What Is Acne?
Acne vulgaris is a chronic inflammatory disease of the pilosebaceous follicle, characterized by comedones (blackheads and whiteheads), papules, pustules, nodules, and, in severe forms, cysts. It is the most common skin disease worldwide, affecting roughly 85% of adolescents and persisting into or starting in adulthood in a significant proportion of patients.
Acne results from four main factors: sebum hypersecretion (driven by androgens), follicular hyperkeratinization (follicle obstruction), proliferation of Cutibacterium acnes, and inflammation. These factors interact in complex ways, and effective treatment must address multiple mechanisms.
Although often trivialized, acne can cause permanent scarring and profound psychological impact. Studies show that its effect on quality of life is comparable to conditions such as asthma, epilepsy, and diabetes. Adult acne, especially in women, is rising in prevalence.
Sebum Hypersecretion
Androgens stimulate the sebaceous glands, increasing sebum production — the fuel of acne.
Follicular Hyperkeratinization
Keratinocytes in the follicular canal proliferate excessively, blocking sebum outflow and forming a comedone.
Inflammation and C. acnes
C. acnes proliferates in the obstructed follicle and activates innate immunity via toll-like receptors, driving inflammation.
Pathophysiology
Acne formation begins with hyperkeratinization of the follicular infundibulum, which obstructs sebum outflow and produces the microcomedone — the invisible precursor lesion. The microcomedone progresses to a closed comedone ("whitehead") or an open comedone ("blackhead" — the dark color comes from melanin oxidation, not from dirt).
In the obstructed, sebum-rich follicle, Cutibacterium acnes (formerly Propionibacterium acnes) proliferates and produces lipases, proteases, and chemotactic factors. Activation of toll-like receptor 2 (TLR-2) on keratinocytes and macrophages triggers release of IL-1beta, TNF-alpha, and IL-8, recruiting neutrophils and producing visible inflammation.
In adult female acne, androgen-receptor sensitivity in the sebaceous glands is the predominant factor, even when serum androgen levels are normal. Insulin resistance and high-glycemic-index diets can amplify androgenic signaling by raising IGF-1 and lowering SHBG.
Symptoms
Acne presents as a spectrum of lesions ranging from non-inflammatory comedones (blackheads and whiteheads) to inflammatory lesions (papules, pustules, nodules, and cysts). The most common location is the face, followed by the back, anterior chest, and shoulders — areas rich in sebaceous glands.
Types of Acne Lesions
- 01
Open comedones ("blackheads")
Dilated follicles with a visible opening. The dark color comes from oxidized melanin and lipids, not dirt. These are non-inflammatory lesions.
- 02
Closed comedones ("whiteheads")
Obstructed follicles with no visible opening. They precede inflammatory lesions and are the target of retinoids.
- 03
Papules and pustules
Superficial inflammatory lesions. Papules are solid reddish elevations; pustules contain purulent material. They are the most common presentation.
- 04
Nodules and cysts
Deep, painful inflammatory lesions with high risk of scarring. Cysts may coalesce, forming sinus tracts (acne conglobata).
- 05
Post-inflammatory hyperpigmentation
Dark patches that persist for weeks to months after inflammatory lesions resolve. More prominent in dark skin.
- 06
Scarring
Atrophic scars (ice pick, boxcar, rolling) or hypertrophic scars, caused by inflammatory damage to the dermis. Without treatment, they are permanent.
SEVERITY CLASSIFICATION
| GRADE | DESCRIPTION | PREDOMINANT LESIONS |
|---|---|---|
| Mild (comedonal) | Predominance of comedones, few papules | Open and closed comedones |
| Moderate (papulopustular) | Frequent papules and pustules | Papules, pustules + comedones |
| Severe (nodulocystic) | Painful nodules, cysts | Nodules, cysts, high scarring risk |
| Very severe (conglobata) | Coalescing nodules, sinus tracts | Abscesses, tracts, extensive scarring |
Diagnosis
Diagnosis is clinical. Laboratory tests are not necessary for typical acne but are indicated in women with signs of hyperandrogenism (hirsutism, menstrual irregularity, alopecia), late-onset acne, or treatment-resistant acne.
In adult women with suspected androgen excess, order total and free testosterone, DHEA-S, 17-OH-progesterone, and, when indicated, cortisol. Polycystic ovary syndrome (PCOS) is the most common endocrine cause of adult female acne.
Differential Diagnosis
Acne is a clinical diagnosis, but several dermatologic conditions can mimic its lesions. Comedones are the most specific finding and distinguish true acne from most alternative diagnoses.
DIAGNÓSTICO DIFERENCIAL
Differential Diagnosis
Rosacea
Read more →- Central facial erythema
- No comedones
- Telangiectasias
Perioral Dermatitis
- Eruption around the mouth
- Topical corticosteroid use
Bacterial Folliculitis
- Pustules with central hair
- No comedones
- Bacterial
Testes Diagnósticos
- Culture
Rosacea Fulminans
- Sudden onset
- Young women
- No comedones
- Explosive onset = urgent dermatologic evaluation
Drug-Induced Acne
- Use of corticosteroids, lithium, androgens
- Onset coincides with medication
Rosacea vs. Acne: Key Differences
Rosacea and acne share pustules and facial erythema but differ in fundamental ways. In rosacea, persistent central erythema, telangiectasias, and flushing dominate, while acne features comedones — a finding absent in rosacea. Rosacea also predominantly affects adults over age 30 and worsens with vasomotor triggers such as heat, alcohol, and sun.
Treatment diverges significantly: antibiotics and topical retinoids are used in both, but systemic isotretinoin — a mainstay for severe acne — can exacerbate rosacea at high doses. A medical acupuncturist evaluates these conditions together, weighing inflammatory and vasomotor components in each case.
Folliculitis and Perioral Dermatitis: When to Suspect
Bacterial folliculitis presents with pustules centered on hairs, distributed in areas of friction or occlusion, and without comedones. Perioral dermatitis, frequently linked to prolonged use of facial topical corticosteroids, presents as a papulopustular eruption around the mouth, nose, and eyes, with a halo of spared skin around the lips.
Bacterial culture helps differentiate folliculitis caused by atypical agents (gram-negatives, Malassezia). In perioral dermatitis, withdrawing the corticosteroid is an essential part of treatment, though it causes transient worsening — the so-called "rebound effect" that must be communicated to the patient.
Drug-Induced Acne: Trace the Pharmacologic History
Systemic corticosteroids, lithium, anabolic androgens, iodides, and antiepileptics are the main triggers of drug-induced acne. The pattern is typically monomorphic (predominantly papules or pustules at a similar stage), and the temporal relationship with starting the medication is essential for diagnosis.
Drug-induced acne from anabolic steroids in athletes deserves special attention: it can be severe, with nodules and cysts on the trunk, and discontinuing the offending agent is indispensable for therapeutic response. A medical acupuncturist systematically reviews the medication history of every patient with acne.
Treatment
Treatment is stepped according to severity and must address multiple pathogenic mechanisms simultaneously. Combination therapy (retinoid + antimicrobial) is superior to monotherapy. Oral isotretinoin remains the most effective treatment for moderate to severe acne.
Mild (comedonal)
First-line topicalTopical retinoid (adapalene 0.1-0.3% or tretinoin 0.025-0.05%) — the cornerstone of treatment and prevention of new lesions. Add benzoyl peroxide (2.5-5%) as an antimicrobial. Use a fixed-dose combination if available.
Moderate (papulopustular)
Topical combination ± oralTopical retinoid + benzoyl peroxide ± topical antibiotic (clindamycin). If insufficient: oral antibiotic (doxycycline 100 mg/day for 3-4 months) plus topicals. Never an oral antibiotic alone without a retinoid.
Severe (nodulocystic)
Oral isotretinoinIsotretinoin 0.5-1.0 mg/kg/day for 5-7 months (cumulative dose 120-150 mg/kg). Cure rate 80-85%. Requires strict contraception (teratogenic) and monitoring of lipids and transaminases.
Adult female acne
Hormonal therapyCombined oral contraceptive with cyproterone, drospirenone, or dienogest. Spironolactone 50-200 mg/day: effective off-label antiandrogen. May be combined with topical retinoids.
Acupuncture as Treatment
Acupuncture is studied as a complementary therapy in acne, with focus on its anti-inflammatory, sebum-regulating, and stress-modulating effects. Experimental studies suggest that acupuncture may reduce sebum production by modulating the hypothalamic-pituitary-gonadal axis and androgenic signaling.
Proposed mechanisms (mostly derived from preclinical studies) include reducing pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-8), modulating toll-like receptor activity, regulating hormones (lowering circulating androgens and improving insulin resistance), and modulating stress — a recognized factor in acne flares.
In clinical practice, acupuncture may be considered as a complementary therapy, especially for patients with stress-related or hormonally driven acne, and for those who wish to reduce antibiotic use. It does not replace topical retinoids, isotretinoin, or hormonal treatment when indicated.
Prognosis
Most adolescent acne cases improve spontaneously by 20-25 years of age. Isotretinoin produces prolonged remission in 80-85% of severe cases. However, 20% of patients relapse after isotretinoin and may require a second course.
The main long-term negative prognostic factor is scarring, which is permanent and difficult to treat. Treating inflammatory acne early and adequately is the best strategy to prevent scarring. Patients with nodules and cysts should be promptly referred for isotretinoin treatment.
Myths and Facts
Myth vs. Fact
Acne is caused by poor hygiene or dirty skin.
Acne is not caused by dirt. The dark color of open comedones comes from melanin oxidation, not dirt. Washing the face excessively can irritate the skin and worsen acne.
Myth vs. Fact
Chocolate and fatty foods cause pimples.
The relationship between specific foods and acne is more complex than once thought. Evidence suggests that high-glycemic-index diets and excess skim dairy may worsen acne, but chocolate itself is not a proven trigger.
Myth vs. Fact
Isotretinoin causes depression.
Large population studies do not confirm a causal link between isotretinoin and depression. In fact, clearing severe acne with isotretinoin generally improves mental health. Psychological monitoring is prudent, but depression is not a contraindication.
When to Seek Care
Frequently Asked Questions
Frequently Asked Questions
Acne can be controlled very effectively and, in many cases, treated definitively — especially with isotretinoin for severe forms. Most adolescents improve spontaneously by the end of puberty. Adult acne tends to be more persistent and may require prolonged maintenance treatment.
No. Manipulating lesions increases local inflammation, prolongs healing time, and significantly raises the risk of scarring and post-inflammatory hyperpigmentation. Topical retinoids are the most effective and safest way to clear comedones without trauma.
Most topical treatments take 8 to 12 weeks to produce significant results. Oral isotretinoin typically shows visible improvement starting at 4-6 weeks. Stick with the regimen your dermatologist prescribes and do not stop it early.
Yes, but less directly than was once believed. Current evidence suggests that high-glycemic-index diets (sugar, white bread, soft drinks) and excess skim dairy may worsen acne in susceptible individuals by raising IGF-1 and lowering SHBG. A low-glycemic, balanced diet can help as a complementary measure.
Clinical studies suggest that acupuncture, used as a complementary therapy, can reduce inflammatory lesion counts and improve skin oiliness. Mechanisms include reducing pro-inflammatory cytokines, modulating hormones, and lowering stress — a recognized factor in acne flares. A medical acupuncturist can assess the individual benefit in each case.
Large population studies do not confirm a causal link between isotretinoin and depression. In practice, clearing severe acne generally improves psychological well-being. Careful mood monitoring is prudent during treatment, but depression is not an absolute contraindication — it must be assessed case by case with the dermatologist.
Oral antibiotics for acne should be used for a limited time — generally 3 to 4 months — and always combined with a topical retinoid and benzoyl peroxide to prevent bacterial resistance. They are not indicated as monotherapy or as prolonged maintenance. Your dermatologist will assess whether to extend or modify the regimen.
Yes. Atrophic scars (ice pick, boxcar, rolling) result from inflammatory damage to the dermis and are permanent without specific treatment. Treating inflammatory lesions — especially nodules and cysts — early and adequately is the best preventive strategy. Once formed, scars require dermatologic procedures (laser, microneedling, subcision) to improve.
Hormonal acne, more common in adult women, tends to settle on the jawline and neck, worsens premenstrually, and is frequently associated with polycystic ovary syndrome (PCOS). Common adolescent acne predominates on the face, back, and chest. Hormonal treatment (combined oral contraceptive, spironolactone) is especially effective for hormonal acne.
Comedogenic sunscreens can worsen acne, but modern oil-free sunscreens with fluid or gel textures are safe and indicated even for acne-prone skin. Sun protection is especially important during retinoid use (which increases photosensitivity) and to prevent post-inflammatory hyperpigmentation in patients with darker skin.
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