Reduce Sebum Production Naturally

Oily Skin Solution

If you know what the annoyances of oily skin are, you will want this book; no question about it. If you struggle with skin that just always feels a little bit greasy no matter what and is constantly fighting acne, you will want this guide. This ebook gives you the ingredients to start making your skin feel a little more like every else's, and gets rid of the unsightly blemishes as a result of acne or other oily side-effects. Patricia Evens shows you that tradition, commercial moisturizers really won't do anything for you You will not be able to fight skin grease with those. Learn what you Really need to do to start repairing your skin and getting better-feeling skin. You don't need to spend a lot of money to help you All it takes is the information in this book! Don't suffer from oily skin Start improving now! More here...

Oily Skin Solution Overview


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Sebum Secretion and Acne

COMPOSITION OF HUMAN SEBUM Sebum is synthesized in sebaceous glands, which are part of the pilosebaceous units of the skin (1). Sebaceous glands are epidermal appendages found in all regions of the skin, except the palmar and plantar surfaces however, the greatest density of glands is found in the scalp and facial areas. As sebocytes move from the basal layer at the periphery of the gland toward the lumen, they synthesize neutral lipids, which accumulate as lipid droplets, and eventually all of the carbon-based components of the cell are converted into lipid. The composition of sebum is species-specific. Human sebum, as it is synthesized in the gland (2), consists of squalene (15 ), wax esters (25 ), cholesterol esters (2 ), triglycerides (57 ), and cholesterol (1 ). The small proportion of free cholesterol and cholesterol esters are thought to be derived from cholesterol in the basal sebo-cyte plasma membrane. Differentiating sebocytes do not express the enzymes of the cholesterol...

Function of Sebum

In animals, sebum may provide odor it contains pheromones and may also condition the hair. However, in humans, the function of sebum is unclear (5) and it has been speculated that the sebaceous glands are vestigial (20). There is now an increasing body of evidence indicating that the sebaceous gland and the components of sebum play a crucial role in the homeostasis of skin (6). Sebum transports vitamin E, a lipophilic antioxidant, to the skin surface where it may play a key role in protecting skin surface lipids from peroxidation (62). Glycerol, a major component of sebaceous triglycerides, may play a role in maintaining epidermal barrier function, since asebic mice lacking sebum and, therefore, glycerol have a poorly functioning epidermal barrier (63). Other proposed functions include antibacterial, lubrication, and or to provide precursor substrates for epidermal metabolism and synthesis of lipids and or vitamin D (5). In equine follicles, the sebaceous gland and sebum are required...

Sebaceous Glands

Sebaceous32 (see-BAY-shus) glands produce an oily secretion called sebum (SEE-bum). They are flask-shaped, with short ducts that usually open into a hair follicle (fig. 6.11c), although some of them open directly onto the skin surface. These are holocrine glands with little visible lumen. Their secretion consists of broken-down cells that are replaced by mitosis at the base of the gland. Sebum keeps the skin and hair from becoming dry, brittle, and cracked. The sheen of well-brushed hair is due to sebum distributed by the hairbrush. Ironically, we go to great lengths to wash sebum from the skin, only to replace it with various skin creams and hand lotions made of little more than lanolin, which is sheep sebum.

Growth Factors and Neuropeptides

EGF, TGF-a, basic FGF, and keratinocyte growth factor (KGF) all inhibit lipogenesis and with the exception of KGF are mitogenic in cultured hamster sebocytes (133,151). In organ culture of human sebaceous glands, EGF produced a dose-dependent inhibition of lipid synthesis and inhibited DNA synthesis (152), and removal of EGF from the medium caused an increase in the rate of lipogenesis without affecting cell turnover (113). In vivo, the presence of EGF inhibited the sebaceous gland differentiation in sheep (153), and in hamster ears, it stimulated the sebaceous glands to proliferate (154). Receptors for EGF are found in sebaceous glands (155). Based on this evidence, Kealey and colleagues proposed that EGF may be, in part, responsible for sebaceous gland atrophy observed during acne lesion formation (7,152). EGF can also induce changes in sebum composition. Ridden (156), reported that there was a fall in the amount of squalene and a corresponding rise in cholesterol, although this was...

Peroxisome Proliferatoractivated Receptors Are Activated By A Diverse Array Of Compounds

FIGURE 4 Peroxisome proliferator activated receptor (PPARa), PPAR S, and PPARy protein is detectable in freshly isolated human sebaceous glands. Sebaceous glands were isolated and processed for immunoblotting as previously described. Approximate protein sizes are indicated. This micrograph is representative of n 3 subjects. Abbreviations KC, primary human keratinocytes PPAR, peroxisome proliferator activated receptor SG, human sebaceous glands. Source From Ref. 41.

Peroxisome Proliferatoractivated Receptor Activity In The Epidermis And Pilosebaceous Unit

Terminal differentiation of the cells of the human pilosebaceous unit is not dissimilar from that of the epidermal keratinocytes. Like epidermal keratinocytes, the matrix cells of the hair follicle and the sebocytes of the sebaceous gland terminally differentiate to die, forming the hair fibre or releasing their cell content as sebum, respectively. This program includes a biochemical differentiation, the expression of various structural proteins, and the processing and reorganization of lipids. A wealth of data has been collected to date, suggesting that PPARs have specific roles in these complex processes. In contrast, in organ maintained human sebaceous glands, PPARy and PPARa selective ligands inhibited total sebaceous lipogenesis (Table 1) and also reduced the production of the sebum-specific lipids, squalene and triacylglycerol (Table 2). Further, arachidonic, linoleic, linolenic, and oleic acid, which are less specific in their PPAR subtype activation, also inhibited sebaceous...

Approach To Hormonal Therapy In Female Acne

Hormonal therapy is an excellent option for treatment of women whose acne is not responding to conventional therapy. If there are signs of hyperandrogenism, an endocrine evaluation is indicated, consisting of tests such as DHEAS, total- and free-testosterone, and an LH FSH ratio. Although hyperandrogenism is an indication for hormonal therapy, women with normal serum androgen levels also respond well to treatment. The mainstays of hormonal therapy include oral contraceptives and spironolactone. Other agents to choose from include cyproterone acetate, flutamide, and glucocorticoids. Hormonal agents work best as part of a combination regimen including topical retinoids or topical or oral antibiotics depending upon the severity of the acne. In some women, the additional of hormonal therapy has improved acne to the point where subsequent treatment with iso-tretinoin was no longer necessary. As more is learned about the hormones involved in acne, their source of production and the...

Regulation of Pilosebaceous Unit Activity

Perhaps the most profound and well-known effect of hormones on the pilosebaceous unit is the one caused by androgens, more specifically in causing sebaceous gland enlargement, sebocyte proliferation, and lipid metabolism (91,92). It is well established that the increase in lipid production and enlargement of the sebaceous glands at puberty is attributable to an increase in circulating androgens from the testes in males, the ovaries in females, and the adrenal glands of both sexes. Androgen-insensitive subjects do not produce sebum (93). Furthermore, the local application of testosterone to skin resulted in a 15-fold increase in sebum excretion rate, although admittedly this was a small study in which 2 testosterone cream was applied to the foreheads of prepubertal boys. In fact, three subjects failed to respond, but this study does demonstrate that skin can respond to local androgens (94). Androgen sensitivity of pilosebaceous units has been confirmed by the positive detection of...

Cell Biology of the Pilosebaceous Unit

Follicular Duct

This chapter reviews the structure and function of the pilosebaceous unit and the controlling influences on the pilosebaceous unit and sebum secretion. The chapter is divided into three sections. Section I gives an account of the structure and function of the normal pilosebaceous unit Section II describes the biochemistry and regulation of pilosebaceous unit biology and finally, Section III deals briefly with the biochemical changes occurring in the pilosebaceous duct in acne. In humans, pilosebaceous units or pilosebaceous follicles are found on all skin surfaces, apart from the palms of the hands and soles of the feet. Essentially, they are invaginations of the epidermis into the dermis. Each comprises a duct, which ends in the dermal papilla, a hair fiber (or pilus) produced by the dermal papilla, a sebaceous gland and its associated sebaceous duct. The duct supports and protects the hair fiber and also drains sebum produced by the sebaceous gland and carries it to the skin...

Overview of the Pathogenesis of Acne

Physical agents may also enhance comedogenesis. Favre-Racouchaut syndrome consists of severe photodamage accompanied by open comedones on the face (9). Mills et al. (10,11) have demonstrated that UV irradiation will enhance the comedo formation in the rabbit ear engendered by squalene, cocoa butter, sebum, and some sunscreens. Another potential cause of comedo formation is the lipid contents of the follicle itself. Bacterial lipolysis will liberate fatty acids from sebaceous triglycerides that are comedogenic, but the presence of microcomedones in the skin of prepuber-tal children (who have no follicular microflora and no sebum) argues against a major role of bacterial action in early comedogenesis (15). Strauss et al. (16) have shown that the sebum of acne patients is relatively deficient in linoleic acid, perhaps reflective of high sebum secretion rates and have suggested that local linoleic acid deficiency may be involved in comedo formation. Further study of this possibility is...

Structure of the Pilosebaceous Duct

Cornification Pilosebaceous Duct

The pilosebaceous duct is lined by a stratified, squamous epithelium consisting of keratinocytes. The duct lumen is frequently colonized by bacteria that rely on the keratinocytes and sebum as a source of nutrients. Several distinct anatomical parts of the duct can be recognized. The opening of the duct onto the surface of the skin is the orifice or ostium. The sebaceous follicles on the back frequently group together and emerge through one orifice (25), while those on the face and chest show no such grouping (26). Grouped follicles may be more prone to bacterial colonization, which may, in turn, have important implications for follicular diseases. The size of the duct orifice can decrease by as much as 50 in conditions of high humidity due to hydration of keratin in the pilosebaceous duct (27). During this time, sebum excretion is significantly reduced, but then increases above its original level when the duct reverts to its original size. In terminal follicles, the whole of the...

Proposed Hybrid Method

The biggest obstacle to accurate measurement of sebum secretion rates is the need to deplete the sebaceous follicles. This can be overcome by 12 to 14 hours of adsorption onto bentonite prior to measurement. Once the reservoir is depleted, the Sebutape method is appealing for the actual sebum secretion measurement. The collection time could be shortened to one hour, and a digitized image of the Sebu-tape on its black backing should be captured immediately. Subsequently, this image can be analyzed to estimate the sebum secretion rate from the total black area. In addition, information on the number, the pattern and the activity of individual glands can be obtained. The Sebutape can be removed from the backing and the lipids can be extracted and examined by thin-layer chromatography in conjunction with photodensitometry. In this way, one could obtain two measures of the sebum secretion rate, the overall lipid class composition and information on the pore density and variation in the...

The Molecular Biology of Retinoids and Their Receptors

Pml Rar Alfa Acido Retinoico

Acne vulgaris is a multifactorial disease of the skin in areas rich in sebaceous follicles. It is characterized by seborrhea, hypercornification of the infundibulum (the neck of the sebaceous gland), and the presence of comedones and inflammatory lesions such as papules and pustules. The inflammatory pathway is mediated by antigenic and inflammatory products of Propionibacterium acnes (1). Although acne is mostly associated with puberty, persistent or late onset acne may be similar in physiology to pubertal acne, with hyperandrogenicity and increased sebogenesis, being the key factors (2). The hyperproliferation of the infundibulum keratinocytes, characterized by the expression of the hyperproliferative marker proteins, Ki67 and K6 16, and the resulting immature stratum corneum does not desquamate efficiently, leading to clumps of squames that attach to the hair follicle causing a blockage to sebum flow. Hypercornification of the infrainfundibulum is an early feature of the...

Androgen Metabolism Within the Skin

Androgens within sebaceous glands (9). Such insights may be of benefit in the design of new acne therapies. The skin and sebaceous gland are capable of producing and metabolizing androgens (9). DHEAS is the major adrenal androgen precursor. It circulates in the blood stream in relatively high levels compared with other hormones with the exception of cortisol. In fact, in for review, see Ref. postmenopausal women, all sex steroids made in the skin are from adrenal steroid precursors, especially DHEA. Secretion of this precursor steroid by the adrenals decreases progressively from age 30 to less than 50 of its maximal value at age 60 (10). The enzyme 3 -hydroxysteroid dehydrogenase (3 -HSD) acts on DHEA to convert it to androstenedione (Fig. 1). This conversion may take place in the adrenal gland and tissues such as the sebaceous gland, where activity of the 3 -HSD enzyme has been identified by several investigators (11-13). The reversible conversion of androstenedione into testosterone...

The Sebaceous Gland Is a Steroidogenic Tissue

The skin and sebaceous glands are capable of synthesizing cholesterol de novo from acetate (22-24). Although this cholesterol is utilized in cell membranes, in the formation of the epidermal barrier, and is secreted in sebum, its use as a substrate for steroid hormone synthesis had not been established until recently. In order for steroid synthesis to occur, cholesterol needs to be translocated from the outer to the inner mitochondrial membrane. This process is regulated by the steroidogenic acute regulatory protein (25). Additional enzymes and cofactors needed to convert cholesterol into a steroid include P450 cholesterol side chain cleavage, adrenodoxin reductase, cytochrome P450c17, and steroidogenic factor-1. Expression of each of these proteins was found in human facial skin, sebocytes, and in a recently developed simian virus (SV) 40-immortalized human sebocyte cell line (SEB-1) (26). These data demonstrate that the skin is in fact a steroidogenic tissue. The clinical...

Changes in the Pilosebaceous Unit in Acne

There is no doubt that sebum plays an important etiological role in acne (99,168170). Patients with acne secrete more sebum than unaffected individuals and sebo-suppressive treatments alleviate acne the greater the inhibition the more profound the clinical response. In addition to elevated sebum excretion, it is well-established that acne is associated histologically and clinically with hypercornification of the duct epithelium (7,38,171). Ductal hypercornification results initially in the formation of microcomedones and eventually comedones, a process termed comedo-genesis. On the basis of a detailed histological study Kligman (7) concluded that comedogenesis began in the infrainfundibulum and was closely followed by hyper-keratosis of the sebaceous duct. This is now generally accepted to a reasonable description of what is likely to happen. Essentially, microcomedones are those follicles containing impactions, follicular casts, or sebaceous filaments of corneocytes, bacteria, sebum,...

Structure of the Pilosebaceous Gland

All sebaceous glands are similar in structure. They consist of either a single lobule (acinus) or a collection of acini. The glands are separated from the dermis by a connective tissue capsule, consisting of fine collagen fibers, fibroblasts, and a capillary plexus. The ultrastructure of human sebaceous cells does not vary significantly from one skin site to another nor does the ultrastructure of sebocytes of prepubertal children differ significantly from that of adults, implying that increased levels of androgens at puberty do not induce gross ultrastructural changes (50). In human skin, the cells of sebaceous glands, called sebocytes, which are modified keratinocytes, can be divided into three major cell types determined by structure undifferentiated or dividing, differentiated, and mature. The undifferen-tiated cells are attached to the basement membrane by hemidesmosomes. These cells tend to be cuboidal and are characterized by the possession of large nuclei, numerous...

Phototherapy and Laser Therapy of Acne

Although there was a clear clinical benefit, sebum secretion and P. acnes populations were measured to be unchanged. Inhibition of Sebum Production Sebum is, in a sense, the central problem in acne. Without it, P. acnes cannot proliferate and acne would not exist. The most effective drug for the disease isotretinoin exerts the majority of its effects on sebum secretion. A light-based treatment that targets sebum production would have the potential to cure acne. Could one do without sebaceous glands Most likely. The function of sebum is unknown it may serve to inhibit invading bacteria such as dermatophytes and streptococci, but children do well with no sebum and adults have little-to-no sebaceous activity on the extremities with no ill effects. Anderson et al. (6) have reported a series of 22 patients with acne of the back, who were sensitized aggressively with ALA and then irradiated with a potent dose of broadband (550-700 nm) light. Pain, erythema, and evidence of...

Role Of Antimicrobial Peptides In Acne

From the published studies to date, it is clear that -defensins are expressed in regions of the pilosebaceous unit that are exposed to microorganisms and moreover, in regions that may provide access routes for these organisms into the skin. Moreover, it is also apparent that some -defensins are upregulated in acne (9). What, therefore, is the role of antimicrobial peptides in acne Major factors in the pathogenesis of acne include hypercornification of the distal ORS and the pilosebac-eous duct in concert with increased sebum production and abnormalities of the microbial flora (34).

Biochemical Changes in the Infundibulum During Comedogenesis

Although it is clear that we now know a great deal about the pilosebaceous unit at the structural, biochemical, and physiological levels, there are still considerable gaps in our understanding. Much of the early work was descriptive biology of the structure obtained using immunohistochemical studies. Over the last decade, several in vitro models systems (isolated organ culture, cultured sebocytes) have made it easier to study the cellular processes in the follicle, including sebum production and the effect of inhibitors and stimulators. There is also now a good deal of information about the chemistry and biosynthesis of sebum components, and we also have a much better understanding of the cell biology of the pilosebac-eous duct. Even so, we are still unable to precisely define the cause of one of the most common skin diseases, namely acne, which affects a very large proportion of the population globally. 19. Pierard GE. Follicle to follicle heterogeneity of sebum excretion....

Squalene Biosynthesis

Human sebum contains a high percentage of squalene, in contrast to the epidermal lipids, which contain a higher proportion of cholesterol. In the sebaceous glands, therefore, the cholesterol biosynthetic pathway appears to be partly arrested in the steps after the production of squalene. This may be due to low activity of squa-lene epoxidase, or other enzyme of cholesterol biosynthesis, or the availability of substrates. For example, a ready supply of acetate appears to direct lipogenesis toward squalene biosynthesis, while glucose, glutamine, and isoleucine preferentially result in more triacylglyceride production in vitro (71). Limiting levels of NADPH had previously been suggested, but this is not believed to be responsible for the low levels of cholesterol produced. Since squalene is unique to sebum, it is often used as a marker to differentiate sebaceous lipids from epidermal lipids. The activity of HMG CoA reductase in sebocytes regulates the amount of squalene produced. This...


Human sebum is quite distinct in composition and biological complexity compared to that of other animals, and also compared to epidermal lipids synthesized by keratinocytes. It is unique in containing high levels of squalene and characteristic free fatty acids, for which the rate-limiting enzymes of the biosynthetic pathways are 3-hydroxy-3-methylglutaryl (HMG) CoA reductase and acetyl CoA carboxylase, respectively. Both enzymes are inactivated by phosphorylation through a cAMP-activated protein kinase. Comparison of the kinetic parameters for these enzymes with those previously described in the literature found in other organs, indicates that the sebaceous gland enzymes have similar affinities for substrates and similar responses to allosteric effectors such as citrate. However, there are key points of differences and these will be discussed in turn.

Instrumental Methods

In 1970, Schaefer and Kuhn-Bussius (27) demonstrated that sebum secretion could be measured by collecting it on a frosted glass plate and measuring the transparency. As sebum is adsorbed on the rough surface, it spreads and fills the microscopic pockets within the glass. This smooths the surface and will result in less light scattering when the plate is illuminated with a beam of light. The relationship between the amount of adsorbed lipid and light transmission was quantitated and shown to be nonlinear. Subsequently, several instruments based on this principle have become commercially available. The first of this is the Lipometre introduced by L'Oreal (Aulnay's Bois, France). More recently, the Sebumeter has been introduced by Courage & Khazaka (Koln, Germany). These instruments allow measurements of the amount of sebum on the skin surface or the sebum secretion rate, which can be made easily within a few minutes. However, calibration can be difficult, and unless the sebaceous...


FIGURE 3 Peroxisome proliferator activated receptors are expressed in freshly isolated human sebaceous glands. RNA was extracted and reverse transcription polymerase chain reaction (PCR) performed as previously described. Lanes 1 to 3 show PCRs performed on freshly isolated glands derived from three different subjects. Individual lane numbers in each of the PCR refer to cDNA obtained from the same subject. For example the PCR shown in lane 1 in each gel was performed using an aliquot from the same sample of cDNA. Abbreviations GAPDH, glyceraldehyde-3-phosphate dehydrogenase PPAR, peroxisome proliferator activated receptors. Source From Ref. 41. Further, mRNA expression of the three PPAR subtypes was demonstrated in cultured human sebocytes (39), as well as the protein expression of PPARy. In accordance, mRNA and protein expression of PPARa, PPAR 8, and PPARy was shown in isolated human sebaceous glands (Figs. 3 and 4, respectively) (41). Although no differences in mRNA levels could be...


Since the completion of this manuscript, more research has been done into examining the effects of PPAR ligands on sebaceous lipogenesis. The PPAR ligands GW7647, GW0742, GW2433, rosiglitazone, and GW4148 significantly increased lipogenesis in SEB-1 sebocytes (121), confirming earlier reports referenced in this chapter. Interestingly, patient data collected in the same paper showed increased sebum secretion in patients receiving fibrates for hyperlipidemia or thialzolidienediones for diabetes. However, this is in contrast to observation in healthy volunteers, and one might argue that these patients are treated for metabolic diseases of the liver and pancreas, which may also effect sebaceous gland metabolism, and therefore these data should be treated with caution. In addition, PPAR involvement in the prostaglandin pathway has been shown in a recent paper where PPARy activation has been implicated in oxidative stress-mediated prostaglandin E(2) production in SX95 human sebaceous cells...


In normal human skin, AM is expressed in suprabasal layers of the epidermis, in melanocytes, and in sweat and sebaceous glands (8,21). In the hair follicle, AM protein is expressed in the basal and suprabasal layers of the hair bulb and the proximal ORS. Whereas, in the distal ORS AM becomes increasingly supra-basal, especially in proximity to the bulge region. In contrast to defensins, AM immunoreactivity (IR) is absent from the basal cells of the bulge. The CRLR is expressed in a similar pattern to that of AM. In contrast, the L1 IR receptor is only expressed in suprabasal cells (21).

Androgens In Acne

An essential role for androgens in stimulating sebum production is supported by several lines of evidence. For example, the development of acne in the prepuber-tal period has been associated with elevated serum levels of DHEAS, a precursor for testosterone (3,4). Androgen-insensitive subjects who lack functional androgen receptors do not produce sebum and do not develop acne (5). Tumors of the ovary or the adrenal that produce androgens are often associated with the development of acne. Systemic administration of testosterone and dehydroepian-drosterone increases the size and secretion of sebaceous glands (6), and we know that severe acne is often associated with elevated serum androgens (7,8).

Estrogens In Acne

Very little is known about the role of estrogens in modulating sebum production. Any estrogen given systemically in sufficient amounts will decrease sebum production. The dose of estrogen required to suppress sebum production, however, is greater than the dose required to suppress ovulation (27). The major active estrogen is estra-diol, which is produced from testosterone by the action of the enzyme aromatase. Aromatase is active in the ovary, adipose tissue, and other peripheral tissues. Estradiol can be converted to the less potent estrogen, estrone, by the action of the 17 -HSD enzyme. Both aromatase and 17 -HSD are present in the skin (17,28). Estrogens may act by several mechanisms they may (i) directly oppose the effects of androgens locally within the sebaceous gland, (ii) inhibit the production of androgens by gonadal tissue via a negative feedback loop on pituitary gonadotrophin release, and (iii) regulate genes that negatively influence sebaceous gland growth or lipid...


Oral spironolactone decreases sebum excretion rate by 30 to 50 . Recommended doses are 50 to 100 mg taken with meals (36,37). However, many women with sporadic outbreaks of inflammatory lesions or isolated cysts respond well to 25 mg twice daily and some even respond to just 25 mg a day. These low doses in healthy young women are generally well-tolerated. However, if this drug is used in older women who may have other medical problems, or if higher doses are used for conditions such as hirsutism or androgenetic alopecia, serum electrolytes should be monitored. Side effects of spironolactone include breast tenderness and menstrual irregularities. Additionally, it is important that pregnancy be avoided during treatment with spironolactone due to the potential for abnormalities of the male fetal genitalia such as hypospadias.

Oral Contraceptives

Oral contraceptives generally contain an estrogen (most commonly ethinyl estra-diol) and a progestin. In their early formulations, oral contraceptives contained over 100 mg of estrogen. In these and higher doses, estrogens themselves can suppress sebum production. Estrogens also act on the liver to increase the synthesis of sex hormone-binding globulin that binds testosterone and lowers the circulating levels of free testosterone. In addition, oral contraceptives inhibit the ovarian production of androgens by suppressing ovulation. This, in turn, decreases serum androgen levels and reduces sebum production. The concentrations of estrogen in oral contraceptives have decreased over the years from 150 to 35 mg, and in the most recent forms, to 20 mg, in order to reduce the side effects associated with estrogen (41). Oral contraceptives containing low doses of estrogen are listed in Table 1.

Use And Side Effects

Dispensed and equally divided over two index fingers, which then dab the medication evenly onto opposite sides of the face and spread the medication into a thin layer until no visible product remains (21). Hands should be washed afterwards to avoid retinoid dermatitis (21). Application should first occur every other night for one to two weeks depending on the skin type so as to minimize the initial irritation that may otherwise discourage adherence to the treatment regimen (1,21). Oily skin is better able to tolerate the potential irritating effects of the retinoids and, as such, a shorter introductory period may be utilized (21). Non-comedogenic moisturizers can be used to minimize xerosis, erythema, and stinging (2). Patients should be instructed that as long as four to six weeks of use may be required before the onset of efficacy and that an initial flare in acne may occur following two to four weeks of use due to an accelerated evolution of preexisting microcomedones (3). Periodic...

Mechanism Of Action

Topical retinoids act to clear and prevent the formation of the microcomedo, the precursor to acneiform lesions. The microcomedo is formed from the occlusion of the follicular ostium by the androgen-induced production of sebum and the accumulation of stratum corneum cells (5). In normal skin, the corneocytes of the hair follicle's infrainfundibular region are small and form a noncontinuous, incoherent layer of cells that easily desquamate individually into the follicular canal (1,2,6). They then travel to the surface of the skin through the secretion of lipid-rich sebum (6). In contrast, the follicular epithelium of the microcomedo demonstrates abnormal, hyperactive keratinization, resulting in hypergranulosis and hyperkeratosis (2,5). Corneocytes are more cohesive and less able to migrate to the skin surface and instead become lodged within the follicle, occluding the expulsion of sebum, distending the follicular ostia, and thus forming the comedo (1,6). The anaerobic environment...


Expression of IL-1a and b was demonstrated in sebaceous glands by immunohis-tochemistry (162), and mRNA for IL-1a was detected in cultured sebocytes (163). No change in staining pattern was observed when sebum was extracted from the samples, indicating that IL-1 is not associated with sebum. The function of IL-1 in normal sebaceous glands is unclear, although in vitro IL-1a and tumor necrosis factor a, inhibited sebaceous lipogenesis in sebaceous gland organ culture and induced de-differentiation of human sebocytes into a keratinocyte-like phenotype (152). In organ culture, IL-1a at 1 ng mL promoted ductal cornification (164) and

Retinoid Types

The dose-dependent epidermal acanthosis results from increased number of cell layers, not from hypertrophy of individual cells (9). There is no change in structure or size of sebaceous glands after treatment with topical retinoids (9). All of the above factors demonstrate that comedolysis is retinoid-specific, not simply secondary to desquamation (3).

Thyroid Hormones

Thyroid hormones exert an effect on sebum secretion since thyroidectomy decreases the rate of sebum secretion in rats and administration of thyroxine reverses this effect (140). Increases in sebum secretion rate were observed when thyroxine was given to hypothyroid patients (141), and immunohistochem-ical localization of thyroid hormone nuclear receptors has been demonstrated in human scalp follicles in the nuclei of the outer root sheath cells, dermal papilla cells, sheath cells, and sebaceous gland cells (142). Other than this, little attention has been paid to the effect of thyroid hormones on sebum secretion.


Acne is generally accepted by clinicians to be a multifactorial disease and it is believed that acne is associated with seborrhea, the excess production of sebum by the sebaceous gland (49,113). Further, Propionibacferinm acnes is a major bacterium implicated in the pathogenesis of acne (114). Acne is characterized by the presence of noninflammatory lesions, termed comedones (47,50). The earliest pathological change in acne is altered follicular epithelial differentiation, resulting in a follicular retention hyperkeratosis the microcomedo (50). In addition to the noninflammatory lesions, inflammatory lesions can develop when such microcomedos are colonized by P. acnes. For inflammatory lesions such as papules, pustules, and nodulocystic lesions to occur, a variety of pathogenic factors are involved, including besides P. acnes, inflammatory mediators, and host immunity (115). In vitro experiments on organ maintained human infudibula have identified a number of cyto-kines that can model...

Effects Of Retinoids

The mechanism of action of isotretinoin has however remained elusive, as it does not bind itself to the retinoid receptors. Multiple actions have been proposed from inhibition of sebaceous gland activity, inhibition of the growth of P. acnes, inhibition of inflammation, and improvements in follicular epithelial differentiation. More recently, it has been shown that isotretinoin competitively inhibits 3 alpha-hydroxysteroid oxidation by retinol dehydrogenase, resulting in reduced formation of dhihydrotestosterone and thereby reduced sebogenesis (33). Retinoids are reported to increase the expression of transforming growth factor (TGF beta 1-3), and these inhibit keratinocyte proliferation. However, TGF beta-2 and 3, but not TGF beta-1, reduce cell proliferation and lipogenesis in human sebaceous glands in organ culture studies, suggesting that these growth factors may also contribute to the effects of retinoids on sebaceous glands (34 -37).

Free Fatty Acids

Sebum contains numerous fatty acids and many are quite unique in structure, including a wide variety of straight, branched, saturated, and unsaturated fatty acids (77). In human sebum, about 27 of fatty acids chains are saturated, with the greatest proportion being unsaturated (68 ). The vast majority of these are monounsaturated (64 ) and about 4 are diunsaturated, with the remainder being composed of fatty acid chains longer than 22 carbons (78). Monounsaturated fatty acids of sebum have a double bond usually inserted at position A9. However, in human sebum there is an unusual placing of the double bond at A6 to produce sapienic acid. Sapienic acid is a very abundant and important monounsaturated fatty acid with 16-carbons and a cis double bond located at the sixth carbon from the carboxyl terminal. This fatty acid has been implicated in acne and is produced by an enzyme unique to sebaceous glands, the A6 desaturase, which has recently been isolated from human skin, and its...


More recently, Sebutape (Cuderm Corporation, Dallas, Texas, U.S.A.) has been introduced for assessment of pore patterns and sebum secretion (22,23). This adsor-bant polymeric tape is white but turns transparent at the points where sebum is adsorbed. This tape is used after clearing sebum from the surface, but not depletion of the follicular reservoir, although there is no fundamental reason why this could notbe done. Typically, the Sebutape is removed from the forehead after three hours, although it has been suggested that one hour would be adequate (24), and placed on a black background. The pore pattern then appears as black dots on a white background, and the total black area determined by image analysis is proportional to the amount of sebum secreted (25). One can qualitatively assign the pore pattern to one of five categories, referring to images provided by the manufacturer prepubertal, pubertal, acne, mature, or senescent (26). It is also possible to extract lipids from the...


As mentioned earlier, all skin areas excluding the glabrous skin, that is, the palmar (palms) and plantar (soles), possess pilosebaceous units. Although the number of secreting follicles, and consequently sebum output, varies greatly between individuals, the distribution and shape of follicles tend to follow the same pattern over the human body (19). The highest density of sebaceous and vellus follicles is found on the face, especially on the forehead, where there may be as many as 900 glands cm2 in some areas (20), but the number varies according to the study Blume et al. (21) determined a density of 423 follicles cm2, Pagnoni et al. (22) found 455 follicles cm2 on the lateral forehead and up to 1220 follicles cm2 in the nose area, and most recently, Otberg et al. (23) determined a number of 292 follicles cm2 on the forehead. Nevertheless, there is agreement that sebum output is maximal on the forehead, nose, and chin, the so-called t-zone and decreases toward the outer edges of the...

StearoylCoA desaturase SCD

To date, four murine isoforms of SCD (SCD1-4) have been identified 72-75 . Although the four isoforms share considerable sequence homology (> 80 amino acid sequence identity) and catalyze the same biochemical transform, their tissue distribution varies. For example, SCD1 is expressed in lipogenic tissues, such as liver, adipose, and sebaceous glands 76 . SCD2 is ubiquitously expressed in most tissues, with the exception of liver 76 , while SCD3 is found in the Harderian gland 74 and SCD4 primarily in the heart 75 . Additionally, two human SCD genes with > 85 homology to murine SCD1 have been identified 77,78 .

Anatomy And Function Of Skin

The dermis is predominantly formed of connective tissue and is responsible for the skin's elasticity and strength. The dermis is vascular, and supplies nutrients to the avascular epidermis. It also contains hair follicles, sweat glands, sebaceous glands and nerve endings.

Role of Environmental Factors

Several environmental factors can influence the course of disease in AD. One of the most important, yet often obscure, factors is climate. Individuals will respond differently to various climatic influences. Most authors report disease intensification during the winter months and patients having the most comfort during the months of summer. Rajka has reported that improvement during the summer may be due to better sebum and sweat secretion, ultraviolet (UV) rays from sun exposure, exposure to water during swim activities, reduced exposure to indoor allergens (i.e., dust mite and molds), less exposure

Clinical Clues to Diagnosis of Anaerobic Infections

The source of bacteria involved in most of the anaerobic infections is the normal indigenous flora of an individual. The mucous surfaces of the child becomes colonized with aerobic and anaerobic flora within a short time after birth (3,4). Anaerobic bacteria are the most common residents of the skin and mucous membrane surfaces (5) and outnumber aerobic bacteria in the normal oral cavity and gastrointestinal tract at a ratio of 10 1 and 1000 1, respectively (6). Examples of these mucous and skin surfaces are the oral, and nasal cavities, the gastrointestinal lumen and the conjunctiva, the skin surfaces of different locations, and the sebaceous glands. It is not surprising, therefore, that a large proportion of anaerobic bacteria that are part of the normal mucous membrane flora can be recovered from infection in proximity to these sites.

Association of Kallikreins with Human Diseases

The epidermis forms the external surface of the skin and is composed of differentiated keratinocytes that form four layers the stratum basale, the stratum spinosum, the stratum granulosum, and the stratum corneum, where keratinocytes have been transformed into corneocytes. The stratum corneum functions as the protective, virtually water-impermeable skin barrier against external insults including desiccation and the entry of noxious chemicals and microbes. To maintain this barrier, old corneocytes are continuously desquamated from the stratum corneum by both stratum corneum trypsin-like and stratum corneum chymotrypsin-like enzymes 202 . The expression of hK5 and hK7 203 and of several kallikrein mRNAs 204 in the upper epidermis (the stratum granulosum or the stratum corneum), indicate that kallikreins may be the stratum corneum serine proteases responsible for the desquamation of corneocytes 205 . A quantitative ELISA assay showed high concentrations of hK7 206 and hK8 78 in skin...

Clinically Studied Inhibitors 31 5LO and FLAP inhibitors

Reduce Corneum

Zileuton (1) is the only marketed 5-LO inhibitor and is approved for the treatment of asthma 44 . The treatment of mild asthmatics with zileuton (600 mg qid, 2 weeks) resulted in a 96 increase in plasma thromboxane B2 from baseline levels and a corresponding 62 increase in spontaneous platelet aggregation, suggesting a shunting of arachidonic acid metabolism to the cyclooxygenase pathway 45 . In a small clinical trial, zileuton provided a magnitude of prophylaxis in exercise-induced asthma (as measured by FEV1) equivalent in magnitude but considerably shorter in duration than salmeterol, montelukast and zafirlukast 46 . Zileuton inhibited bronchoalveolar lavage (BAL) fluid eosinophil counts by 68 upon antigen challenge in a sub-population of allergic asthmatics who exhibited a significant increase in BAL leukotrienes and inflammatory cytokines, but not in those patients where leukotriene levels were unchanged upon antigen challenge 47 . Zileuton provided minimal efficacy 48 or no...

Infections in or around Hair Follicles

Folliculitis, furunculosis, and carbundes are localized abscesses either in or around hair follicles. These infections are distinguishable from one another based on size and the extent of involvement in subcutaneous tissues. Table 60-2 summarizes each infection's respective clinical features. For the most part, these infections are predpitated by blockage of the hair follide with skin oils (sebum), or minor trauma resulting from friction

The Dermis

The dermis ranges from 0.2 mm thick in the eyelids to about 4 mm thick in the palms and soles. It is composed mainly of collagen but also contains elastic and reticular fibers, the usual cells of fibrous connective tissue (described in chapter 5), and blood vessels, sweat glands, sebaceous glands, hair follicles, and nail roots (see fig. 6.1). It also contains sensory nerve endings, discussed later in this chapter (p. 199), and muscular tissue. Smooth muscle cells associated with hair follicles make the hairs stand on end in response to cold or fear, cause goose bumps, and wrinkle the skin in areas such as the scrotum and areola in response to cold or touch. In the face, skeletal muscles attach to dermal collagen fibers and produce such expressions as a smile, a wrinkle of the forehead, and the wink of an eye.

Systemic treatments

Terbinafine (1), a representative of the allylamine class of antifungal agents, inhibits squalene epoxidase 16,17 and thereby prevents the biosynthesis of ergos-terol, a key ingredient in the fungal cell wall. Terbinafine is active against dermatophytes, M. furfur, Aspergillus species and some Candida species including C. parapsilosis however, it is fungistatic against C. albicans 2 . A single oral dose of 250 mg terbinafine given to humans produces peak plasma concentrations of 1 mg mL within two hours 14 . It is > 99 protein bound and has a half-life of about 36 hours. It is administered at a dose of 250mg once daily for 6 weeks for finger nails or 12 weeks for toe nails 14 . One study showed that terbinafine localizes in the stratum corneum via sebum 18 . Terbinafine has a cLogP of 6.5 and a molecular weigh of 292 Da. itraconazole also localizes in the stratum corneum via sebum but at much lower levels 18,19 . Itraconazole has a cLogP of 3.3 and molecular weight of 706 Da.

Skin and Hair

The dermis is made up of connective tissue and contains structures such as hair follicles, sweat glands, sebaceous glands (which produce an oily substance called sebum), blood vessels, lymph vessels (which carry lymph into and out of the lymph glands), and nerves. Your skin also has some other important roles, including sensation such as touch, temperature, and pain and regulation of body temperature through perspiration and dilation (widening) and constriction (narrowing) of blood vessels.

Anatomy Of The Skin

Above the subcutaneous tissue and fasdal membranes lies the deimis, which comprises dense connective tissue that is rich in blood and nerve supply. Shorter hair follicles and sebaceous (oil-producing) glands originate in the dermis. Finally, die epidermis, which is the outermost layer of skin, is made of layered squamous epithelium. Hair follicles, sebaceous glands, and sweat glands open to the skin surface, through the epidermis.

Groin And Pubic Area

The penile skin often contains visible Fordyce glands, which are sebaceous (fat-producing) glands (Swartz, 2002) to keep the penile skin lubricated. They can be easily mistaken for genital warts or molluscum contagiosum, despite being little fatty lumps under the skin. The sebaceous glands can become blocked or form into sebaceous cysts, and rarely may become infected. The patient needs to be reassured about their presence.

Physical Findings

Another prominent physical finding in patients with AD is an impaired sweating mechanism. Several investigators have documented this phenomenon, with patients demonstrating less sweating under periods of stimulation. In addition, patients frequently complain of increased pruritus during periods of sweating. Increased transepidermal water loss has also been noted in patients with AD. This has been attributed to fewer sebaceous glands and less total lipid content of AD skin. All of these findings contribute to the clinical manifestations of dry skin and increased pruritus.


Flutamide does not interfere with ovulation and is generally well tolerated. The only common complaint of patients given flutamide is dry skin, attributable to reduced sebum production. Liver toxicity is an uncommon, but potentially severe, risk with this drug (24). On the whole, from several points of view, flutamide is probably the best available antiandrogen drug. However, this drug should be used with caution for the treatment of hirsutism, and in these cases serum transaminases should be carefully monitored.

Nails And Glands

Fig. 6.2 Nails and glands Helpful ''things added'' to the skin. (A) Dorsal aspect of the thumb. (B) Sweat and sebaceous glands near hair follicles. Fig. 6.2 Nails and glands Helpful ''things added'' to the skin. (A) Dorsal aspect of the thumb. (B) Sweat and sebaceous glands near hair follicles. Sebaceous (sih-BAY-shus) glands ''involve or pertain to'' (-ous) ''grease'' (sebac). The great majority of the several million sebaceous glands within the dermis are attached to the sides of hair follicles (see Figure 6.2,B). The sebaceous glands continually produce and secrete sebum (SEE-bum) or skin ''grease'' (seb). Sebum plays an often-underappreciated role in lubricating the hairs and skin surface. (Think about what happens to the skin on the hands of many people, such as nurses, who have to wash their hands often. Especially in the winter, not having enough sebum results in dry, red, painfully cracked skin )

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