What Is Smoker's Melanosis?
Smokers' melanosis is basically a physiologic and benign oral brownish to black hyperpigmentation observed in chronic smokers. Both smokeless forms like dry snuff, gutka, plain tobacco, and smoke forms like pipe smoke, beedi, hookah, etc., contain toxic nitrosamines and carcinogens that affect the gingiva, periodontal ligament, and alveolar jaw bone. In this condition, the recommendation is to select mucosal areas of the oral cavity like the lip, gingiva, palate, or buccal mucosa.
The color of gingival tissue is determined in an individual (usually healthy pink in color with or without melanization) by the degree of keratinized tissue, the thickness of the underlying epithelium, presence of pigments like hemoglobin and oxyhemoglobin, etc.
If melanin deposition is present in the gingival tissue, it is usually a result of melanocytes seen within the basal layer of the gingival epithelium. Increased melanin deposition in the gums can be seen in various conditions ranging from trauma, inflammatory disorders like (lichen planus, pemphigoid, lichenoid reactions), infections, the effect of certain drugs (tetracycline, ketoconazole, clotrimazole, etc.), and in systemic conditions like Peutz jeghers syndrome, Albright's disease, and Addison disease.
In smoking as well, melanin deposition is increased in the oral epithelial layers because the melanin in the case of smokers acts rather as a protective adaptation of mucosal changes that occur in response to the inflammatory mediators and potential carcinogenic effect caused by nicotine in any tobacco product. The use of nicotine either in the form of tobacco smoke in cigarettes or tobacco products or in the form of nicotine-based drugs is related to the release of benzopyrenes, which are polycyclic chemical compounds that stimulate melanocyte cells and in turn result in melanin production. Similarly, tobacco snuff and nicotine-containing tablets have also been shown to produce oral hyperpigmentation as a direct effect.
What Are the Causes And Pathogenesis of Smoker’s Melanosis?
Women are more commonly affected than men in smoker's melanosis with a diffuse brownish-black pigmentation. Its incidence is in about 25 to 30% of smokers globally or, rather specifically, in users of tobacco. A characteristic brown pigmentation feature by multiple coalescing or discrete brownish colored macules occurs upon the gingiva on the labial surfaces of the lower teeth more often and may also be seen in the palate and buccal mucosa. Though smokers' metabolism itself is a benign, self-resolving condition with the stoppage of tobacco products and does not cause cancer, it still is important for the patient to consult the dental surgeon regarding the same. This is because the melanin is protective in function, and in a few cases where the smokers are used to having the glowing part of cigars in their mouths, the mucosa gets depigmented.
In reverse smokers as well, melanin depigmentation can be observed. The loss of protective melanin in these smokers by virtue of the habit or the style of smoking results in the development of potential inflammatory red or white lesions of the oral cavity occurring in the deployments surfaces that would, in turn, predispose the individual to be precancerous or cancerous lesions. Thus, it is essential to observe if the hyperpigmented oral mucosa is self-healing or persisting for a long time, even after the cessation of the smoking habit.
Like sun-tanned skin, in smokers melanosis, the black or brown pigmentation seen in the oral or gingival mucosa is a hyperpigmentation of the oral epithelium in the affected area. This might be attributed to the clearance of toxic chemicals like tobacco that penetrate the epithelium and is cleared by the oral cavity's natural defense mechanism of the aging epithelium to move faster or closer to the outer surface. That is the same kind of mechanism observed in individuals who have higher amounts of melanin, where the pigment is transported to the mucosal surface. In the oral cavity, similarly, the transport of melanin is through the melanocytes producing melanin granules in the oral mucosal surface as observed in electron microscopy.
Current research also suggests that the use of tobacco is indicative directly of causing hyperpigmentation of any skin surface exposed to tobacco. Smokers melanosis is a phenomenon not affecting just the oral cavity but also the other tissue surfaces exposed to the tobacco content and smoke like the lips and finger skin of smokers.
What Is the Differential Diagnosis of Smoker’s Melanosis?
It is pivotal for the dental or maxillofacial surgeon to assess that the pigmentation observed is indeed smokers melanosis. A detailed medical history and habit history will elicit the patient's frequency, and habituation to the kind of tobacco he or she is exposed to. The patient's medical and oral history should be evaluated thoroughly prior to the confirmed diagnosis of the same. Unless a patient is usually originated from a particular race or ethnicity in which the melanin pigmentation is characteristic, other systemic conditions and cancer-causing lesions need to be differentially diagnosed from melanosis by a biopsy and histopathologic study of the tissue, especially to differentiate it from potential precancerous and cancerous lesions.
Oral nevi, electromagnetic oral malignant melanoma, Addison's disease, Albright syndrome, lichenoid reactions, oral melanotic macule, or drug-induced hyperpigmentations are the differential diagnoses for smokers’ melanosis.
How Is Smoker’s Melanosis Managed?
The lesions are usually self-limiting with cessation of smoking. Chronic users of tobacco might have more detrimental pigmentation that may elicit a cosmetic need for surgical removal of the pigmentation. The dental surgeon will choose to remove the pigmentation observed in smokers' melanosis, usually only for aesthetic reasons and depending on the areas of occurrence.
Lasers are a preferable choice to eliminate the hyperpigmented oral epithelium. The advancement in laser technology in dentistry eliminates the need for suturing, provides better hemostasis, and reduces postoperative complications of pain, swelling, and infection. Other techniques are also adapted by surgeons like scalpel gingivectomy, gingival surgical abrasions, laser vapourization, electrosurgery, cryosurgery, gingival grafts, and accessory chemical methods.
Conclusion:
Though smoker's melanosis may be a benign physiologic condition, the long-lasting detrimental impacts of nicotine can be seen on overall oral and systemic health. Counseling to quit smoking should be advocated by both the physician and dental surgeon to spread community awareness about the deleterious impact of tobacco addiction.
