Acne vulgaris
Definitions & Key takeaways
Acne vulgaris (commonly called acne) is a chronic skin disease that occurs when hair follicles are clogged with dead skin cells and oil from the skin. It is characterized by blackheads or whiteheads, pimples, oily skin, and possible scarring.
It primarily affects areas of the skin with a high number of oil glands, such as the face, chest, shoulders, and back. Acne is self-limiting but can cause significant emotional distress.
Introduction0:00–0:47
With acne vulgaris, acne means “eruption” and vulgaris, means “common”. So acne vulgaris is a common skin eruption that occurs when hair follicles, or pores, get blocked by particles like dead skin cells or oil.
Once hair follicles are blocked, it forms small raised, red bumps on the skin. Acne is particularly common among teenagers because of the skin changes that occur during puberty.
Acne can be categorized into different types based on specific characteristics. For example, mild acne usually consists of whiteheads and blackheads, moderate acne, usually consists of pustules, and severe acne, usually consists of cysts and nodules.
Skin0:47–2:47
Now, the skin is divided into three main layers--the epidermis, dermis, and hypodermis. The epidermis forms the thin outermost layer of skin, and has 5 sublayers: the stratum corneum as the outermost layer followed by the stratum granulosum, the stratum spinosum, and the stratum basale.
In the palms and feet, which are areas with thicker skin, there is a fifth layer called the stratum lucidum which is around one cell layer thick.
Underneath the layers of the epidermis is the dermis, and it’s mainly made up of connective tissue but also contains nerve endings, hair follicles, sweat glands, sebaceous glands, lymphatic vessels and blood vessels.
Focusing on the hair follicles, each one contains a strand of hair, composed of the shaft, root, and bulb that sits in the follicle.
The hair follicle is epidermal tissue that dips down into the dermis, and is associated with other structures like apocrine glands, sebaceous glands, the arrector pili muscle, and nerve receptors.
Now, sebaceous glands, or oil glands, are located in the dermis layer of the skin and are connected to hair follicles. Each sebaceous glands secrete an oily substance called sebum into a nearby hair follicle or through pores that extend directly to the skin surface.
Sebum is a substance made of different fatty acids and waxy esters to help transport nutrients and lubricate the skin. As it turns out, arrector pili muscles surround the sebaceous glands, so when these tiny muscles contract, sebum gets squeezed out.
Sebum softens the hair shaft preventing it from becoming brittle. Sebum also prevents moisture loss from the skin and is slightly acidic, which helps to deter pathogens.
And below all of this is the hypodermis which is made of fat and connective tissue that anchors the skin to the underlying muscle.The cause of acne is not completely understood but we do know that there are a few main factors that contribute to acne formation: keratin plugs, sebum, and bacterial overgrowth.
Pathophysiology2:47–4:55
First, there’s keratin plugs which are tiny clumps made up of dead keratinocytes, the protein keratin, and the pigment melanin.
When keratinocytes in hair follicles overproduce keratin it’s called hyperkeratosis. It leads to more keratin plugs forming, and these little keratin plugs block the opening of the hair follicle.
Second, there’s sebum, which is released by sebaceous glands in response to increased androgen production, like during puberty, in both boys and girls.
The sebum contributes to clogging up the follicles and causes blockage just like the keratin plugs. So when there’s an excess in keratin plugs or sebum or both, it can start to fill up a hair follicle, but not quite plug it up all the way.
If the hair follicle is still open to the surface of the skin, then it’s called an open comedo, and it looks black so it’s also called a blackhead.
Blackheads look black because melanin in the keratin plug ends up getting oxidized when it’s exposed to air and becomes dark in color.
Now, the third factor to consider in acne is bacteria, like Propionibacterium, which are always living within the follicles.
Normally, these bacteria don’t cause any problems; they’re part of the normal skin flora. But if the hair follicle gets completely plugged up with keratin plugs and sebum, then it creates a closed environment, and it’s called a closed comedo, or a whitehead.
In a closed comedo, the bacteria grow and grow - feasting on the keratin plugs and sebum, and they have no place to go - resulting in bacterial overgrowth.
The overwhelming number of bacteria attracts immune cells which head over and start attacking the bacterial cells. The result of this mix of bacterial cells and immune cells is white pus with surrounding red inflammation.
Risk factors4:55–6:09
For example, hyperkeratosis can have a genetic component and often runs in the family. In addition, hormones, as well as using specific physical products and behaviors can also can also lead to hyperkeratosis.
For example, women with polycystic ovarian syndrome, have increased androgen hormone levels which leads to more sebum and therefore more acne.
Physical products and behaviors include the use of certain moisturisers and cosmetics that can block pores. Similarly, doing things like wearing a headband can irritate the skin and block pores - that’s called ‘contact acne’ or ‘acne venenata’.
Also, washing the face excessively can irritate the skin surface, predisposing it to acne formation. Finally, some studies have found links between low fat dairy and acne, as well as a correlation between compounds in chocolate.Acne vulgaris most often occurs on the face, chest, shoulders, and back -- the sites of oil glands, and it can be categorised into four types based on severity.
Manifestation and Classification6:09–7:07
In type 4 or severe acne, there’s severe scarring and nodulocystic acne which has firm lumps called nodules, and cysts which are fluid filled cavities in the skin.
Nodulocystic acne invades deeper into the dermis, forming interconnecting abscesses. Depending on the severity and location of acne, treatments can vary.
Treatment7:07–8:56
For mild acne, topical treatments such as benzoyl peroxide or salicylic acid can help remove comedones by removing the top keratin layer.
In moderate cases, antibiotics such as doxycycline or tetracycline can be used both topically or orally. Occasionally, spironolactone can be used, particularly for hormonal regulation in women.
In more severe cases, isotretinoin, a vitamin A derivative, has been shown to significantly improve facial acne due to its ability to impact sebum secretion.
To minimize the risk of that, a gentle, non-soap facial cleanser should be used, and a non-comedogenic facial moisturizer may help with dry skin.
There’s even laser treatments which can stimulate cell turnover and growth of new epidermal tissue. In women, the oral contraceptive pill can be beneficial.
For some acne sufferers, there can be significant feelings of depression or anxiety, especially when there are severe or frequent bouts of acne.
Psychological counselling can help suffers cope with their condition. In fact, there’s a field called psychodermatology which utilizes strategies like anti-anxiety medications, biofeedback, allergy and immune function testing, and cognitive behavioral therapy.
Review8:56–9:40
Key risk factors are keratin plugs, sebum, and bacterial overgrowth. Open comedones or blackheads develop when the hair follicle is open to the air and there’s oxidization of the melanin within the keratin plug.
Closed comedones or whiteheads develop when the hair follicle gets blocked completely and leads to bacterial overgrowth and inflammation.
There are various oral and topical treatment options available, as well as new areas of psychodermatology which addresses the relationship between emotions and physical changes in the skin.
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- "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
- "Acne vulgaris" BMJ (2013)
- "Epidemiology of acne vulgaris" British Journal of Dermatology (2013)
- "Pathways to inflammation: acne pathophysiology" European Journal of Dermatology (2011)
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