hyperkeratosis

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Related to Hyperkeratinization: keratosis pilaris

hy·per·ker·a·to·sis

 (hī′pər-kĕr′ə-tō′sĭs)
n. pl. hy·per·ker·a·to·ses (-sēz)
Hypertrophy of the cornea or the horny layer of the skin.

hy′per·ker′a·tot′ic (-tŏt′ĭk) adj.

hyperkeratosis

(ˌhaɪpəˌkɛrəˈtəʊsɪs)
n
(Pathology) pathol overgrowth and thickening of the outer layer of the skin
hyperkeratotic adj

hy•per•ker•a•to•sis

(ˌhaɪ pərˌkɛr əˈtoʊ sɪs)

n.
1. proliferation of the cells of the cornea.
2. a thickening of the horny layer of the skin.
[1835–45]
hy`per•ker`a•tot′ic (-ˈtɒt ɪk) adj.
Translations
Hyperkeratose
과각화
References in periodicals archive ?
We now have evidence that inflammation appears even before follicular hyperkeratinization.
Objective: Follicular hyperkeratinization and Propionibacterium acnes colonization are mainly responsible for the pathogenesis of acne.
However, due to the variety of benign lesions, such as bite trauma, or hyperkeratinization, less-obvious lesions may be difficult to distinguish as suspicious for oral cancer.
Histopathological examination of tumor growth revealed hyperkeratinization surrounded by neoplastic squamous cells forming characteristic onion like eosinophilic keratin pearls (cell nests) surrounded by inflammatory cell infilteration (Fig.
It is an inflammatory disease of pilosebaceous unit, and the four major pathophysiological mechanisms are increased sebum production, follicular hyperkeratinization, proliferation of Propionibacterium acnes, and inflammation.
The etiology of acne vulgaris appears to be multifactorial, involving follicular hyperkeratinization, proliferation of Propionibacterium acnes, increased sebum production, and inflammation [29].
6,7] Diffuse hyperkeratinization & desquamation are characteristic of HI.
In addition, the follicle contains immune response mechanism protecting invasion of foreign substances and may respond in an inflammation reaction that will result in hyperkeratinization, will clog the pore and prevent further penetration.
The current hypothesis is that the HS primary event is a hyperkeratinization of the follicular infundibulum, followed by follicular occlusion, dilatation and rupture; the spread of bacterial and cellular remnants would trigger the local inflammatory response (3).
The hallmark of TCDD toxicity in humans is chloracne (Panteleyev and Bickers 2006), characterized by epidermal acanthosis and hyperkeratosis, and hyperkeratinization and metaplasia of the sebaceous glands, with comedone formation.