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PubMed2001

Chronological ageing and photoageing of the human sebaceous gland.

The human sebaceous gland undergoes both extrinsic and intrinsic ageing. The latter is associated with morphological changes and alteration in the sebaceous gland activity. The high androgen-dependent sebum secretion in neonates falls during childhood, starts to rise again during puberty and reaches its maximum in young adults. While the number of sebaceous glands remains the same during life, sebum levels tend to decrease after menopause in females, whereas no major changes appear until the eighth decade of life in men. Reduced androgen levels in aged individuals lead to a slow cellular turnover in the sebaceous glands resulting in hyperplasia of the facial sebaceous glands in advanced age. Ultraviolet radiation and immune suppression (cyclosporin A with corticosteroids) represent cofactors for the development of sebaceous gland hyperplasia. Current molecular findings indicate that overexpression of the ageing-associated gene Smad7 and parathormone-related protein correlate with sebaceous gland hyperplasia, whereas c-myc overexpression is associated with enhanced sebum production. On the other hand, down-regulation of the mismatch repair genes hMLH-1 and hMSH-2 may promote the development of sebaceous gland carcinoma. In addition to spontaneous single tumours, sebaceous gland carcinomas have been reported in immune-suppressed transplant recipients (azathiorpine, cisplatin, cyclosporin A) and in association with the Muir-Torre syndrome. Microsatellite instability with a loss of the mismatch repair gene hMSH-2 has been detected in immune suppressed patients and under photo-induced DNA damage. Topical and systemic oestrogens offer treatment options for skin xerosis in menopausal females. A combination of isotretinoin and interferon-alpha may prevent tumour development in patients with Muir-Torre syndrome.

Androgens↗
PubMed1998

Oxidative activity of the type 2 isozyme of 17beta-hydroxysteroid dehydrogenase (17beta-HSD) predominates in human sebaceous glands.

Sebum production is regulated by the opposing effects of androgens and estrogens. The intracrine activity of steroid metabolizing enzymes is important in regulating sebum production because these enzymes can convert weak steroids from the serum into potent androgens and estrogens within the sebaceous gland (SG). 17Beta-hydroxysteroid dehydrogenase (17beta-HSD) interconverts weak and potent sex steroids via redox reactions. In this regard, it may function as a gatekeeping enzyme regulating the hormonal milieu of the SG. Six isozymes of 17beta-HSD have been identified that differ in their substrate preference and their preference to produce weak or potent sex steroids via oxidation or reduction, respectively. The goals of this study are: (i) to identify which isozyme (s) of 17beta-HSD is active in SG; (ii) to determine if its activity differs in facial skin compared with nonacne-prone skin that may account for the regional differences in sebum production; (iii) to compare the activity of 17beta-HSD in intact glands and in SG homogenates; and (iv) to determine if 13-cis retinoic acid inhibits 17beta-HSD activity. Human SG were assayed for 17beta-HSD activity using estrogens, androgens, and progestins as substrates. Oxidative activity of the type 2 isozyme predominated in all samples tested. Although transcripts for the types 1, 2, 3, and 4 isozymes were detected using reverse transcriptase-polymerase chain reaction, only mRNA for the predominant type 2 isozyme and the type 4 isozyme were detected in northern analysis. Greater reductive activity of 17beta-HSD was noted in SG from facial areas compared with nonacne-prone areas, suggesting an increased net production of potent androgens in facial areas. Oxidation was more predominant over reduction in intact SG compared with homogenized SG, thus supporting the hypothesis that 17beta-HSD protects against the effects of potent androgens in vivo. Activity of the type 2 17beta-HSD was not inhibited by 13-cis retinoic acid. In conclusion, SG possess the cellular machinery needed to transcribe the genes for the type 1-4 isozymes of 17beta-HSD. At the protein level, however, oxidative activity of the type 2 isozyme predominates, suggesting that 17beta-HSD isozyme activity may be translationally regulated.

17-Hydroxysteroid Dehydrogenases↗
PubMed2000

Topical ALA-photodynamic therapy for the treatment of acne vulgaris.

Topical aminolevulinic acid is converted into a potent photosensitizer, protoporphyrin, in human hair follicles and sebaceous glands. Photodynamic therapy with topical aminolevulinic acid was tested for the treatment of acne vulgaris, in an open-label prospective human study. Each of 22 subjects with acne on the back was treated in four sites with aminolevulinic acid plus red light, aminolevulinic acid alone, light alone, and untreated control. Half of the subjects were treated once; half were treated four times. Twenty percent topical aminolevulinic acid was applied with 3 h occlusion, and 150 J per cm2 broad-band light (550-700 nm) was given. Sebum excretion rate and auto-fluorescence from follicular bacteria were measured before, and 2, 3, 10, and 20 wk after, treatment. Histologic changes and protoporphyrin synthesis in pilosebaceous units were observed from skin biopsies. Aminolevulinic acid plus red light caused a transient acne-like folliculitis. Sebum excretion was eliminated for several weeks, and decreased for 20 wk after photodynamic therapy; multiple treatments caused greater suppression of sebum. Bacterial porphyrin fluorescence was also suppressed by photodynamic therapy. On histology, sebaceous glands showed acute damage and were smaller 20 wk after photodynamic therapy. There was clinical and statistically significant clearance of inflammatory acne by aminolevulinic acid plus red light, for at least 20 wk after multiple treatments and 10 wk after a single treatment. Transient hyperpigmentation, superficial exfoliation, and crusting were observed, which cleared without scarring. Topical aminolevulinic acid plus red light is an effective treatment of acne vulgaris, associated with significant side-effects. Aminolevulinic acid plus red light causes phototoxicity to sebaceous follicles, prolonged suppression of sebaceous gland function, and apparent decrease in follicular bacteria after photodynamic therapy. Potentially, aminolevulinic acid plus red light may be useful for some patients with acne.

Acne Vulgaris↗
PubMed1993

Interaction of Propionibacterium acnes with skin lipids in vitro.

Propionibacterium acnes is the predominant microbial resident within the pilosebaceous follicles of sebum-rich areas of human skin. This study investigated the effects of known hydrophobic components of sebum on the physiology and nutrition of this microorganism, grown anaerobically at 33 degrees C, under defined conditions using continuous culture techniques. The medium used was chemically defined, comprising eight amino acids, with glucose as the main carbon energy source, and the culture pH was maintained at 5.6. The range of sebum lipids assayed was based on the C18 monounsaturated fatty acid 9-cis-octadecenoic acid (oleic acid). Stock micronized solutions were aseptically pulsed into continuous cultures in the presence and absence of glucose, and nutritional effects monitored. None of the lipid substrates significantly affected P. acnes growth either in terms of maximum specific growth rate (mu max) or final culture biomass yield. Glycerol (3 mg ml-1) was found to be a poor carbon/energy source in comparison to glucose. Bacterial cells did, however, adhere with varying degrees, to the different lipid species, with maximum adherence occurring with the free fatty acid. This observation was confirmed by preliminary uptake experiments using [14C]oleic acid. The interactive site for cell adherence may be the lipid-fibrillar layer associated with the cell surface of P. acnes, as discerned in electron microscopical studies. The findings of this investigation suggest that one function of the P. acnes lipase may be to aid colonization within the pilosebaceous follicle, by promoting cell adherence to components such as oleic acid.

Glucose↗
PubMed2005

Unsaturated fatty acids induce calcium influx into keratinocytes and cause abnormal differentiation of epidermis.

Abnormal follicular keratinization is involved in comedogenesis in acne vulgaris. We recently demonstrated that calcium influx into epidermal keratinocytes is associated with impaired skin barrier function and epidermal proliferation. Based on these results, we hypothesized that sebum components affect calcium dynamics in the keratinocyte and consequently induce abnormal keratinization. To test this idea, we first observed the effects of topical application of sebum components, triglycerides (triolein), saturated fatty acids (palmitic acid and stearic acid), and unsaturated fatty acids (oleic acid and palmitoleic acid) on hairless mouse skin. Neither triglyceride nor saturated fatty acids affected the skin surface morphology or epidermal proliferation. On the other hand, application of unsaturated fatty acids, oleic acid, and palmitoleic acid induced scaly skin, abnormal keratinization, and epidermal hyperplasia. Application of triglycerides and saturated fatty acids on cultured human keratinocytes did not affect the intracellular calcium concentration ([Ca(2+)](i)), whereas unsaturated fatty acids increased the [Ca(2+)](i) of the keratinocytes. Moreover, application of oleic acid on hairless mouse skin induced an abnormal calcium distribution in the epidermis. These results suggest that unsaturated fatty acids in sebum alter the calcium dynamics in epidermal keratinocytes and induce abnormal follicular keratinization.

Acne Vulgaris↗
PubMed2004

The use of pyruvic acid in the treatment of acne.

BACKGROUND: Acne is one of the most common dermatological diseases, affecting about 50% of adolescents. Different chemical peelings are used in local treatment, either alone or in association with other therapies. OBJECTIVE: To evaluate the efficacy and tolerability of chemical peeling with pyruvic acid for treatment of mild to moderate papulo-pustular acne. METHODS: We conducted an open-label study in which patients affected by mild to moderate papulo-pustular acne were treated with 40-50% pyruvic acid every 2 weeks for a total of 3-4 months. Forty patients (26 women and 14 men), ranging in age from 18 to 30 years, were enrolled in the study. Evaluations of sebum production and skin hydration were performed before and after treatment in 24 patients. RESULTS: Complete remission was observed in 16 patients (40%), partial remission was detected in 20 patients (50%), and no improvement was seen in four patients (10%). No side-effects were observed during or after treatment. Post-treatment evaluation of sebum production in 24 patients revealed a reduction in sebum levels in all patients. Post-treatment values of cutaneous hydration did not vary significantly from pretreatment values in the 24 patients evaluated. CONCLUSIONS: The results of our study indicate that peeling with pyruvic acid can be considered an effective, safe and well-tolerated procedure in the treatment of patients affected by mild to moderate papulo-pustular acne.

Acne Vulgaris↗
PubMed2004

Improved efficacy and tolerability of retinoic acid in acne vulgaris: a new topical formulation with cyclodextrin complex psi.

OBJECTIVES: Retinoic acid (RA) has long been used, both topically and systemically, for disorders of keratinization, acne and related disorders. In the present study, the efficacy and tolerability of topical RA prepared as a cyclodextrin beta complex (beta-CD) is investigated in 66 acne vulgaris patients. METHODS: This randomized, double-blind, placebo-controlled study compares nightly topical application of RA/beta-CD complex hydrogel formulation (0.025%), RA/beta-CD complex in moisturizing base (0.025%), hydrogel base, moisturizer base or a commercial RA gel (0.05%) in acne vulgaris patients. Improvement of acne was assessed using a 5-point improvement scale and by measuring sebum and moisture content of the skin using an SM 810 sebumeter/corneometer. RESULTS: After 3 months of treatment, mean scores of acne improvement on the 5-point scale were 4 with the RA/beta-CD complex hydrogel formulation, 4.1 with the RA/beta-CD complex in moisturizing base, 1.2 with hydrogel placebo base, 1.1 with moisturizer placebo base and 3 with the commercial RA product. All patients treated with the commercial product experienced local side-effects. One patient discontinued due to severe irritation. None of the patients treated with the RA/beta-CD complex in the moisturizing base and hydrogel formulation experienced significant local irritation, although the sebum content of the skin decreased after application of the RA/beta-CD preparations. This change was not significant compared to controls. The moisture content of the skin was better preserved in the group treated with the RA/beta-CD complex in the moisturizing base. CONCLUSION: The topical RA/beta-CD complex, in hydrogel and moisturizing base, was more effective than the twice concentrated commercial RA product. There were few topical side-effects with this new formulation, which increases patient compliance. Topical RA/beta-CD (0.025% RA) did not significantly reduce sebum secretion but may help to preserve optimum epidermal moisture content with the proper base formulation. This is the first study in the literature reporting efficacy and tolerability of the topical RA/beta-CD complex in acne vulgaris. We conclude that the topical RA/beta-CD complex displays an improved efficacy and tolerability profile and is an effective treatment alternative for acne vulgaris.

Acne Vulgaris↗
PubMed2004

Novel aspects in cutaneous biology of acetylcholine synthesis and acetylcholine receptors.

Extraneuronal acetylcholine (ACh) has been demonstrated to influence a plethora of cutaneous cell functions in an autocrine, paracrine and endocrine fashion. Through the differentiation-specific expression of its different nicotinic (nACh-R) and muscarinic (mACh-R) receptors, ACh acts upon keratinocyte proliferation and migration, terminal differentiation and barrier formation, sweat and sebum secretion as well as microcirculation and angiogenesis. Only very recently it has been recognized that acetylcholinesterase, but not cholineacetyltransferase, activity is regulated by hydrogen peroxide. Considering that the outer layer of the human skin can be a target for UV-generated H2O2 in the millimolar range, this mechanism needs to be taken into account for the regulation of ACh homeostasis in skin biology. Consequently, ACh can accumulate, as shown, for example, in the depigmentation process in vitiligo. There is a highly regulated distribution of ACh-R in human epidermis and adnexal structures, supporting previously observed effects of cholinergic compounds on keratinocyte biology. Most significantly, the regulated expression of ACh-R in sebaceous glands advocates a role for ACh in sebum production and as a promoter of sebocyte differentiation, thus offering an explanation for skin diseases associated with altered sebum production after chronic nicotine exposure. So far, ACh-induced sweat production has been thought to be under the exclusive control of mACh-R. However, recently, the presence of both different nACh-R and mACh-R in myoepithelial and acinar cells of eccrine sweat glands has been documented, indicating a more complex regulation of sweat production and expulsion.

Acetylcholine↗
PubMed1995

Effect of oral isotretinoin treatment on skin androgen receptor levels in male acneic patients.

An oral daily dose (mean +/- SD, 0.75 +/- 0.05 mg/kg) of isotretinoin was administered for 3 months to six male patients with acne (scores of 4 and 5 according to Rosenfield). The therapy resulted in complete resolution of acne in four patients and improved acne significantly (score 1) in two patients. In accordance with recent findings, no change in serum testosterone and significant decreases in 5 alpha-dihydrotestosterone, 5 alpha-androstane-3 alpha,17 beta-diol glucosiduronate, and androsterone glucosiduronate levels were observed after treatment. Androgen receptor status was investigated in back skin biopsies obtained in acne areas before and after 3 months of isotretinoin treatment. The treatment did not modify the binding affinity constant of skin androgen receptor (0.44 vs. 0.32 nmol/L), but it did induce a 2.6-fold decrease in its binding capacity constant (62 vs. 24 fmol/mg cytosolic protein), as assessed by Scatchard plot and confirmed immunologically by Western blot analysis. These data clearly showed that skin androgen receptor was sensitive to oral isotretinoin administration in acneic patients. The decrease in skin androgen receptor levels (this study) and the recently reported suppression of skin 5 alpha-dihydrotestosterone production by isotretinoin treatment appeared consistent with the involvement of androgen receptor and 5 alpha-dihydrotestosterone in the pathogenesis of acne. Indeed, sebum production is under androgen control, and an abnormal response of the pilosebaceous unit to androgens appears to be implicated in the pathogenesis of acne. These observations were consistent with the absence of sebum in complete androgen-insensitive patients and normal sebum production in male pseudohermaphrodites.

Acne Vulgaris↗
PubMed2002

[Mechanisms and causes of acne].

Three pathogenic factors are closely involved in the mechanism of acne with a sequence beginning with seborrhea, then sebum retention, and finally inflammation. The sebaceous gland is a target of androgens. Acne may be related to an excessive sensitivity of sebaceous end-organs to androgens. However, in women, an ovarian or adrenal hyperandrogenism may be implicated. The cause of sebum retention is the hyperkeratinisation of the infra infundibulum of the sebaceous duct. Many factors, particularly the chemical composition of sebum in acne and the androgens are responsible for this hyperkeratinisation. The inflammation is related to the inflammatory role of the numerous enzymes of Propionibacterium acnes and to the chimiotactism of neutrophils. Other pathogenic factors may have a role in acne, particularly smoking and stress. The knowledge of these pathogenic factors and their evaluation in each patient are a main point for therapeutic strategy, because every available treatment has a special impact on such or such factor.

Acne Vulgaris↗
PubMed1977

Acne vulgaris: recent advances in pathogenesis and treatment.

Hormonal factors, particularly androgens, appear to be important in the pathogenesis of acne vulgaris. The sebaceous glands in acne are more sensitive to normal blood levels of androgens, and are stimulated to produce more sebum. Corynebacterium acnes in the sebaceous follicles act on triglycerides in the sebum to form free fatty acids which might alter the process of keratinization in the follicular canal. A microcomedo is formed which can progress to the clinical lesions of acne. Sebum and its components may also be inflammatory if released into the skin. There are, however, still a number of unanswered questions relating to acne pathogenesis. Currently, therapy of acne vulgaris revolves around topical benzoyl peroxide and retinoic acid and systemic tetracyclines. Benzoyl peroxide and tetracyclines are antibacterial while retinoic acid is comedolytic. Because of these different actions, combined therapy appears to be more effective (benzoyl peroxide and/or tetracyclines together with retinoic acid). Topical antibiotics show promise as new therapeutic agents.

Acne Vulgaris↗
PubMed1984

Lipid composition of the bovine epidermis.

In contrast to skin surface or sebum lipid, cattle epidermis was found to contain a lower proportion of wax ester and unesterified fatty acid and a high proportion of triglyceride. The epidermal triglycerides differed significantly in their fatty acid composition from those of the skin surface and sebum. In particular they contained extremely low levels of linoleic acid. It is concluded that the skin surface triglycerides and most likely the other major lipid fractions of the bovine skin surface are derived mainly from sebum.

Animals↗
PubMed1993

The effect of synthetic dermal secretion on transfer and dissipation of the insecticide aldicarb from granular formulation to fabric.

This research investigated the potential for contamination of fabric by aldicarb (Temik 15) pesticide. Fabric soiled with synthetic perspiration or synthetic sebum was contaminated with Temik granules for various time periods and extracted with methanol. Extracts were analyzed with high performance liquid chromatography. The aldicarb transferred to both soiled and unsoiled fabric; however, the sebum soil and longer contact time increased the transfer of aldicarb to fabric. The dissipation of aldicarb from fabric was affected by the soil type and the formulation of the Temik granule. It is apparent a potential for dermal exposure to granular pesticide exists when the pesticide is trapped in pockets or folds of clothing.

Aldicarb↗
PubMed1983

Vimentin filaments in peritoneal macrophages at various stages of differentiation and with altered function.

Comparative immunofluorescence microscopic, transmission and scanning electron microscopic investigations were carried out to study the arrangement and significance of vimentin filaments in monocytes, macrophages, epithelioid cell equivalents and multinucleate giant cells under various different functional conditions, and in the presence of functional disorders. Uncoated or sebum-coated coverslips were implanted in the peritoneal cavity of Wistar rats. Some of the animals received repeated i.p. injections of colchicine. Rats were killed at various times 1 to 14 days after initiation of the experiment. The number of macrophages, the degree of their activation, and the growth of cells on the coverslips was considerably greater on sebum-coated than on uncoated implants. Various characteristic vimentin distribution patterns were found dependent on the cell cycle, the form and volume of the cell, and on the degree of differentiation and maturity; they were also related to the type and intensity of cell function. These patterns were best developed in ordered multinucleate giant cells. Repeated administrations of colchicine resulted in a marked flattening of the cell body on the coverslips--which correlated with a considerable reduction in the number of vimentin filaments and of cytoplasmic processes--and also in the formation of circumscribed erect, tree-like protuberances. The "trunk" of these structures comprised closely bundled vimentin filaments, and the cell nucleus was located at its base. These morphologic changes, which were associated with a functional insufficiency, proved to be reversible.

Animals↗
PubMed2001

Skin function and skin disorders in Parkinson's disease.

Cutaneous symptoms (seborrhoea and hyperhidrosis) in Parkinson's disease were investigated. In 70 treated patients with Parkinson's disease and 22 control subjects, non-invasive bioengineering methods (sebumetry, corneometry, pH) were carried out on the forehead, sternum and forearm. In addition, concomitant dermatoses and medication were recorded. 18.6% of the patients had seborrhoea on the forehead (>220 microg/cm2), 51.4% showed normal sebum values (100-220 microg/cm2) and 30% a sebostasis (<100 microg/cm2). Males has significantly higher sebum values than females. No relationship between the seborrhoea and the therapy for Morbus Parkinson was found. Patients with hyperhidrosis (n = 36) had significantly lower pH values (p < 0.05) on the forehead than those without hyperhidrosis. 22 patients (31.9%) reported a cold/hot flush and a further 13 (18.8%) had clinical rosacea. Seborrhoea is rare in treated Parkinsonian patients but hyperhidrosis is frequently found. Furthermore, a particular lack of vasostability (flush) appears to be an autonomic dysregulation in the skin related to Morbus Parkinson, which has not been studied to any extent to date.

Aged↗
PubMed2001

Pathogenesis of acne.

Acne vulgaris is a skin disorder of the sebaceous follicles that commonly occurs in adolescence and in young adulthood. The major pathogenic factors involved are hyperkeratinization, obstruction of sebaceous follicles resulting from abnormal keratinization of the infundibular epithelium, stimulation of sebaceous gland secretion by androgens, and microbial colonization of pilosebaceous units by Propionibacterium acnes, which promotes perifollicular inflammation. The clinical presentation of acne can range from a mild comedonal form to severe inflammatory cystic acne of the face, chest, and back. At the ultrastructural level, follicular keratinocytes in comedones can be seen to possess increased numbers of desmosomes and tonofilaments, which result in ductal hypercornification. The increased activity of sebaceous glands elicited by androgen causes proliferation of P. acnes, an anaerobe present within the retained sebum in the pilosebaceous ducts. The organism possesses a ribosome-rich cytoplasm and a relatively thick cell wall, and produces several biologically active mediators that may contribute to inflammation, for instance, by promoting leukocyte migration and follicular rupture. In inflamed lesions, numerous neutrophils and macrophages infiltrate around hair follicles and sometimes phagocytose P. acnes. To examine the participation of neurogenic factors in the pathogenesis of acne, we quantitatively assessed the effects of neuropeptides on the morphology of sebaceous glands in vitro using electron microscopy. Substance P, which can be elicited by stress, promoted the development of cytoplasmic organelles in sebaceous cells, stimulated sebaceous germinative cells, and induced significant increases in the area of sebaceous glands. It also increased the size of individual sebaceous cells and the number of sebum vacuoles for each differentiated sebaceous cell, all of which suggests that substance P promotes both the proliferation and the differentiation of sebaceous glands. In this review, we introduce the general concept of pathogenic factors involved in acne, including typical electron microscopic findings and recent evidence of stress-induced exacerbation of acne from a neurological point of view. An improved understanding of the pathogenesis of acne should lead to a rational therapy to successfully treat this skin disease.

Acne Vulgaris↗
PubMed1975

A sebotrophic stimulus in benign and malignant breast disease.

The sebum-excretion rate (S.E.R.) has been found to be increased in patients with benign as well as malignant breast disease. The S.E.R. was not increased in patients undergoing surgery for other diseases. It is considered that the sebotrophic hormone may also be mammotrophic. Drugs such as reserpine and the phenothiazines which increase sebum production may perhaps provoke benign as well as malignant breast disease.

Acne Vulgaris↗