Oral cancer
BMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7190.1051 (Published 17 April 1999) Cite this as: BMJ 1999;318:1051
All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
This review (1)summarised some of the important points relating to
oral
cancer but failed particularly to highlight the importance of second
primary tumours in these patients. These may be synchronous elsewhere in
the upper aerodigestive tract in up to 15% and metachronous in up to
40%(2,3). Oral examination alone is therefore inadequate in the planning
of
care or follow-up. Patients with oral cancer may present with a local
lesion but many are exposing themselves systemically to carcinogens or
inadequate nutrition, and there is growing evidence of a familial and
sometimes genetic background in some(4,5).
1. Zakrzewska JM. Oral Cancer. Br Med J 1999; 318: 1051-1054.
2.Vikram B. Changing patterns of failure in advanced head and neck
cancer.
Arch Otolaryngol. 1984 ;110(9):564-5.
3.Licciardello JT, Spitz MR, Hong WK. Multiple primary cancer in
patients
with cancer of the head and neck:second cancer of the head and neck,
esophagus, and lung.Int J Radiat Oncol Biol Phys 1989 ;17(3):467-76
4. Copper MP, Jovanovic A, Nauta JJ. Role of genetic factors in the
etiology of squamous cell carcinoma of the head and neck. Arch Otol Head
and Neck Surg. 1995; 121: 157-160.
5. Goldstein AM, Blot WJ, Greenberg RS. Familial risk in oral and
pharyngeal cancer. Oral Oncol. 1994; 30B: 319-322.
NO CONFLICT OF INTEREST
Professor Crispian Scully
MD,PhD,MDS,FDSRCS,FDSRCPS,FFDRCSI,FDSRCSE,FRCPath,FMedSci
Dean, Director of Studies and Research
International Centres for Excellence in Dentistry
Eastman Dental Institute for Oral Health Care Sciences
University of London
256 Gray's Inn Road
LONDON WC1X 8LD
UK
Tel; 441719151038
Fax; 441719151039
Competing interests: No competing interests
EDITOR - The Review published by Zakrzewska (1) is inadequate and misleading.
Method
A Medline search using the terms "mouth" & "neoplasm" will not
yield the necessary data for such a review as the specific anatomical
divisions of the oral cavity will not be detected by such a search.
Definition and Classification
Neoplasms of the oral cavity must of necessity fall into the
U.I.C.C's subdivisions which I will briefly refer to below (2). To state
that tumours of the salivary glands are rare is misleading as they are the
most common tumours of the hard palate (3). The inaccuracy of the review
will become apparent when the oral cavity is properly defined.
Oral Cavity (2)
1. Buccal mucosa
i. mucosal surface of upper and lower lips
ii. mucosal surface of the cheeks
iii. retromolar areas
iv. Bucco-alveolar sulci, upper and lower.
2. Upper alveolus and gingiva.
3. Lower alveolus and gingiva.
4. Hard Palate.
5. Tongue.
i. Dorsal surface and lateral borders anterior to
vallate papillae (anterior two-thirds)
ii. Inferior surface.
6. Floor of mouth.
Management
The previous edition of "Practical Radiotherapy Planning" by Dobbs
& Barrett (3) could correct the wrong impression conveyed by
Sakrzewska's article (1).
"Radical radiation therapy is used to treat squamous cell carcinomas
of the oral cavity, with surgery for recurrent disease. Local control
rates for T1 tumours are about 80% with 60-75% control for T2 tumours. For
large tumours the control rate falls to considerably less than 50%.
Retrieval of surgical failures by radiotherapy is usually unsuccessful.
However, primary surgery is indicated for small T1 lesions of the tongue,
which can be excised without deformity, and for large tumour masses or
those with bone involvement, where there is a low cure rate with
radiotherapy. Surgery, involving a partial or total glossectomy and
mandibulectomy, may result in difficulty with speech and mastication.
Melanomas, adenocarcinomas and tumours in areas of premalignant change are
treated with surgery. Salivary gland tumours form the commonest neoplasm
in the hard palate and are treated surgically" (3)
Dobson and Barrett have brought out a new edition with Dan Ash as a
co-author which is not yet generally available (4). Furthermore the above
authors distinguish between treatment for the tongue, the floor of mouth,
the buccal mucosa,lower alveolus and the retromolar trigone (3).
When Zabrzewska (1) states "the prognosis for large oral neoplasms
remains poor" it is difficult to understand as there is no anatomical
definition or staging system used or referred to in her article. It would
have been helpful to glean assistance from a good Head and Neck Clinic as
I am sure exists at the Royal Marsden Hospital as well as in many other
centres in Great Britain.
Sincerely,
L. Reinecke
References:
1. Zakrzewska JM Oral Cancer A Fornightly review
BMJ 1999;318:1051-1054.
2. UICC TNM Atlas Spiessl B, Beahrs OH et al. 3rd Edition. 1990:12-19
3. Dobbs J & Barrett A. Practical Radiotherapy Planning - Royal
Marsden Hospital Practice. Edward Arnold - A division of Hodder &
Stoughton. 1988: 51-39
4. Personal communication - Ann Barrett.
Competing interests: No competing interests
Excellent discussion and the best quality photos I have ever
seen published! The electronic version allowed this article to be an
excellent educational experience for me.
H2
Competing interests: No competing interests
Dear Sir,
Stephan Larssen in his response to Zakrzewskas' article on Oral
Cancer (1) asserts that there is 'little or no evidence' to support the
'surgical' view that oral cancer or indeed head and neck cancer is treated
to a large extent by surgery or surgery in combination with radiotherapy.
The statement he makes that in the U.K. radiotherapy is the primary
curative treatment modality for head and neck cancer is not in keeping
with the findings of a recently published Head and Neck Audit from
multiple centres in the South and West of England (2).
The audit shows that of 494 new cases of head and neck cancer treated by
surgery, radiotherapy or a combination, in 1997, a minority (45%) were
treated by radiotherapy alone
in spite of nearly 1/3 of these cases having tumours of the larynx (in
which the primary modality was of course radiotherapy).
However, the article by Zakrzewska was about oral cancer. Out of 147
new cases treated by surgery, radiotherapy or combination in the same
year, a minority (27%) were treated by radiotherapy alone. Breaking this
down further, 22% of stage I and II disease and 40% of stage III and IV
disease were treated by radiotherapy alone.
The assertion that surgery only has a role to play in very small or
very advanced lesions is also not borne out by the audit results. The
majority of cases (68%) of stage II and III disease (73% of all cases)
were treated with surgery, with or without radiotherapy.
Head and neck cancer is a difficult disease to treat, and no
treatment modality should be rejected by dogma. The way forward in the
management of these cases is by assessment in multidisciplinary clinics,
with individually tailored treatment plans being formulated.
1) Zakrzewska JM. Oral Cancer. BMJ 1999; 318: 1051-4
2) South and West Head and Neck Report. Cancer Intelligence Unit, March
1999
Competing interests: No competing interests
Dear Editor
It was disappointing to read the review article on oral cancer1 and
find little emphasis on the role of alcohol limitation in the prevention
of oral cancer. Whilst the role of alcohol consumption in the aetiology of
oral cancer is complicated by several factors, most commonly the
difficulty in separating the effects of heavy consumption of alcohol from
those of smoking. There are a number of studies that support the link
between consumption of alcohol and oral cancer2,3. It is ironic that in
the same issue there was also a letter (BMJ 1999; 318: 1078) highlighting
one of the problems associated with the high alcohol levels (37%) in
mouthrinses, although the issue of alcohol in mouthrinses and oral cancer
is controversial 4,5. Further coincidence was provided in the
medicopolitical digest column highlighting the BMJ's policy statement on
alcohol and children. If the rise in young drinkers continues will this
lead to an increase in the number of oral cancers or merely lead to the
possibility of mouthrinses becoming a fashionable "designer drink" ?
Yours sincerely
Andrew Smith
Lecturer/ Hon. Specialist Registrar Microbiology.
Glasgow Dental Hospital & School, 378 Sauchiehall Street, Glasgow
References
1 Zakrzewska JM. Oral Cancer. BMJ 1999; 318: 1051-4.
2 Blot WJ, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston-Martin
S, et al. Smoking and drinking in relation to oral and pharyngeal cancer.
Cancer Res 1988; 48; 3282-7.
3 International Agency for Research on Cancer. Alcoholic beverages. Lyons:
IARC , 1989(Monograph 42.)
4 Winn DM, Blot WJ, McLaughlin JK, Austin DF, Greenberg RS, Preston-Martin
S, et al. Mouthwash use and oral conditions in the risk of oral and
pharyngeal cancer. Cancer Res 1991; 51:3044-7.
5 Elmore JG, Horwitz RI. Oral cancer and mouthwash use: evaluation of the
epidemiologic evidence. Otolaryngol Head Neck Surg 1995; 113:253-61
Competing interests: No competing interests
Madam,
Your article on oral cancer is illustrative and to the point. Tobacco
use is the major causal agent in oral cancers, although no one super-
carcinogen has been elucidated to date. Benzpyrene, long thought to play a
major role on tobacco related cancers, is a combustion product, possibly
from DDT. However, chewing and other non-combusted tobacco products are
also associated with oral cancers. Benzpyrene can play no role here.
Aflatoxin,a profound carcinogen and the protypical mutator of the p53
tumor suppressor gene, has been shown to regularly inhabit tobacco. Many
oral cancers have p53 mutations. If mutations at codon 249 in p53, the
hallmark of aflatoxin contamination, can be shown in users of non-
combusted tobacco products, a major breakthrough will have been achieved
in elucidating the causality of tobacco related carcinogenesis for all
tobacco products.
I suggest a multicenter study be undertaken to test this theory as
samples are readily available and the ramifications are significant.
Competing interests: No competing interests
Dear Sir,
I read Dr Zakrzewska's paper on oral cancer with interest.
The sections on Epidemiology and Prevention were lucid and concise, and
the clinical photographs are excellent.
In the Management section, however, I must question the following
assertions:
"Treatment for oral cancer is principally surgical. Few patients are
treated solely with radiotherapy and even fewer with chemotherapy" and
"Radiotherapy is rarely used as a primary treatment; it is used either to
debulk the tumour before surgery or to prevent recurrences and eliminate
residual tissue after an incomplete resection."
In fact, here in Canada and in most of the UK, radiotherapy is the
primary curative treatment modality for head and neck cancers, especially
those of the oral cavity, and pharynx. Surgery has a role to play in the
primary excision of very small lesions and in the combined modality
management of very advanced lesions, but these patients are in the
minority.
Nothing in the data presented, nor the references quoted, gives me
any reason to believe that her assessment of the role of radiotherapy is
an accurate one. Unfortunately, the primarily surgical view of the
management of head and neck cancer is a common one - amongst surgeons -
btu there is little or no evidence to support it.
Competing interests: No competing interests
Smoking and Oral Cancer
Dear Editor,
Tobacco consumption and excess alcohol use are the major risk factors
for cancers of the oral cavity and pharynx(1).
Tobacco dependence is recognised as a life-threatening disorder with
serious oral health consequences which responds to treatment in the form
of behavioural support and medication. While cigarette smoking is the most
hazardous and prevalent form of tobacco use in the west, consideration
also needs to be given to other forms such as bidi smoking in India,
reverse smoking by several rural populations and use of snuff and chewing
tobacco.
The evidence that the use of tobacco is the major risk factor for
oral cancer and potentially malignant lesions of the mouth is clear.
Counseling to quit smoking is not applied in a systematic or frequent
manner to people presenting with potentially malignant lesions of the oral
cavity.
Tobacco smoke contains many carcinogenic combustion products.
In developed countries, approximately 30–40% of smokers make an
attempt to stop smoking in any year. However, without formal assistance,
only about 2–3% of smokers making a quit attempt on their own, succeed in
abstaining for at least a year. Recognition of the tenacious nature of
nicotine addiction and the great difficulty most tobacco users have in
overcoming it despite interest in stopping has finally galvanised the
health care system in some countries to fund formal cessation programmes.
Recommendations for a successful intervention for tobacco users were
proposed in the US Clinical Practice Guidelines; the “5A’s” approach (Ask,
Advise, Assess, Assist, Arrange follow-up).
The first step (Ask) is to identify tobacco users by considering
tobacco use as one of the “vital signs”. It is important to ask the
patient regularly whether he or she uses tobacco and if they do, to assess
their willingness to make a serious attempt to stop. Tobacco use should be
clearly identified in the case notes to prompt clinicians to intervene now
or at a later stage.
Having asked about tobacco use, all users should be strongly advised
to stop. Clinicians need to make it clear that the goal is complete
cessation of all forms of tobacco use, and should emphasize the benefits
of quitting through personalised reference to the individuals own health
and their family situation.
The third “A” involves assessing motivation and interest in stopping
which can be done very simply by a couple of direct questions. e.g. “Do
you want to stop?” and “Are you interested in making a serious attempt in
the near future?”(3).
Sincerely
Dr. Murat Enoz
References
1- C. La Vecchia, A. Tavani, S. Franceschi, F. Levi, G. Corrao and E.
Negri, Epidemiology and prevention of oral cancer, Oral Oncol. 33 (1997),
pp. 302–312.
2- G. Shanks and D.M. Burns, Disease consequences of cigar smoking,
Smoking and tobacco control monograph 9. Cigars health effects and trends,
National Cancer Institute, Bethesda, MD (1998), pp. 105–158.
3- R. West, Assessment of tobacco dependence and motivation to stop
smoking, Br. Med. J. 328 (2004), pp. 338–339.
Competing interests:
None declared
Competing interests: No competing interests