Acne

Acne Treatment at Prescription Skin

Acne is a chronic inflammatory disease of the pilosebaceous unit—the hair follicle and its sebaceous gland—characterised by comedones, papules, pustules, and, in more severe cases, nodules or cysts. It most commonly affects the face and upper trunk and more than 80% of people experience it at some point in life. Early, guideline-based treatment matters because persistent inflammation increases the risk of dyspigmentation and permanent scarring [1]–[4].

What causes acne?

Acne isn’t just “dirty skin.” It develops from four processes that interact with each other:

1. 1. Oil glands make more sebum [skin oil] under the influence of androgens (hormones). This fills hair follicles with oil and lowers oxygen, which sets the stage for acne [2]–[4],[15]–[17].

   2. The lining cells inside the pore don’t shed smoothly. Instead, they stick together and form a tiny plug (a “microcomedone”), which blocks the pore and traps oil and debris [2]–[4],[15]–[17].

   3. In these blocked pores, the skin’s bacteria shift toward more inflammatory strains of Cutibacterium acnes and form biofilms (sticky bacterial layers). This change encourages irritation and swelling [2]–[4],[15]–[17].

   4. The immune system ramps up. Pattern-sensing pathways (like TLR2), early “priming” signals (IL-1), and an inflammation switch (the NLRP3 inflammasome) drive Th1/Th17 immune responses. If the pore wall breaks, the trapped material leaks into the skin and creates tender red bumps, whiteheads, pustules, and deeper nodules or cysts [2]–[4],[15]–[17].

Your baseline risk can be higher if acne runs in the family or you have a polygenic (many-gene) predisposition, and day-to-day factors—cosmetics, tight clothing or helmets (occlusion), certain medications, and climate—can worsen or improve how much acne you see and how severe it is [3],[13]–[16].

Why is it worse in some people?

Severity is the sum of biology and exposure. Higher baseline sebum output, a stronger tendency to follicular hyperkeratinisation, the presence of inflammatory C. acnes phylotypes, and a more reactive immune milieu all push disease toward greater inflammation and scarring risk. Genetics contribute substantially—heritability estimates around 70–80% are typical—and truncal involvement, earlier onset, and nodulocystic lesions predict a more persistent, relapse-prone course [2]–[4],[13]–[16],[18]–[20].

Why does acne continue after puberty for some?

Acne frequently persists into adulthood, particularly in women, either as persistent disease from adolescence or as late-onset acne. Fluctuating androgens, occlusive or comedogenic skincare and makeup, occupations or sports involving friction and sweat, and an individual’s immunologic set-point sustain low-grade but chronic inflammation. Adult female acne commonly concentrates along the lower face and jawline; topical retinoids and benzoyl peroxide (BPO) remain foundational, and carefully selected hormonal therapies can help where androgen signalling and oiliness drive flares [3],[4],[6].

A medical approach that targets the four drivers

The fastest, most durable improvements happen when treatment covers each of the four core processes rather than chasing lesion types. We build plans around a nightly retinoid backbone to normalise keratinisation and dampen inflammation, then add agents to address dysbiosis and, where relevant, sebum control. When antibiotics are needed, they are time-limited and always paired with BPO to minimise resistance, and escalation to oral isotretinoin is considered early where nodules, truncal burden or scarring risk are present [4]–[7],[9],[18]–[20].

Sebum overproduction (androgen-driven)

Excess sebum enriches a low-oxygen niche that fuels congestion and bacterial lipase activity. Oral isotretinoin directly shrinks sebaceous glands and normalises sebum quality and quantity, producing prolonged remissions in severe, scarring or refractory acne; relapse risk is influenced by sex, age, total cumulative dose and whether a maintenance retinoid or hormonal regimen is used [2],[4],[18]–[19]. In adult females, combined oral contraceptives and spironolactone reduce androgen signalling and sebum-driven flares when chosen appropriately and monitored carefully [4],[6]. Topical retinoids are not anti-androgens, but by preventing microcomedones they mitigate the congestion that sebum excess otherwise sustains [4],[7],[20].

Abnormal follicular keratinisation (retention hyperkeratosis)

Microcomedones are the “seed” of every acne lesion. Topical retinoids (adapalene or tretinoin) are therefore first-line for almost all patients because they normalise desquamation, open existing microcomedones and prevent new ones. This comedolytic effect underpins both active treatment and long-term maintenance once clear. Retinoids also exert direct anti-inflammatory effects, which improves clinical response beyond decongestion alone [4],[7],[20]. When retinoids are contraindicated, poorly tolerated, or during pregnancy, azelaic acid (15–20%) offers a comedolytic and anti-inflammatory alternative with the added advantage of improving post-inflammatory hyperpigmentation [4],[8].

Cutibacterium acnes bacteria

Shifts in C. acnes bacteria on the skin promote inflammatory cascades in obstructed follicles. Benzoyl peroxide is rapidly antibactericidal without inducing resistance and is the essential partner whenever topical or systemic antibiotics are used. Systemic antibiotics (for example doxycycline) are reserved for moderate to severe inflammatory or truncal disease, prescribed for the shortest effective course (typically ≤12 weeks), and always combined with a topical retinoid ± BPO to sustain control and reduce resistance selection pressure [4]–[6],[9]. Everyday product choices matter too: non-comedogenic sunscreens and moisturisers, and avoiding heavy occlusive cosmetics, help keep the follicular environment unfavourable to dysbiosis [15]–[17].

Inflammation (TLR2, IL-1, NLRP3; Th1/Th17)

Inflammation is present from the earliest microcomedone stage and intensifies with follicular rupture. Retinoids and azelaic acid reduce inflammatory signalling while also correcting keratinisation. BPO combined with a topical antibiotic reduces inflammatory lesions more effectively than an antibiotic alone and curbs resistance; antibiotic monotherapy should be avoided. When inflammatory burden is high or there is extensive truncal disease, short courses of systemic antibiotics can be useful, but topical agents must continue during and after the course to prevent rebound. For nodulocystic or scarring-risk acne—or for disease that fails to respond to appropriate combinations—oral isotretinoin offers comprehensive disease modification across sebum, keratinisation and inflammation [2],[4]–[9],[18]–[19].

What to expect and when

With consistent use, early reductions in tender papules and pustules usually appear within two to four weeks, particularly where BPO or a fixed retinoid/BPO combination is included; transient “purging” reflects microcomedones surfacing and generally settles with continued therapy and sensible moisturiser use. By six to twelve weeks, comedones fall, texture and tone improve, and most patients are ready to taper any systemic antibiotics while maintaining their nightly retinoid. Between three and six months, control consolidates; azelaic acid can be layered to manage colour change, and isotretinoin is considered earlier in the course whenever scarring risk is evident [4],[6]–[9],[18]–[20].

Adjunctive lifestyle notes

Diet is supportive rather than determinative. Low-glycaemic eating patterns modestly reduce lesion counts, likely via IGF-1 signalling, while evidence linking dairy to acne is observational and heterogeneous; we use shared decision-making rather than strict prohibitions. Sleep, stress management, and avoiding friction and heavy occlusion on acne-prone sites reduce triggers that otherwise complicate care [10]–[12].

Why prescription treatments are better

Prescription care delivers therapeutic-level actives and combinations—retinoids, fixed-dose adapalene/BPO, time-limited systemic therapy, hormonal options and, when needed, isotretinoin—implemented within resistance-aware protocols and monitored over time. This process-first approach treats what drives acne rather than masking flares, reduces relapse, and protects against scarring [4]–[7],[9],[18]–[20].

How Prescription Skin can help you

Start with a quick online skin assessment and a medical review. We personalise your formulation to your skin tone, sensitivity and goals, then adjust strengths and companions over follow-ups. For example, we titrate retinoids to tolerance, choose appropriate BPO or azelaic acid strengths, and decide when to add, continue or stop systemic therapy. For adult female acne we assess suitability for hormonal therapy; for scarring-risk disease we discuss isotretinoin early and coordinate care safely. Clear, step-by-step instructions ensure you know what to use, when to use it, and how to manage temporary irritation while results build.

Start with a quick skin assessment →