Whiteheads, Pus-filled Acne, and Acne Marks
Table of Contents
Acne generally progresses through the following stages:
- Increased sebum secretion
- P. acnes proliferation
- Increased keratinization around pores
- Pore occlusion and the formation of comedones, including whiteheads
- Inflammation of comedones, progressing to pustular lesions
- Acne scars
Increased Sebum Secretion and its Relation to Hormones
Increased sebum secretion is deeply related to hormones, such as androgens. An increase in androgens boosts sebum production in the sebaceous glands and simultaneously leads to increased keratinization of keratinocytes. This results in clogged pores and sebum accumulation, progressing to P. acnes proliferation and inflammation.
Comedones are classified as blackheads or whiteheads depending on whether the pore is open or closed, but essentially, both refer to a situation where sebum is trapped inside the pore and cannot escape.
Inflammatory Acne and Immune Response
As immune responses and inflammatory reactions due to P. acnes progress, they develop into pustular and inflammatory acne. Changes in androgens can lead to hyperandrogenism, such as polycystic ovary syndrome (PCOS) particularly in women, which can exacerbate inflammatory acne.
Skin Immune Function and Cytokines
Beyond merely producing sebum, sebaceous glands also play a role in skin immune function. Cytokines secreted by sebaceous glands trigger inflammatory responses and periporal keratinization, accelerating acne progression.
Sebaceous glands and sebocytes are part of the immune system capable of detecting pathogens and secreting various cytokines in response.
Onset of Inflammation and NLRP3 Inflammasome
Inflammation begins with the recognition of PAMPs, DAMPs, etc., which then leads to the secretion of various cytokines, creating an inflammatory environment. Receptors such as TLRs are present in sebocytes and can secrete cytokines involved in inflammation. The NLRP3 inflammasome plays a crucial role in the initiation of inflammation.
In conclusion, when endocrine factors and P. acnes proliferation stimulate sebocytes to send inflammatory cytokine signals, these cytokines in turn induce inflammation and follicular hyperkeratosis, leading to inflammatory acne.
Therefore, treatment should also proceed by considering these aspects.
