1. GENERAL OVERVIEW
Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit. It is one of the most common dermatological conditions worldwide, affecting approximately 9.4% of the global population.
The condition typically develops during puberty, when hormonal changes increase sebaceous gland activity, leading to increased sebum production. The accumulation of sebum, combined with dead skin cells, can obstruct hair follicles, resulting in comedone formation and triggering an inflammatory response.
2. PATHOPHYSIOLOGY
Acne vulgaris develops through the interaction of four major mechanisms: increased sebum production, abnormal follicular keratinization, proliferation of Cutibacterium acnes (C. acnes), and inflammation.
a) Increased Sebum Production
Elevated androgen levels or excessive sebaceous gland sensitivity to androgens stimulate sebaceous gland activity and increase sebum production.
In addition, insulin-like growth factor 1 (IGF-1) contributes to the stimulation of sebum secretion. Excessive sebum creates favorable conditions for acne development and may worsen disease severity.
b) Follicular Obstruction Due to Abnormal Keratinization
In individuals with acne, keratinocytes within the hair follicles undergo abnormal proliferation and adhesion.
When combined with sebum, these cells form obstructive plugs within the follicles, leading to the formation of microcomedones, which subsequently develop into whiteheads or blackheads.
c) The Role of Cutibacterium acnes
When hair follicles become obstructed, the resulting lipid-rich, oxygen-poor environment provides favorable conditions for C. acnes proliferation.
This bacterium produces lipase enzymes that break down sebum into free fatty acids, which irritate the skin and promote inflammatory responses.
d) Inflammation and Immune Responses
The presence of C. acnes activates the immune system, triggering the release of pro-inflammatory mediators such as IL-1β, TNF-α, and IL-17. These mediators recruit immune cells to the affected areas.
Persistent inflammation may cause follicular wall rupture, resulting in inflammatory lesions ranging from superficial lesions, such as papules and pustules, to deeper lesions, including nodules and cysts.
In addition to these primary mechanisms, acne severity may be influenced by several other factors, including genetics, high-glycemic-index diets, dairy consumption (particularly skimmed milk), psychological stress, hot and humid environments, and the use of inappropriate cosmetic products.
3. CLINICAL MANIFESTATIONS
a) Non-Inflammatory Lesions
These represent the early stages of acne and develop when hair follicles become obstructed by sebum and keratinized cells.
Closed comedones (whiteheads): Hair follicles become completely blocked, producing small, white bumps on the skin's surface.
Open comedones (blackheads): The follicular openings remain exposed to the skin surface, allowing sebum to oxidize and develop its characteristic black appearance.
b) Inflammatory Lesions
When inflammation develops, acne may progress into more severe forms of lesions.
Inflammatory papules and pustules: Red, tender bumps or lesions containing pus develop as a result of inflammation within the hair follicles.
Nodules: Deep, large inflammatory lesions that are often painful to the touch and carry a risk of scarring.
Cysts: Severe lesions containing thick purulent material mixed with blood. They may rupture easily and frequently leave scars after healing.
c) Post-Acne Sequelae
After active acne lesions subside, several persistent skin changes may remain.
Post-inflammatory hyperpigmentation and post-inflammatory erythema: These appear as dark spots or persistent areas of redness following acne lesions.
Atrophic scars: Deep tissue damage results in the loss of the skin's supporting structure. Common types include ice-pick scars, rolling scars, and boxcar scars.
Hypertrophic scars and keloids: These develop due to excessive fibrous tissue formation during wound healing. They commonly occur on the chest, back, shoulders, jawline, and face.
d) Special Clinical Presentations and Complications
In certain cases, acne may be associated with hormonal disorders or progress into severe clinical forms.
Signs of hyperandrogenism in women: These may include hirsutism, male-pattern hair loss, menstrual irregularities, a deeper voice, or clitoromegaly.
Acne fulminans: A severe form characterized by the sudden appearance of large inflammatory nodules and cysts, ulceration, and hemorrhagic crusting, sometimes accompanied by fever or musculoskeletal pain.
Acne conglobata: Characterized by large inflammatory nodules and cysts connected by subcutaneous sinus tracts, with draining openings that release purulent or bloody discharge and frequently result in severe scarring.
Excoriated acne: Oft en associated with psychological factors, in which repeated picking or scratching of acne lesions causes skin erosion and subsequent scarring.
Other complications may include Gram-negative folliculitis and solid facial edema.
4. SEVERITY CLASSIFICATION
In clinical practice, to facilitate disease assessment and treatment selection, the Vietnamese Ministry of Health classifies acne severity into two main categories: mild acne and moderate-to-severe acne.
This classification is based on lesion type, degree of inflammation, the presence of deep lesions, and residual skin changes.
a) Mild Acne
Mild acne is generally characterized by small, localized lesions without evidence of deep tissue involvement.
Key features include:
The presence of whiteheads, blackheads, inflammatory papules, or small pustules (less than 5 mm) in limited numbers and scattered distribution.
No nodular lesions.
No acne scars or long-term residual skin changes.
The affected area is usually limited to one body region. If lesions are more widespread, their number in each affected area remains relatively small.
At this stage, appropriate treatment and skincare can help control the condition and prevent progression to more severe inflammatory acne.
b) Moderate-to-Severe Acne
Moderate-to-severe acne is characterized by more prominent clinical manifestations, a greater number of lesions, increased inflammation, and a higher risk of scarring.
Key features include:
Numerous whiteheads, blackheads, inflammatory papules, or pustules.
Possible development of nodules and cysts due to inflammation extending into deeper skin layers.
The presence of acne scars, indicating damage to the skin's structural integrity.
Lesions distributed across multiple body regions, with a significant number of lesions in each affected area.
5. TREATMENT
General Principles of Treatment
Target the underlying causes of acne
Treatment should address the major pathogenic mechanisms, including excessive sebum production, abnormal follicular keratinization, C. acnes proliferation, and inflammation.
Initiate treatment early and appropriately
Early intervention helps control existing lesions, prevent disease progression, and reduce complications such as acne scarring, post-inflammatory hyperpigmentation, and erythema.
Individualize treatment according to disease severity
Accurate assessment of acne severity is essential for selecting an appropriate treatment regimen for each patient.
Continue treatment after acne has been controlled
Following the initial treatment phase, maintenance therapy should be continued, with topical retinoids generally preferred to help prevent recurrence.
Combine different treatment approaches
Appropriate combinations of topical medications, oral medications, and non-pharmacological interventions can improve treatment outcomes and disease control.
Supportive skincare measures include:
Washing the face twice daily with a gentle cleanser.
Using non-comedogenic moisturizers.
Applying sunscreen.
Avoiding self-extraction or picking of acne lesions.
Additional procedures, such as comedone extraction, chemical peels, and light-based therapies, may also be considered.
Pharmacological Treatment
a) Topical Treatment
Topical Retinoids: Adapalene, Tretinoin, Tazarotene, and Trifarotene
Retinoids help normalize follicular keratinization, unclog pores, reduce comedone formation, and exert anti-inflammatory effects.
They are also important components of maintenance therapy for preventing acne recurrence.
These medications are generally applied once daily in the evening to clean, dry skin.
Common adverse effects include skin dryness, irritation, peeling, and increased photosensitivity.
Tazarotene is contraindicated during pregnancy. Other topical retinoids should also generally be avoided during pregnancy because of insufficient safety data.
Daily sunscreen application is recommended throughout treatment.
Benzoyl Peroxide
Benzoyl peroxide kills C. acnes by releasing free oxygen radicals. It also helps reduce inflammation and promotes mild exfoliation of the outermost layer of the skin.
Commonly used concentrations range from 2.5% to 5%.
Because benzoyl peroxide has a low tendency to induce bacterial resistance, it is frequently combined with antibiotics to minimize the development of antimicrobial resistance.
Common adverse effects include skin dryness and irritation. It may also bleach fabrics and hair.
Topical Antibiotics: Clindamycin, Erythromycin, and Minocycline
These medications help reduce C. acnes populations and control inflammation.
However, they should not be used as monotherapy or for prolonged periods because of the increased risk of antimicrobial resistance.
They should preferably be combined with benzoyl peroxide, with treatment effectiveness reassessed after approximately 3–4 months.
Other Topical Medications
Azelaic acid: Exhibits antibacterial and anti-inf lammatory properties and helps reduce post-inflammatory hyperpigmentation. It is suitable for sensitive skin and may be used during pregnancy.
Clascoterone: Acts as a topical androgen receptor inhibitor, reducing the effects of androgens on sebaceous glands.
Topical dapsone: Exhibits antibacterial and anti-inflammatory properties.
Salicylic acid: Helps remove dead skin cells, clear follicular openings, and reduce pore obstruction.
b) Systemic Treatment
Systemic therapy is generally indicated for moderate-to-severe acne, widespread lesions, or cases that do not respond adequately to topical treatment.
Oral Antibiotics
Newer-generation tetracyclines are generally preferred, including:
Doxycycline.
Minocycline.
Treatment duration is usually limited to approximately 3–4 months. These antibiotics should not be used for long-term maintenance therapy.
When tetracyclines cannot be used, such as in pregnant women or young children, macrolides such as azithromycin or erythromycin may be considered.
Oral antibiotics should not be used as monotherapy. They should be combined with benzoyl peroxide or topical retinoids.
Oral Isotretinoin
Isotretinoin is a potent systemic medication generally indicated for:
Severe nodular or cystic acne.
Acne that does not respond to conventional treatment.
Acne associated with scarring or significant psychological distress.
It is the only medication capable of targeting all four major pathogenic mechanisms of acne:
Reducing sebum production.
Normalizing follicular keratinization.
Reducing C. acnes proliferation.
Suppressing inflammation.
Treatment generally begins at a low dose, followed by gradual dose escalation according to patient tolerability.
The usual initial dose is 0.25–0.5 mg/kg/day, which may subsequently be increased to 0.5–1 mg/kg/day depending on tolerability.
The target cumulative dose is approximately 120–150 mg/kg, with treatment generally lasting 4–6 months.
Because isotretinoin carries a serious risk of fetal abnormalities, it is contraindicated during pregnancy and breastfeeding.
Women of childbearing potential must have a negative pregnancy test before starting treatment and undergo monthly pregnancy testing during therapy. Effective contraception is required for at least one month before treatment begins and for one month after discontinuation.
Liver enzymes and blood lipid levels should also be monitored throughout treatment.
Concomitant use with tetracyclines should be avoided because of the increased risk of intracranial hypertension.
Hormonal Therapy (in Women)
Hormonal therapy is suitable for women whose acne is associated with hormonal disturbances or tends to flare in relation to the menstrual cycle.
Combined Oral Contraceptives (COCs)
These contain estrogen combined with progestins that possess antiandrogenic activity. They help reduce androgen-mediated effects and consequently decrease sebum production.
Spironolactone
Spironolactone is an antiandrogen medication that can improve hormonally driven acne in adult women.
It is contraindicated during pregnancy. Serum potassium levels should be monitored, and potential adverse effects such as menstrual irregularities should be considered.
REFERENCES
Ministry of Health of Vietnam. (2023). Guidelines for the Diagnosis and Treatment of Dermatological Diseases. Issued under Decision No. 4416/QĐ-BYT dated December 6, 2023.
Ogé, Linda K., Alan Broussard, and Marilyn D. Marshall. (2019). Acne vulgaris: Diagnosis and treatment. American Family Physician, 100(8), 475–484.
Vasam, Mallikarjun, Satyanarayana Korutla, and Raghvendra Ashok Bohara. (2023). Acne vulgaris: A review of the pathophysiology, treatment, and recent nanotechnology-based advances. Biochemistry and Biophysics Reports, 36, 101578. DOI: 10.1016/j.bbrep.2023.101578.
Reynolds, Rachel V., et al. (2024). Guidelines of care for the management of acne vulgaris. Journal of the American Academy of Dermatology, 90(5), 1006.e1. DOI: 10.1016/j.jaad.2023.12.017.
Jaiswal, Sharwari, et al. (2024). Recent trends in the management of acne vulgaris: A review focusing on clinical studies in the last decade. Cureus, 16(3). DOI: 10.7759/cureus.56596.
Heng, Anna Hwee Sing, and Fook Tim Chew. (2020). Systematic review of the epidemiology of acne vulgaris. Scientific Reports, 10(1), 5754. DOI: 10.1038/s41598-020-62715-3.
Authors:
MSc. Kim Ngoc Son
MSc. Dinh Thi Thuy Ha
Publication date: October 15, 2026
