Acne vulgaris is a disorder of the sebaceous follicles, which are special pilosebaceous units (relating to the hair follicles and sebaceous glands) located on the face, chest, and back. It is an extremely common skin disorder, which affects nearly all adolescents and adults at least once during life [1, 2]. According to Brown et al (1998), the incidence of acne peaks at age 18; however, a substantial amount of men and women aged 20-40 are also affected by the disorder. Acne is a disease rarely associated with systemic medical problems; however, the importance and morbidity of acne should not be underestimated because its disfiguring can have important negative psychosocial consequences for affected individuals including diminished self-esteem, social embarrassment, social withdrawal, depression and even unemployment [1, 3].

1. Food/Diet
Foods such as nuts, cola, milk, cheese, fried foods and iodised salts have been implicated as triggers of acne vulgaris; however, the connections between nutrition and acne has not definitely been proven as they are rarely supported by good analytical, epidemiological or therapeutic studies [4, 5]. On the other hand, recurrent acne as noted by Niemeier et al (2006) may be a cutaneous sign of an underlying eating disorder.

2. Genetics
A genetic background is supported by a case control study by Goulden et al, as noted by Rzany et al (2006). This stated that the risk of adult acne vulgaris in relatives of patients with acne as compared with those of patients without acne is significantly higher [4].

3. Hormones
According to Rzany et al (2006), hormonal influences on acne vulgaris are undisputed as shown by the higher incidence of acne in male adolescents. Premenstrual flare has also been recorded as causing acne [5].

4. Nicotine
Smoking has also been named as a risk factor for acne vulgaris; however, conflicting data exists as to the link between smoking and acne. Some population based studies have found links between smoking and acne whilst some others have not [4].

Important!
Contrary to popular misconceptions by young patients and occasionally their parents, acne does not come from bad behaviour nor is it a disease of poor hygiene. It also has nothing to do with lack of cleanliness [2].

There are two main types of acne vulgaris, inflammatory and non-inflammatory; these can be manifested in different ways,
1. Comedonal acne, which is a non-inflammatory acne
2. Papules and pustules of inflammatory acne
3. Nodular acne (inflammatory acne)
4. Inflammatory acne with hyperpigmentation (this occurs more commonly in patients with darker skin complexions) [1]

In general, acne is limited to the parts of the body, which have the largest and most abundant sebaceous glands such as the face, neck, chest, upper back and upper arms. Among dermatologists, it is almost universally accepted that the clinical manifestation of acne vulgaris is the result of four essential processes as described below [1, 6],

1. Increased sebum production in the pilosebaceous follicle. Sebum is the lipid-rich secretion product of sebaceous glands, which has a central role in the development of acne and also provides a growth medium for Propionibacterium acnes (P acnes), an anaerobic bacterium which is a normal constituent of the skin flora. Compared with unaffected individuals, people with acne have higher rates of sebum production. Apart from this, the severity of acne is often proportional to the amount of sebum produced [1, 6].

2. Abnormal follicular differentiation, which is the earliest structural change in the pilosebaceous unit in acne vulgaris [1].

3. Colonisation of serum-rich obstructed follicle with Propionibacterium acnes (P acnes). P acnes is an anaerobic bacterium which is a normal constituent of the skin flora and which populates the androgen-stimulated sebaceous follicle [androgen is a steroid hormone such as testosterone or androsterone, that controls the development and maintenance of masculine characteristics]. Individuals with acne have higher counts of P acnes compared with those without acne [1, 6].

4. Inflammation. This is a direct or indirect result of the rapid and excessive increase of P acnes [1].

Non-inflammatory acne lesions include open and closed comedones, which are thickened secretions plugging a duct of the skin, particularly sebaceous glands. Open comedones, also known as blackheads, "appear as flat or slightly raised brown to black plugs that distend the follicular orifices". Closed comedones, also known as whiteheads, "appear as whitish to flesh-coloured papules with an apparently closed overlying surface" [1].

Inflammatory lesions on the other hand include papules, pustules, and nodules; papules and pustules "result from superficial or deep inflammation associated with microscopic rupture of comedones". Nodules are large, deep-seated abscesses, which when palpated may be compressible. In addition to the typical lesions in acne, other features may also be present. These include scarring and hyperpigmentation, which can result in substantial disfigurement [1].

Numerous psychological problems such as diminished self-esteem, social embarrassment, social withdrawal, depression and even unemployment stem from acne. However, differential diagnosis from a psychosomatic point of view indicates two serious psychological problems, which can arise from acne. These are,
1. Psychogenic excoriation, and
2. Body dysmorphic disorder (BDD)

Psychogenic excoriation also referred to as neurotic excoriation, pathological or compulsive skin picking "is characterised by excessive scratching or picking of normal skin or skin with minor irregularities" [5]. According to Niemeier et al (2006) it is estimated to occur in 2% of dermatological patients. Patients with this disorder can also have psychiatric disorders such as mood and anxiety disorders, as well as associated disorders such as obsessive compulsive disorder, substance abuse disorder, obsessive compulsive personality disorder, compulsive buying, eating disorder, and borderline personality disorder, to mention a few [5].

Body dysmorphic disorder (BDD) "is a condition characterised by an extreme level of dissatisfaction or preoccupation with a normal appearance that causes disruption in daily functioning" [3]. Niemeier et al (2006) described it as "a syndrome characterised by distress, secondary to imagined or minor defects in one's appearance." The onset of BDD is usually during adolescence, and it occurs equally in both male and female. Common areas of concern include the skin, hair and nose, with acne being one of the most common concerns with BDD patients [3].

According to the Diagnostic and Statistics Manual of Mental Disorders (2000), BDD has three diagnostic criteria,
1. A preoccupation with an imagined defect in appearance; where a slight physical anomaly is present, the person's concern is markedly excessive,
2. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning,
3. The preoccupation is not caused by another mental disorder (e.g. Anorexia Nervosa)
Characteristic behaviours include skin picking, mirror checking, and camouflaging by wearing a hat or excessive make up. Apart from these, patients often seek reassurance frequently by asking questions such as "Can you see this pimple?" or "Does my skin look okay?" Some patients also have a tendency to doctor shop, which is essentially going from one specialist to another in search of a dermatologist or plastic surgeon, willing to carry out a desired procedure or dispense a certain drug, to improve their perceived defect [3, 5].

Although it is a relatively common disease, BDD is still an under diagnosed psychiatric disorder and is estimated to affect 0.7 to 5% of the general population. Other psychiatric conditions associated with BDD include major depression, anxiety, and obsessive compulsive disorder. It is also associated with high rates of functional impairment and suicide attempts, high levels of perceived stress, and markedly poor quality of life [3, 5, 8].

1. Topical treatment, particularly for individuals with non-inflammatory comedones or mild to moderate inflammatory acne (See types of acne vulgaris). Medications include tretinoin (available as gels, creams, and solutions), adapalene gel, salicylic acid (available as solutions, cleansers, and soaps), isotretinoin gel, azelaic acid cream, benzoyl peroxide (available as gels, lotions, creams, soaps, and washes), to mention a few [1, 2].

2. Oral treatment, particularly for acne that is resistant to topical treatment or which manifests as scarring or nodular lesions. Medications include oral antibiotics (e.g. tetracycline, doxycycline, minocycline, erythromycin, and co-trimoxazole), oral isotretinoin, and hormonal agents (e.g. oral contraception, oral corticosteroid, cyproterone acetate, or spironolactone) [1, 2].

3. Physical or surgical methods of treatment, which are sometimes useful as adjuvant to medical therapy. Methods include comedo extraction, intralesional injections of corticosteroids, dermabrasion, chemical peeling, and collagen injections, to mention a few [1, 9].

4. Sun exposure, reported by up to 70% of patients to have a beneficial effect on acne [10].

5. Light therapy, which is becoming more popular due to the growing demand for a convenient, low risk and effective therapy, as many patients fail to respond adequately to treatment or develop side effects, from the use of various oral and topical treatments available for the treatment of acne [11]. Methods include the use of visible light (e.g. blue light, blue/red light combinations, yellow light, and green light), laser treatment and monopolar radiofrequency [11]. Many of these light therapy treatments can be used at home.

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1. Brown SK, Shalita AR. Acne vulgaris. Lancet 1998; 351:1871-1876.

2. Webster GF. Acne vulgaris. Br Med J 2002; 325: 475-479.

3. Bowe WP et al. Body dysmorphic disorder symptoms among patients with acne vulgaris. J Am Acad Dermatol 2007; DOI: 10.1016/j.jaad.2007.03.030.

4. Rzany B, Kahl C. Epidemiology of acne vulgaris. JDDG 2006; DOI: 10.1111/j.1610-0387.2006.05876.x

5. Niemeier V, Kupfer J, Gieler U. Acne vulgaris-Psychosomatic aspects. JDDG 2006; DOI: 10.1111/j.1610-0387.2006.06110.x

6. Gollnick H. Current perspectives on the treatment of acne vulgaris and implications for future directions. Eur Acad Dermatol Venereol 2001; 15 (Suppl. 3):1-4.

7. American Psychiatric Association. Diagnostic and Statistics Manual of Mental Disorders. 4th Ed. Accessed via: BehaveNet® Clinical CapsuleTM; http://www.behavenet.com/capsules/disorders/bodydysdis.htm. Accessed on: 28th June 2007.

8. Phillips KA et al. A retrospective follow-up study of body dysmorphic disorder. Comprehensive Psychiatry 2005; 46: 315-321.

9. Taub AF. Procedural treatments of acne vulgaris. Dermatol Surg 2007; 33: 1-22.

10. Cunliffe WJ, Goulden V. Phototherapy and acne vulgaris.Br J Dermatol 2000; 142 (5): 855-856.

11. Dierickx CC. Lasers, Light and Radiofrequency for treatment of acne. Med Laser Appl 2004; 19: 196-204.

This article is only for informative purposes. It is not intended to be a medical advice and is not a substitute for professional medical advice. Please consult your doctor for all your medical concerns. Kindly follow any information given in this article only after consulting your doctor or qualified medical professional. The author is not liable for any outcome or damage resulting from any information obtained from this article.