Hubbry Logo
Sebaceous glandSebaceous glandMain
Open search
Sebaceous gland
Community hub
Sebaceous gland
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Sebaceous gland
Sebaceous gland
Sebaceous gland
View on Wikipedia
from Wikipedia

Schematic view of hair follicle and sebaceous gland
Cross-section of all skin layers. A hair follicle with associated structures. (Sebaceous glands labeled at center left.)
Identifiers
MeSHD012627
TA98A16.0.00.030
A15.2.07.044
TA27082
FMA59160
Anatomical terminology

A sebaceous gland or oil gland[1] is a microscopic exocrine gland in the skin that opens into a hair follicle to secrete an oily or waxy matter, called sebum, which lubricates the hair and skin of mammals.[2] In humans, sebaceous glands occur in the greatest number on the face and scalp, but also on all parts of the skin except the palms of the hands and soles of the feet. In the eyelids, meibomian glands, also called tarsal glands, are a type of sebaceous gland that secrete a special type of sebum into tears. Surrounding the female nipples, areolar glands are specialized sebaceous glands for lubricating the nipples. Fordyce spots are benign, visible, sebaceous glands found usually on the lips, gums and inner cheeks, and genitals.

Structure

[edit]

Location

[edit]

In humans, sebaceous glands are found throughout all areas of the skin, except the palms of the hands and soles of the feet.[3] There are two types of sebaceous glands: those connected to hair follicles and those that exist independently.[4]

Sebaceous glands are found in hair-covered areas, where they are connected to hair follicles. One or more glands may surround each hair follicle, and the glands themselves are surrounded by arrector pili muscles, forming a pilosebaceous unit. The glands have an acinar structure (like a many-lobed berry), in which multiple glands branch off a central duct. The glands deposit sebum on the hairs and bring it to the skin surface along the hair shaft. The structure, consisting of hair, hair follicles, arrector pili muscles, and sebaceous glands, is an epidermal invagination known as a pilosebaceous unit.[4]

Sebaceous glands are also found in hairless areas (glabrous skin) of the eyelids, nose, penis, labia minora, the inner mucosal membrane of the cheek, and nipples.[4] Some sebaceous glands have unique names. Sebaceous glands on the lip and mucosa of the cheek, and on the genitalia, are known as Fordyce spots, and glands on the eyelids are known as meibomian glands. Sebaceous glands of the breast are also known as Montgomery's glands.[5]

Development

[edit]

Sebaceous glands are first visible from the 13th to the 16th week of fetal development, as bulgings off hair follicles.[6] Sebaceous glands develop from the same tissue that gives rise to the epidermis of the skin. Overexpression of the signalling factors Wnt, Myc and SHH all increase the likelihood of sebaceous gland presence.[5]

The sebaceous glands of a human fetus secrete a substance called vernix caseosa, a waxy, translucent white substance coating the skin of newborns.[7] After birth, activity of the glands decreases until there is almost no activity during ages two–six years, and then increases to a peak of activity during puberty, due to heightened levels of androgens.[6]

Function

[edit]

Relative to keratinocytes that make up the hair follicle, sebaceous glands are composed of huge cells (sebocytes) with many large vesicles that contain the sebum.[8] These cells express Na+ and Cl− ion channels, ENaC and CFTR (see Fig. 6 and Fig. 7 in reference[8]).

Sebaceous glands secrete the oily, waxy substance called sebum (Latin for 'fat, tallow') that is made of triglycerides, wax esters, squalene, and metabolites of fat-producing cells. Sebum lubricates the skin and hair of mammals.[9] Sebaceous secretions in conjunction with apocrine glands also play an important thermoregulatory role. In hot conditions, the secretions emulsify the sweat produced by the eccrine sweat glands and this produces a sheet of sweat that is not readily lost in drops of sweat. This is of importance in delaying dehydration. In colder conditions, the nature of sebum becomes more lipid, and in coating the hair and skin, rain is effectively repelled.[10][11]

Sebum is produced in a holocrine process, in which sebocyte cells within the sebaceous gland rupture and disintegrate as they release the sebum and the cell remnants are secreted together with the sebum.[12][13] The cells are constantly replaced by mitosis at the base of the duct.[4]

Sebum

[edit]

Sebum is secreted by the sebaceous gland in humans. It is primarily composed of triglycerides (≈41%), wax esters (≈26%), squalene (≈12%), and free fatty acids (≈16%).[7][14] The composition of sebum varies across species.[14] Wax esters and squalene are unique to sebum and not produced as final products anywhere else in the body.[5] Sapienic acid is a sebum fatty acid that is unique to humans, and is implicated in the development of acne.[15] Sebum is odorless, but its breakdown by bacteria can produce strong odors.[16]

Sex hormones are known to affect the rate of sebum secretion; androgens such as testosterone have been shown to stimulate secretion, and estrogens have been shown to inhibit secretion.[17] Dihydrotestosterone acts as the primary androgen in the prostate and in hair follicles.[18][19]

Immune function and nutrition

[edit]

Sebaceous glands are part of the body's integumentary system and serve to protect the body against microorganisms. Sebaceous glands secrete acids that form the acid mantle. This is a thin, slightly acidic film on the surface of the skin that acts as a barrier to microbes that might penetrate the skin.[20] The pH of the skin is between 4.5 and 6.2,[21] an acidity that helps to neutralize the alkaline nature of contaminants.[22] Sebaceous lipids help maintain the integrity of the skin barrier[10][23][24] and supply vitamin E to the skin.[25]

Unique sebaceous glands

[edit]

During the last three months of fetal development, the sebaceous glands of the fetus produce vernix caseosa, a waxy white substance that coats the skin to protect it from amniotic fluid.[26]

The areolar glands are in the areola that surrounds the nipple in the female breast. These glands secrete an oily fluid that lubricates the nipple, and also secrete volatile compounds that are thought to serve as an olfactory stimulus for the newborn. During pregnancy and lactation these glands, also called Montgomery's glands, become enlarged.[27]

Meibomian glands, in the eyelids, secrete a form of sebum called meibum onto the eye, that slows the evaporation of tears.[28] They also serve to create an airtight seal when the eyes are closed, and their lipid quality also prevents the eyelids from sticking together. They attach directly to the follicles of the eyelashes, which are arranged vertically within the tarsal plates of the eyelids.

Fordyce spots, or Fordyce granules, are ectopic sebaceous glands found on the genitals and oral mucosa. They show themselves as yellowish-white milia (milk spots).[29]

Earwax is partly composed of sebum produced by glands in the ear canal. These secretions are viscous and have a high lipid content, which provides good lubrication.[30]

Clinical significance

[edit]
Conditions of sebaceous glands

Sebaceous glands are involved in skin problems such as acne and keratosis pilaris. In the skin pores, sebum and keratin can create a hyperkeratotic plug called a comedo.

Acne

[edit]
Main article: Acne

Acne is a common occurrence, particularly during puberty in teenagers, and is thought to relate to an increased production of sebum due to hormonal factors. The increased production of sebum can lead to a blockage of the sebaceous gland duct. This can cause a comedo (commonly called a blackhead or a whitehead), which can lead to infection, particularly by the bacteria Cutibacterium acnes. This can inflame the comedones, which then change into the characteristic acne lesions. Comedones generally occur on the areas with more sebaceous glands, particularly the face, shoulders, upper chest and back. Comedones may be "black" or "white" depending on whether the entire pilosebaceous unit, or just the sebaceous duct, is blocked.[31] Sebaceous filaments—innocuous build-ups of sebum—are often mistaken for whiteheads.

There are many treatments available for acne from reducing sugars in the diet, to medications that include antibiotics, benzoyl peroxide, retinoids, and hormonal treatments.[31] Retinoids reduce the amount of sebum produced by the sebaceous glands.[32] Should the usual treatments fail, the presence of the Demodex mite could be looked for as the possible cause.[33]

Other

[edit]

Other conditions that involve the sebaceous glands include:

History

[edit]

The word sebaceous, meaning 'consisting of sebum', was first termed in 1728 and comes from the Latin for 'tallow'.[40] Sebaceous glands have been documented since at least 1746 by Jean Astruc, who defined them as "...the glands which separate the fat."[41]: viii  He describes them in the oral cavity and on the head, eyelids, and ears, as "universally" acknowledged.[41]: 22–25 viii  Astruc describes them being blocked by "small animals" that are "implanted" in the excretory ducts[41]: 64  and attributes their presence in the oral cavity to apthous ulcers, noting that "these glands naturally [secrete] a viscous humour, which puts on various colours and consistencies... in its natural state is very mild, balsamic, and intended to wet and lubricate the mouth".[41]: 85–86  In The Principles of Physiology 1834, Andrew Combe noted that the glands were not present in the palms of the hands or soles of the feet.[42]

In animals

[edit]
Example of a gular gland in a male black bonneted bat[43]
Example of a gular gland in a male black bonneted bat[43]

The preputial glands of mice and rats are large modified sebaceous glands that produce pheromones used for territorial marking.[5] These and the scent glands in the flanks of hamsters have a similar composition to human sebaceous glands, are androgen responsive, and have been used as a basis for study.[5] Some species of bat, including the Mexican free-tailed, have a specialized sebaceous gland occurring on the throat called a "gular gland".[44] This gland is present more frequently in males than females, and it is hypothesized that the secretions of the gland are used for scent-marking.[45]

Sebaceous adenitis is an autoimmune disease that affects sebaceous glands. It is mainly known to occur in dogs, particularly poodles and akitas, where it is thought to be generally autosomal recessively inherited. It has also been described in cats, and one report describes this condition in a rabbit. In these animals, it causes hair loss, though the nature and distribution of the hair loss differs greatly.[46]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Sebaceous gland

View on Grokipedia
from Grokipedia
Sebaceous glands are microscopic, exocrine glands embedded in the of mammalian , primarily associated with hair follicles to form pilosebaceous units, where they secrete an oily substance known as sebum that lubricates and protects the and . These glands are absent on the palms, soles, and certain mucosal surfaces but are densely distributed on the , face, and upper trunk, with each typically connected to multiple sebaceous lobules via a short duct that opens into the upper portion of the follicle. Structurally, sebaceous glands consist of clusters of sebocytes—specialized epithelial cells—arranged in pear-shaped lobules, where peripheral undifferentiated cells proliferate and mature centrally, accumulating until they undergo to release sebum in a manner. Histologically, the glands exhibit a characteristic "foamy" appearance under due to their high content, which stains poorly with standard hematoxylin and but can be highlighted using lipid-specific dyes like ; the entire maturation process from proliferation to typically spans about one week. Sebum, comprising approximately 90% of the skin's surface , is a complex mixture of triglycerides, wax esters, , , and free fatty acids derived from the breakdown of sebocytes. The primary functions of sebaceous glands extend beyond to include maintaining barrier integrity by preventing moisture loss, providing defense through fatty acids and proteolytic enzymes that inhibit bacterial and fungal growth, and modulating the skin's endocrine environment by metabolizing androgens such as testosterone into . Dysregulation of sebaceous gland activity is implicated in common dermatological conditions, including acne vulgaris—characterized by excessive sebum production leading to follicular hyperkeratinization and inflammation—and , underscoring their role in and disease.

Anatomy and Structure

Location and Distribution

Sebaceous glands are microscopic exocrine glands situated in the mid-dermal layer of the skin, where they form an integral component of the pilosebaceous unit alongside . Their short duct typically opens into the upper portion of the canal, near the bulge region, facilitating the delivery of sebum to the skin surface as emerges. This close association underscores their role in coating shafts and lubricating the surrounding epidermis.30869-1/fulltext) Sebaceous glands are present across nearly all body regions, with the notable exceptions of the palms and soles, which lack both glands and follicles due to their unique epidermal structure. They exhibit the highest prevalence in androgen-sensitive areas, including the face (particularly the , , and ), , upper chest, and upper back, where environmental and hormonal factors promote robust glandular activity. In contrast, distribution is markedly sparser on the extremities, such as the arms, legs, and especially the lower legs, reflecting lower influence and fewer pilosebaceous units in these regions. Quantitative variations in glandular density highlight these regional differences, with up to 400–900 glands per square centimeter reported on the face and , compared to far fewer—often below 100 per square centimeter—on the limbs and trunk extremities. These disparities contribute to differences in sebum output and skin oiliness across the body.30869-1/fulltext) While predominantly linked to hair follicles, sebaceous glands also occur independently in certain non-hair-bearing sites, such as the tarsal plates of the eyelids (as modified Meibomian glands) and the of the lips (as ectopic ).

Histology and Cellular Composition

Sebaceous glands are glands characterized by a lobular architecture, consisting of clusters of sebocytes organized into acini that are connected to short excretory ducts opening into follicles or, in specialized cases, directly onto the skin or mucosal surface. Each lobule is enveloped by a thin capsule of fibers, which provides structural support and separates the glandular units. The glands are embedded in the mid-dermis, forming part of the pilosebaceous unit in most regions. The cellular composition primarily involves sebocytes, which undergo a differentiation process from the periphery to the center of each lobule. Undifferentiated peripheral sebocytes are small, cuboidal cells with basophilic and large nuclei, exhibiting high mitotic activity to replenish the . As they mature centrally, sebocytes accumulate lipid droplets in their , leading to a foamy appearance on histological sections due to lipid extraction during staining; these cells develop pyknotic nuclei and lose organelles before disintegrating in a manner to release sebum. This lipid accumulation contributes to the composition of sebum, the 's secretory product. The ductal components are brief, lined by continuous with the hair follicle's infundibulum, facilitating the transport of sebum without additional glandular elements. Sebaceous glands receive a rich blood supply from dermal vessels, essential for delivering nutrients to the metabolically active sebocytes. They are also innervated by cutaneous nerves, which release neuropeptides and neurotransmitters to regulate glandular activity and secretion.

Embryological Development

Sebaceous glands originate from the ingrowth of ectodermal cells into the underlying , forming as solid cellular buds that protrude from the developing during early fetal life. This process begins between weeks 13 and 16 of , coinciding with the initial stages of , where the sebaceous gland anlage emerges as a bulge-like structure attached to the outer root sheath of the follicle. By the 14th to 15th week, these buds differentiate into immature sebaceous glands capable of production, contributing to the that protects the fetal . The differentiation of sebaceous progenitor cells is tightly regulated by reciprocal interactions between the epithelial cells and underlying mesenchymal signals from dermal fibroblasts and specialized condensate cells. Key transcription factors, including (PPARγ) and (SREBP1), drive sebocyte maturation by promoting lipogenic gene expression and secretion pathways. These molecular cues ensure the glands integrate into the pilosebaceous unit, with PPARγ particularly essential for terminal differentiation and lipid accumulation in sebocytes. Following birth, sebaceous glands remain relatively quiescent until , when surging levels, such as testosterone and , induce rapid proliferation and of the glands. This hormonal stimulation transforms prepubertal vellus follicles into mature sebaceous follicles, markedly increasing gland size and sebum output to support skin lubrication during . Developmental anomalies of sebaceous glands can result in , often associated with ectodermal dysplasias where genetic defects impair ectodermal-derived formation, leading to absent or hypoplastic glands. Conversely, hyperplasia may occur in conditions like nevus sebaceus, a hamartomatous arising from postzygotic mutations in or genes that disrupt normal ectodermal development and cause localized overgrowth of sebaceous elements.

Physiology and Function

Sebum Production and Composition

Sebaceous glands produce sebum through a secretion process, in which undifferentiated sebocytes proliferate and differentiate within the gland's secretory acini, progressively accumulating in cytoplasmic droplets until the mature cells undergo , rupture, and release their entire contents—including , cellular debris, and breakdown products—into the ductal lumen to form sebum. This mechanism, which involves and lysosomal degradation facilitated by enzymes like DNase2 for nuclear breakdown, ensures the complete conversion of sebocyte contents into sebum without residual cellular structures, contributing to the gland's role in skin . The entire differentiation and cycle typically spans about one week, with sebum then transported to the skin surface via the duct. Sebum production rates vary by skin site, age, and hormonal influences, with the highest output occurring on the face and during due to stimulation. In adults, the average sustainable secretion rate is approximately 1 mg per 10 cm² of skin every 3 hours, equating to roughly 8 mg daily per that area, though rates can range from less than 0.5 mg/10 cm²/3 hours in dry skin to over 1.5 mg/10 cm²/3 hours in oily conditions. Production declines with age, particularly in women after , and is lower on extremities compared to sebum-rich areas like the . The of sebum primarily occurs through de novo lipogenesis (DNL) within sebocytes, where derived from glucose metabolism is carboxylated by (ACC) to form , which then serves as the substrate for (FAS) to elongate and synthesize saturated and monounsaturated s, such as and sapienic acid, that form the building blocks of triglycerides, wax esters, and other components. This DNL pathway accounts for 80-85% of sebum's content, distinguishing sebaceous synthesis from other tissues, and is upregulated by androgens while being a target for therapeutic inhibition in conditions of excess production. Key enzymes like ACC and FAS are highly expressed in sebocytes, driving the unique profile that includes branched-chain and odd-numbered species not found in dietary . Freshly produced sebum in the glandular lumen consists primarily of nonpolar , with triglycerides comprising about 57%, wax esters 25-26%, 12-13%, cholesterol esters 3-4.5%, free 1.5-3%, and free fatty acids around 1-2%, along with minor cellular remnants. These proportions reflect the output before surface modification by microbial lipases, which hydrolyze triglycerides into diglycerides and free fatty acids, altering the composition on the skin. , a unique to sebum at high levels, provides properties, while wax esters contribute to the emollient quality. Sebum's film, formed by mixing with epidermal , aids in maintaining the skin's hydrophobic barrier against loss.

Role in Skin Barrier and Lubrication

Sebaceous glands play a crucial role in forming the skin surface film by secreting sebum, which mixes with sweat to create the acidic mantle, a protective layer with a of approximately 4.5 to 5.5 that repels and environmental pathogens. This mantle enhances the skin's hydrophobicity, preventing excessive moisture loss and ingress while maintaining an optimal acidic environment for barrier integrity. The lipid-rich composition of sebum, including free fatty acids and triglycerides, contributes directly to this film's formation, ensuring a cohesive interface between the skin and external factors. In addition to barrier formation, sebum provides essential lubrication for the skin and , reducing during movement and preventing dryness that could lead to cracking or irritation. This lubricating effect is achieved through sebum's wicking along the hair shaft and direct coating of the epidermal surface, which also aids in by facilitating even distribution of heat and moisture across the skin. By sealing in hydration, sebum helps preserve the skin's suppleness and flexibility, countering the desiccating effects of low humidity or wind exposure. Sebum's antioxidant properties further bolster the skin barrier, particularly through , a unique that neutralizes free radicals generated by (UV) exposure. This compound acts as a natural of , mitigating oxidative damage to lipids and proteins that could compromise . Squalene's high penetration efficiency allows it to distribute effectively within the upper layers, providing a protective shield against photo-induced stress without relying on external agents. Sebum interacts with the to enhance overall by modulating the organization of intercellular , such as ceramides and . These sebum-derived penetrate the , influencing the lipid composition and phase behavior in the to form a more robust, orthorhombic-packed structure that impedes . Areas with higher sebaceous gland density exhibit elevated levels of barrier-essential like cholesterol sulfate, underscoring sebum's role in fine-tuning the skin's permeability barrier for sustained protection.

Immune and Antimicrobial Roles

Sebaceous glands contribute to innate immunity through the delivery of antimicrobial lipids in sebum, primarily free fatty acids such as lauric acid, palmitic acid, and oleic acid, as well as squalene, which exhibit bactericidal effects against skin pathogens. These lipids disrupt bacterial cell membranes and inhibit the growth of Propionibacterium acnes and Staphylococcus epidermidis, key contributors to cutaneous infections, thereby enhancing the skin's self-disinfection capacity. For instance, free fatty acids upregulate the expression of human β-defensin-2 (hBD-2), an antimicrobial peptide that further bolsters defense against microbial invasion. Squalene, abundant in human sebum, provides additional protection by peroxidizing under oxidative stress to form compounds toxic to pathogens. Beyond direct action, sebum serves as a source for the , selectively supporting the proliferation of commensal while restricting pathogenic overgrowth. components like and monounsaturated fatty acids nourish beneficial Gram-negative species, such as those in the order, fostering microbial equilibrium essential for . This selective nutrition is modulated by (ILCs), which regulate sebum production to prevent excessive availability that could favor pathogens like Staphylococcus aureus. In ILC-deficient models, elevated sebum levels create an acidic environment that limits Gram-positive commensals, indirectly curbing pathogen dominance. Sebocytes, the primary cells of sebaceous glands, facilitate with immune cells by expressing Toll-like receptors (TLRs), including TLR2, TLR4, and TLR6, which detect microbial components and initiate inflammatory signaling. Upon recognition of ligands from P. acnes, these receptors trigger cytokine production, such as IL-1β and IL-8, recruiting neutrophils and other effectors to sites of potential . This immunoregulatory function positions sebaceous glands as active participants in the skin's adaptive innate response, coordinating with surrounding immune elements to maintain barrier integrity without overinflammation. In , sebum-derived factors from sebaceous glands promote keratinocyte proliferation, aiding re-epithelialization and tissue repair. and associated peptides stimulate the migration and division of epidermal , accelerating closure of cutaneous injuries while minimizing scarring. This regenerative support underscores the gland's broader role in post-injury recovery, integrating defense with proliferative cues.

Specialized Forms and Variations

Meibomian and Glandular Variations

Meibomian glands represent a specialized form of sebaceous glands embedded within the tarsal plates of the , numbering approximately 25 to 40 in the upper and 20 to 30 in the lower . These glands secrete meibum, a -rich substance that forms the outermost layer of the tear film, stabilizing it by reducing and maintaining ocular surface lubrication. Unlike typical sebaceous sebum, meibum is enriched in nonpolar , including esters, esters, and triacylglycerols, which contribute to its higher and thermoregulatory properties suited for the ocular environment. Glands of Zeis, another eyelid-associated sebaceous variant, are smaller structures directly connected to follicles, with one to two glands per . They produce an oily secretion that lubricates the shafts and adjacent lid margin, preventing dryness and facilitating smooth eyelid movement. These glands open into the mid-portion of the canal, integrating their output with the pilosebaceous unit to support localized hydration without contributing significantly to the broader tear film. Montgomery glands, located on the surrounding the , function as large sebaceous glands that during and to secrete protective . Their oily , rich in free fatty acids and sebum-like components, lubricates and antimicrobializes the -areola complex, reducing friction and infection risk during . This adaptation ensures nipple suppleness and barrier integrity in the mammary region, distinct from the moisturizing role of general skin sebaceous glands. These glandular variations exhibit morphological adaptations relative to standard sebaceous glands, including larger lobules in Meibomian and Montgomery forms to accommodate site-specific secretory demands. Such features enhance their efficiency in specialized niches, like the eyelid's dynamic or the areola's protective needs, while maintaining the core mechanism of sebaceous activity.

Fordyce Spots and Ectopic Glands

Fordyce spots, also known as Fordyce granules, are the most common cause of small, yellowish-white granules or bumps ("粒粒") in the mouth, particularly on the inner cheeks (buccal mucosa), lips, or other oral mucosa. They represent a common form of ectopic sebaceous glands that occur independently of hair follicles, primarily manifesting on the vermilion border of the lips, buccal mucosa, and genital regions such as the labia minora or glans penis. These appear as small, painless, yellowish-white granules or papules, typically measuring 1-3 mm in diameter, and are often arranged in clusters giving a floral or scattered appearance. They are harmless, non-contagious, and considered a normal anatomical variant rather than a pathological condition. The prevalence of Fordyce spots is high, affecting 70-90% of adults, with visibility increasing after puberty due to glandular maturation and hormonal changes, though they are likely congenital. They are more prominent in males and can be bilateral on the buccal mucosa or lips, but they cause no symptoms and require no treatment unless for cosmetic reasons. Occasionally, they are misidentified as warts, genital warts, or sexually transmitted infections, leading to unnecessary concern or interventions. Although Fordyce spots are the typical benign explanation for such appearances, other causes may include irritation, infections, or cysts; individuals should consult a healthcare professional if the spots become painful, change in appearance, or cause concern to rule out alternative conditions. Histologically, Fordyce spots consist of mature sebaceous lobules or small clusters of sebaceous glands situated in the submucosa, lacking any association with hair follicles and almost always without ductal connections to the surface epithelium, which results in minimal sebum secretion and accumulation beneath the mucosa. Overlying the glands is typically parakeratotic stratified squamous epithelium, confirming their benign, non-proliferative nature similar to normal cutaneous sebaceous glands but in an aberrant location. Beyond oral and genital sites, ectopic sebaceous glands can rarely occur in other locations such as the esophagus or conjunctiva, where they are typically incidental findings during endoscopic or ophthalmologic examinations. In the esophagus, they present as small yellowish plaques or nodules, with a reported prevalence of 0.005-0.05%, showing no clinical symptoms or malignant potential and consisting of lobulated sebaceous structures without hair follicles. Conjunctival ectopics are even less common, often asymptomatic and discovered incidentally, maintaining the same benign histologic profile.

Regional and Hormonal Influences

Sebaceous gland activity exhibits significant regional variations across the , with the highest density and output observed in areas such as the face, , and upper trunk. On the face, the T-zone—encompassing the , , and —displays markedly higher sebum production compared to the U-zone (cheeks), primarily due to elevated expression of androgen receptors (AR) in sebaceous glands of these regions. In vivo studies reveal stronger AR immunostaining and a higher of AR-positive nuclei in differentiated sebocytes of T-zone glands, while analyses show T-zone sebocytes expressing 4.8-fold more AR protein and 5.2-fold higher AR mRNA levels than those from U-zones. Additionally, the activity of type 1 , which converts testosterone to the more potent (DHT), is substantially higher in facial and sebaceous glands than in non-acne-prone areas like the arms or legs, further contributing to localized sebum hypersecretion. Hormonal regulation plays a central role in modulating sebaceous gland function, with androgens serving as the primary stimulators. Testosterone and DHT bind to AR in sebocytes, promoting gland growth, sebocyte proliferation, and synthesis through activation of the sterol regulatory element-binding protein (SREBP) pathway. This involves upregulation of SREBP-1 mRNA and its rapid nuclear translocation following androgen exposure, which in turn enhances expression of lipogenic enzymes such as , , and fatty acyl-CoA reductase, leading to increased production of esters, triglycerides, and . Estrogens, conversely, generally inhibit sebaceous activity by reducing sebocyte proliferation and sebum output, as evidenced by historical observations of gland in estrogen-treated models and clinical benefits of estrogen-containing contraceptives in reducing sebum levels. Progesterone's effects are more nuanced, with limited human data suggesting minimal direct impact on sebocyte proliferation or production, though it may indirectly modulate activity through interactions with pathways. Age-related changes in sebaceous gland activity follow a tied to hormonal shifts. In childhood, secretion remains minimal due to low levels, with glands exhibiting small size and limited output. Pubertal onset triggers a surge in activity driven by rising , peaking in late teens and early adulthood, where sebum production stabilizes at high levels in both sexes. In men, this elevated activity persists relatively unchanged through adulthood and into , up to 80 years. Women, however, experience a gradual decline post-menopause, attributed to reduced ovarian production, though levels plateau after the seventh decade without further significant drop. Despite these changes, glands maintain responsiveness to exogenous throughout life. Environmental factors, including diet and stress, influence sebaceous gland activity primarily through insulin-like growth factor-1 (IGF-1) signaling. High-glycemic-load diets elevate serum insulin and IGF-1 levels, which activate the PI3K/AKT/ pathway in sebocytes, suppressing FoxO1 and derepressing SREBP-1c to boost and sebum production. Clinical trials demonstrate that low-glycemic diets reduce sebaceous gland size, IGF-1 , and inflammatory markers after 10 weeks. Stress exacerbates this by increasing release (e.g., IL-1β, IL-6, TNF-α) and potentially elevating IGF-1 via hypothalamic-pituitary-adrenal axis activation, further upregulating and lipogenic genes in sebocytes.

Clinical Significance

Acne and Seborrheic Disorders

Acne vulgaris is a chronic inflammatory disorder primarily affecting the pilosebaceous unit, where sebaceous gland hyperactivity plays a central role in its pathogenesis. Androgens, such as testosterone and insulin-like growth factor-1 (IGF-1), stimulate sebaceous gland proliferation and increase sebum production, leading to seborrhea that contributes to follicular obstruction. This excess sebum, combined with abnormal desquamation and hyperkeratosis of the follicular epithelium, promotes the formation of microcomedones, the initial lesions in acne development. Subsequent proliferation of Cutibacterium acnes (formerly Propionibacterium acnes), a commensal bacterium that thrives in the lipid-rich environment, triggers an inflammatory cascade through the release of lipases, proteases, and chemotactic factors, exacerbating the condition. Acne manifests in two main forms: comedonal and inflammatory. Comedonal acne, the non-inflammatory variant, features open comedones (blackheads) and closed comedones (whiteheads) due to retained sebum and within follicles. Inflammatory acne involves papules, pustules, nodules, and cysts, arising from rupture of comedones and intense immune-mediated inflammation. The disorder affects 80-90% of adolescents, with global prevalence estimates ranging from 35% to nearly 100% during this period, driven by pubertal hormonal surges. Key risk factors include , with heritability estimated at 50-90% and a threefold increased risk among those with affected first-degree relatives; dietary influences, such as high-glycemic-load foods and consumption, which may elevate IGF-1 levels and sebum output; and puberty-related increases. Seborrheic dermatitis is an inflammatory condition predominantly occurring in areas rich in sebaceous glands, such as the , face, and upper trunk, where sebum provides a nutrient-rich milieu for microbial overgrowth. The pathogenesis centers on an aberrant immune response to species, lipophilic yeasts that are normal but proliferate excessively in seborrheic regions. These yeasts metabolize sebum triglycerides via lipases and phospholipases, releasing irritant free fatty acids that penetrate the , induce hyperproliferation of , and provoke inflammation characterized by , scaling, and pruritus. Unlike , seborrheic dermatitis involves neither follicular hyperkeratosis nor C. acnes dominance but shares sebaceous hyperactivity as a predisposing factor, often linked to genetic susceptibility and environmental triggers like stress. Prevalence peaks in adolescence and early adulthood, aligning with sebaceous gland maturation.

Neoplasms and Tumors

Sebaceous gland neoplasms encompass both benign and malignant proliferations arising from sebaceous cells, with benign lesions being far more common than their malignant counterparts. represents a frequent benign condition characterized by the enlargement of sebaceous glands, presenting as soft, yellow papules, typically 2 to 9 mm in diameter, with a central umbilication, most often on the central face such as the , cheeks, and in middle-aged to elderly individuals. This benign proliferation involves an increased number of mature sebaceous lobules surrounding hair follicles, without atypical features, and affects approximately 1% of the general population, with higher prevalence in those on long-term immunosuppressive therapy like cyclosporine. Another benign entity is nevus sebaceus, a congenital of the pilosebaceous unit, appearing at birth as a solitary, smooth, yellow-orange plaque, commonly on the , , or face, which becomes thickened and verrucous during due to hormonal influences on sebaceous gland maturation. Histologically, it features immature sebaceous glands with malformed ducts and increased lobules in a background of epidermal and follicular abnormalities, carrying a low risk (<1%) of secondary benign tumors like trichoblastomas, though is rare. Malignant neoplasms of sebaceous glands primarily include sebaceous , a rare and aggressive adnexal tumor that accounts for about 0.2% to 0.8% of all skin malignancies, with an incidence of approximately 0.16 to 0.32 per 100,000 person-years, showing a rising trend particularly among males and White individuals over the past two decades. It predominantly affects the eyelids (periocular sites in 75% of cases), presenting as a slowly growing, yellowish nodule or irregular thickening, though extraocular occurrences on the head, neck, or trunk are possible. Risk factors include chronic (UV) radiation exposure, (e.g., in solid organ transplant recipients), older age (peak 60-79 years), and male sex, with a 1.4:1 male-to-female ratio. Notably, up to 30% of cases are associated with Muir-Torre (MTS), a variant of Lynch syndrome caused by mutations in genes like MLH1 or MSH2, linking sebaceous carcinoma to internal malignancies, particularly colorectal and other gastrointestinal cancers, necessitating genetic screening and oncologic surveillance. Histopathologically, sebaceous neoplasms are distinguished by their cellular composition, featuring peripheral basaloid cells—small, hyperchromatic undifferentiated cells with scant —and central mature sebocytes containing intracytoplasmic vacuoles that impart a foamy appearance. In benign lesions like or adenomas, the architecture is well-circumscribed with orderly lobules connected to the , lacking or mitoses, whereas sebaceous carcinoma exhibits irregular, infiltrative lobules with pagetoid spread, nuclear pleomorphism, high mitotic activity, and , often mimicking other adnexal tumors. Definitive diagnosis for all sebaceous neoplasms requires , typically incisional for larger lesions, with immunohistochemical stains (e.g., adipophilin for confirmation) aiding in confirmation, especially to differentiate from mimics like . Self-removal or home remedies (e.g., squeezing, popping, or using over-the-counter methods) for sebaceous neoplasms are not safe and should be avoided. These practices risk infection, scarring, incomplete removal, and spreading of cancer if the growth is malignant. Professional medical evaluation and intervention are essential.

Diagnostic and Treatment Approaches

Diagnosis of sebaceous gland disorders typically begins with a clinical examination by a dermatologist, who identifies characteristic lesions such as yellowish papules for or nodular masses for potential neoplasms based on appearance, location, and patient history. Dermoscopy may assist in confirming features like central umbilication in hyperplasia or irregular borders in suspicious tumors, aiding differentiation from similar conditions like . For definitive diagnosis, particularly in suspected malignancies, a is performed to allow histological examination, revealing enlarged sebaceous lobules in or atypical cells with vacuoles in sebaceous . Sebum excretion rate (SER) measurement, using devices like the Sebumeter, quantifies sebum production on the or cheeks after site degreasing, providing objective data on glandular hyperactivity relevant to disorders like or seborrhea. Imaging modalities such as high-frequency are employed for deeper evaluation of tumors, delineating size, depth, and to guide surgical planning, especially in periocular sebaceous carcinoma where margins must be preserved. Treatment approaches for sebaceous gland-related disorders target underlying hyperactivity or neoplastic growth, tailored to the specific condition. For and seborrheic disorders involving excessive sebum production, topical retinoids like tretinoin normalize follicular keratinization and reduce gland activity, while benzoyl peroxide provides antimicrobial effects against Cutibacterium acnes. Oral , a systemic , dramatically shrinks sebaceous glands and decreases sebum output by up to 90%, serving as a cornerstone for severe unresponsive to topicals. In hormonal cases, particularly in women, anti-s such as block androgen receptors in sebaceous glands, reducing sebum synthesis and alleviating symptoms. Management of sebaceous neoplasms prioritizes complete removal to prevent recurrence and . Self-removal or home remedies for these neoplasms are not safe, risking infection, scarring, incomplete removal, and potential cancer spread if malignant; professional medical intervention is required. Wide with margins of 5-6 mm is standard for accessible lesions, but Mohs micrographic surgery is preferred for facial or eyelid tumors due to its tissue-sparing precision and recurrence rates below 5%. For advanced or recurrent sebaceous carcinoma, or in non-surgical candidates, delivers localized doses of 50-60 Gy to control local disease, often as post-excision. Emerging therapies focus on minimally invasive options for benign overgrowths like . Laser treatments, including CO2 or 1450-nm diode , ablate enlarged glands with high efficacy, achieving 75% improvement and reduction in multiple sessions with minimal scarring. Microbiome-targeted interventions, such as topical or oral containing Lactobacillus species, modulate the skin and to suppress pathogenic overgrowth and inflammation in and seborrheic dermatitis, showing promise in reducing severity through sebaceous gland regulation.

Historical and Comparative Perspectives

Discovery and Key Milestones

Early observations of skin conditions later associated with sebaceous gland activity date back to , where in the 4th century BCE described eruptions linked to puberty, akin to acne vulgaris. These accounts focused on the clinical presentation, though the glands themselves were not yet anatomically identified. In the , provided one of the first detailed anatomical descriptions of skin structures in his seminal 1543 work De Humani Corporis Fabrica, marking a shift toward empirical dissection-based . The 19th century brought focused histological studies, with Paul Gerson Unna in 1896 observing microbial elements within comedones and linking sebaceous gland hyperactivity to pathogenesis through histopathological analysis. Concurrently, Raymond Sabouraud advanced concepts of seborrhea in the 1890s, proposing that excessive sebaceous secretion, influenced by microbial factors like , underlies conditions such as seborrheic , integrating clinical and mycological perspectives. These insights established the sebaceous gland as central to inflammatory diseases. In the 20th century, research progressed to biochemical characterization, with early analyses circa 1910 elucidating sebum's lipid composition, revealing triglycerides, wax esters, and squalene as key components produced by holocrine secretion. A major therapeutic milestone occurred in the 1980s with the development of isotretinoin, a retinoid that dramatically reduces sebaceous gland size and sebum output, revolutionizing acne treatment after its synthesis and clinical trials by Hoffmann-La Roche in the 1970s. Modern advancements since the 1990s have uncovered molecular regulators, such as (PPARγ), which drives sebocyte differentiation and lipid synthesis, as demonstrated in studies of human sebaceous gland models. In the , investigations highlighted the sebaceous microbiome's role, showing how sebum shape microbial communities like Cutibacterium acnes and influence homeostasis and disease susceptibility in and seborrhea. Since the 2020s, single-cell sequencing has revealed cellular heterogeneity within sebaceous glands, enhancing understanding of their role in skin disorders like acne vulgaris (as of 2025).

Structure and Function in Animals

Sebaceous glands exhibit significant variations across mammalian species, reflecting adaptations to diverse ecological niches. In carnivores and other terrestrial mammals, these glands are often denser and more prominent, particularly in regions involved in scent communication. For instance, preputial glands in , which are specialized sebaceous structures, secrete pheromones that facilitate scent marking for territorial and social purposes. Similarly, in canids such as dogs, modified sebaceous glands contribute to the production of odorous secretions used in demarcation. In contrast, aquatic mammals like whales display reduced or absent sebaceous glands, correlating with their hairless, streamlined adapted for hydrodynamic efficiency and minimal need for lubrication in a fully aquatic environment. This loss is evident in cetaceans, where genes associated with sebum production have undergone complete inactivation during their evolutionary transition from land to water. Outside of mammals, sebaceous-like glands are rudimentary or absent in other classes. In birds, the serves as a functional analog, functioning as a bilobate sebaceous organ that produces waxy for feather waterproofing and maintenance during behaviors. This gland, located at the base of the tail, exhibits secretion similar to mammalian sebaceous glands but is absent in flightless or aquatic species to varying degrees. In reptiles and amphibians, true sebaceous glands are lacking; instead, these groups rely on mucous glands for hydration and granular glands for defense, with lipid barriers formed primarily through epidermal keratinization rather than glandular secretion. Functionally, sebaceous glands in animals primarily secrete sebum to lubricate skin and appendages, but their roles diverge by species. In dogs, these glands produce musk-like secretions that aid in olfactory signaling for territory and social interactions, often in conjunction with apocrine elements in specialized areas. By comparison, in humans, sebaceous glands emphasize lubrication and emollience of the skin and hair, with less emphasis on pheromonal communication. Evolutionarily, the secretions of sebaceous glands represent an adaptation that likely originated in the synapsid ancestors of mammals, predating the full development of follicles and aiding in integumental during the transition to terrestrial life in early tetrapods. This mechanism enhanced barrier function against , building on primitive layers in reptilian around 300 million years ago. In mammals, these glands became integral to pilosebaceous units, supporting and microbial defense through sebum's properties.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK499819/
  2. https://www.ncbi.nlm.nih.gov/books/NBK482237/
  3. https://www.sciencedirect.com/topics/medicine-and-dentistry/sebaceous-gland
  4. https://pmc.ncbi.nlm.nih.gov/articles/PMC6068117/
  5. https://accessmedicine.mhmedical.com/Content.aspx?bookid=392&sectionid=41138784
  6. https://histology.siu.edu/intro/IN043b.htm
  7. https://www.kenhub.com/en/library/anatomy/sebaceous-gland
  8. https://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/sebaceous-gland
  9. https://pubmed.ncbi.nlm.nih.gov/31970855/
  10. https://pubmed.ncbi.nlm.nih.gov/33354858/
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC5595243/
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC9775059/
  13. https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1029818/full
  14. https://academic.oup.com/edrv/article/21/4/363/2423841
  15. https://www.ncbi.nlm.nih.gov/medgen/1706541
  16. https://rarediseases.org/rare-diseases/schimmelpenning-syndrome/
  17. https://www.sciencedirect.com/science/article/pii/S0022202X16325349
  18. https://pmc.ncbi.nlm.nih.gov/articles/PMC5605215/
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC9428133/
  20. https://www.science.org/doi/10.1126/scitranslmed.aau8465
  21. https://www.nature.com/articles/s42003-025-08105-9
  22. https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/sebum
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC5821166/
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC7167948/
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC3051853/
  26. https://doi.org/10.1038/jid.2009.384
  27. https://doi.org/10.1038/jid.2009.93
  28. https://www.cell.com/cell/fulltext/S0092-8674(18)31645-3
  29. https://doi.org/10.1194/jlr.R700015-JLR200
  30. https://doi.org/10.1016/j.micinf.2006.04.001
  31. https://doi.org/10.1111/j.0022-202X.2005.23705.x
  32. https://doi.org/10.1016/j.stem.2013.07.010
  33. https://eyewiki.org/Meibomian_Gland_Dysfunction_%28MGD%29
  34. https://www.aao.org/eye-health/anatomy/meibomian-glands
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC3183971/
  36. https://www.ncbi.nlm.nih.gov/books/NBK537278/
  37. https://vitreum.ro/en/ophthalmological-dictionary/ocular-sebaceous-glands/
  38. https://morancore.utah.edu/section-07-orbit-eyelids-and-lacrimal-system/what-is-a-stye-and-how-do-you-treat-it/
  39. https://www.sciencedirect.com/topics/medicine-and-dentistry/gland-of-montgomery
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC2761488/
  41. https://www.ncbi.nlm.nih.gov/books/NBK148970/
  42. https://www.reviewofophthalmology.com/article/the-form-and-function-of-meibomian-glands
  43. https://www.pathologyoutlines.com/topic/oralcavityfordyce.html
  44. https://dermnetnz.org/topics/fordyce-spots
  45. https://my.clevelandclinic.org/health/diseases/24140-fordyce-spots
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC11086941/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC3283840/
  48. https://www.pathologyoutlines.com/topic/esophagusectopicsebaceousglands.html
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC3369260/
  50. https://onlinelibrary.wiley.com/doi/full/10.1111/exd.12291
  51. https://pubmed.ncbi.nlm.nih.gov/7636302/
  52. https://onlinelibrary.wiley.com/doi/10.1034/j.1600-0625.2003.00014.x
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC5821152/
  54. https://pubmed.ncbi.nlm.nih.gov/448169/
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC4507494/
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC5318522/
  57. https://www.ncbi.nlm.nih.gov/books/NBK459173/
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC10709101/
  59. https://www.nature.com/articles/s41598-020-62715-3
  60. https://www.aafp.org/pubs/afp/issues/2015/0201/p185.html
  61. https://dermnetnz.org/topics/seborrhoeic-dermatitis
  62. https://www.ncbi.nlm.nih.gov/books/NBK562148/
  63. https://www.ncbi.nlm.nih.gov/books/NBK482493/
  64. https://pubmed.ncbi.nlm.nih.gov/27720512/
  65. https://www.ncbi.nlm.nih.gov/books/NBK610689/
  66. https://www.ncbi.nlm.nih.gov/books/NBK513271/
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC10217338/
  68. https://www.healthline.com/health/can-i-stick-a-needle-in-a-sebaceous-cyst
  69. https://my.clevelandclinic.org/health/diseases/22670-sebaceous-hyperplasia
  70. https://www.mayoclinic.org/diseases-conditions/sebaceous-carcinoma/symptoms-causes/syc-20577038
  71. https://pmc.ncbi.nlm.nih.gov/articles/PMC10483949/
  72. https://ijdvl.com/sebumeter/
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC10765351/
  74. https://journals.lww.com/dmms/fulltext/2020/15030/ultrasonography%2C_doppler%2C_and_elastograhic_imaging.28.aspx
  75. https://www.mayoclinic.org/diseases-conditions/acne/diagnosis-treatment/drc-20368048
  76. https://www.aafp.org/pubs/afp/issues/2012/1015/p734.html
  77. https://www.hopkinsmedicine.org/health/conditions-and-diseases/acne
  78. https://pubmed.ncbi.nlm.nih.gov/16295039/
  79. https://my.clevelandclinic.org/health/diseases/24087-sebaceous-carcinoma
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC6805970/
  81. https://pubmed.ncbi.nlm.nih.gov/32484621/
  82. https://www.nature.com/articles/s41598-024-53016-0
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC8953587/
  84. https://www.sciencedirect.com/science/article/pii/S2352647516300284
  85. https://www.britannica.com/topic/De-humani-corporis-fabrica-libri-septem
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC6534434/
  87. https://accessmedicine.mhmedical.com/content.aspx?bookid=392&sectionid=41138717
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC2835893/
  89. https://www.dermatologytimes.com/view/isotretinoins-discovery-and-development
  90. https://www.sciencedirect.com/science/article/pii/S0022202X15326099
  91. https://pmc.ncbi.nlm.nih.gov/articles/PMC6920876/
  92. https://www.nature.com/articles/s41586-023-06645-7
  93. https://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/preputial-gland
  94. https://www.sciencedirect.com/topics/veterinary-science-and-veterinary-medicine/scent-gland
  95. https://www.frontiersin.org/journals/marine-science/articles/10.3389/fmars.2020.592375/full
  96. https://academic.oup.com/mbe/article/36/6/1270/5415914
  97. https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/uropygial-gland
  98. https://www.sciencedirect.com/topics/medicine-and-dentistry/skin-gland
  99. https://www.merckvetmanual.com/integumentary-system/integumentary-system-introduction/the-integumentary-system-in-animals
  100. https://pmc.ncbi.nlm.nih.gov/articles/PMC10740688/
  101. https://journals.biologists.com/jeb/article/209/2/202/16270/Water-relations-of-tetrapod-integument
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC10277264/
Add your contribution
Related Hubs
User Avatar
No comments yet.