Discuss the inflammatory progression of acne vulgaris by integrating your understanding of the pilosebaceous unit and epithelial dynamics. Your answer should cover:

What is the sebaceous follicle?

A follicle that contains a vellus-sized hair but has extensive sebaceous glands attached. Found on the face, chest and back.

What is the vellus follicle?

Produces fine, colourless 'peach fuzz'. The follicle only reaches to the upper dermis. Functions: thermoregulation, sensation, and distributing sebum.

What is the terminal follicle?

Thick, long, pigmented hair with a deeper root structure extending to the subcutaneous layer. Involved in temperature regulation and skin protection. Found on the scalp, face, armpit and pubic regions.

How is a sebaceous follicle structurally different to a vellus and terminal follicle?

The sebaceous follicle has a small (vellus-sized) hair but extensive sebaceous glands attached. The vellus follicle is shallow (reaches only the upper dermis) and produces fine colourless hair. The terminal hair is thick, long and pigmented, with the deepest root structure (extending to the subcutaneous layer)

Why does acne primarily form on the face, chest and back?

Because these areas contain sebaceous follicles — follicles with extensive sebaceous glands attached. Since acne involves hyperactive sebaceous glands producing excess sebum, these gland-rich regions are where acne forms.

What are the four key mechanisms of acne formation?

1. Hyperkeratinisation — epithelial cells in the upper hair follicle overproduce and retain keratin, plugging the follicle.

2. Sebum overproduction — sebaceous glands become hyperactive (largely driven by androgens during puberty); excess sebum mixes with retained keratin, thickening the plug.

3. Bacterial overgrowth — Cutibacterium acnes proliferates in the oxygen-poor plugged follicle; it secretes lipases that break down sebum triglycerides into pro-inflammatory fatty acids.

4. Inflammation — immune cells infiltrate and release pro-inflammatory cytokines, damaging surrounding tissue.

What are the different types of acne lesions?

Papules — raised, red, no pus. Pustules — contain pus (dead neutrophils + bacteria). Nodules/cysts — deep, painful, inflammatory lesions which scar.

What are the different acne treatment options?

Topical retinoids; benzoyl peroxide; antibiotics; hormonal therapy (e.g. oral contraceptives).

How does each treatment treat acne?

Topical retinoids — decrease keratinocyte cohesion/turnover. Benzoyl peroxide — anti-microbial peeling agent. Antibiotics — reduce C. acnes and inflammation. Hormonal therapy — decrease sebum.

What is the pilosebaceous unit?

The hair's functional unit, made up of the hair follicle (the tunnel structure the hair strand grows from), the sebaceous gland (which lubricates the hair strand), and the arrector pili muscle (which erects the hair).

How does acne inflammation progress?

In the oxygen-poor plugged follicle, C. acnes proliferates and secretes lipases that break down sebum triglycerides into pro-inflammatory fatty acids. Bacterial antigens (e.g. toll-like receptors) activate local immune cells. Neutrophils, macrophages and T-cells infiltrate the follicle and release pro-inflammatory cytokines, increasing inflammation and damaging surrounding tissue. This produces the visible lesions, and the inflammation disrupts epithelial integrity, causing further damage and post-inflammatory pigmentation or scarring.