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Earwax is produced by glands in the ear canal. Although scientists are still not completely sure why we have earwax, it does trap dust and other small particles and prevent them from reaching and possibly damaging or infecting the eardrum. Normally, the wax dries up and falls out of the ear, along with any trapped dust or debris. Everyone makes ear wax, but the amount and type are genetically determined just like hair color or height. Smaller or oddly shaped ear canals may make it difficult for the wax our ears make naturally to get out of the canal. This can lead to wax impactions. This is earwax buildup.
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Basal cell carcinoma (BCC) accounts for 90% of all malignant cutaneous lesions in the head and neck region and is therefore the most common type of skin cancer on the ear. It makes up one fifth of neoplasms that involve the ear and the temporal bone [20]. The vast majority of BCC occurs on the auricular helix and periauricular area which are especially susceptible as they are exposed to the most UV light. Nevertheless 15% arise in the external auditory canal. Five different clinical forms are distinguished in the literature: nodular-ulcerative, pigmented, cystic, superficial multicentric and morphealike. The most common type is the nodular-ulcerative. The lesion is a flesh-colored scaling papule, mostly erythematous to pink, sometimes pigmented, with a surrounding capillary network. It has a pearly border and can show a central ulcer (Fig. 3). This most frequent form may infiltrate the cartilage. Although metastases of BCC are extremely rare, the invasive character of the tumor can cause extensive local tissue destruction. The second most common type is the morphealike or sclerosing subtype. It is more troublesome as it has indistinct margins and infiltrates along deep tissue planes. It spreads centrifugally with a finger-like growth pattern which complicates therapy. The lesion can potentially extend to the temporal bone or parotid gland and remain undetected.
The patients report an asymmetric flat hyperpigmentation or a raised nodular lesion which has changed in color and size. Amelanotic (non-pigmented) variants exist as well. The three most described subtypes are the superficial spreading melanoma, the nodular melanoma and the lentigno maligna melanoma. Each type has its characteristic growth pattern with a horizontal and a vertical growth phase. All over the body, the superficial spreading melanoma is the most common type (Fig. 6). It shows an intermediate radial growth phase before starting to invade the dermis.
Winkler disease. Ulcerated nodule with overlying crust. The surrounding skin is inflamed as indicated by the red color. Remark: If painful ulcerated nodules are present at the external ear, Winkler disease has to be kept in mind.
Cylindroma is benign, solitary or group-like skin colored or light red, bulging, protuberand tumors with a flat, shining surface. They are usually located at the head and neck (turban tumor) and can potentially involve the ear (Fig. 12). They most likely represent very primitive sweat gland tumors originating from eccrine or apocrine glands. Histologically they show apocrine, eccrine, secretory, and ductal features, and the exact cellular origin of cylindromas remains unknown. Although benign, malignant transformation (cylindrocarcinoma) has been reported, in which case surgical excision is the treatment of choice [77].
Leukoplakia could be classified as mucosal disease, and also as a premalignant condition. Although the white color in leukoplakia is a result of hyperkeratosis (or acanthosis), similarly appearing white lesions that are caused by reactive keratosis (smoker's keratosis or frictional keratoses e.g. morsicatio buccarum) are not considered to be leukoplakias.[15] Leukoplakia could also be considered according to the affected site, e.g. oral leukoplakia, leukoplakia of the urinary tract, including bladder leukoplakia or leukoplakia of the penis, vulvae, cervix or vagina.[16][17] Leukoplakia may also occur in the larynx, possibly in association with gastro-esophageal reflux disease.[18] Oropharyngeal leukoplakia is linked to the development of esophageal squamous cell carcinoma,[18] and sometimes this is associated with tylosis, which is thickening of the skin on the palms and soles of the feet (see: Leukoplakia with tylosis and esophageal carcinoma). Dyskeratosis congenita may be associated with leukoplakia of the oral mucosa and of the anal mucosa.[18]
Non-homogeneous leukoplakia is a lesion of non-uniform appearance. The color may be predominantly white or a mixed white and red. The surface texture is irregular compared to homogeneous leukoplakia, and may be flat (papular), nodular or exophytic.[9][15] "Verrucous leukoplakia" (or "verruciform leukoplakia") is a descriptive term used for thick, white, papillary lesions. Verrucous leukoplakias are usually heavily keratinized and are often seen in elderly people. Some verrucous leukoplakias may have an exophytic growth pattern,[2] and some may slowly invade surrounding mucosa, when the term proliferative verrucous leukoplakia may be used. Non-homogeneous leukoplakias have a greater risk of cancerous changes than homogeneous leukoplakias.[9]
Erythroleukoplakia (also termed speckled leukoplakia, erythroleukoplasia or leukoerythroplasia) is a non-homogeneous lesion of mixed white (keratotic) and red (atrophic) color. Erythroplakia (erythroplasia) is an entirely red patch that cannot be attributed to any other cause. Erythroleukoplakia can therefore be considered a variant of either leukoplakia or erythroplakia since its appearance is midway between.[22] Erythroleukoplakia frequently occurs on the buccal mucosa in the commissural area (just inside the cheek at the corners of the mouth) as a mixed lesion of white nodular patches on an erythematous background,[22] although any part of the mouth may be affected. Erythroleukoplakia and erythroplakia have a higher risk of cancerous changes than homogeneous leukoplakia.[22]
Most cases of leukoplakia cause no symptoms,[9] but infrequently there may be discomfort or pain.[2] The exact appearance of the lesion is variable. Leukoplakia may be white, whitish yellow or grey.[29] The size can range from a small area to much larger lesions.[29] The most common sites affected are the buccal mucosa, the labial mucosa and the alveolar mucosa,[30] although any mucosal surface in the mouth may be involved.[2] The clinical appearance, including the surface texture and color, may be homogeneous or non-homogeneous (see: classification). Some signs are generally associated with a higher risk of cancerous changes (see: prognosis).
The exact underlying cause of leukoplakia is largely unknown,[1] but it is likely multifactorial, with the main factor being the use of tobacco.[29] Tobacco use and other suggested causes are discussed below. The mechanism of the white appearance is thickening of the keratin layer, called hyperkeratosis. The abnormal keratin appears white when it becomes hydrated by saliva, and light reflects off the surface evenly.[29] This hides the normal pink-red color of mucosae (the result of underlying vasculature showing through the epithelium).[1] A similar situation can be seen on areas of thick skin such as the soles of the feet or the fingers after prolonged immersion in water. Another possible mechanism is thickening of the stratum spinosum, called acanthosis.[29]
The epithelium may show hypertrophy (e.g. acanthosis) or atrophy. Red areas within leukoplakia represent atrophic or immature epithelium which has lost the ability to keratinize.[1] The transition between the lesion and normal surrounding mucosa may be well-demarcated, or poorly defined. Melanin, a pigment naturally produced in oral mucosa, can leak from cells and give a grey color to some leukoplakia lesions.[29]
Almost all oral white patches are usually the result of keratosis.[3] For this reason, oral white patches are sometimes generally described as keratoses, although a minority of oral white lesions are not related to hyperkeratosis, e.g. epithelial necrosis and ulceration caused by a chemical burn (see: Oral ulceration#Chemical injury).[3] In keratosis, the thickened keratin layer absorbs water from saliva in the mouth and appears white in comparison with normal mucosa. Normal oral mucosa is a red-pink color due to the underlying vasculature in the lamina propria showing through the thin layer of epithelium. Melanin produced in the oral mucosa also influences the color, with a darker appearance being created by higher levels of melanin in the tissues (associated with racial/physiologic pigmentation, or with disorders causing melanin overproduction such as Addison's disease).[29] Other endogenous pigments can be overproduced to influence the color, e.g. bilirubin in hyperbilirubinemia or hemosiderin in hemochromatosis, or exogenous pigments such as heavy metals can be introduced into the mucosa, e.g. in an amalgam tattoo.
Leukoplakia cannot be rubbed off the mucosa,[14] distinguishing it readily from white patches such as pseudomembraneous candidiasis, where a white layer can be removed to reveal an erythematous, sometimes bleeding surface underneath. The white color associated with leukoedema disappears when the mucosa is stretched. A frictional keratosis will generally be adjacent to a sharp surface such as a broken tooth or rough area on a denture and will disappear when the causative factor is removed. Some have a suggested as general rule that any lesion that does not show signs of healing within 2 weeks should be biopsied.[38] Morsicatio buccarum and linea alba are located at the level of the occlusal plane (the level at which the teeth meet). A chemical burn has a clear history of placing an aspirin tablet (or other caustic substance such as eugenol) against the mucosa in an attempt to relieve toothache. Developmental white patches usually are present from birth or become apparent earlier in life, whilst leukoplakia generally affects middle aged or elderly people. Other causes of white patches generally require pathologic examination of a biopsy specimen to distinguish with certainty from leukoplakia.
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