About Pathophysiology of Acne Vulgaris

Acne vulgaris pathophysiology and pathogenesis - The pathophysiology of acne vulgaris is genetic and multifactorial. The pathogenesis of acne vulgaris recent advances but the acne develops as a result of these 4 factors which are influencing each other:

1. The overproduction of sebum.
2. The follicular colonization of cutibacterium acne which was propionibacterium acne before.
3. The releasing of inflammation mediators into the skin (acne vulgaris involves inflammation of the sebaceous follicles).
4. Hyperkeratinization of the follicle with subsequent follicular blockage.

If you don't know what this disease is, please read the link below.

👉 Acne vulgaris definition and epidemiology

Acne Vulgaris Pathophysiology and Pathogenesis

Research has shown that the response of the inflammation actually happens before the hyperkeratinization. The cytokines which are produced by the CD4+ T cells and macrophages activate the local endothelial cells in order to set up the inflammatory mediators, such as human leukocyte antigen (HLA)–DR, intercellular adhesion molecule-1 (ICAM-1), and also vascular cell adhesion molecule-1 (VCAM-1) in the blood vessels around the pilosebaceous follicles.

The Follicular hyperkeratinization is involving decreased desquamation and increased keratinocyte proliferation which leads to micro comedones which are filled with sebum and keratin. Acne vulgaris organism: C acne which was P acne before. It is an anaerobic organism that is found in acne lesions. The presence of C acne triggers inflammation through various mechanisms. C acne stimulates the inflammation by producing pro-inflammatory mediators which diffuse through follicle walls. A study has shown that C acne is able to activate toll-like receptor 2 on neutrophils and monocytes. The toll-like receptor 2 activation then leads to the production of some pro-inflammatory cytokines, including tumor necrosis factor and interleukins 12 and 8.

If a person is hypersensitive to C acne, it explains why some people develop inflammatory acne while others do not so. The excess sebum is another factor why acne vulgaris develops. The production of sebum and excretion is set up by a number of different mediators as well as different hormones. Specifically, androgen hormones increase the production and releasing of sebum. The level of comedonal acne in pre-pubertal girls is related to the circulating levels of the adrenal androgen dehydroepiandrosterone sulfate or also known as DHEAS.

A number of other receptors and mediators, such as an insulin-like growth factor, growth hormones, and also peroxisome proliferator-activated receptors set up the sebaceous and able to contribute to the acne development. Moreover, the sebaceous glands play a role as a neuroendocrine-inflammatory organ which is activated via corticotrophin-releasing hormones as a response to normal functions and stress.

The History of Acne Vulgaris

Acne vulgaris usually affects the skin area with the densest sebaceous follicles’ population. For example, back, face, and also upper chest. This kind of acne is characterized by inflammatory papules, pustules, and nodules, closed or open non-inflammatory comedones. The symptoms of acne vulgaris can be tenderness, erythema, and pain. But acne rarely causes any systemic symptoms. In a severe case, this acne is able to cause acne conglobata, with highly inflammatory nodulocystic acne and interconnected abscesses.

Acne fulminans is even worse than acne conglobata. The systemic symptoms of acne fulminans are general malaise, fever, and joint pain. Acne vulgaris can psychologically affect the sufferers, regardless of how severe the disease or the level. That is the information about acne vulgaris that might be useful for you. We hope you know about acne vulgaris pathogenesis and this disease needs assessment and treatment based on its history.

Reference

Acne Vulgaris Medscape - emedicine

Acne Vulgaris AAFP (American Academy of Family Physicians)

Acne problem

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