Sie sind auf Seite 1von 3

This article appeared in a journal published by Elsevier.

The attached
copy is furnished to the author for internal non-commercial research
and education use, including for instruction at the authors institution
and sharing with colleagues.
Other uses, including reproduction and distribution, or selling or
licensing copies, or posting to personal, institutional or third party
websites are prohibited.
In most cases authors are permitted to post their version of the
article (e.g. in Word or Tex form) to their personal website or
institutional repository. Authors requiring further information
regarding Elsevier’s archiving and manuscript policies are
encouraged to visit:
http://www.elsevier.com/copyright
Author's personal copy

Oral Oncology 47 (2011) 920–921

Contents lists available at ScienceDirect

Oral Oncology
journal homepage: www.elsevier.com/locate/oraloncology

Letter to the Editor

A new classification for potentially malignant disorders of the IIb: Chronic inflammation caused by external factors.
oral cavity
1. Chronic mucosal trauma10
2. Lichenoid reactions11
Potentially malignant disorders (PMD) of oral cavity were classi-
3. Poor oral hygiene12
fied as ‘lesions’ and ‘conditions’ by WHO in 1978.1 It was considered
4. Chronic infections13,14
that in ‘lesions’, the cancer would correspond with the site of PMD.
 Chronic bacterial infections
On the other hand, in ‘conditions’, cancer may arise in any anatom-
 Chronic viral infections
ical site of the oral cavity. It is now known that even the clinically
 Chronic fungal infections
‘normal’ appearing mucosa in patients harboring a precancerous le-
5. Other pathologies associated with prolonged untreated
sion may have dysplasia on the contralateral anatomic site2 or
chronic inflammation of the oral cavity.
molecular aberrations in other oral mucosal sites suggestive of a
pathway to malignant transformation, and that cancer could subse-
Group III: Inherited disorders that do not necessarily alter the
quently arise in apparently normal tissue.3 Hence, the current
clinical appearance of local tissue but are associated with a
Working Group (WHO) does not favor such subdivisions and refers
greater than normal risk of PMD or malignant transformation.
to all the clinical presentations that carry the risk of oral squamous
cell carcinoma (OSCC) as ‘potentially malignant disorders’.4
1. Inherited cancer syndromes15
The present paper attempts to suggest a new classification sys-
 Xeroderma pigmentosum
tem for PMDs which is based on authors’ opinions. All the disor-
 Ataxia telangiectasia
ders included either carry some risk and/or predispose the oral
 Bloom syndrome
mucosa to OSCC development.
 Fanconi’s anemia
 Li Fraumeni syndrome
Group I: Morphologically altered tissue in which external factor
is responsible for the etiology and malignant transformation.
2. Dyskeratosis congenita
3. Epidermolysis bullosa
4. White sponge nevus
1. Habit related
5. Darier’s disease
a. Tobacco associated lesions
6. Hailey–Hailey disease
 Leukoplakia
 Tobacco pouch keratosis
 Stomatitis palatine nicotini Group IV: No clinically evident lesion but oral cavity is
susceptible to OSCC.
b. Betel nut associated
1. Immunosupression
 Oral submucous fibrosis  AIDS16
c. Sanguinaria-associated keratosis  Immunosupression therapy (for malignancy or organ
transplant)
2. Non-habit related 2. Alcohol consumption and abuse
 Actinic cheilosis 3. Nutritional deficiency17,18
 Chronic candidiasis⁄  Sideropenic dysphagia

Certain strains of Candida have been shown to produce nitros-  Deficiency of micronutrients
amines, a chemical carcinogen (external factor) and hence, candi-
diasis is included under Group I.5 The proposed classification is based on pathogenesis and also
has therapeutic basis to some extent. Group I disorders are treated
Group II: Morphologically altered tissue in which chronic by discontinuation of the habit (except for candidiasis and actinic
inflammation is responsible for malignant transformation keratosis). Group IIa comprises immunologically mediated disor-
(chronic inflammation mediated carcinogenesis).7–9 ders and requires treatment that will modify the immune system.
Group IIb disorders require mainly anti-inflammatory and anti-
IIa. Chronic inflammation caused by internal derangement. microbial therapy (for infections), along with removal of etiologi-
1. Lichen planus6 cal factor (for chronic mucosal trauma and lichenoid reaction).
2. Discoid lupus erythematosus Group III comprises inherited cancer syndromes and other hered-
itary disorders which probably will be treated by gene therapy in

1368-8375/$ - see front matter Ó 2011 Elsevier Ltd. All rights reserved.
doi:10.1016/j.oraloncology.2011.06.005
Author's personal copy

Letter to the Editor / Oral Oncology 47 (2011) 920–921 921

future. In Group IV, immunosupression is inevitable and hence 16. Flaitz CM, Nichols CM, Adler-Storthz K, Hicks MJ. Intraoral squamous cell
other factors associated with the etiology of oral cancer should carcinoma in human immunodeficiency virus infection: a clinicopathologic
study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;80:55–62.
be controlled (except for alcohol abuse and nutritional deficiency). 17. De Stefani E, Ronco A, Mendilaharsu M, Deneo-Pellegrini H. Diet and risk of
The classification is based on the authors’ opinions with the cancer of the upper aerodigestive tract-I. Foods. Oral Oncol 1999;35:17–21.
hope of further suggestions from readers. 18. De Stefani E, Ronco A, Mendilaharsu M, Deneo-Pellegrini H. Diet and risk of
cancer of the upper aerodigestive tract-II. Nutrients. Oral Oncol 1999;35:22–6.
References
Sachin C. Sarode
1. World Health Organization. Report of a meeting of investigators on the Department of Oral Pathology and Microbiology,
histological definition of precancerous lesions. Geneva: World Health Dr. D.Y. Patil Dental College and Hospital,
Organization, 1973, Can/731. Maheshnagar, Pimpri, Pune 411018,
2. Thompson PJ. Field change and oral cancer: new evidence for widespread
carcinogenesis? Int J Oral Maxillofac Surg 2002;31:262–6.
Maharashtra, India
3. Bremmer JF, Braakhuis BJM, Ruijter-Schippers HJ, et al. A noninvasive genetic Tel.: +91 9922491465/9823871462
screening test to detect oral preneoplastic lesions. Lab Invest 2005;85:1481–8. E-mail address: drsachinsarode@gmail.com
4. Warnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and
classification of potentially malignant disorders of the oral mucosa. J Oral Gargi S. Sarode
Pathol Med 2007;36:575–80. Department of Oral Pathology and Microbiology,
5. O’Grady JF, Reade PC. Candida albicans as a promoter of oral mucosal neoplasia. Dr. D.Y. Patil Dental College and Hospital,
Carcinogenesis 1992;13:783–6.
Maheshnagar, Pimpri, Pune 411018,
6. Mignogna MD, Fedele S, Lo Russo L, Lo Muzio L, Bucci E. Immune activation and
chronic inflammation as the cause of malignancy in oral lichen planus: is there
Maharashtra, India
any evidence ? Oral Oncol 2004;40:120–30. Tel.: +91 9823871462
7. Kawanishi S, Hiraku Y, Pinlaor S, Ma N. Oxidative and nitrative DNA damage in E-mail address: gargi14@gmail.com
animals and patients with inflammatory disease in relation to inflammation-
related carcinogenesis. Biol Chem 2006;387:365–72. Swarada Karmarkar
8. Kundu JK, Surh YJ. Inflammation: gearing the journey to cancer. Mutat Res Department of Oral Pathology and Microbiology,
2008;659:15–30. Dr. D.Y. Patil Dental College and Hospital,
9. Keibel A, Singh V, Sharma MC. Inflammation, microenvironment, and the
Maheshnagar, Pimpri,
immune system in cancer progression. Curr Pharm Des 2009;15:1949–55.
10. Piemonte ED, Lazos JP, Brunotto M. Relationship between chronic trauma of the Pune 411018, India
oral mucosa, oral potentially malignant disorders and oral cancer. J Oral Pathol Tel.: +91 9890048796
Med 2010;39:513–7. E-mail address: dr.swarada86@gmail.com
11. van der Meij EH, Mast H, van der Waal I. The possible premalignant character of
oral lichen planus and oral lichenoid lesions: a prospective 5 year follow-up Jagdish V. Tupkari
study of 192 patients. Oral Oncol 2007;43:742–8. Department of Oral Pathology and Microbiology,
12. Bloching M, Reich W, Schubert J, Grummt T, Sandner A. The influence of oral Government Dental College and Hospital,
hygiene on salivary quality in the Ames test, as a marker for genotoxic effects.
Mumbai,
Oral Oncol 2007;43:933–9.
13. Hooper SJ, Wilson MJ, Crean SJ. Exploring the link between microorganisms and Maharashtra, India
oral cancer: a systematic review of the literature. Head Neck 2009;31:1228–39. Tel.: +91 9820241603
14. Kuper H, Adami HO, Trichopoulos D. Infections as a major preventable cause of E-mail address: jvtupkari@gmail.com
human cancer. J Intern Med 2000;248:171–83.
15. Prime SS, Thakker NS, Pring M, Guest PG, Paterson IC. A review of inherited
cancer syndromes and their relevance to oral squamous cell carcinoma. Oral
Available online 28 June 2011
Oncol 2001;37:1–16.

Das könnte Ihnen auch gefallen