Encyclopedia of Pathology

Living Edition
| Editors: J.H.J.M. van Krieken

Smoker’s Keratosis

  • Jacqueline E. van der WalEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-28845-1_778-1



A lesion due to the use of smokeless tobacco, used as snuff/spit or chewing tobacco. The development of the lesion is influenced by the type of smokeless tobacco, the amount of tobacco used, the brand of tobacco, and the duration of the contact between tobacco and oral mucosa.

Clinically, it is characterized by a white or gray-white, translucent lesion at the site where the smokeless tobacco is held in the oral cavity. The alterations can be graded by a 3- (Greer and Poulson) or 4- (Axèll, Mörnstad, Sundström) grade system, depending on the amount of color change, wrinkling, and thickening of the mucosa.

Clinical Features

  • Incidence: Estimated prevalence of 6% with in some areas of southeastern United States of 21%.

    A white lesion is present in 15% of chewing tobacco users and 60% of snuff/spit tobacco users. In India, smokeless tobacco may be combined with other products, such as betel leaves, areca nuts, and slaked lime.

  • Age: Starting between the ages of 9 and 16 years.

  • Sex: Chewing tobacco mostly by males, dry snuff by females.

  • Site: Labial mucosa, buccal mucosa, and any other intraoral area in continuous contact with the tobacco.

  • Treatment: Cessation of tobacco use.

  • Outcome: Lesions resolve within 1–2 weeks after cessation of tobacco use. The risk of carcinogenesis in continuation of the use of smokeless tobacco is unknown and controversial.


Thickening of the mucosa due to acanthosis and hyperkeratosis, with or without intracellular vacuolization of glycogen-rich superficial cells. Parakeratin chevrons may be present (Fig. 1). Dysplasia is not a common finding.
Fig. 1

Hyperkeratosis of the lower lip in a pipe-smoking man (hematoxylin-eosin)

Subepithelial vascularity is often increased with vessel engorgement. A deposition of amorphous eosinophilic material may be present in the subjacent connective tissue and salivary glands.

Differential Diagnosis

  • Leukoplakia

  • Stomatitis nicotina

References and Further Reading

  1. Axèll, T., Mörnstad, H., & Sundström, B. (1976). The relationship of the clinical picture to the histopathology of snuff dipper’s lesions in a Swedish population. Journal of Oral Pathology, 5, 229–236.CrossRefPubMedGoogle Scholar
  2. Greer, R. O., & Poulson, T. C. (1983). Oral tissue alterations associated with the use of smokeless tobacco by teenagers. Oral Surgery, 56, 275–284.CrossRefGoogle Scholar
  3. Kaugars, G. E., Riley, W. T., Brandt, R. B., et al. (1992). The prevalence of oral lesions in smokeless tobacco users and an evaluation of risk factors. Cancer, 70, 2579–2585.CrossRefPubMedGoogle Scholar
  4. Taybos, G. (2003). Oral changes associated with tobacco use. The American Journal of the Medical Sciences, 326, 179–182.CrossRefPubMedGoogle Scholar
  5. Warnakulasuriya, K. A., & Ralhan, R. (2007). Clinical, pathological, cellular and molecular lesions caused by oral smokeless tobacco – a review. Journal of Oral Pathology & Medicine, 36, 63–77.CrossRefGoogle Scholar

Copyright information

© Springer International Publishing AG 2018

Authors and Affiliations

  1. 1.Department of Pathology, Antoni van Leeuwenhoek HospitalThe Netherlands Cancer InstituteAmsterdamThe Netherlands