Acne/Breakouts

(Acne Vulgaris)

Acne develops from the following four factors:

Follicular epidermal hyper-proliferation (Blocked Pores) with subsequent plugging of the follicle Excess sebum production

Presence and activity of the bacteria Cutibacterium acnes (formerly Propionibacterium acnes)

Inflammation

Genetics

The pathogenesis of acne vulgaris is multifactorial. Acne develops as a result of an interplay of the following four factors

Release of inflammatory mediators into the skin

Inflammatory responses actually occur before hyperkeratinization

Cytokines produced by CD4+ T cells and macrophages activate local endothelial cells to up-regulate inflammatory mediators such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and human leukocyte antigen (HLA)–DR in the vessels around the pilosebaceous follicle.

Follicular hyperkeratinization with subsequent plugging of the follicle.

Cutibacterium acnes follicular colonisation

C acnes is an anaerobic organism present in acne lesions. The presence of C acnes promotes inflammation through a variety of mechanisms.
C acnes stimulates inflammation by producing pro-inflammatory mediators that diffuse through the follicle wall.

Studies have shown that C acnes activates the toll-like receptor 2 on monocytes and neutrophils.

Activation of the toll-like receptor 2 then leads to the production of multiple pro-inflammatory cytokines, including interleukins 12 and 8 and tumour necrosis factor.

Hypersensitivity to C acnes may also explain why some individuals develop inflammatory acne vulgaris while others do not.

Excess sebum production

Excess sebum is another key factor in the development of acne vulgaris. Sebum production and excretion are regulated by a number of different hormones and mediators. In particular, androgen hormones promote sebum production and release. The degree of comedonal acne in prepubertal girls correlates with circulating levels of the adrenal androgen dehydroepiandrosterone sulphate (DHEAS).

Numerous other mediators and receptors, including growth hormone and insulin like growth factor, as well as peroxisome proliferator-activated receptors also regulate the sebaceous gland and may contribute to the development of acne. Furthermore, the sebaceous gland acts a neuroendocrine-inflammatory organ that is activated via corticotrophin-releasing hormones in response to stress and normal functions.

Follicular hyperkeratinization involves increased keratinocyte proliferation and decreased desquamation, leading to sebum- and keratin-filled microcomedones.

How Microneedling helps

Microneedling:

Normalises the keratinocyte function and reduces hyperkeratinization

Normalises sebocyte function

Triggers an immune response that not only controls bacteria, but also is anti inflammatory.