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Clinical Presentation

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Identifying various forms of acne – Information on the clinical presentation of acne

  • Acne lesions begin with an initial inflammatory event, triggered by an infiltration of inflammatory cells
  • Hyperproliferation of the keratinocytes with an increase of cohesiveness then occurs in which keratinocytes and sebum build up in a follicle1-3
  • The initial lesion is referred to as a microcomedone2,4
  • The microcomedone progresses to a comedone, and at this point, lesions may take either an inflammatory or a non- inflammatory course2,4

Types of acne lesions

Non-inflammatory lesions

Closed Comedones (Whiteheads)2

Closed comedones may be difficult to visualise. They appear as pale, slightly elevated, pin point papules, and do not have a clinically visible orifice.2,5

clinical presentation_closed comedones

Open Comedones (Blackheads)2 The open comedone can appear as a flat or slightly raised lesion. The dark-coloured appearance of the lesions may result from oxidation of a central follicular impaction of keratin and lipid or interference of the transmission of light through compacted epithelial cells.2,4,5

clinical presentation_open comedones

Inflammatory Acne Lesions

Inflammatory lesions are characterised by the presence of one or more of the following types of lesions:6

Papules: a solid raised lesion that has distinct borders and is less than 1 cm in diameter

Pustules: a circumscribed elevation of the skin that contains pus

Nodules: a raised solid lesion of more than 1cm, which may be in the epidermis, dermis, or subcutaneous

clinical presentation_papulopustular acne

Papulopustular acne

clinical presentation_nodularcystic acne

Nodularcystic acne

Pathogenesis of acne – Key causes of acne


Adolescence is a period of dramatic physiological changes.
Comedonal acne, particularly of the central face, is often the first sign of pubertal maturation. At puberty, increased sebum production caused by androgenic stimulation of sebaceous glands, is a major factor in the pathogenesis of acne.

In its mildest form, which is often seen in early adolescence, lesions are limited to comedones on the central area of the face.4

Lesions may also involve the chest and upper back: more severe lesions on the body are most often seen in males.4

After lesions heal, there is a risk of hyperpigmentation and scarring, the latter can be pitted, atrophic or hypertrophic, depending on the severity and length of time the acne has been present.4

clinical presentation_PIH

Post-inflammatory hyperpigmentation

clinical presentation_acne scarring

Acne scarring


Adult acne can be categorized into two types:8

  • Persistent: adolescent acne that lasts beyond the age of 25 years
  • Late-onset: acne that develops for the first time after the age of 25

Adult acne is usually mild-to-moderate and mainly affects the face. There are two clinical forms of acne most prominent in females:9

  • Most common: an inflammatory form comprising papulopustules and nodules on the lower part of the face
  • Less common: a retentional form made up of blackheads and micro cysts with hyperseborrhoea

The causes of acne in adults are thought to be related to hormones, resistant bacteria, the use of cosmetics, drugs, smoking and chronic stress.8,10

Genetics are another factor: around 50% of female acne sufferers have a first-degree relative with post-adolescent acne.10

Adult acne differs from teenage acne: in adolescent acne, males tend to be affected more commonly and show the most severe forms of the disease, whereas post-adolescent acne mainly affects females and is more inflammatory8 – comedonal lesions are typically absent or sparse.10


Classification of acne – Key factors in diagnosing acne

Physically, acne is categorized as mild, moderate, or severe, but other factors, including the extent of acne and scarring, are also taken into account:11-13

  • Mild: characterized by the presence of comedones(whiteheads and blackheads), few papules and pustules(generally <10), but no nodules (whiteheads and blackheads)
  • Moderate: presence of several to many papules and pustules (10 to 40) along with comedones (10 to 40). The presence of >40 papules and pustules along with larger, deeper nodular inflamed lesions (up to five) denotes moderately severe acne
  • Severe: presence of numerous or extensive papules and pustules as well as many (more than five) nodular lesions;also includes scarring, which has occurred as a result of previous severe acne

However, it isn’t just the physical aspects of acne that determine the severity of a patient’s acne. There is increasing evidence that factors other than objective (clinical) severity of disease contribute to the overall impact on a patient’s quality of life, including patient age and the patient’s self-perception of their acne.14

According to current European guidelines:

“Quality of life measures can influence the choice of therapy: in patients with a severe impact on their quality of life, a more aggressive therapy may be justified.”12

Read the guidelines in full


  1. Zager SH. Acne Vulgaris and Acne Rosacea. In: Rakel D, ed.Integrative Medicine. 3rd ed. Philadelphia, PA: SaundersElsevier; 2012 Accessed June 2015
  2. Habif TP. Acne, Rosacea, and Related Disorders. In: HabifTP, ed. Clinical Dermatology. 5th ed. Edinburgh: MosbyElsevier; 2010; 217–263
  3. Jeremy AH, Holland DB, Roberts SG, Thomson KF, CunliffeWJ. Inflammatory events are involved in acne lesioninitiation. J Invest Dermatol 2003;121(1):20–27
  4. Morelli JG. Acne. In: Kliegman RM, ed. Kliegman: NelsonTextbook of Pediatrics. 19th ed. Philadelphia, PA: SaundersElsevier; 2011. Accessed June 2015
  5. Zaenglein AL, Graber EM, Thiboutot DM. Acne vulgaris andacneiform eruptions. In: Goldsmith LA, Katz SI, GilchrestBA, Paller AS, Leffell DJ, Dallas NA, eds. Fitzpatrick'sDermatology in General Medicine. 8th ed. New York, NY:McGraw-Hill; 2012. Accessed June 2015.
  6. Williams. Primary Care Dermatology Module:Nomenclature of Skin Lesions. 2015. Last accessed August2015.
  7. Krakowski AC, et al. Practical considerations in acnetreatment and the clinical impact of topical combinationtherapy. Pediatr Dermatol 2008;25 Suppl 1:1–1414.
  8. Khunger N, et al. A clinico-epidemiological study of adultacne: is it different from adolescent acne? Indian JDermatol Venereol Leprol 2012;78(3):335–41.
  9. Preneau S, et al. Female acne – a different subtype of teenageracne? JEADV 2012; 26: 277–282.
  10. Williams C, et al. Persistent acne in women: implications forthe patient and for therapy. Am J Clin Dermatol 2006; 7 (5): 281–290.
  11. National Health Service. Acne. NHS Web site UpdatedSeptember, 2014. Accessed July 2015.
  12. Nast A, et al. European evidence-based (S3) guidelines for thetreatment of acne. J Eur Acad Dermatol Venereol 2012;26 Suppl1:1–29.
  13. Ferri: Ferri's Clinical Advisor 2013, 1st ed. Elsevier Inc.Philadelphia.
  14. Lasek RJ, et al. Acne vulgaris and the quality of life of adultdermatology patients. Arch Dermatol 1998;134:454–458.

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