| DERMONUTRITION | ARTICLE Normally, acne is related to increased and altered
sebum production and follicular cell hyperproliferation under hormonal control (or increased androgen receptor sensitivity) that causes follicular blocking with comedo formation. When the blockage is complete, the lesions
are referred to as Ôclosed comedonesÕ, while
incomplete blockage results in Ôopen comedonesÕ . Inflammatory lesions occur when Propionibacterium acnes, usually detectable on the skin, colonises the pilosebaceous unit, with follicular rapture, release of inflammatory mediators, and the subsequent activation of neutrophil cascade1 scientific studies2
. As shown in a number of , human sebaceous glands express Its distribution is correlated to the body areas with the
highest density of these glands (i.e. face, neck, upper chest, shoulders and back)2
. Acne manifests in early
puberty with more seborrhoea and comedones than adult populations, in whom more inflammatory lesions are usually visible. Even though it is not a life-threatening condition, it can cause physical and emotional scars, such as low self-esteem, social withdrawal, and depression3
.
Pathogenesis of acne It is well established that acne is influenced by a genetic predisposition, but that the onset of the disease is mediated by environmental factors, such as endogenous and exogenous hormones, diet and cigarette smoke.
Formation of skin pimples and acne Sebaceous duct gland Clogged duct
Figure 1 Presentation of acne on the face
functional receptors for different neuropeptides, such as corticotropin-releasing hormone (CRH) (explaining the correlation between acne and stress), melanocortins, substance P, and many other nonreproductive hormones, such as growth hormone (GH), that are able to modulate immunoreactivity by increasing inflammatory cytokine production, cellular proliferation and differentiation, lipogenesis, and androgen metabolism in sebocytes. For this reason, α-melanocyte-stimulating hormone and insulin-like growth factor 1 (IGF-1) can induce sebocyte differentiation and lipogenesis. In fact, IGF-1 is able to influence androgen regulation in the skinÕs intracrine system and potentiate the androgen signal by inducing 5α-reductase activity and enhancing androgen receptor sensitivity. The pilosebaceous unit is also an immunocompetent
organ. Keratinocytes and sebocytes may act as immune cells and may be activated by P. acnes through innate immunity molecules, such as toll-like receptors (TLR-2 and -4). These cells can also recognise altered sebum lipid content after inflammatory cytokine production and are also able to produce many antimicrobial
Androgens
have a significant role in acne pathogenesis. While hormonal serum levels do not correlate with disease severity, they may have a permissive role in the onset of the pathology.
Healthy follicle
Duct clogged by dead cells, sebum starts to accumulate
Bacterial infection, inflammation
triggered — pimple
Follicle ruptures, pustule with fluid formed — acne
prime-journal.com | July/August 2012 ❚ 41
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