All you need to know about the physiology and function of sebaceous glands.

Sebaceous glands are specialized exocrine structures of the skin.

Sebaceous glands belong to the pilosebaceous apparatus, forming with the hair follicle and the arrector pili muscle a functional unit called thepilosebaceous unit. They are located in the deep dermis and have a lobular structure, grouped around an excretory duct that opens into the hair follicle. This duct enables sebum produced by the sebaceous glands at the base of the hair to readily reach the skin surface.

Note : There are also free sebaceous glands that are not associated with a hair, but these are relatively uncommon.

Sebaceous glands are composed primarily of specialized sebaceous cells, derived from the proliferation of keratinocytes in the outer root sheath of the hair follicle. These cells, called sebocytes, undergo a differentiation process culminating in programmed cell death. During this maturation, they synthesize a complex mixture of lipids that is then released into the excretory duct: the sebum. Composed of approximately 50% triglycerides, 20% wax esters, 15% squalene, as well as small amounts of cholesterol and its esters and vitamin E, which exhibits protective and moisturizing properties.

The density and size of sebaceous glands vary significantly by body location. They are abundant on the face, particularly on the forehead, nose, and chin, corresponding to the famous T-zone, but also on the scalp, chest, and back, areas known for high sebum production. In contrast, sebaceous glands are absent from the palms of the hands and the soles of the feet.

The production of sebum by the sebaceous glands relies on a specific physiological process called holocrine secretion. This process is distinguished by the fact that sebum release does not occur simply by exocytosis but by the complete destruction of the cells that produced it. At the periphery of the sebaceous gland are immature sebaceous cells corresponding to undifferentiated sebocytes. They exhibit a flattened shape and are in an active proliferation phase. Gradually, these cells migrate toward the center of the gland, entering a maturation phase. During this stage, they become engorged with lipid droplets originating from the intracellular synthesis of various fatty compounds that will later be found in the sebum.

As they progress through this internal migration, sebocytes increase in volume and their lipid content becomes increasingly dense. Upon reaching the central zone near the excretory duct, sebocytes reach the end of their life cycle: their cell membrane weakens and then ruptures, fully releasing their lipid content. Once released, sebum travels through the pilosebaceous canal to reach the skin surface. It then deposits both on the hair shaft and on the stratum corneum, where it mixes with epidermal lipids and sweat. This complex mixture will later form the hydrolipidic film.

This perpetual renewal mechanism enables the sebaceous glands to continuously produce a natural lipid barrier, protecting and hydrating the skin.

The activity of the sebaceous glands is regulated by a complex network of hormonal signals, growth factors, and neuropeptide interactions. Androgens are particularly central to this regulation, beginning with 5α-dihydrotestosterone (5α-DHT), which is produced by the type I 5α-reductase isoenzyme acting on testosterone. With a high affinity for the androgen receptor in the sebaceous glands, 5α-DHT activates this receptor and promotes sebocyte proliferation. Conversely, estrogens exert an inhibitory effect on sebaceous gland activity and sebum synthesis, acting as a counterbalance to androgenic effects.

Alongside sex hormones, certain growth factors influence sebaceous physiology. Growth hormone (GH) and IGF-I (insulin-like growth factor-I) are particularly involved, as evidenced by the increase in sebum secretion observed during adolescence, when GH and IGF-I reach their maximum plasma concentrations. IGF-I directly stimulates sebocyte lipogenesis by activating the transcription factor SREBP-1, a regulator of the genes involved in fatty acid synthesis. This activation occurs through the PI3K/Akt and MAPK/ERK signaling pathways. Correlations have been established between IGF-I levels and acne severity, as well as with plasma levels of 5α-DHT and DHEAS, highlighting the interconnection between lipid metabolism, androgens, and IGF-I signaling.

Another notable player is fibroblast growth factor receptor 2b (FGFR-2b), whose expression is regulated by androgens and which is involved in keratinocyte proliferation. In certain conditions such as nevus acneiformis, a malformation characterized by epidermal hyperplasia, activating mutations in FGFR-2b lead to sebaceous hyperactivity and to an alteration of the pilosebaceous unit. Experimental models have shown that postnatal deletion of FGFR-2b leads to complete atrophy of the sebaceous glands, confirming its structural role.

Regulation of sebaceous glands extends beyond hormones and growth factors. MicroRNAs, small noncoding sequences of about 21 nucleotides, provide an additional level of control by modulating gene expression post-transcriptionally. Some microRNAs, such as miR-574-3p targeting the nuclear receptor RXRα, can significantly increase lipid synthesis when overexpressed. Others, involved in sebaceous gland tumors, influence the NF-κB, PTEN, and TGF-β pathways, thereby affecting cell proliferation and transformation.

Finally, although the sebaceous gland is richly vascularized to meet its high demands for nutrients and lipid precursors, its innervation remains less well characterized. Nerve networks surround the hair follicle and lie in close proximity to the gland, but the direct penetration of nerve fibers into it is still under debate. However, the presence of receptors for various neuropeptides, such as CRH (corticotropin-releasing hormone), α-MSH, or β-endorphin, suggests a heightened sensitivity to neuroendocrine signals. For example, CRH released in a circadian manner by the hypothalamus modulates the secretion of ACTH and POMC-derived peptides, which can directly influence the proliferation and differentiation of sebaceous glands.

The physiology of sebaceous glands thus relies on a dynamic balance between hormonal signals, growth factors, post-transcriptional regulation, and neuropeptide responses, each contributing to the modulation of cell proliferation and sebum production.

Although sebaceous glands are primarily recognized for their ability to produce sebum, this is not their only function.

Sebum produced by the sebaceous glands obviously plays a hydrating and protective role, helping to reduce water evaporation from the stratum corneum, prevent friction and the penetration of pathogenic microorganisms, allergens, and irritants, but it also serves to transport antioxidants, such as vitamin E, to the skin surface, protecting the skin’s lipids. To some extent, this contributes to natural photoprotection of the skin. Moreover, sebum possesses antibacterial activity thanks to certain free fatty acids that disrupt the membranes of pathogenic bacteria. It is therefore essential to the balance of the skin microbiota.

Sebaceous glands also participate in modulation of skin inflammation. They produce pro- and anti-inflammatory molecules depending on the context, contributing both to the immune response against insults and to the restoration of homeostasis. They also play a role in neutralizing certain xenobiotics, foreign compounds to the body, by regulating their local metabolism. In addition, sebaceous glands are actively involved in wound healing: after an injury, they secrete lipid mediators and growth factors that promote epidermal regeneration.

This multifunctional role of the sebaceous glands is closely linked to their ability to produce steroid hormones locally, notably androgens. They contain all of the enzymes required to convert cholesterol into active steroids, as well as to transform adrenal precursors—such as dehydroepiandrosterone sulfate (DHEA-S)—into DHEA, then into androstenedione, testosterone, and ultimately dihydrotestosterone. This process, catalyzed in part by type I 5α-reductase, is especially active in the sebaceous glands of the face and scalp. This local hormone production directly regulates sebocyte differentiation and the amount of sebum secreted.

Finally, sebaceous glands interact closely with the cutaneous nervous system. They express receptors for CRH, a molecule released in response to stress by nerves and certain skin cells. CRH modulates lipid production by sebocytes and influences the expression of enzymes involved in steroidogenesis. In parallel, other neuropeptides, such as substance P, released by perisudoral nerve fibers, can stimulate peripheral sebocytes, enhancing local secretion and inflammation. These interactions partly explain why psychological stress can exacerbate certain seborrheic conditions, notably acne.

The proper functioning of the sebaceous glands is essential for skin homeostasis. When their activity is altered, whether through overproduction, insufficient production, or qualitative changes in sebum, the balance of the skin microbiota, the barrier function, and the inflammatory regulation of the skin can be compromised. These sebaceous gland imbalances are involved in numerous inflammatory dermatoses, ranging from acne to eczema, including rosacea, psoriasis and seborrheic dermatitis.

• The link between sebaceous glands and acne.

  Affecting up to 85% of adolescents and often persisting into adulthood, acne is the most prevalent skin disease. It is characterized by hyperactivity of the sebaceous glands driven by androgens at puberty. In acne lesions, the sebaceous glands exhibit overexpression of the enzyme 11β-hydroxysteroid dehydrogenase type I, which locally increases cortisol and promotes lipid synthesis. Beyond the quantity, sebum composition can also be altered: reduced linoleic acid, excess squalene whose oxidation triggers inflammation, and low vitamin E levels. This phenomenon is known as dyseborrhea. These changes perpetuate comedogenesis and skin inflammation. Treatments that reduce sebaceous gland activity, such as isotretinoin, confirm this role: the decrease in sebum production is accompanied by fewer lesions but also by a degree of skin dryness, both linked to reduced sebaceous function.

• The relationship between sebaceous glands and eczema.

  Eczema is characterized by a alteration of the skin barrier, with an elevated pH of the stratum corneum, increased transepidermal water loss, and reduced hydration. While most studies focus on keratinocyte-derived ceramide deficiency, sebaceous function impairment is also significant. In patients with atopic dermatitis, sebum production is often reduced, contributing to skin dryness and fragility of the hydrolipid film. Histologically, both lesional and non-lesional skin exhibit sebaceous hypoplasia, and in infantile eczema the glands are underdeveloped, with small basal cells devoid of lipids and lacking secretory activity. Sebaceous secretion then increases during adolescence, which explains why many children outgrow atopic dermatitis as sebaceous activity normalizes.

• The link between sebaceous glands and psoriasis.

  Psoriasis is a chronic inflammatory dermatosis affecting up to 8.5% of adults. Although the histological and immunological changes in psoriasis are well documented, alterations in the sebaceous glands remain poorly studied. On the psoriatic scalp, lesions often present a marked atrophy of the sebaceous glands, with a reduction in their size and number, sometimes complete in more than half of cases. However, gland size does not appear to correlate with clinical severity or inflammatory signs, and the average sebum content in psoriatic skin is comparable to that in healthy skin. Some hypotheses suggest that growth factors such as TGF-α and epidermal growth factor, which are overexpressed in psoriasis, may inhibit sebocytes, but further research on this topic is needed.

• The link between sebaceous glands and rosacea.

  Rosacea is a common chronic skin condition characterized primarily by diffuse redness. In patients with papulopustular rosacea, the skin’s barrier function is impaired, with increased pH and reduced skin hydration. However, total sebum amount and sebum excretion rate on the forehead do not differ significantly from those of healthy subjects, nor do they correlate with disease severity. Nevertheless, the lipid composition of sebum appears to have an influence. Indeed, individuals with rosacea typically exhibit increased levels of myristic acid (C14:0) and decreased levels of long-chain and very long-chain saturated fatty acids. This lipid imbalance likely contributes to skin barrier dysfunction.

• The link between sebaceous glands and seborrheic dermatitis.

  Seborrheic dermatitis is an inflammatory skin disorder that preferentially affects areas rich in sebaceous glands, such as the scalp, face, and upper trunk. Contrary to what its name implies, this condition is not directly linked to excessive sebum production. The role of sebaceous glands in its development is rather attributed to the sebaceous lipid metabolism by the fungus Malassezia, whose lipases hydrolyze the triglycerides in sebum, reducing their concentration and increasing that of irritating free fatty acids. This leads to disruption of the skin barrier, inflammation, and scaling. Seborrheic dermatitis therefore results from an interaction between the sebaceous glands, the fungal microbiota, and individual susceptibility, without a significant change in the total lipid quantity.

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