reported smok‐

1 (25)

ing and alcohol use, well‐established risk factors for developing oral
0
0
0
0

cancer.14 Lesion size and homogeneity have also been associated

with greater risk of MT but were not reported at sufficiently high
% of patients

rates to analyse in this study, although we have reported on a parallel

patient cohort in the past which showed that a non‐homogeneous
72.8
50.7

14.6

3.9
3.9
4.9

lesion was a significant independent indicator for underlying OED.7

Excisional biopsies

The proportions of OED, another MT risk factor, were surprisingly

No. of patients

low. Sixty per cent of the OSCCs involved either the tongue or floor
of mouth, both sites being associated with higher MT risk.8
The transformed patients in this cohort were aged above
102

55 years, although Patient 1 was substantially younger than the

15
75

4
5
4

overall cohort, having developed OSCC at 40 years of age. This pa‐

No. patients under‐

tient is part of a growing cohort of patients developing OSCC at a

younger age, 20 earlier than the time the impact of risk factors such
going MT (%)

as smoking would be expected to manifest. This suggests a poten‐

Details of biopsy type as related to OED diagnosis

2 (1.32)
3 (1.49)

tial genetic basis for the propensity of such OPMDs to transform.

1 (20)

Unfortunately, there are few high‐quality genomic studies investi‐

0
0
0

gating early‐onset OSCC to shed light on this issue, and those to

date which have focused on tongue SCC have not found much age‐
% of patients

based distinction. A Singaporean study found a tendency towards

increased mutations in PIK3CA and MLL2/KMT2A in late‐onset ver‐
14.8
74.9
100

2.5
3.0
3.9

sus early‐onset OSCC whilst another US‐based study found minimal

genomic differences between the two groups. 20,21
No. of patients

Interestingly, two out of three of our biopsy‐proven OLK patients

All biopsies

who underwent MT had an initial lesion that was histopathologically

assessed as non‐dysplastic. This is an unusual result as typically OED
202
152

is associated with a higher risk of MT, and higher grades of OED are
30
8
5
6

correlated with higher risk. This has been demonstrated in a meta‐

analysis and in a range of studies where MT rates have been esti‐
OED severe
OED NOS
OED mod
TA B L E 3

OED mild

mated at 0.012% for non‐dysplastic lesions, 3.8%‐15% for mild OED,

No OED

15%‐18% for moderate OED and 26%‐39% for severe OED. 2,15,22,23
Total

There is certainly evidence for OSCC arising from non‐dysplastic

6 |
(A) (B)
(C) (D)
(E) (F)
lesions; Hsue et al24 found that 3.5% of lesions diagnosed with hy‐
perkeratosis/hyperplasia underwent MT versus 4.8% of lesions diag‐
24,25
nosed with OED and there are other examples.
There are a number of possibilities to explain why OED lesions
are relatively under‐represented in our transformed cohort. The cur‐
rent gold standard for identifying lesions at high risk of MT is surgical
biopsy and histopathological evaluation; however, the determination
of OED, particularly mild OED, is notoriously subjective, with po‐
tentially large inter‐observer variability. 26 In our study however, an
experienced oral pathologist reassessed the slides of the initial le‐
sions that underwent transformation and was largely in agreement
with the original diagnosis. The choice of lesion site, particularly in
large heterogeneous lesions, can also influence the diagnosis, and
27
regions of dysplasia or even malignancy can be missed by biopsy.
Another possibility is that OED lesions are under‐represented in our
transformed cohort due to the prevailing management strategy of
excision of such lesions.
In lesions where dysplasia is present, full excision of the lesion,
if practicable, is recommended to reduce MT risk, although there
are those who support the “wait and watch” approach for mild OED.
There is variable evidence for the efficacy of lesion excision in pre‐
venting MT, with some studies suggesting that it has no statistically
19
significant benefit ; however in a meta‐analysis, OED lesions that
were excised underwent MT at a much lower rate than those that
were not excised (14.6% vs 5.4%).15 A further potential benefit of
SHEARSTON et al.
F I G U R E 2 Representative clinical
and/or histopathological presentation of
Patient 1 (A; year 2000, B; year 2005),
Patient 2 (C, D) and Patient 3 (E, F) who
underwent malignant transformation
and for whom clinical photographs and
histopathological slides were available for
assessment
excision is that in heterogeneous lesions, it allows assessment of the
entire lesion histologically; Chiesa et al reported that in post‐exci‐
sion assessment, 10% of lesions previously identified as benign were
reassessed as malignant. 28 A recent Cochrane review concluded that
there was insufficient evidence to validate any intervention in the
treatment of leukoplakia, including surgical modalities. This was due
to the fact that there have been no randomised clinical trials assess‐
ing the effect of surgical excision on the development of oral cancer
that include a control arm with no treatment, due to the associated
ethical issues. 29 The position can certainly be argued that lesions
displaying any grade of OED should, where possible, be excised and
this approach has mostly been taken with the current cohort under
investigation. 2
In this cohort, half of the patients presenting with OLK (50.7%)
had their lesion fully excised, frequently after an initial incisional bi‐
opsy, and this was more likely in patients with any grade of OED
(27.3% of fully excised lesions displayed OED vs 21.4% of lesions
that had only an incisional biopsy). Of the lesions that displayed
OED, 50% of mild OED were fully excised; however, this increased
with OED grade, with 62.5% of moderate OED and 80% of severe
OED fully excised. Non‐dysplastic lesions, primarily those diagnosed
with hyperkeratosis/hyperplasia, were fully excised at a similar rate
to mild OED (49%), as befitting their apparently lower risk status.
Nonetheless, the majority of the cohort (75.5%) were diagnosed
with non‐dysplastic lesions.
SHEARSTON et al.
The fact that two of our three patients undergoing MT had no
histopathological evidence of OED in the last biopsy prior to devel‐
oping OSCC highlights the need for objective molecular biomarkers
of MT. The molecular profiling of OLK lesions would allow more ac‐
curate characterisation of their relationship to OSCC. Shared chro‐
mosomal alterations have been identified in progressive leukoplakia
and their matching OSCCs, with DNA aneuploidy being strongly
linked with increased dysplasia, and increased risk of MT. 22,30,31 A
recent study by our group has shown that the gene expression pro‐
file of OLK with dysplasia is indeed distinct from that of OLK with‐
out dysplasia,32 and this not only provides insight into the processes
that regulate malignant transformation of OLK, but also assist with
determining a set of unbiased biomarkers with which to predict le‐
sions at higher risk of MT. In future, single‐cell transcriptomics may
offer even greater value in understanding pre‐malignant lesions,
where changes in gene expression are limited to a relatively small
proportion of cells which may be too subtle to detect in bulk RNA se‐
quencing. This has been demonstrated in pre‐malignant lung lesions
among other cancers.33
Relatively, few OPMDs will undergo MT, and clinical obser‐
vation and histopathological assessment alone do not allow ac‐
curate prediction of which lesions will progress to malignancy.
Exomic studies of OPMDs and their comparison with OSCC would
allow an understanding of the process of oral carcinogenesis, in
particular the accumulation and timing of specific mutations asso‐
ciated with malignancy. This has been performed in oesophageal
SCC where mutational profiles were compared between matched
sets of pre‐malignant lesions and their matching SCCs, as well as
with dysplastic samples from patients without cancer. 34 More re‐
cently, we have shown that exomic sequencing of dysplastic and
non‐dysplastic leukoplakia has demonstrated that progressive leu‐
koplakia can be differentiated from non‐progressive leukoplakia
using the frequency of exomic variants, particularly in DNA dam‐
age repair pathway genes, implicating the Fanconi anemia/BRCA
double‐strand break pathway in malignant transformation of OED
to OSCC. 35
A greater understanding of the molecular pathways involved in
oral carcinogenesis would also allow for more effective and per‐
sonalised treatment of potentially malignant lesions such as OLK.
The recent “Erlotinib Prevention of Oral Cancer” (EPOC) trial was
an early example of the potential of chemotherapeutic treatment
of high‐risk pre‐malignant lesions identified by loss of heterozy‐
gosity (LOH). Whilst this particular drug was ultimately not benefi‐
cial, it provided a useful proof of concept study and highlighted the
importance of molecular markers to both identify high‐risk lesions
and to be able to offer targeted treatments most likely to be of
benefit. 36
Our study has several limitations that may cause it to underes‐
timate the overall rate of MT. Firstly, the number of cases reported
is small, the study is retrospective in design, and patients drawn
from a single clinic. Secondly, any patients who left the state of
Queensland and subsequently developed OSCC would not be
included in the Queensland Cancer Registry and therefore not
| 7
be included in our follow‐up data. Thirdly, given that it may take
5‐7 years to undergo MT, there is a group of patients who may
develop OSCC in the future but have not yet reached that stage;
42% of our cohort have 0‐ to 5‐year follow‐up. A future follow‐
up study should address these issues to confirm the reported MT
rates, whilst confirmation in another Australian cohort would be
beneficial.
In conclusion, our audit finds that oral leukoplakia in an Australian
cohort undergoes malignant transformation at a rate that is within
the range of similar studies reported worldwide, but at a rate lower
than the average. Patients with leukoplakic lesions which trans‐
formed to OSCC were more likely to exhibit risk factors including
increased age, female gender, smoking and alcohol use, with lesions
present on the tongue or floor of mouth. The rate of dysplasia in the
original lesions was low, with two thirds of our patients who trans‐
formed having leukoplakia classified as non‐dysplastic. Whilst this
cannot be tested within the scope of the current study, we suggest
that the under‐representation of dysplastic lesions in the cohort
that developed cancer, and the comparatively low MT rate, could be
related to the management approach of excising dysplastic lesions
where practicable. The transformation of OLK without dysplasia
also highlights the difficulty in identifying and treating suspicious
lesions with current clinical tools, placing greater emphasis on the
molecular profiling of leukoplakia to drive novel treatment and man‐
agement strategies for improved patient care.
AC K N OW L E D G E M E N T S
The authors thank the Queensland Cancer Registry for retrieval of
data.
ORCID
Camile S. Farah https://orcid.org/0000-0002-1642-6204
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How to cite this article: Shearston K, Fateh B, Tai S, Hove D,
Farah CS. Malignant transformation rate of oral leukoplakia
in an Australian population. J Oral Pathol Med. 2019;00:1–8.
https​://doi.org/10.1111/jop.12899​