Oral Pathology in Clinical Dental Practice. Robert E. Marx

Oral Pathology in Clinical Dental Practice - Robert E. Marx


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       Smokeless tobacco keratosis from chewing tobacco.

      Non–Betel Nut/Slaked Lime Smokeless Tobacco Keratosis

      Nature of disease

      A reactive nondysplastic hyperkeratosis of the mucosa due to inflammation and stimulation from various smokeless tobacco products.

      Predilections

      May occur in anyone who uses such products but has a higher incidence in the western United States and the Scandinavian countries due to cultural traditions. More common in men also because of cultural acceptance. No racial predilection is known.

      Clinical features

      The area corresponding to the placement of the tobacco product (usually the mandibular attached gingiva and mucosa of the vestibule) will appear as an irregular and often leathery white patch referred to as a “snuffle dippers patch.” It is usually nonpainful unless the area is inflamed.

      Radiographic presentation

      None.

      Differential diagnosis

      The clinician is advised to ask the patient about use of betel nut/slaked lime use versus true smokeless tobacco products. Betel nut/slaked lime keratosis is premalignant, whereas other true tobacco-containing, topical smokeless tobacco products are not. Additionally, clinicians should also consider epithelial dysplasia, carcinoma in situ, invasive squamous cell carcinoma, and even lichen planus and hypertrophic candidiasis.

      Microscopic features

      Nondysplastic epithelium will be present with a thick layer of pale-staining cells occupying the superficial half of the keratinocyte layer along with significant hyperkeratosis.

      Suggested course of action

      Confirm that the patch is not the result of betel nut/slaked lime use. Incisional biopsy is indicated to document the absence of dysplasia. Counsel the patient about tobacco cessation, particularly as it relates to erosion of the mucosa and gingiva as well as staining of the teeth.

      Treatment

      No specific treatment other than cessation of smokeless tobacco use.

       Trismus, buccal mucosa hyperkeratosis, and fibrosis from betel nut/slaked lime use.

      Betel Nut/Slaked Lime Keratosis

      Nature of disease

      A dysplastic premalignant transformation of mucosal epithelial cells due to the carcinogenic effects of slaked lime. Additionally, the Areca catechu chemical in the betel nut often causes a concomitant submucosal fibrosis.

      Predilections

      Mostly seen in individuals from India, Sri Lanka, and East Asian countries, where the produce is called quid or pan and used for oral gratification much like chewing gum in the United States.

      Clinical features

      A white patch is usually seen on either buccal mucosa. There is often a limited jaw opening due to the submucosal fibrosis. Induration around the white patch is common.

      Radiographic presentation

      None.

      Differential diagnosis

      The clinician is advised to ask the patient specifically about betel nut/slaked lime use versus use of smokeless tobacco products, as the latter are not carcinogenic to a significant degree. Other considerations include squamous cell carcinoma, actinomycosis, lichen planus, and hypertrophic candidiasis.

      Microscopic features

      Various degrees of epithelial dysplasia up to invasive carcinoma may be seen together with hyperkeratosis. Dense, poorly cellular collagen is usually seen in the submucosa. Inflammatory cells are variably present.

      Suggested course of action

      Incisional biopsy to assess for dysplasia or carcinoma or referral to an oral and maxillofacial surgeon.

      Treatment

      If only premalignant changes are seen on the biopsy, a wide local excision together with skin grafting the defect is accomplished. If invasive carcinoma is identified on the biopsy, a wide local excision and ipsilateral neck dissection is accomplished together with flap reconstruction.

      Dyskeratosis Congenita

      Nature of disease

      A very rare autosomal dominant disorder involving mutations in six genes that code for telomerase, thereby increasing a cell’s life span. Forty percent of oral lesions gradually progress to invasive squamous cell carcinoma.

      Predilections

      Begins in childhood. No sex or racial predilection is known.

      Clinical features

      Oral lesions of the labial and buccal mucosa will appear white and are frequently thick. Lesions become thicker with age. Skin telangiectasias are common as well as a smooth dorsal tongue surface from loss of filiform papillae. Atrophic nail beds may also be seen.

      Radiographic presentation

      None.

      Differential diagnosis

      In younger individuals, hereditary benign intraepithelial dyskeratosis, white sponge nevus, and pachyonychia congenita are considerations. In adults, lichen planus and squamous cell carcinoma are added to these.

      Microscopic features

      In early lesions, acanthosis and hyperkeratosis are seen. As lesions age, epithelial dysplasia and squamous cell carcinoma may be seen.

      Suggested course of action

      Close follow-up observing for clinical suggestions of premalignant or malignant changes (ie, ulceration, induration, pain, increase in size, lymphadenopathy, etc). Biopsy as necessary, or refer to an oral and maxillofacial surgeon.

      Treatment

      Excision of lesions as they show signs of malignant transformation.

       Erythroleukoplakia representing carcinoma in situ.

      Epithelial Dysplasia/Carcinoma in Situ


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