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Pilosebaceous glands

Additionally, Propionibacterium acnes, which thrives in the pilosebaceous glands of the skin, secretes enzymes that cause local skin irritation and inflammation, and is generally accepted to play a role in the dermatologic condition, acne (178). The role of other microbiota in the development of acne, however, is still under investigation. [Pg.98]

Demodicosis is thought to be caused by an over-infestation of the mite in the follicles and pilosebaceous glands of the eyelids. These parasites cause destruction of the epithelial and glandular tissue, producing follicular distension, hyperplasia, increased keratinization, and acute inflammation. Dead mites and keratinization may play a role in the stagnation of secretions, which adds to the overall disease process. No current studies adequately prove the minimum number of mites necessary to produce symptoms therefore their role in pathogenesis remains imclear. It has been postulated that Demodex... [Pg.397]

Mixtures of pesticides and UV are also phototoxic. Hairless dogs treated with maneb (a fungicide) and UVA showed epidermal degradation, vasodilation, and intradermal infiltration of inflammatory cells. Animals treated with zineb (a general use pesticide) and UVA produced comedones with well-developed pilosebaceous glands, f181... [Pg.250]

Hair follicles and their associated sebaceous glands (pilosebaceous glands), eccrine glands, apocrine glands, and finger and toenails are all considered skin appendages. Hair follicles are found everywhere within the skin except for the soles of the feet, the palms of the hand, the red portion (vermilion border) of the lips, and the external genitalia. All are formed from fetal epidermal cells. Hair differs markedly in its prominence from place to place over the body. Delicate primary hair is found on the fetus secondary hair or down covers the adult forehead terminal hair ordinarily blankets the scalp and is found as pubic... [Pg.49]

Acne vulgaris, commonly called acne, is inflammation of the pilosebaceous glands. These are the glands which produce oil for the hair. Acne is more likely to occur in adolescent males and is associated with testosterone level and the ingestion of greasy foods—food containing trans-fatty acids (TEA). TEA are synthetic alterations of naturally fatty acids and are present in processed foods, candies, and potato chips. [Pg.398]

Inflammation of the pilosebaceous glands form papules, nodules, and cysts on the face, neck, shoulders, and back as a result of keratin plugs at the base of the pilosebaceous oil glands near the hair follicles. [Pg.399]

Acne vulgarisis is an inflammation of the pilosebaceous glands and is treated by using a cleansing agent and applying topical anti-acne medication. [Pg.407]

The pilosebaceous unit of the skin consists of a hair follicle and the surrounding sebaceous glands. An initial acne lesion called a comedo forms when there is a blockage in the pilosebaceous unit.8... [Pg.960]

The major barrier of the skin is the outermost dead layer, the stratum corneum. A number of routes of penetration of a drug, across this region can be identified. First, the appendages, the pilosebaceous and eccrine glands, form a potential shunt route across the stratum corneum. The relative surface area of these is very small (<0.1%) and there has been little conclusive evidence to suggest that this is a major route. Second, the penetrant could diffuse across the entire stratum corneum through the dead cells, the corneocytes. A large surface area is available but the... [Pg.121]

The pathogenesis of juxtaclavicular beaded lines is unclear. Some authors have reported a prevalence of 16% in heart transplant patients, but only in men. Becanse ciclosporin is highly lipophilic, it has many adverse effects associated with alterations of pilosebaceous follicles, snch as hypertrichosis and acne. In this case the authors postulated that the combined effect of prednisone and ciclosporin may have induced sebaceous gland hyperplasia. [Pg.753]

A woman had received intralesional paramethasone and other topical glucocorticoids several times for alopecia between the ages of 7 and 18 years (381). When she was 30 she was again treated with intralesional paramethasone for a relapse of alopecia. She developed pruritus after the first intralesional injection and erythema, edema, and vesicles 6-8 hours later. A biopsy showed spongiform lymphocytic folliculitis with spongiosis and exocytosis in the sweat gland ducts and in the pilosebaceous unit. She was treated with triamcinolone cream and her skin lesions resolved. Patch tests were positive for paramethasone, with cross-reactivity to tixocortol pivalate, hydrocortisone, and hydrocortisone butyrate. [Pg.942]

Acne vulgaris is the result of several factors combined. The condition arises in the pilosebaceous units in the dermis, which consist of a hair follicle and associated sebaceous gland. These glands secrete sebum, a mixture of fats and waxes that protect the skin and hair by retarding water loss and forming a barrier against external agents. The hair follicle is lined with epithelial cells that become keratinised as they mature. [Pg.163]

Skin repair after a peel to the reticular dermis is slower, as all the basal layer keratinocytes have been destroyed and the skin can only rely on the differentiated keratinocytes of the pilosebaceous units and the intradermal excretory ducts of the sweat glands. To repair the dermis, the sebocytes in the pilosebaceous units must dedifferentiate, and horizontal growth is required to close the skin quickly. Next comes a phase of vertical growth whose purpose is to regenerate a physiologically sound epidermis that will maintain homeostasis and restore the vital barrier function after the keratinocytes have differentiated into corneocytes. [Pg.330]

Acne vulgaris is a disease of the pilosebaceous unit (i.e., the sebaceous glands and adjacent hair follicle). [Pg.1755]

Androgenic activity drives sebum production in the sebaceous glands however, most acne patients do not have an endocrine abnormality. Acne-affected pilosebaceous units apparently have a hyperresponsiveness to circulating androgens. Increased sebum production per se is not necessarily responsible for acne, but may rather be viewed as an underlying factor. [Pg.1755]

Acne vulgaris is a disease of the pilosebaceous unit (i.e., the sebaceous gland and adjacent hair follicle). Sebaceous glands, predominant on the face, chest, and upper back, respond to androgen stimulation. These glands provide sebum to the follicular canal and eventually to the skin surface through the foUicular opening (the pore). Follicular canal contents inclnde keratinocytes, Propionibacterium acnes (P. acnes), and free fatty acids. [Pg.1756]

Pilosebaceous—Sebaceous gland and adjacent hair follicle. [Pg.2689]


See other pages where Pilosebaceous glands is mentioned: [Pg.195]    [Pg.199]    [Pg.201]    [Pg.203]    [Pg.206]    [Pg.210]    [Pg.53]    [Pg.318]    [Pg.45]    [Pg.52]    [Pg.54]    [Pg.79]    [Pg.195]    [Pg.199]    [Pg.201]    [Pg.203]    [Pg.206]    [Pg.210]    [Pg.53]    [Pg.318]    [Pg.45]    [Pg.52]    [Pg.54]    [Pg.79]    [Pg.5]    [Pg.460]    [Pg.43]    [Pg.423]    [Pg.424]    [Pg.426]    [Pg.50]    [Pg.221]    [Pg.85]    [Pg.2418]    [Pg.7]    [Pg.23]    [Pg.91]    [Pg.177]    [Pg.67]    [Pg.787]    [Pg.21]    [Pg.166]    [Pg.34]   
See also in sourсe #XX -- [ Pg.45 , Pg.49 , Pg.52 , Pg.54 , Pg.56 , Pg.62 ]




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