COM Nov. 2007 Diagnosis

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In 1985, Hanson et al coined the term proliferative verrucous leukoplakia (PVL) to describe a type of oral leukoplakia that was relentless in its persistence, recurrences and potential transformation to verrucous carcinoma and squamous cell carcinoma (SCC) (1). Most of the 30 cases reported in Hanson’s study presented as flat white patches and progressed to verrucous leukoplakia. Twenty four of the 30 patients were females, mostly over 60 years of age, with a few patients in their thirties. Eighteen out of 30 patients had used tobacco in their lifetime, though ten had never used tobacco; twelve had superficial candidiasis. This disease was not caused by a specific etiology, which made treatment, control of the progression, and prediction of behavior difficult. Since then, many more reports have emerged, some suggesting new etiology such as human papilloma virus types 16 and 18. The clinical profile, however, did not change: this lesion is far more common in females, especially older females. PVL is a progressive disease, usually presenting as benign hyperkeratosis and progressing to squamous cell carcinoma within five to a ten-year period. Gingiva and palate are the most common locations for PVL-related SCC, where 80% of cases occur, followed by the buccal mucosa, tongue and floor of mouth. Treatment includes scalpel surgery, laser surgery, radiation, chemotherapy, Vitamin A derivatives therapy, surgery combined with antiviral systemic medications and other combination therapies have been tried, some with success. Most commonly used therapies include scalpel and laser surgery. Verrucous carcinomas and SCC arising in PVL are treated more aggressively and according to the stage of the disease. PVL can be a very aggressive and persistent disease, some lasting for 20 years and others dying of the disease. The original study by Hanson demonstrated 13 out of 30 patients died of the disease and 14 out of 30 alive with the disease—rendering it very aggressive in behavior. Other reports however present a less aggressive picture for example Bagan et al (2-3) had a much lower mortality rate in their multiple oral SCC patients—where one of seven died of the disease over an average of about six years with a TNM stage two. The current less aggressive behavior may be interpreted to be the result of more awareness of the disease. Given the persistent nature of this disease, close follow-up visits of at least six month duration and even closer in the more aggressive behaving lesions are recommended. We also recommend removal of all the white lesions using the conventional or laser surgery. The histology may represent a stage of PVL but the disappearance of most of the disease upon tobacco cessation is not supportive of PVL.

Nicotinic stomatitis, also known as “smoker’s palate,” or stomatitis nicotina is caused by the heat and chemicals generated by smoked tobacco. Heat is suggested to play a significant role in the production of this lesion. It is a condition that is virtually only presents in heavy tobacco users especially in heavy pipe and cigar smokers and progressively more in heavy cigarette smokers. The palatal clinical changes in this population tend to be benign. However the nicotinic stomatitis changes described in reverse smokers has the potential for malignant transformation. Reverse smoking is rare in the United States but is practiced in countries such as the Philippines, Latin America, the Caribbean countries and India (5). Cigarettes are usually homemade and are short and the lighted part is held inside the mouth with the lips closed. The heat generated by this process is believed to be stronger than that generated by the conventional pipe and cigar/cigarette smoking. It is suggested that heat when combined with the tobacco carcinogens plays a significant factor in leading to cell transformation (4-5). 

Clinically, in conventional heavy smokers, NS presents as a diffuse white plaque involving the middle hard palate (usually behind the palatal rugae and involving the palatal marginal gingiva and intradental papilla. The depth of the white color and consistency varies depending on the thickness of the keratin layer. The latter can be so thick that it would give a fissured appearance. The white palate is uniformly interspersed with red spots representing dilated minor salivary gland ducts. Occasionally saliva can be seen oozing from the dilated ducts. 

The palatal epithelial changes in reverse smokers should be viewed with some caution since these patients are at a higher risk for epithelial dysplasia and squamous cell carcinoma of the palate than the conventional cigarette smokers (4-5). The clinical changes can be similar to those of the conventional heavy smokers in that the hard palate mainly and hard and soft palate occasionally would demonstrate a variety of lesions including the presence of thick white or yellow patches to thick patches with fissures. The lesions may also present as red patches or non-healing ulcers. Frequently these lesions are associated with brown pigmentation. In India, the frequency of reverse smoking was 6.23 times higher in females than in males. This study also showed that palatal lesions including nicotinic stomatitis was 7.13 times higher in reverse smokers than in regular smokers (5).

Nicotinic stomatitis in the conventional smokers is usually benign in that the mucosa shows evidence of hyperkeratosis and acanthosis with connective tissue fibrosis and chronic inflammation. The salivary gland ducts usually show evidence of ductal ectasia, epithelial metaplasia and hyperplasia. Treatment therefore should include smoking cessation, the palatal changes regress within a few weeks of tobacco cessation. More importantly, the patient posterior areas such as the retromolar pad areas, oro and nasopharyngeal areas as well as the “high-risk” locations, i.e. ventral-lateral tongue, floor of mouth, lips (where the pipe and cigarette is held) and soft palate areas should be evaluated for epithelial neoplastic changes.

Nicotinic stomatitis in reverse smokers (and in this case smoker’s keratosis), since the typical clinical features of NS were not completely met can be benign, premalignant or malignant (4-5). The histology would include benign hyperkeratosis and acanthosis to hyperkeratosis accompanied with graded epithelial dysplasia or invasive squamous cell carcinoma. The salivary gland ducts would show evidence of ductal ectasia, epithelial metaplasia, hyperplasia and may be even dysplasia depending on the overlying epithelial changes. Treatment depends on the histology and may range from tobacco cessation and close observation for the benign cases to surgical removal with clean margins for the graded epithelial dysplasia cases to a more radical treatment for the invasive squamous cell carcinoma cases.

Treatment

Under local anesthesia, both plaques were surgically removed. The patient was advised to continue the tobacco cessation. 

References

1. Hansen LS, Olson JA et al. Proliferative verrucous leukoplakia. A long-term study of thirty patients. Oral. Surg. Oral. Med. Oral. Pathol. 1985; 60: 285-298.
2. Bagan JV, Jimenez Y et al. Proliferative verrucous leukoplakia: high incidence of gingival squamous cell carcinoma. J. Oral. Pathol. Med. 2003; 32: 379–382.
3. Bagán JV, Murillo J, et al. Proliferative verrucous leukoplakia: unusual locations of oral squamous cell carcinomas, and field cancerization as shown by the appearance of multiple OSCCs. Oral Oncol 2004; 40: 440-443.
4. Ramulu C, Raju MV, VenkatarathnamG, Reddy CR. Nicotine stomatitis and its relation to carcinoma of the hard palate in reverse smokers of chuttas. J Dent Res. 1973 Jul-Aug;52(4):711-8.
5. Gavarasana S, Susarla MD. Palatal mucosal changes among reverse smokers in an Indian village. Jpn J Cancer Res. 1989 Mar;80(3):209-11.
6. Spiro RH. Verrucous carcinoma, then and now. Am J Surg. 1998 Nov;176(5):393-7.
7. R.V. Kolbusz and L.H. Goldberg, Verrucous carcinoma of the oral cavity, Int J Dermatol 33 (1994), pp. 618–622.
8. Miller CS, White DK. Human papillomavirus expression in oral mucosa, premalignant conditions, and squamous cell carcinoma: a retrospective review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Jul;82(1):57-68. Review.
9. Warshaw EM, Templeton SF, Washington CV. Verrucous carcinoma occurring in a lesion of oral lichen planus. Cutis. 2000 65(4):219-22.
10. Sherman RG, Oral candidosis. Quintessence Int. 2002; 33(7):521-32.
11. Lynch DP. Oral candidiasis. Oral Surg Oral Med Oral Pathol. 1994 Aug;78(2):189-93.

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Verrucous carcinoma is a rare low-grade malignant neoplasm of the surface epithelium that was first reported by Ackerman to affect the oral cavity. It was subsequently described in the larynx, esophagus, nasal fossae, vagina and rectum. It is not common representing 1-10% of oral epithelial malignant neoplasms (6). It is generally a slow growing, exophytic and warty in appearance, non-metastasizing, superficially invasive and laterally spreading neoplasm that responds well to thorough local excision.

It affects males, 60-70 years of age. It is most commonly occur on the buccal mucosa, gingiva and alveolar ridge and occasionally, it involves the palate and floor of mouth. It presents as sessile, papillary or rough surfaced, grayish-white in color with sharply demarcated margins. It grows laterally rather than vertically. If it involves the alveolar ridge, it extends into the periosteum and slowly destroys the underlying bone but in a shallow depth within one mm or so of depth of the periosteum (7-8). Sometimes palpable lymph nodes are noted but they represent inflammation and not tumor metastasis. The etiology of oral verrucous carcinoma is strongly associated with the use of chewing tobacco, snuff dipping, and heavy cigarette smoking. Ackerman noted in his seminal report that more than one-third of the patients in the study with verrucous carcinoma used chewing tobacco; since then, many more studies have confirmed this connection.(6) In India, where the prevalence of verrucous carcinoma is comparatively high, the chewing of pan is another important etiological factor (7). Numerous types of Human Papilloma Viruses (HPV) have also been implicated in both the oral and the extraoral forms of the disease. Although HPV tends to be found more often in non-oral verrucous carcinoma, a literature review in 1996 indicated that HPV is typically found in 27% of cases of oral verrucous carcinoma. (6) A 2000 study further suggested that chronic inflammation, as in lichen planus (9), may play a role in the etiology of this disease. (7). Histologically, it is made up of papillary and proliferative surface epithelium with hyperparakeratosis and keratin plugging and downward growth of bulbous rete pegs with sparse mitosis. Pleomorphism and other malignant changes are absent. Inflammatory infiltrate may or may not be present. Surgery is the treatment of choice. Radiation has been used with some success. However, radiation is reported in some instances to cause anaplastic transformation of this low-grade malignancy and for that reason, some suggest against using it as a treatment modality. Chemotherapy has been used in combination with surgery. 

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Oral candidiasis is a common opportunistic infection of the mouth and is the most common human fungal infection. It is most common in the elderly population who wear full upper and lower dentures 24 hours a day and do not pay close attention to hygiene. Candida albicans is the most common type affecting the mouth (10). Candida albicans is normally found in the oral cavity of human of all ages; it is present in the mouth of 50-65% of the healthy adult population. Given the fact that it is one of the most common opportunistic diseases, it is especially important to rule out systemic diseases such as diabetes mellitus and compromised immune system. Oral candidiasis represents an overgrowth of a yeast-like fungus. It most commonly occurs in immune-compromised patients especially AIDS, chemotherapy and cancer metastasis patients. Two types are described and these are acute and chronic candidiasis with further classification into acute pseudomembranous, acute atrophic, chronic hyperplastic and chronic atrophic candidiasis. 

This case would best fit the chronic hyperplastic candidiasis given the thick white plaques that did not wipe off. Chronic hyperplastic candidiasis characteristically presents in heavy smokers as firm, white, persistent plaque on the tongue and buccal mucosa (11). This patient qualifies for heavy smoker but the lesions were only present on the hard palate, an unusual location for chronic hyperplastic candidiasis. Neither the histology nor the clinical presentation support the diagnosis of chronic hyperplastic candidiasis.