Smoker's melanosis | |
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Smoker's melanosis in gums base |
Smoker's melanosis is seen with the naked eye as a brown to black pigmentation of the oral tissue i.e. the gums, [1] cheeks or palate [2] as well as in larynx. [3] [4] It is most often seen in the lower labial gingiva of tobacco users. Most easily it is found in Caucasians, due to their lack of a genetically caused melanin pigmentation. [5] [6]
The brown to black colour is melanin. In skin, melanin prevents harmful UV-light from reaching deeper, sensible parts of the tissue. If UV-light penetrates deeply, some of the toxic substances caused by UV-light damage to cells are bound to melanin in the epithelial cells and travel with the ageing cells to the skin surface, where they are expelled from the tissue surface. In this way the melanocytes and keratinocytes together protect the tissue, with melanin serving as a toxic defence and cleaning agent.
In the oral mucosa, where the ageing epithelial cells move faster to the surface compared to skin, a similar defence-mechanism seems to be present, cleaning the mucosa from different toxic chemicals penetrating the epithelium. Besides chemicals in tobacco also antimalaria-drugs cause an oral pigmentation. Smoker's melanosis is like the genetic melanin pigmentations, a defence-system in action.
The microscope shows smoker's melanosis to be characterized by a melanin hyperpigmentation of the lower part of the oral epithelium, similar to sun-tanned skin. The hyperpigmentation consists of melanin granules which have the shape and colour of "coffea beans". They are produced by the dendritic, octopus-like melanocytes, seen between the epithelial cells situated closest to the epithelium/connective tissue border. [7]
In tobacco-users the melanocytes are stimulated to produce melanin granules and to distribute them out to the surrounding epithelial cells for further transport to the mucosal surface, like the mechanism in melanin-pigmented skin.
Small amounts of melanin-like granules together with other electron-dense particles can also be seen within large melanosome complexes in the underlying connective tissue. [8] If the granules derive from the epithelium, a phenomenon known as melanin incontinence, is not known. [9] In Caucasians these granules are not expected to influence on the clinically observed degree of smoker's melanosis.
Smoking or the use of nicotine-containing drugs is the cause to Smoker's melanosis,. [10] [11] Also tar-components (benzopyrenes) are known to stimulate melanocytes to melanin production, and other unknown toxic agents in tobacco may also be the cause. These chemical agents have a polycyclic, chain-like structure. Environmental tobacco smoke from parents is causing smoker's melanosis in their children [12] [13] Swedish snuff causes a small elevation of oral melanin pigmented individuals from 3.0% to 4.7%. [2] Nicotine tablets have shown to stimulate to melanin pigmentation of the oral mucosa. [11]
Lesions usually disappear between 3 months to 3 years for those who stop smoking. [2] [14] Smoker's melanosis is a benign, normal physiological reaction, and does not develop into cancer. If it does not disappear, however, a biopsy can verify the diagnosis. If smoker's melanosis is destroyed by excessive smoking, as in the hard palate of reverse smokers, who smoke with the glowing part of the cigarette inside the mouth for different reasons, a pale depigmented surface is first seen, indicating the loss of the protecting melanin. Then a red inflammation sometimes occurs and cancer development may follow. [15] In reverse smokers it is important to regularly inspect the areas with smoker's melanosis to detect any melanin destruction, in order to stop smoking in time and thus prevent cancer development.
A study in Sweden [2] showed that 21.5% of smokers and 3% of nonsmokers (genetic pigmentation or unknown cause) had lesions that could be classified as an oral melanin pigmentation. A gingival melanin index in 4 degrees was established. [5] Already with a consumption of 1-3 cigarettes a day 9.3% of all 20.333 examined showed a smoker's melanosis. Pipe smokers had smoker's melanosis in 16.8%. One year after the start of cigarette smoking a clinically visible smoker's melanosis could be seen in 12.3% of women, and 17% among men.
In cigarette smokers who quit smoking, the number of individuals with smoker's melanosis becomes slowly less frequent after 2–3 months, but can still be seen in a few former smokers three years after smoking stop.
Although clinically visible genetic melanin pigmentations in the mouth are present in several ethnic groups all over the world, more mucosal areas will be melanin-pigmentet if tobacco products are used. Smoker's melanosis is found in India, [12] [15] Italy, [16] Japan, [17] Nigeria, [18] Sweden, Turkey, [19] [20] USA, [21] [22] and several other countries. [23]
Smoker's melanosis is expected to be found also in other tissue surfaces exposed to tobacco and tobacco smoke, for instance lips and in skin of the fingers holding the cigarette. Future studies will also show if the use of tobacco exaggerates the pigmentation of skin.
Nicotine is a naturally produced alkaloid in the nightshade family of plants and is widely used recreationally as a stimulant and anxiolytic. As a pharmaceutical drug, it is used for smoking cessation to relieve withdrawal symptoms. Nicotine acts as a receptor agonist at most nicotinic acetylcholine receptors (nAChRs), except at two nicotinic receptor subunits where it acts as a receptor antagonist.
Oral leukoplakia is a potentially malignant disorder affecting the oral mucosa. It is defined as "essentially an oral mucosal white lesion that cannot be considered as any other definable lesion." Oral leukoplakia is a white patch or plaque that develops in the oral cavity and is strongly associated with smoking. Leukoplakia is a firmly attached white patch on a mucous membrane which is associated with increased risk of cancer. The edges of the lesion are typically abrupt and the lesion changes with time. Advanced forms may develop red patches. There are generally no other symptoms. It usually occurs within the mouth, although sometimes mucosa in other parts of the gastrointestinal tract, urinary tract, or genitals may be affected.
The gums or gingiva consist of the mucosal tissue that lies over the mandible and maxilla inside the mouth. Gum health and disease can have an effect on general health.
Nevus is a nonspecific medical term for a visible, circumscribed, chronic lesion of the skin or mucosa. The term originates from nævus, which is Latin for "birthmark"; however, a nevus can be either congenital or acquired. Common terms, including mole, birthmark, and beauty mark, are used to describe nevi, but these terms do not distinguish specific types of nevi from one another.
The periodontal ligament, commonly abbreviated as the PDL, is a group of specialized connective tissue fibers that essentially attach a tooth to the alveolar bone within which it sits. It inserts into root cementum on one side and onto alveolar bone on the other.
Periodontology or periodontics is the specialty of dentistry that studies supporting structures of teeth, as well as diseases and conditions that affect them. The supporting tissues are known as the periodontium, which includes the gingiva (gums), alveolar bone, cementum, and the periodontal ligament. A periodontist is a dentist that specializes in the prevention, diagnosis and treatment of periodontal disease and in the placement of dental implants.
The oral mucosa is the mucous membrane lining the inside of the mouth. It comprises stratified squamous epithelium, termed "oral epithelium", and an underlying connective tissue termed lamina propria. The oral cavity has sometimes been described as a mirror that reflects the health of the individual. Changes indicative of disease are seen as alterations in the oral mucosa lining the mouth, which can reveal systemic conditions, such as diabetes or vitamin deficiency, or the local effects of chronic tobacco or alcohol use. The oral mucosa tends to heal faster and with less scar formation compared to the skin. The underlying mechanism remains unknown, but research suggests that extracellular vesicles might be involved.
Tobacco products, especially when smoked or used orally, have negative effects on human health, and concerns about these effects have existed for a long time. Research has focused primarily on cigarette smoking.
Stomatitis nicotina is a diffuse white patch on the hard palate, usually caused by tobacco smoking, usually pipe or cigar smoking. It is painless, and it is caused by a response of the palatal oral mucosa to chronic heat. A more pronounced appearance can occur with reverse smoking, sometimes distinguished from stomatitis nicotina by the term reverse smoker's stomatitis. While stomatitis nicotina that is caused by heat is not a premalignant condition, the condition that is caused by reverse smoking is premalignant.
Melanosis coli, also pseudomelanosis coli, is a disorder of pigmentation of the wall of the colon, often identified at the time of colonoscopy. It is benign and may have no significant correlation with disease. The brown pigment is lipofuscin in macrophages, not melanin.
Leukoedema is a blue, grey or white appearance of mucosae, particularly the buccal mucosa ; it may also occur on the mucosa of the larynx or vagina. It is a harmless and very common condition. Because it is so common, it has been argued that it may in fact represent a variation of the normal appearance rather than a disease, but empirical evidence suggests that leukoedema is an acquired condition caused by local irritation. It is found more commonly in black skinned people and tobacco users. The term is derived from the Greek words λευκός leukós, "white" and οἴδημα oídēma, "swelling".
Gingival and periodontal pockets are dental terms indicating the presence of an abnormal depth of the gingival sulcus near the point at which the gingival tissue contacts the tooth.
The junctional epithelium (JE) is that epithelium which lies at, and in health also defines, the base of the gingival sulcus. The probing depth of the gingival sulcus is measured by a calibrated periodontal probe. In a healthy-case scenario, the probe is gently inserted, slides by the sulcular epithelium (SE), and is stopped by the epithelial attachment (EA). However, the probing depth of the gingival sulcus may be considerably different from the true histological gingival sulcus depth.
Smoking is a practice in which a substance is burned and the resulting smoke is typically breathed in to be tasted and absorbed into the bloodstream. Most commonly, the substance used is the dried leaves of the tobacco plant, which have been rolled into a small rectangle of rolling paper to create a small, round cylinder called a cigarette. Smoking is primarily practised as a route of administration for recreational drug use because the combustion of the dried plant leaves vaporizes and delivers active substances into the lungs where they are rapidly absorbed into the bloodstream and reach bodily tissue. In the case of cigarette smoking, these substances are contained in a mixture of aerosol particles and gases and include the pharmacologically active alkaloid nicotine; the vaporization creates heated aerosol and gas into a form that allows inhalation and deep penetration into the lungs where absorption into the bloodstream of the active substances occurs. In some cultures, smoking is also carried out as a part of various rituals, where participants use it to help induce trance-like states that, they believe, can lead them to spiritual enlightenment.
Gum depigmentation, also known as gum bleaching, is a procedure used in cosmetic dentistry to lighten or remove black spots or patches on the gums consisting of melanin. Melanin in skin is very common in inhabitants in many parts of the world due to genetic factors. Melanin pigmentation in skin, oral mucosa, inner ear and other organs is a detoxification mechanism. Some toxic agents bind to melanin and will move out of the tissue with the ageing cells and are expelled to the tissue surfaces. Also in the gums and oral mucosa a visible pigmentation is most often caused by genetic factors, but also by tobacco smoking or in a few cases by long-term use of certain medications. If stopping smoking or change of medication do not solve the problem with a disfigurating melanin pigmentation, a surgical operation may be performed. The procedure itself can involve laser ablation techniques.
Plasma cell gingivitis is a rare condition, appearing as generalized erythema (redness) and edema (swelling) of the attached gingiva, occasionally accompanied by cheilitis or glossitis. It is called plasma cell gingivitis where the gingiva (gums) are involved, plasma cell cheilitis, where the lips are involved, and other terms such as plasma cell orifacial mucositis, or plasma cell gingivostomatitis where several sites in the mouth are involved. On the lips, the condition appears as sharply outlined, infiltrated, dark red plaque with a lacquer-like glazing of the surface of the involved oral area.
Oral pigmentation is asymptomatic and does not usually cause any alteration to the texture or thickness of the affected area. The colour can be uniform or speckled and can appear solitary or as multiple lesions. Depending on the site, depth, and quantity of pigment, the appearance can vary considerably.
Tissue engineering of oral mucosa combines cells, materials and engineering to produce a three-dimensional reconstruction of oral mucosa. It is meant to simulate the real anatomical structure and function of oral mucosa. Tissue engineered oral mucosa shows promise for clinical use, such as the replacement of soft tissue defects in the oral cavity. These defects can be divided into two major categories: the gingival recessions which are tooth-related defects, and the non tooth-related defects. Non tooth-related defects can be the result of trauma, chronic infection or defects caused by tumor resection or ablation. Common approaches for replacing damaged oral mucosa are the use of autologous grafts and cultured epithelial sheets.
Gingival cyst, also known as Epstein's pearl, is a type of cysts of the jaws that originates from the dental lamina and is found in the mouth parts. It is a superficial cyst in the alveolar mucosa. It can be seen inside the mouth as small and whitish bulge. Depending on the ages in which they develop, the cysts are classified into gingival cyst of newborn and gingival cyst of adult. Structurally, the cyst is lined by thin epithelium and shows a lumen usually filled with desquamated keratin, occasionally containing inflammatory cells. The nodes are formed as a result of cystic degeneration of epithelial rests of the dental lamina.