A sebaceous gland or oil gland[1] is a microscopic
exocrinegland 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 nipple,
areolar glands are specialized sebaceous glands for lubricating the nipple.
Fordyce spots are
benign, visible, sebaceous glands found usually on the lips, gums and inner cheeks, and
genitals.
Structure
Location
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 follicle, arrector pili muscles, and sebaceous gland, is an epidermal invagination known as a pilosebaceous unit.[4]
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]
Relative to keratinocytes that make up the hair follicle, sebaceous glands are composed of huge cells 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: 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 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
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]
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]
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]
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
Other conditions that involve the sebaceous glands include:
Seborrhoea refers to overactive sebaceous glands, a cause of oily skin[5] or hair.[16]
Sebaceous hyperplasia, referring to excessive proliferation of the cells within the glands, and visible macroscopically as small papules on the skin, particularly on the forehead, nose and cheeks.[34]
Seborrheic-like psoriasis (also known as "Sebopsoriasis",[36] and "Seborrhiasis") is a skin condition characterized by
psoriasis with an overlapping seborrheic dermatitis.[3]: 193
Sebaceous cyst is a term used to refer to both an
epidermoid cyst and a
pilar cyst, though neither of these contain sebum, only keratin and do not originate in the sebaceous gland and so are not true sebaceous cysts. A true sebaceous cyst is relatively rare and is known as a
steatocystoma.[38]
Nevus sebaceous, a hairless region or plaque on the scalp or skin, caused by an overgrowth of sebaceous glands. The condition is congenital and the plaque becomes thicker into adulthood.[39]
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]
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]
^
abJames, William D.; Berger, Timothy; Elston, Dirk M. (2006). Andrews' Diseases of the Skin: Clinical dermatology. Saunders Elsevier. p. 7.
ISBN978-0-7216-2921-6.
^
abcdYoung, Barbra; Lowe, James S; Stevens, Alan; Heath, John W; Deakin, Philip J (March 2006). Wheater's Functional Histology (5 ed.). Elsevier Health Sciences. pp. 175–178.
ISBN978-0-443-06850-8.
^Dellmann's textbook of veterinary histology (405 pages), Jo Ann Coers Eurell, Brian L. Frappier, 2006, p.29, weblink:
Books-Google-RTOCArchived 24 February 2024 at the
Wayback Machine.
^Wilkinson, P.F.; Millington, R. (1983). Skin (Digitally printed ed.). Cambridge: Cambridge university press. p. 151.
ISBN978-0-521-24122-9.
^Monika-Hildegard Schmid-Wendtner; Korting Schmid-Wendtner (2007).
Ph and Skin Care. ABW Wissenschaftsverlag. pp. 31–.
ISBN978-3-936072-64-8. Retrieved 19 June 2012.
^Zlotogorski A (1987). "Distribution of skin surface pH on the forehead and cheek of adults". Arch. Dermatol. Res. 279 (6): 398–401.
doi:
10.1007/bf00412626.
PMID3674963.
S2CID3065931.
^McCulley, JP; Shine, WE (March 2004). "The lipid layer of tears: dependent on meibomian gland function". Experimental Eye Research. 78 (3): 361–5.
doi:
10.1016/s0014-4835(03)00203-3.
PMID15106913.
^Dorland's (2012). Dorland's Illustrated Medical Dictionary (32nd ed.). Elsevier Saunders. p. 802.
ISBN978-0-19-856878-0.
^Roeser, RJ; Ballachanda, BB (December 1997). "Physiology, pathophysiology, and anthropology/epidemiology of human earcanal secretions". Journal of the American Academy of Audiology. 8 (6): 391–400.
PMID9433685.
^
abColledge N, Walker B, Ralston S, eds. (2010). Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 1267–1268.
ISBN978-0-7020-3085-7.
^Farrell LN, Strauss JS, Stranieri AM (December 1980). "The treatment of severe cystic acne with 13-cis-retinoic acid. Evaluation of sebum production and the clinical response in a multiple-dose trial". Journal of the American Academy of Dermatology. 3 (6): 602–11.
doi:
10.1016/S0190-9622(80)80074-0.
PMID6451637.
^Neville BW, Damm DD, Allen CA, Bouquot JE (2002). Oral & maxillofacial pathology (2nd ed.). Philadelphia: W. B. Saunders. p. 31.
ISBN978-0-7216-9003-2.
^Dobson, G. E. (1878). Catalogue of the Chiroptera in the collection of the British Museum. Order of the Trustees.
^Gutierrez, Mercedes; Aoki, Agustin (1973). "Fine structure of the gular gland of the free-tailed bat Tadarida brasiliensis". Journal of Morphology. 141 (3): 293–305.
doi:
10.1002/jmor.1051410305.
PMID4753444.
S2CID3093610.