Different types of Acne Vulgaris: A: Cystic acne on the face, B: Subsiding tropical acne of trunk, C: Extensive acne on chest and shoulders.
The term acne comes from a corruption of the Greek (acne in the sense of a skin eruption) in the writings of Atius Amidenus. Used by itself, the term “acne” refers to the presence of pustules and papules. The most common form of acne is known as “acne vulgaris”, meaning “common acne”. Many teenagers get this type of acne. Use of the term “acne vulgaris” implies the presence of comedones.
The term “acne rosacea” is a synonym for rosacea, however some individuals may have almost no acne comedones associated with their rosacea and prefer therefore the term rosacea. Chloracne is associated with exposure to polyhalogenated compounds.
Causes of acne
Acne develops as a result of blockages in follicles. Hyperkeratinization and formation of a plug of keratin and sebum (a microcomedo) is the earliest change. Enlargement of sebaceous glands and an increase in sebum production occur with increased androgen (DHEA-S) production at adrenarche. The microcomedo may enlarge to form an open comedone (blackhead) or closed comedone (whitehead). Whiteheads are the direct result of sebaceous glands becoming clogged with sebum, a naturally occurring oil, and dead skin cells. In these conditions the naturally occurring largely commensal bacteria Propionibacterium acnes can cause inflammation, leading to inflammatory lesions (papules, infected pustules, or nodules) in the dermis around the microcomedo or comedone, which results in redness and may result in scarring or hyperpigmentation.
A 16 year-old teenager with acne on his cheek.
Acne is known to be partly hereditary, but no particular genetic cause has been identified. Acne is not contagious or infectious. Several factors are known to be linked to acne:
Family/Genetic history. The tendency to develop acne runs in families. For example, school-age boys with acne often have other members in their family with acne as well. A family history of acne is associated with an earlier occurrence of acne and an increased number of retentional acne lesions.
Hormonal activity, such as menstrual cycles and puberty. During puberty, an increase in male sex hormones called androgens cause the follicular glands to grow larger and make more sebum.
Inflammation, skin irritation or scratching of any sort will activate inflammation.
Stress. While the connection between acne and stress has been debated, scientific research indicates that “increased acne severity” is “significantly associated with increased stress levels.” The National Institutes of Health (USA) list stress as a factor that “can cause an acne flare.” A study of adolescents in Singapore “observed a statistically significant positive correlation  between stress levels and severity of acne.”
Hyperactive sebaceous glands, secondary to the three hormone sources above.
Bacteria in the pores. Propionibacterium acnes (P. acnes) is the anaerobic bacterium that causes acne. In-vitro resistance of P. acnes to commonly used antibiotics has been increasing.
Use of anabolic steroids.
Exposure to certain chemical compounds. Chloracne is particularly linked to toxic exposure to dioxins, namely Chlorinated dioxins.
Acne on an arm.
Several hormones have been linked to acne: the androgens testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), as well as insulin-like growth factor 1 (IGF-I).
Development of acne vulgaris in later years is uncommon, although this is the age group for Rosacea which may have similar appearances. True acne vulgaris in adult women may be a feature of an underlying condition such as pregnancy and disorders such as polycystic ovary syndrome or the rare Cushing’s syndrome. Menopause-associated acne occurs as production of the natural anti-acne ovarian hormone estradiol fails at menopause. The lack of estradiol also causes thinning hair, hot flashes, thin skin, wrinkles, vaginal dryness, and predisposes to osteopenia and osteoporosis as well as triggering acne (known as acne climacterica in this situation).
The popular belief that chocolate intake, in and of itself, is a cause of acne is not supported by scientific studies. As discussed below, various studies point not to chocolate, but to the high glycemic nature of certain foods containing simple carbohydrates as a cause of acne. Chocolate itself has a low glycemic index.
Recently, three epidemiological studies from the same group of scientists found an association between acne and consumption of partially skimmed milk, instant breakfast drink, sherbet, cottage cheese, and cream cheese. The researchers hypothesize that the association may be caused by hormones (such as several sex hormones and bovine insulin-like growth factor 1 (IGF-1)) or even iodine present in cow milk.
The long-held belief that there is no link between diets high in refined sugars and processed foods, and acne, has recently been challenged. The previous belief was based on earlier studies (some using chocolate and Coca-Cola) that were methodologically flawed. The recent low glycemic-load hypothesis postulates that rapidly digested carbohydrate foods (such as soft drinks, sweets, white bread) produce an overload in blood glucose (hyperglycemia) that stimulates the secretion of insulin, which in turn triggers the release of IGF-1. IGF-1 has direct effects on the pilosebaceous unit (and insulin at high concentrations can also bind to the IGF-1 receptor) and has been shown to stimulate hyperkeratosis and epidermal hyperplasia. These events facilitate acne formation. Sugar consumption might also influence the activity of androgens via a decrease in sex hormone-binding globulin concentration.
In support of this hypothesis, a randomized controlled trial of a low glycemic-load diet improved acne and reduced weight, androgen activity and levels of insulin-like growth factor binding protein-1. High IGF-1 levels and mild insulin resistance (which causes higher levels of insulin) had previously been observed in patients with acne. High levels of insulin and acne are also both features of polycystic ovarian syndrome.
According to this hypothesis, the absence of acne in some non-Westernized societies could be explained by the low glycemic index of these cultures’ diets. It is possible that genetic reasons account for there being no acne in these populations, although similar populations (such as South American Indians or Pacific Islanders) do develop acne. Note also that the populations studied consumed no milk or other dairy products.
Further research is necessary to establish whether a reduced consumption of high-glycemic foods, or treatment that results in increased insulin sensitivity (like metformin) can significantly alleviate acne, though consumption of high-glycemic foods should in any case be kept to a minimum, for general health reasons. Avoidance of “junk food” with its high fat and sugar content is also recommended.
Vitamins A and E
Studies have shown that newly diagnosed acne patients tend to have lower levels of vitamin A circulating in their bloodstream than those who are acne free. In addition people with severe acne also tend to have lower blood levels of vitamin E.
Acne is not caused by dirt. This misconception probably comes from the fact that blackheads look like dirt stuck in the openings of pores. The black color is not dirt but simply oxidized keratin. In fact, the blockages of keratin that cause acne occur deep within the narrow follicle channel, where it is impossible to wash them away. These plugs are formed by the failure of the cells lining, the duct, to separate and flow to the surface in the sebum created there by the body. Built-up oil of the skin can block the passages of these pores, so standard washing of the face could wash off old oil and help unblock the pores.
There are many products available for the treatment of acne, many of which are without any scientifically proven effects. Generally speaking, successful treatments show little improvement within the first two weeks, instead taking a period of approximately three months to improve and start flattening out. Many treatments that promise big improvements within two weeks are likely to be largely disappointing. However, short bursts of cortisone can give very quick results, and other treatments can rapidly improve some active spots, but usually not all active spots.
Modes of improvement are not necessarily fully understood but in general treatments are believed to work in at least 4 different ways (with many of the best treatments providing multiple simultaneous effects):
normalising shedding into the pore to prevent blockage
killing Propionibacterium acnes
A combination of treatments can greatly reduce the amount and severity of acne in many cases. Those treatments that are most effective tend to have greater potential for side effects and need a greater degree of monitoring, so a step-wise approach is often taken. Many people consult with doctors when deciding which treatments to use, especially when considering using any treatments in combination. There are a number of treatments that have been proven effective:
Benzoyl peroxide cream.
Proper washing and skin care can help to remove bacteria and oils which cause acne. Some anecdotal reports indicate placing a clean towel over one’s pillow each night can help prevent contaminating the pillow with the bacteria that causes acne, and reintroducing it to the face. Additionally, cleaning the hands before touching the affected area can prevent transmission of the bacteria from one part of the body to another.
Widely available OTC bactericidal products containing benzoyl peroxide may be used in mild to moderate acne. The gel or cream containing benzoyl peroxide is applied, twice daily, into the pores over the affected region. Bar soaps or washes may also be used and vary from 2% to 10% in strength. In addition to its therapeutic effect as a keratolytic (a chemical that dissolves the keratin plugging the pores) benzoyl peroxide also prevents new lesions by killing P. acnes. In one study, roughly 70% of participants using a 10% benzoyl peroxide solution experienced a reduction in acne lesions after six weeks. Unlike antibiotics, benzoyl peroxide has the advantage of being a strong oxidizer and thus does not appear to generate bacterial resistance. However, it routinely causes dryness, local irritation and redness. A sensible regimen may include the daily use of low-concentration (2.5%) benzoyl peroxide preparations, combined with suitable non-comedogenic moisturisers to help avoid overdrying the skin.
Care must be taken when using benzoyl peroxide, as it can very easily bleach any fabric or hair it comes in contact with.
Other antibacterials that have been used include triclosan, or chlorhexidine gluconate. Though these treatments are often less effective, they also have fewer side-effects.
Products containing azeleic acid are also used in the treatment of P. acnes. It is available in the United States as a 20% concentration and does not generate bacterial resistance.
Prescription-strength benzoyl peroxide preparations do not necessarily differ with regard to the maximum concentration of the active ingredient (10%), but the drug is made available dissolved in a vehicle that more deeply penetrates the pores of the skin.
Externally applied antibiotics such as erythromycin, clindamycin or tetracycline kill the bacteria that are harbored in the blocked follicles. While topical use of antibiotics is equally as effective as oral use, this method avoids possible side effects including upset stomach and drug interactions (e.g. it will not affect use of the oral contraceptive pill), but may prove inefficient to apply over larger areas than just the face alone.
Oral antibiotics used to treat acne include erythromycin or one of the tetracycline antibiotics (tetracycline, the better absorbed oxytetracycline, or one of the once daily doxycycline, minocycline, or lymecycline). Trimethoprim is also sometimes used (off-label use in UK). However, reducing the P. acnes bacteria will not, in itself, do anything to reduce the oil secretion and abnormal cell behaviour that is the initial cause of the blocked follicles. Additionally the antibiotics are becoming less and less useful as resistant P. acnes are becoming more common. Acne may return soon after the end of treatmentays later in the case of topical applications, and weeks later in the case of oral antibiotics. Furthermore, side effects of tetracycline antibiotics can include yellowing of the teeth and an imbalance of gut flora, so are only recommended after topical products have been ruled out.
It has been found that sub-antimicrobial doses of antibiotics such as minocycline also improve acne. It is believed that minocycline’s anti-inflammatory effect also prevents acne.
In females, acne can be improved with hormonal treatments. The common combined estrogen/progestogen methods of hormonal contraception have some effect, but the antiandrogen, Cyproterone, in combination with an oestrogen (Diane 35) is particularly effective at reducing androgenic hormone levels. Diane-35 is not available in the USA, but a newer oral contraceptive containing the progestin drospirenone is now available with fewer side effects than Diane 35 / Dianette. Both can be used where blood tests show abnormally high levels of androgens, but are effective even when this is not the case. Along with this, treatment with low dose spironolactone can have anti-androgenetic properties, especially in patients with polycystic ovarian syndrome.
If a pimple is large and/or does not seem to be affected by other treatments, a dermatologist may administer an injection of cortisone directly into it, which will usually reduce redness and inflammation almost immediately. This has the effect of flattening the pimple, thereby making it easier to cover up with makeup, and can also aid in the healing process. Side effects are minimal, but may include a temporary whitening of the skin around the injection point; and occasionally a small depression forms, which may persist, although often fills eventually. This method also carries a much smaller risk of scarring than surgical removal.
A group of medications for normalizing the follicle cell lifecycle are topical retinoids such as tretinoin (brand name Retin-A), adapalene (brand name Differin), and tazarotene (brand name Tazorac). Like isotretinoin, they are related to vitamin A, but they are administered as topicals and generally have much milder side effects. They can, however, cause significant irritation of the skin. The retinoids appear to influence the cell creation and death lifecycle of cells in the follicle lining. This helps prevent the hyperkeratinization of these cells that can create a blockage. Retinol, a form of vitamin A, has similar but milder effects and is used in many over-the-counter moisturizers and other topical products. Effective topical retinoids have been in use over 30 years but are available only on prescription so are not as widely used as the other topical treatments. Topical retinoids often cause an initial flare up of acne and facial flushing.
Main article: isotretinoin
A daily oral intake of vitamin A derivative isotretinoin (marketed as Accutane, Amnesteem, Sotret, Claravis, Clarus) over a period of 46 months can cause long-term resolution or reduction of acne. It is believed that isotretinoin works primarily by reducing the secretion of oils from the glands, however some studies suggest that it affects other acne-related factors as well. Isotretinoin has been shown to be very effective in treating severe acne and can either improve or clear well over 80% of patients. The drug has a much longer effect than anti-bacterial treatments and will often cure acne for good. The treatment requires close medical supervision by a dermatologist because the drug has many known side effects (many of which can be severe). About 25% of patients may relapse after one treatment. In those cases, a second treatment for another 46 months may be indicated to obtain desired results. It is often recommended that one lets a few months pass between the two treatments, because the condition can actually improve somewhat in the time after stopping the treatment and waiting a few months also gives the body a chance to recover. Occasionally a third or even a fourth course is used, but the benefits are often less substantial. The most common side effects are dry skin and occasional nosebleeds (secondary to dry nasal mucosa). Oral retinoids also often cause an initial flare up of acne within a month or so, which can be severe. There are reports that the drug has damaged the liver of patients. For this reason, it is recommended that patients have blood samples taken and examined before and during treatment. In some cases, treatment is terminated or reduced due to elevated liver enzymes in the blood, which might be related to liver damage. Others claim that the reports of permanent damage to the liver are unsubstantiated, and routine testing is considered unnecessary by some dermatologists. Blood triglycerides also need to be monitored. However, routine testing are part of the official guidelines for the use of the drug in many countries. Some press reports suggest that isotretinoin may cause depression but as of September 2005 there is no agreement in the medical literature as to the risk. The drug also causes birth defects if women become pregnant while taking it or take it while pregnant. For this reason, female patients are required to use two separate forms of birth control or vow abstinence while on the drug. Because of this, the drug is supposed to be given to females as a last resort after milder treatments have proven insufficient. Restrictive rules (see iPledge program) for use were put into force in the USA beginning in March 2006 to prevent misuse, causing occasioned widespread editorial comment.
Sulfur has an inhibitory effect on the growth of Propionibacterium acnes and, when combined with sodium sulfacetamide (5% and 10%, respectively) has been shown to reduce acne with only mild side effects.
Dermabrasion is a cosmetic medical procedure in which the surface of the skin is removed by abrasion (sanding). It is used to remove sun-damaged skin and to remove or lessen scars and dark spots on the skin. The procedure is very painful and usually requires a general anaesthetic or “twilight anaesthesia”, in which the patient is still partly conscious Afterward, the skin is very red and raw-looking, and it takes several months for the skin to regrow and heal. Dermabrasion is useful for scar removal when the scar is raised above the surrounding skin, but is less effective with sunken scars.
In the past, dermabrasion was done using a small, sterilized, electric sander. In the past decade, it has become more common to use a CO2 or Er:YAG laser. Laser dermabrasion is much easier to control, much easier to gauge, and is practically bloodless compared to classic dermabrasion.
Microdermabrasion comes from the above mentioned technique dermabrasion. Microdermabrasion is a more natural skin care that is a gentler, less invasive technology for doing an exfoliation on the skin. The goal of the microdermabrasion is to eliminate the superficial layer of the skin called the epidermis. If the surface of the abraded skin is touched, a roughness of the skin will be noticed. The roughness is keratinocytes, which are better hydrated than the surface corneocytes. Keratinocytes appear in the basal layer from the proliferation of keratinocyte stem cells. They are pushed up through the cells of the epidermis, experiencing gradual specialization until they reach the stratum corneum where they form a layer of dead, flattened, strongly keratinized cells called squamous cells. This layer creates an efficient barrier to the entry of foreign matter and infectious elements into the body and reduces moisture loss. Keratinocytes are shed and restored continuously from the stratum corneum.
The time of transit from basal layer to shedding is generally one month. Corneocytes are cells derived from keratinocytes in the late stages of terminal specialization of squamous epithelia. The microdermabrasion is done to eliminate some of the corneocytes. These cells are responsible for the impermeability of the skin. The minimizing or elimination of scars, skin lesions, blotchiness and stretch marks from the skin can be an easy process with the use of skin exfoliation. The result depends on how well the procedure known as “skin remodeling” works. Results are optimal and fewer treatments are needed with more recent and/or superficial scars. Still, microdermabrasion can be used on scars that showed up during puberty or many years later.
‘Blue’ and red light
Light exposure has long been used as a short term treatment for acne. Recently, visible light has been successfully employed to treat mild to moderate acne (phototherapy or deep penetrating light therapy) – in particular intense violet light (405-420 nm) generated by purpose-built fluorescent lighting, dichroic bulbs, LEDs or lasers. Used twice weekly, this has been shown to reduce the number of acne lesions by about 64% and is even more effective when applied daily. The mechanism appears to be that a porphyrin (Coproporphyrin III) produced within P. acnes generates free radicals when irradiated by 420 nm and shorter wavelengths of light. Particularly when applied over several days, these free radicals ultimately kill the bacteria. Since porphyrins are not otherwise present in skin, and no UV light is employed, it appears to be safe, and has been licensed by the U.S. FDA.
The treatment apparently works even better if used with a mixture of the violet light and red visible light (660 nanometer) resulting in a 76% reduction of lesions after three months of daily treatment for 80% of the patients; and overall clearance was similar or better than benzoyl peroxide. Unlike most of the other treatments few if any negative side effects are typically experienced, and the development of bacterial resistance to the treatment seems very unlikely. After treatment, clearance can be longer lived than is typical with topical or oral antibiotic treatments; several months is not uncommon. The equipment or treatment, however, is relatively new and reasonably expensive to buy initially, although the total cost of ownership can be similar to many other treatment methods (such as the total cost of benzoyl peroxide, moisturizer, washes) over a couple of years of use.
In addition, basic science and clinical work by dermatologists Yoram Harth and Alan Shalita and others has produced evidence that intense blue/violet light (405-425 nanometer) can decrease the number of inflammatory acne lesion by 60-70% in four weeks of therapy, particularly when the P. acnes is pretreated with delta-aminolevulinic acid (ALA), which increases the production of porphyrins. However this photodynamic therapy is controversial and apparently not published in a peer reviewed journal. A phase II trial, while it showed improvement occurred, failed to show improved response compared to the blue/violet light alone.
For patients with cystic acne, boils can be drained through surgical lancing.
Subcision is a process used to treat deep rolling scars left behind by acne or other skin diseases. Essentially the process involves separating the skin tissue in the affected area from the deeper scar tissue. This allows the blood to pool under the affected area, eventually causing the deep rolling scar to level off with the rest of the skin area. Once the skin has leveled, treatments such as laser resurfacing, microdermabrasion or chemical peels can be used to smooth out the scarred tissue.
Laser surgery has been in use for some time to reduce the scars left behind by acne, but research has been done on lasers for prevention of acne formation itself. The laser is used to produce one of the following effects:
to burn away the follicle sac from which the hair grows
to burn away the sebaceous gland which produces the oil
to induce formation of oxygen in the bacteria, killing them
Since lasers and intense pulsed light sources cause thermal damage to the skin, there are concerns that laser or intense pulsed light treatments for acne will induce hyperpigmented macules (spots) or cause long-term dryness of the skin.
In the United States, the FDA has approved several companies, such as Candela Corp., to use a cosmetic laser for the treatment of acne. However, efficacy studies have used very small sample sizes (fewer than 100 subjects) for periods of six months or less, and have shown contradictory results. Also, laser treatment being relatively new, protocols remain subject to experimentation and revision, and treatment can be quite expensive. Also, some Smoothbeam laser devices had to be recalled due to coolant failure, which resulted in painful burn injuries to patients.
Less widely used treatments
Aloe vera: there are treatments for acne mentioned in Ayurveda using herbs such as Aloe vera, Neem, Haldi (Turmeric) and Papaya. There is limited evidence from medical studies on these products. Products from Rubia cordifolia, Curcuma longa (commonly known as Turmeric), Hemidesmus indicus (known as ananthamoola or anantmula), and Azadirachta indica (Neem) have been shown to have anti-inflammatory effects, but not aloe vera.
Azelaic acid (brand names Azelex, Finevin and Skinoren) is suitable for mild, comedonal acne.
Calendula used in suspension is used as an anti-inflammatory agent.
Cortisone injection into spots, also cortisone pills are sometimes used.
Hydrogen Peroxide oxidizes acne which kills bacteria.
Heat: local heating may be used to kill the bacteria in a developing pimple and so speed healing.
Naproxen or ibuprofen are used for some moderate acne for their anti-inflammatory effect.
Nicotinamide, (Vitamin B3) used topically in the form of a gel, has been shown in a 1995 study to be of comparable efficacy to topical clindamycin topical antibiotic used for comparison. Topical nicotinamide is available both on prescription and over-the-counter. The property of topical nicotinamide’s benefit in treating acne seems to be its anti-inflammatory nature. It is also purported to result in increased synthesis of collagen, keratin, involucrin and flaggrin and may also according to a cosmetic company be useful for reducing skin hyperpigmentation (acne scars), increased skin moisture and reducing fine wrinkles.
Pantothenic acid, (high dosage Vitamin B5)
Rofecoxib was shown to improve premenstrual acne vulgaris in a placebo controlled study.
Tea tree oil (melaleuca oil) dissolved in a carrier (5% strength) has been used with some success, where it is comparable to benzoyl peroxide but without excessive drying, kills P. acnes, and has been shown to be an effective anti-inflammatory in skin infections.
Zinc: Orally administered zinc gluconate has been shown to be effective in the treatment of inflammatory acne, although less so than tetracyclines.
Detoxification is a common method used by alternative medicine practitioners for the treatment of acne, although there have been no studies to prove its success. Detoxification is the process of cleansing the body of toxins purportedly caused by the environment, pharmaceutical drugs, food, and cosmetics.
History of some acne treatments
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The history of acne reaches back to the dawn of recorded history. In Ancient Egypt, it is recorded that several pharaohs were acne sufferers. From Ancient Greece comes the English word ‘acne’ (meaning ‘point’ or ‘peak’). Acne treatments are also of considerable antiquity:
Ancient Rome: bathing in hot, and often sulfurous, mineral water was one of the few available acne treatments. One of the earliest texts to mention skin problems is De Medicina by the Roman writer Celsus.
1800s: Nineteenth century dermatologists used sulphur in the treatment of acne. It was believed to dry the skin.
1920s: Benzoyl Peroxide is used
1930s: Laxatives were used as a cure for what were known as ‘chastity pimples’. Radiation also was used.
1950s: When antibiotics became available, it was discovered that they had beneficial effects on acne. They were taken orally to begin with. Much of the benefit was not from killing bacteria but from the anti-inflammatory effects of tetracycline and its relatives. Topical antibiotics became available later.
1960s: Low Radiation treatments are widely used.
1970s: Tretinoin (original Trade Name Retin A) was found effective for acne. This preceded the development of oral isotretinoin (sold as Accutane and Roaccutane) in 1980.
1980s: Accutane is introduced in the United States, and later found to be a teratogen, highly likely to cause birth defects if taken during pregnancy. In the United States more than 2,000 women became pregnant while taking the drug between 1982 and 2003, with most pregnancies ending in abortion or miscarriage. About 160 babies with birth defects were born.
1990s: Laser treatment introduced
2000s: Blue/red light therapy
A vaccine against inflammatory acne has been tested successfully in mice, but it is not certain that it would work similarly in humans.
A 2007 microbiology article reporting the first genome sequencing of a Propionibacterium acnes bacteriophage (PA6) said this “should greatly enhance the development of a potential bacteriophage therapy to treat acne and therefore overcome the significant problems associated with long-term antibiotic therapy and bacterial resistance.”
Talarozole, a retinoic acid metabolism blocking agent, is currently under investigation for acne therapy in combination with tretinoin.
Preferred treatments by types of acne vulgaris
Comedonal (non-inflammatory) acne: local treatment with azelaic acid, salicylic acid, topical retinoids, benzoyl peroxide.
Mild papulo-pustular (inflammatory) acne: benzoyl peroxide or topical retinoids, topical antibiotics (such as erythromycin).
Moderate inflammatory acne: benzoyl peroxide or topical retinoids combined with oral antibiotics (tetracyclines). Isotretinoin is an option.
Severe inflammatory acne, nodular acne, acne resistant to the above treatments: isotretinoin also known as Accutane, can be prescribed by a doctor, or contraceptive pills with cyproterone for females with virilization or drospirenone.
Acne often leaves small scars where the skin gets a “volcanic” shape.
Physical acne scars are often referred to as “Icepick” scars. This is because the scars tend to cause an indentation in the skin’s surface. There are a range of treatments available. Although quite rare, the medical condition Atrophia Maculosa Varioliformis Cutis also results in “acne like” depressed scars on the face.
Ice pick scars: Deep pits, that are the most common and a classic sign of acne scarring.
Box car scars: Angular scars that usually occur on the temple and cheeks, and can be either superficial or deep, these are similar to chickenpox scars.
Rolling scars: Scars that give the skin a wave-like appearance.
Hypertrophic scars: Thickened, or keloid scars.
Pigmented scars is a slightly misleading term as it suggests a change in the skin’s pigmentation and that they are true scars; however, neither is true. Pigmented scars are usually the result of nodular or cystic acne (the painful ‘bumps’ lying under the skin). They often leave behind an inflamed red mark. Often, the pigmentation scars can be avoided simply by avoiding aggravation of the nodule or cyst. When sufferers try to ‘pop’ cysts or nodules, pigmentation scarring becomes significantly worse, and may even bruise the affected area. Pigmentation scars nearly always fade with time taking between three months to two years to do so, although rarely can persist.
On the other hand, some peoplearticularly those with naturally tanned skino develop brown hyperpigmentation scars due to increased production of the pigment melanin. These too typically fade over time.
There are multiple grading scales for grading the severity of acne vulgaris, three of these being: Leeds acne grading technique: Counts and categorises lesions into inflammatory and non-inflammatory (ranges from 0-10.0). ‘Cook’s acne grading scale: Uses photographs to grade severity from 0 to 8 (0 being the least severe and 8 being the most severe). Pillsbury scale: Simply classifies the severity of the acne from 1 (least severe) to 4 (most severe).
List of cutaneous conditions
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One study has estimated the incidence of suicidal ideation in patients with acne as 7.1%:
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^ Grow Your Own Drugs – BBC2 James Wong
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^ Leeds, Cook’s and Pillsbury scales obtained from here
Review articles and guidelines
Webster GF (August 2002). “Acne vulgaris”. BMJ 325 (7362): 4759. doi:10.1136/bmj.325.7362.475. PMID 12202330.
Gollnick H, Cunliffe W, Berson D, et al. (July 2003). “Management of acne: a report from a Global Alliance to Improve Outcomes in Acne”. Journal of the American Academy of Dermatology 49 (1 Suppl): S137. doi:10.1067/mjd.2003.618. PMID 12833004.
Feldman S, Careccia RE, Barham KL, Hancox J (May 2004). “Diagnosis and treatment of acne”. American Family Physician 69 (9): 212330. PMID 15152959.
Haider A, Shaw JC (August 2004). “Treatment of acne vulgaris”. JAMA 292 (6): 72635. doi:10.1001/jama.292.6.726. PMID 15304471.
Katsambas, A; Cunliffe, W (2004). “Commentary: Acne and its treatment”. Clinics in Dermatology 22: 359. doi:10.1016/j.clindermatol.2004.03.003.
James WD (April 2005). “Clinical practice. Acne”. The New England Journal of Medicine 352 (14): 146372. doi:10.1056/NEJMcp033487. PMID 15814882.
“Drugs for acne, rosacea and psoriasis”. Treatment Guidelines from the Medical Letter 3 (35): 4956. July 2005. PMID 15961971. http://www.medicalletter.org/scripts/articlefind.cgi?issue=35&page=49.
Sinclair W, Jordaan HF (November 2005). “Acne guideline 2005 update”. South African Medical Journal 95 (11 Pt 2): 88192. PMID 16344888. http://blues.sabinet.co.za/WebZ/Authorize?sessionid=0:autho=pubmed:password=pubmed2004&/AdvancedQuery?&format=F&next=images/ejour/m_samj/m_samj_v95_n11_a21.pdf.
Zaenglein AL, Thiboutot DM (September 2006). “Expert committee recommendations for acne management”. Pediatrics 118 (3): 118899. doi:10.1542/peds.2005-2022. PMID 16951015.
Purdy S, de Berker D (November 2006). “Acne”. BMJ 333 (7575): 94953. doi:10.1136/bmj.38987.606701.80. PMID 17082546.
Strauss JS, Krowchuk DP, Leyden JJ, et al. (April 2007). “Guidelines of care for acne vulgaris management”. Journal of the American Academy of Dermatology 56 (4): 65163. doi:10.1016/j.jaad.2006.08.048. PMID 17276540.
Reference books and chapters
Plewig, Gerd; Kligman, Albert M. (2000). Acne and rosacea (3rd ed.). New York: Springer-Verlag. ISBN 3-540-66751-2.
Cunliffe, William J.; Gollnick, Harald P. M. (2001). Acne : diagnosis and management. London: Martin Dunitz. ISBN 1-85317-206-5.
Thiboutot, Diane M.; Strauss, John S. (2003). “Diseases of the sebaceous glands”. in Burns, Tony; Breathnach, Stephen; Cox, Neil; Griffiths, Christopher. Fitzpatrick’s dermatology in general medicine (6th ed.). New York: McGraw-Hill. pp. 67287. ISBN 0-07-138076-0.
Zaenglein, Andrea L.; Thiboutot, Diane M. (2003). “Acne vulgaris”. in Bolognia, Jean L.; Jorizzo, Joseph L.; Rapini, Ronald P. (eds.). Dermatology. London: Mosby. pp. 53144. ISBN 0-32302-4092.
Habif, Thomas P. (2004). “Acne, rosacea, and related disorders”. Clinical dermatology : a color guide to diagnosis and therapy (4th ed.). Edinburgh: Mosby. pp. 162208. ISBN 0-323-01319-8.
Simpson, Nicholas B.; Cunliffe, William J. (2004). “Disorders of the sebaceous glands”. in Burns, Tony; Breathnach, Stephen; Cox, Neil; Griffiths, Christopher. Rook’s textbook of dermatology (7th ed.). Malden, Mass.: Blackwell Science. pp. 43.175. ISBN 0-632-06429-3.
James, William D.; Berger, Timothy G.; Elston, Dirk M. (2006). “Acne”. Andrews’ diseases of the skin: clinical dermatology (10th ed.). Philadelphia: Saunders Elsevier. pp. 23150. ISBN 0-7216-2921-0.
Wikimedia Commons has media related to: Acne
Acne vulgaris: more than skin deep (on the psychological effects of acne)
Acne photo library at Dermnet
Acne from the U.S. National Library of Medicine
Story on Acne from the Better Health Channel
“AcneNet”. American Academy of Dermatology. http://www.skincarephysicians.com/acnenet. – Dermatologist-reviewed information about acne.
Q&A about Acne, from the National Institutes of Health.
v d e
Acne-treating agents (D10)
Azelaic acid Benzoyl peroxide Blue light therapy Tea tree oil
Glycolic acid Salicylic acid Sulfur Benzoyl peroxide
Aspirin Ibuprofen Red light therapy
Clindamycin Dapsone Erythromycin Sulfacetamide Minocycline Tetracyclines
Adapalene Isotretinoin Tazarotene Tretinoin
ZIANA Duac BenzaClin PLEXION Epiduo
v d e
Diseases of the skin and appendages by morphology
wart callus seborrheic keratosis acrochordon molluscum contagiosum actinic keratosis squamous cell carcinoma basal cell carcinoma merkel cell carcinoma nevus sebaceous trichoepithelioma
Freckles lentigo melasma nevus melanoma
epidermal inclusion cyst hemangioma dermatofibroma keloid lipoma neurofibroma xanthoma Kaposi’s sarcoma infantile digital fibromatosis granular cell tumor leiomyoma lymphangioma circumscriptum myxoid cyst
contact dermatitis atopic dermatitis seborrheic dermatitis stasis dermatitis lichen simplex chronicus Darier’s disease glucagonoma syndrome langerhans cell histiocytosis lichen sclerosus pemphigus foliaceus Wiskott-Aldrich syndrome Zinc deficiency
psoriasis tinea (corporis cruris pedis manuum faciei) pityriasis rosea secondary syphillis mycosis fungoides systemic lupus erythematosus pityriasis rubra pilaris parapsoriasis ichthyosis
herpes simplex herpes zoster varicella bullous impetigo acute contact dermatitis pemphigus vulgaris bullous pemphigoid dermatitis herpetiformis porphyria cutanea tarda epidermolysis bullosa simplex
scabies insect bite reactions lichen planus miliaria keratosis pilaris lichen spinulosus transient acantholytic dermatosis lichen nitidus pityriasis lichenoides et varioliformis acuta
acne vulgaris acne rosacea folliculitis impetigo candidiasis gonococcemia dermatophyte coccidioidomycosis subcorneal pustular dermatosis
tinea versicolor vitiligo pityriasis alba postinflammatory hyperpigmentation tuberous sclerosis idiopathic guttate hypomelanosis leprosy hypopigmented mycosis fungoides
drug eruptions viral exanthems toxic erythema systemic lupus erythematosus
cellulitis abscess boil erythema nodosum carcinoid syndrome fixed drug eruption
urticaria erythema (multiforme migrans gyratum repens annulare centrifugum ab igne)
thrombocytopenic purpura actinic purpura
disseminated intravascular coagulation vasculitis
scleroderma/morphea granuloma annulare lichen sclerosis et atrophicus necrobiosis lipoidica
telogen effluvium androgenic alopecia trichotillomania alopecia areata systemic lupus erythematosus tinea capitis loose anagen syndrome lichen planopilaris folliculitis decalvans acne keloidalis nuchae
onychomycosis psoriasis paronychia ingrown nail
aphthous stomatitis oral candidiasis lichen planus leukoplakia pemphigus vulgaris mucous membrane pemphigoid cicatricial pemphigoid herpesvirus coxsackievirus syphilis systemic histoplasmosis squamous cell carcinoma
v d e
Disorders of skin appendages (L60-75, 700-709)
thickness: Onychogryphosis Onychauxis
color: Beau’s lines Yellow nail syndrome Leukonychia Azure Lunula
shape: Koilonychia Clubbing
other: Ingrown nail Anonychia
Alopecia areata (Alopecia totalis, Alopecia universalis, Ophiasis)
Androgenic alopecia Hypotrichosis Telogen effluvium Traction alopecia Lichen planopilaris Trichorrhexis nodosa
Acneiform eruption (Acne vulgaris, Chloracne, Blackhead) Rosacea (Perioral dermatitis, Rhinophyma)
Epidermoid cyst Trichilemmal cyst Sebaceous cyst Steatocystoma multiplex
Pseudofolliculitis barbae Hidradenitis suppurativa Folliculitis
eccrine (Miliaria, Anhidrosis) apocrine (Body odor, Chromhidrosis, Fox-Fordyce disease)
skin appendage navs: anat, noncongen/congen/neoplasia, symptoms+signs/eponymous, proc
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