Print this page Email this page | Users Online: 523
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
CASE REPORT
Year : 2013  |  Volume : 4  |  Issue : 1  |  Page : 35-38

Early invasive squamous cell carcinoma of the tongue


1 Department of Prosthodontics and Implantology, Bhojia Dental College, Baddi, Himachal Pradesh, India
2 Department of Oral Pathology & Microbiology, Bhojia Dental College, Baddi, Himachal Pradesh, India
3 Department of Oral Medicine and Radiology, Government Dental College, Bangalore, Karnataka, India

Date of Web Publication22-Aug-2013

Correspondence Address:
Charu Kapoor
Department of Oral Medicine and Radiology, Bhojia Dental College, Budd, Baddi, District Solan, Himachal Pradesh
India
Login to access the Email id


DOI: 10.4103/0976-433X.116830

Rights and Permissions
  Abstract 

Oral cancer is the sixth most common cancer for both sexes in the general population. Squamous cell carcinoma is defined as "a malignant epithelial neoplasm exhibiting squamous differentiation as characterized by the formation of keratin and/ or the presence of intercellular bridges" (Pindborg et al., 1977).[1] It is the most common neoplasm of the oral cavity. We present a case of oral SCC emphasizing on the invasive nature of the lesion and importance of correct biosy and histopathological examination.

Keywords: Correct diagnosis, early invasive, squamous cell carcinoma


How to cite this article:
Vaidya S, Kapoor C, Ohri N. Early invasive squamous cell carcinoma of the tongue. SRM J Res Dent Sci 2013;4:35-8

How to cite this URL:
Vaidya S, Kapoor C, Ohri N. Early invasive squamous cell carcinoma of the tongue. SRM J Res Dent Sci [serial online] 2013 [cited 2019 Jul 18];4:35-8. Available from: http://www.srmjrds.in/text.asp?2013/4/1/35/116830


  Introduction Top


Oral cancer is the sixth most common cancer for both sexes in the general population. Squamous cell carcinoma is defined as "a malignant epithelial neoplasm exhibiting squamous differentiation as characterized by the formation of keratin and/ or the presence of intercellular bridges" (Pindborg et al., 1977). [1] It is the most common neoplasm of the oral cavity. Although it may occur at any intraoral site, certain sites are more frequently involved than others. The lateral border, the ventral surface of the tongue and the lips are the most commonly affected areas, followed by floor of the mouth, the gingiva, the alveolar mucosa and the palate. [2] Oral squamous cell carcinoma (OSCC) occurs more frequently in men than in women and usually around 60 years of age. [3] Clinically, almost all oral cancers, except those in the earliest stages have two very characteristic features in the form of ulceration and an indurated margin.


  Case Report Top


A 32-year-old male patient reported to the department of Oral and Maxillofacial Pathology, with the complaint of ulcer on the right side of the tongue associated with pain. The history of present illness dates back to 1 year when the patient noticed ulceration with reference to the right side of tongue. Patient went to the dentist and underwent biopsy twice in 1 year duration which was diagnosed as epithelial hyperplasia and had a habit of Gutkha chewing, 1-2 packets for last 10 years.

On intraoral examination, an ulcerative growth was seen with reference to the right lateral border of tongue, measuring 1 cm × 1 cm × 1 cm in dimensions, irregular in shape with indurated and raised margins [Figure 1].
Figure 1: Intraoral view showing an ulcer on the lateral border of tongue

Click here to view


A provisional diagnosis of squamous cell carcinoma, verrucous carcinoma with clinical staging of T1N0M0 was given (based on the size of the lesion, lymphadenopathy). An incisional biopsy was performed. Lesional tissue measuring 6 mm × 2 mm, irregular in shape, creamish white in color was sent for the microscopic examination.

Microscopic examination showed [Figure 2] hyperplastic stratified squamous epithelium with its basal end proliferating and pushing downward as large islands [Figure 3]. A part of these large islands showed cellular and nuclear pleomorphism with enlarged hyperchromatic nuclei. The epithelium around these areas was showing loss of cohesiveness and nucleoli count was abnormal, some showing 6-7 nucleoli. The connective tissue was very minimal in the given section. The features were suggestive of Severe Epithelial Dysplasia.
Figure 2: H and E ×10 showing hyperplastic epithelium with bulbous rete ridges

Click here to view
Figure 3: H and E ×40 view showing nuclear pleomorphism with enlarged hyperchromatic nuclei

Click here to view


Based on the histopathological findings, the patient underwent excisional biopsy. A margin of 6 mm normal tissue was included in the surgery. The specimen measuring 1.5 cm × 1.5 cm, irregular in shape, with white superior surface and brownish inferior surface was received from the excisional biopsy [Figure 4].
Figure 4: A single soft tissue specimen measuring 1.5 cm × 1.5 cm irregular in shape, white superior surface and brownish inferior surface received after excisional biopsy

Click here to view


The histopathology of the excised specimen showed epithelial cells arranged in the form of islands and sheets in the connective tissue stroma. Epithelial cells were showing dysplastic features such as cellular and nuclear pleomorphism, increase in the number of nucleoli and prominent nucleoli. The formation of small and large keratin pearls was also evident within the epithelial islands [Figure 5]. Numerous engorged feeder ducts were seen in the stroma and also a dense chronic inflammatory cell infiltrate was seen. Invasion was seen up to the muscle tissue.
Figure 5: H and E ×10 view showing epithelial islands and keratin pearls, invasion in the form of epithelial strands dense chronic inflammatory cell infiltrate is seen

Click here to view


The margin of the tumor showed certain dysplastic features, such as increase in number of nucleoli and prominent nucleoli. Tumor free margin was evident at three high power fields from the site of invasion.

Immunohistochemistry was performed with monoclonal p53 [Figure 6]. Peripheral Island of tumor cells was positive for p53 and showed mild to moderate staining intensity.
Figure 6: Tumor cells showing mild to moderate p53 intensity ×10

Click here to view


The diagnosis of early invasive squamous cell carcinoma of the Tongue with margins free from invasion was given.


  Discussion Top


Squamous cell carcinoma represents about 90% of oral cancers and accounts for 3-5% of all cancers. Incidence of tongue cancer in India is second highest in the world. [4] About half of the patients afflicted die within 5 years of diagnosis while surviving patients may be left with the severe esthetic and/or functional compromise. [5]

OSCC generally occurs in elderly men during the fifth to eighth decades of life. The incidence of OSCC in young adults accounts for 0.4-3.6% of all cases of this disease. [2] The risk of intraoral cancer increases with increasing age with a male preponderance. Our case was seen in younger age group.

The most common site of intraoral carcinoma involvement is the tongue, usually the postero lateral and ventral surfaces. [6] In our patient, the site of involvement was similar. The lateral borders and base of the tongue are the most "cancer-prone" areas and along with the floor of the mouth, make up the common intraoral sites for cancer in most populations. It has been suggested that this site predilection for intraoral cancer is due to the pooling of carcinogens in saliva in these food channels and reservoirs [1] or "gutter zones." [2],[3] This theory has been referred to as Lederman's hypothesis. [2]

The cause of OSSC is believed to be multifactorial. Extrinsic factors implicated are tobacco smoke, alcohol, syphilis, poor oral hygiene and sunlight (vermilion cancers only). Intrinsic factors include systemic or generalized disorders such as malnutrition, general resistance and iron-deficiency anemia. [6] In our case, we observed a history of tobacco intake and constant trauma from the adjacent teeth as the main etiological factors. In a study by Gibbel, around 4.8% of the lingual carcinomas occurred in juxtaposition to ill-fitting dentures, carious teeth, thus stressing the role of trauma as a risk factor, [7] but any recent study does not support such hypothesis.

Tobacco and alcohol are the two most important known risk factors for the development of oral cancer. In the present case also, the patient was a habitual Gutkha chewer.

The risk of OSCC from long-term Shiga like toxin use is elevated for some products, and much of this risk has been attributed to the presence of Tobacco specific Nitrosamines (TSNAs). There are four principal compounds: N-nitrosonornicotine (NNN), 4-methyl-N-nitrosamino-1-(3-pyridyl)-1-butanone (NNK), N-nitrosoanatabine, and N-nitrosoanabasine. Only two TSNAs, NNN and NNK, are considered to be potential carcinogens. [8] Continuous local irritation by pan masala, Gutkha or areca nut can lead to injury-related chronic inflammation, oxidative stress and cytokine production. Oxidative stress and subsequent reactive oxygen specimen (ROS) generation can induce cell proliferation, cell senescence or apoptosis, depending upon the level of ROS production. During the chronic exposure, these events can lead to preneoplastic lesions in the oral cavity and subsequently to malignancy. [9]

Family history of head and neck cancer can be attributed as another risk factor for oral cancer. It has been suggested that the ability to repair deoxyribonucleic acid damaged by tobacco carcinogens, such as benzo-(a)-pyrene diol epoxide, is defective in some patients with the head and neck cancer. Some patients might show an increased susceptibility to chromosome damage by mutagens. [10]

Viruses, most notably the human papillomavirus (HPV), have also long been linked to oral carcinogenesis. Previous studies have reported the presence of HPV types 16 and 18 in oropharyngeal cancers. These viral types produce oncogenic proteins (E6 and E7) that disrupt p53 and pRb function, respectively and thereby promoting cellular immortalization. [11]

Oral carcinogenesis is considered to be a multistep process in which genetic events lead to the disruption of the normal regulatory pathways that control basic cellular functions including cell division, differentiation, and cell death. [12] Several oncogenes have been implicated in oral carcinogenesis. Aberrant expression of the proto-oncogene epidermal growth factor receptor, members of the ras gene family, c-myc, int-2, hst-1, PRAD-1, contributes toward cancer development. [12] Cell adhesion molecules such as E-Cadherin, P-Cadherin and matrix metalloprotienases are involved in tumor metastasis.

Tumor suppressor genes such as Rb gene, p53, NF1gene, NF 2 gene play an important role in carcinogenesis. p53 gene is located on the short arm (P) of chromosome 17. p53 over-expression is a common finding in oral cancer with mutation observed in over one half of cases. This mutation is often observed as an apparent overexpression of the gene since immunocytochemical staining can detect p53 readily in many oral cancers, but not in normal tissues. In several studies, the p53 immunoexpression ranged from as high as 76.8% to as low as 36%. No specific correlation has been noted with respect to age, sex and site. In our case, tumor cells in the periphery of the islands showed mild to moderate intensity with p53 staining. [13]

Lymph node metastasis occurs with greater frequency in the tongue. [1] The entire cervical chain of nodes may eventually become involved. [7] Cervical lymph node metastasis was found in 35.6% of T1 and T2 tumors and 62.35% of T3 and T4 tumors. [14] In addition to cervical lymphnode metastasis, distant metastasis is seen in 14.5% of cases. [7]

The prognosis for OSCC depends in large measure, on the site involved, the clinical stage at the time of diagnosis, the width of the tumor at its greatest diameter, patient's access to adequate health-care and patient's ability to cope and mount an immunologic response. The lesion was initially diagnosed by previous physicians as an epithelial hyperplasia but was confirmed as OSCC on histopathologic evaluation. Early lesions are often asyptomatic and slow growing. An early diagnosis would lead to better prognosis.


  Conclusion Top


Our case was previously misdiagnosed as epithelial hyperplasia, which was probably due to choosing incorrect site for biopsy, thus in case of small ulcers like these, proper care should be given to select the representative site for biopsy. In young patients with OSCC, the search for predisposing factors should assign greater weight to familial antecedents of malignant neoplasm. This is important to save time and ensure early treatment, which improves the prognosis in especially younger patient like in the present case.

 
  References Top

1.Shafer WG, Hine MK, Levy BM. Textbook of Oral Pathology. 4 th ed. Philadelphia:Saunders; 1983.  Back to cited text no. 1
    
2.Moore SR, Johnson NW, Pierce AM, Wilson DF. The epidemiology of tongue cancer: A review of global incidence. Oral Dis 2000;6:75-84.  Back to cited text no. 2
[PUBMED]    
3.Hirota SK, Braga FP, Penha SS, Sugaya NN, Migliari DA. Risk factors for oral squamous cell carcinoma in young and older Brazilian patients: A comparative analysis. Med Oral Patol Oral Cir Bucal 2008;13:E227-31.  Back to cited text no. 3
[PUBMED]    
4.Murthy NS, Mathew A. Cancer epidemiology, prevention and control. Curr Sci 2004;86:518-527.  Back to cited text no. 4
    
5.Wong DT, Todd R, Tsuji T, Donoff RB. Molecular biology of human oral cancer. Crit Rev Oral Biol Med 1996;7:319-28.  Back to cited text no. 5
[PUBMED]    
6.Orbak R, Recep Orbaka, Cigdem Bayraktara, Fahri Kavruta, Cemal Gündogdub et al. Poor oral hygiene and dental trauma as the precipitating factors of squamous cell carcinoma. Oral Oncol Extra 2005;41:109-13.  Back to cited text no. 6
    
7.Gibbel MI, Cross JH, Ariel IM. Cancer of the tongue; A review of 330 cases. Cancer 1949;2:411-23.  Back to cited text no. 7
[PUBMED]    
8.Rodu B, Jansson C. Smokeless tobacco and oral cancer: A review of the risks and determinants. Crit Rev Oral Biol Med 2004;15:252-63.  Back to cited text no. 8
[PUBMED]    
9.Nair U, Bartsch H, Nair J. Alert for an epidemic of oral cancer due to use of the betel quid substitutes gutkha and pan masala: A review of agents and causative mechanisms. Mutagenesis 2004;19:251-62.  Back to cited text no. 9
[PUBMED]    
10.Mehrotra R, Yadav S. Oral squamous cell carcinoma: Etiology, pathogenesis and prognostic value of genomic alterations. Indian J Cancer 2006;43:60-6.  Back to cited text no. 10
[PUBMED]  Medknow Journal  
11.Ringström E, Peters E, Hasegawa M, Posner M, Liu M, Kelsey KT. Human papillomavirus type 16 and squamous cell carcinoma of the head and neck. Clin Cancer Res 2002;8:3187-92.  Back to cited text no. 11
    
12.Williams HK. Molecular pathogenesis of oral squamous carcinoma. Mol Pathol 2000;53:165-72.  Back to cited text no. 12
[PUBMED]    
13.Nylander K, Dabelsteen E, Hall PA. The p53 molecule and its prognostic role in squamous cell carcinomas of the head and neck. J Oral Pathol Med 2000;29:413-25.  Back to cited text no. 13
[PUBMED]    
14.Nithya C, Pandey M, Naik B, Ahamed IM. Patterns of cervical metastasis from carcinoma of the oral tongue. World J Surg Oncol 2003;1:10.  Back to cited text no. 14
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Case Report
Discussion
Conclusion
References
Article Figures

 Article Access Statistics
    Viewed8002    
    Printed31    
    Emailed0    
    PDF Downloaded285    
    Comments [Add]    

Recommend this journal