Etiology
Acne is polygenic and multifactorial. Four main pathogenetic factors contribute to the condition:
Sebaceous gland hyperplasia and excess sebum production: sebaceous follicle size and number of lobules per gland are increased in patients with acne.[14] Androgens stimulate sebaceous glands to enlarge and produce more sebum, a process that is most prominent during puberty.
Abnormal follicular differentiation: in normal follicles, keratinocytes are shed as single cells into the lumen and then excreted. In acne, keratinocytes are retained and accumulate due to their increased cohesiveness.[15]
Cutibacterium acnes colonization: previously named Propionibacterium acnes, these gram-positive, nonmotile rods are found deep in follicles and stimulate the production of proinflammatory mediators and lipases.[16] While there may be increased numbers of C acnes in acne, bacterial counts often do not correlate with acne severity.[17]
Inflammation and immune response: inflammatory cells and mediators efflux into the disrupted follicle, leading to the development of papules, pustules, nodules, and cysts.
External factors may exacerbate acne including diet (although controversial), mechanical trauma, cosmetics, topical corticosteroids, and oral drugs (e.g., corticosteroids, lithium, iodides, some anticonvulsants gender-affirming testosterone therapy).[18]
Endocrine disorders resulting in hyperandrogenism (e.g., polycystic ovary syndrome) may also predispose patients to developing acne.[10]
A family history of severe acne increases its likelihood in subsequent generations.[19] The concordance rate for the prevalence and severity of acne among identical twins is high.[20] One study concluded that 81% of variance in acne was attributable to genetics, and only 19% to environmental factors.[21]
Genome-wide association studies have demonstrated that genetic susceptibility to acne results from a variation in the genes responsible for structure and function of the pilosebaceous unit, which creates an environment prone to bacterial colonization and inflammation, including inherited variation in Toll-like receptors (TLR)-2 and TLR4.[22][23]
Pathophysiology
Acne vulgaris is a common, highly heritable, chronic inflammatory disease of the skin. The onset of acne involves different factors resulting in inflammation and the formation of different types of acne lesions. These factors include the quantitative and qualitative alteration of the sebum during puberty (dysseborrhea), triggered by internal hormonal or genetic factors, and external factors such as comedogenic cosmetics, aggressive detergents or drugs, which may stimulate mechanisms involved in the pathophysiologies of acne.[24]
Dysbiosis, the process which leads to disturbance of the skin barrier, and the disequilibrium of the cutaneous microbiome, resulting in the proliferation of Cutibacterium acnes (C acnes; previously known as Proprionibacterium acnes) strains, are also important processes that trigger acne.[24] C acnes activates innate immunity via the expression of protease activated receptors (PARs), tumor necrosis factors alpha, and Toll-like receptors (TLRs), and the production of interferon y, interleukins (IL-8, IL-12 and IL-1), and matrix metalloproteinases by keratinocytes, resulting in the hyperkeratinization of the pilosebaceous unit.[24]
Genome-wide association studies have demonstrated that genetic susceptibility to acne results from a variation in the genes responsible for structure and function of the pilosebaceous unit, which creates an environment prone to bacterial colonization and inflammation, including inherited variation in TLR-2 and TLR4.[22][23]
Classification
Commonly accepted
There are many acne grading/classifying systems but no standardized approach exists for clinical practice.
Most employ type or severity:
type (comedonal/papular, pustular/nodulocystic), or
severity (mild/moderate/moderately severe/very severe).
Skin lesions can be described as noninflammatory (comedones) or inflammatory (papules, pustules, nodules, and cysts). Comedones and inflammatory lesions are usually considered separately.
Simplified classification[3]
Mild: comedones are the main lesions. Papules and pustules may be present but are small and few in number (generally <10).
Moderate: moderate numbers (10-40) of papules and pustules. Moderate numbers (10-40) of comedones are also present. Sometimes mild truncal disease.
Moderately severe: numerous papules and pustules (40-100), usually with many comedones (40-100) and the occasional (up to 5) larger, deeper nodular inflamed lesions. Widespread affected areas usually involving face, chest, and back.
Very severe: nodulocystic acne and acne conglobata with severe lesions; many large, painful nodular/pustular lesions along with many smaller papules, pustules, and comedones.
Investigator’s Global Assessment (IGA) severity scale[4]
Used primarily for research purposes, an example of which could be:
Grade 0: clear skin with no inflammatory or noninflammatory lesions
Grade 1: almost clear; rare noninflammatory lesions with no more than 1 small inflammatory lesion
Grade 2: mild severity; greater than grade 1; some noninflammatory lesions with no more than a few inflammatory lesions (papules/pustules only, no nodular lesions)
Grade 3: moderate severity; greater than grade 2; up to many noninflammatory lesions and may have some inflammatory lesions, but no more than 1 small nodular lesion
Grade 4: severe; greater than grade 3; up to many noninflammatory and inflammatory lesions, but no more than a few nodular lesions.
Leeds technique[5]
Assessment of severity, using grades 1-12 (mild to severe) for facial acne, and 1-8 for the upper chest and back. Many research studies use the Leeds technique to grade acne; but it is not commonly used in clinical practice.
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