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Home , Actinic cheilitis, Cheilitis, Oral submucous fibrosis

Tobacco induced oral keratosis. Oral sub-mucous . Nicotine . . Actinic Assoc. prof. Zornitsa Mihaylova, DDS, PhD Dept. of Dental, oral and maxillofacial surgery, Faculty of Dental medicine, Medical Universtity- Sofia

Precancerous are morphologically altered tissues that possess greater than normal tissues risk of malignant transformation. The term “potentially malignant disorders” (PMD) is broadly accepted in order to avoid terminological confusion. In significant number of cases the is preceded by a premalignancy. On the other hand PMD may not undergo malignant transformation (especially when the bad habits are ceased and proper treatment with long-term follow up have been conducted). The following risk factors may play a significant role in the development of PMD and cancer: tobacco smoking, smokeless tobacco, betel quid, alcohol consumption (the combination of smoking and alcohol significantly increases the risk of malignant transformation), oral HPV , radiation, vitamin deficiency, bacterial , immunosuppression and immunodeficiency, drugs, poor , chronic trauma. It is well established that the effects of the etiologic factors may vary depending on the geographic region, the lifestyle and the habits of the population.

Tobacco induced oral keratosis

There are three types of smokeless tobacco: dry snuff, moist snuff and chewing tobacco. Smokeless tobacco is mainly used by young males. The long-term/chronic smokeless tobacco use causes local alterations of the oral structures due to the significant nicotine absorption. Some of the most common oral changes related to smokeless tobacco are lesions, periodontal and dental caries.

Clinically asymptomatic white lesions of the oral mucosa are identified. The most common location of the lesions is the mucobuccal fold at the level of the mandibular incisors and molars. These are the most common sites for hronic tobacco placement. The mucosal surface in tobacco induced keratosis appears granular or wrinkled. The lesions might also be described as

gray-white fissured plaques, non-well defined (indistinct borders) and soft to velvet, painless on palpation. The lesions do not cause particular symptoms and are usually identified on a routine examination of the teeth and the oral cavity. Rarely thickening might be seen after long term tobacco application. The periodontal tissues might also be severely damaged, as in advanced cases gingival recessions and alveolar bone loss are found.

Histopathology: and acanthosis, epithelial vacuolization or , as well as inflammatory cells are seen. Epithelial dysplasia is not a common finding. However, mild dysplasia might be identified in long-term smokeless tobacco users.

The severity of the tobacco induced keratosis is strongly related to the duration and the number of the sites of tobacco placement, as well as the amount of the tobacco daily used. The lesions are associated with low risk of malignant transformation. is needed only when thickening, induration, verruciform surface appearance or ulceration are identified. The lesions may transform into oral verrucous or .

The treatment consists of smokeless tobacco use discontinuation and long term monitoring. Normal mucosal appearance is achieved nearly 2 weeks after the cessation of the habit. Lesions persistence requires biopsy and further treatment depending on the histopathological findings.

Oral sub-mucous fibrosis

Oral submucous fibrosis is a chronic PMD appearing with progressive scarring of the connective tissue. Multiple causative factors are thought to be associated with , as most likely the etiology is linked to the chewing of betel quid ( wrapped by betel leaves). This is commonly found in the young adults. The pathogenesis is strongly related to impaired collagen metabolism appearing with excessive collagen maturation, as well as intensive fibroblast proliferation.

The early symptoms of oral submucous fibrosis are burning sensation (stomatopyrosis) of the oral mucosa with intolerance to spicy food. Other early signs identified in the initial stage are dry mouth (), petechiae and vesicles. Afterwards, progressive fibrosis and mucosal

stiffness are found. The most commonly affected sites are the labial, buccal mucosa, retromolar space and the soft (the regions where the submucosal connective tissue is at a higher amount). The tongue may also suffer and it might be clinically presented as diminished and atrophic. The fibrosis progression leads to significant restriction in the lower jaw movements.

Histopathology: submucosal connective tissue fibrosis, inflammatory cells, hyperkeratosis, epithelial and minor salivary glands . Epithelial dysplasia might be seen.

Treatment consists of the following procedures and modalities: intralesional application of corticosteroids, physiotherapy (consists of physical exercises and application of mouth opening devices), surgical management (it consists of excision and splitting). Other medication have also been suggested including vitamins, pentoxifylline, hyaluronidase, collagenase, beta- carotene, etc.

The oral submucous fibrosis does not regress even when the habit is ceased and relapse is a common finding. There is a risk of malignant transformation towards oral squamous cell carcinoma.

Nicotine stomatitis

The smoked tobacco is known to be a chief causative factor for abnormal oral cavity pH, dry mouth, increased temperature of the mouth, decreased resistance to bacterial and fungal infections. Excessive smoked tobacco may induce the development of nicotine stomatitis. It mainly affects older males.

The hard palate is the site usually affected. The clinical features at the initial stage of nicotine stomatitis consist of mucosal followed by hyperkeratosis (the mucosa becomes gray-white). Subsequently with globular shape having a red spot in the central aspect and with a size of 1-2 mm are observed. The papules cannot be scraped off and represent minor and the red center corresponds to the ductal opening (orifice).

Histopathology: hyperkeratosis and acanthosis, connective tissue , squamous dysplasia of the minor salivary gland ducts.

The treatment consists of smoking cessation and clean oral cavity maintenance.

Actinic keratosis (solar keratosis)

Long term UV light exposure is known to cause mutations in tumor suppressor genes and is a chief causative factor for precancerous and cancerous of the exposed non-protected skin regions. Actinic keratosis is a cutaneous PMD and is a PMD observed on the lower , both found in patients with history of chronic UV light exposure (outdoor workers).

Actinic keratosis is seen in the skin regions directly exposed to sun light (face, neck, scalp, etc). The clinical presentation consists of rough hyperkeratotic plaques with whitish or brown color and irregular borders. The size of the lesions is usually up to 10mm and might be surrounded by red halo.

The lesions are usually asymptomatic.

Histopathology: hyperkeratosis, acanthosis, rete ridges, epithelial dysplasia, inflammatory cells.

Treatment: sun exposure avoidance and application of . Surgical excision is recommended for solitary or nodular lesions followed by histopathological examination. In sun- damaged skin with confluent actinic keratosis application of topical agents is the treatment of choice (5-, , etc.), as well as laser of photodynamic therapy. Long term follow up is hardly recommended as actinic keratosis is a precancerous lesion and may progress towards .

Actinic cheilitis (solar cheilosis)

Actinic cheilitis is a chronic inflammatory preneoplastic disorder of the lip, generally caused by solar exposure. It is observed in fair-skinned and older patients with history of long term sun exposure. Other causative factors have also been described including tobacco smoking,

chronic trauma, poor oral hygiene and immunosuppression. The vermilion of the lower lip is predominantly affected. Progression to squamous cell carcinoma might be observed.

Actinic keratosis is a slowly progressive lesion. At the early stage the vermilion seems dry and atrophic. At a late stage the surface of the lip becomes rough, hyperkeratotic, thicken and whitish. The line between the skin and the vermilion is blurred and it is hard to define it.

If thickening and ulceration appear, a biopsy followed by histopathological examination is mandatory in order to reveal the presence of .

Histopathology: hyperkeratosis, acanthosis or epithelial atrophy and inflammatory cell infiltrate. Dysplasia of varying degree might be identified. Solar elastosis of the connective tissue is quite typical.

The treatment of actinic cheilitis consists of limited sun exposure and the application of sun protector lip balms. If , lip thickening or ulceration appears, surgical excision or vermilionectomy are the treatment of choice depending on the size of the lesion. Biopsy is hardly recommended prior the performance of the surgical excision.

QUESTIONS:

1. What are the most common causative factors for the precancerous lesions? 2. Describe the lesion from the image as follows: clinical features, differential DEPT. OF DENTAL, ORAL AND MAXILLOFACIAL diagnosis, diagnosis, treatment. SURGERY Send your answers to the following e- mail: [email protected]

References:

1. Regezi et al. Oral pathology-clinical pathologic correlations. 7-th ed. Elsevier 2017 2. Neville at all. Oral and maxillofacial pathology. 4-th ed. Elsevier 2016 3. Rodu, B., & Jansson, C. (2004). Smokeless tobacco and oral cancer: a review of the risks and determinants. Critical Reviews in Oral Biology & Medicine, 15(5), 252-263. 4. Prabowo, D. M., & Widodo, H. B. (2018). Nicotine stomatitis in smokers: a case report. J Dentomaxillofac Sci, 3(1), 58-60. 5. Zornitsa Mihaylova, Pavel Stanimirov, "Actinic Cheilitis: Literature Data and Case Report", International Journal of Science and Research (IJSR), Volume 6 Issue 2, February 2017, 1569 - 1571