ACNE VULGARIS,

ROSACEA &
PERIORAL DERMATITIS

Presentation by:
Dr. Deeksha N
1 Junior resident
Dept. of Dermatology
AIMS and RC
 OVERVIEW:
 Acne Vulgaris
> Introduction
> Epidemiology
> Pathophysiology
> Classification and Grading
> Syndromes associated
> Variants of acne
> Consequences
> Management
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 Rosacea
 Perioral dermatitis
 Latest updates
INTRODUCTION:
 It can be defined as a chronic, self-limiting, inflammatory disease of the pilosebaceous
unit, manifesting generally in adolescence with pleomorphic lesions like comedones,
papules, pustules, nodules, and cysts and these may lead to scarring.

 Acne vulgaris is well known and easily recognized in adolescents across the globe.

 It is common enough to be called a physiological process but is better regarded as a

disease due to its inflammatory component and the disfigurement it produces on the
face.

 Socially and psychologically the most important part of the body.

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EPIDEMIOLOGY

 Affects 90% of individuals sometime in their lifetime.

 Acne occurs in all races

 Americans > Japanese population and cystic acne more common in whites.

 Age of onset is at puberty or a few months earlier.

 Peak age of incidence is 14–17 years in females and 16–19 years in males.

 In case there is sudden and profuse eruption of lesions at a later age, it calls for
investigations of the pituitary, adrenal cortex, and gonads.
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PATHOPHYSIOLOGY:
 Acne vulgaris is multifactorial in origin and several factors affect the severity of acne:

1. Follicular hyperkeratinisation

2. Androgens

3. Organism(Propionibacterium acnes  Cutibacterium acnes)

4. Inflammation and immune response

5. Other factors
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1. Follicular hyperkeratinisation

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 2. Androgens
 Sebaceous glands enlarge with adrenarche and sebum production increases.

 Androgens increase sebum secretion and also cause sebaceous gland hyperplasia.

 Sex hormone-binding globulin (SHBG) is also important, as it binds free androgen.

 Overall increased androgen production is evidenced by elevation in the levels of

plasma testosterone, 17 alpha hydroxysteroids, androstenedione and DHEA-S.

 Other hormones such as estrogens, GH, insulin, IGF-1, glucocorticoids, ACTH and
melanocortins also regulate sebum production.

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3. Organisms

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4. Inflammation and immune response

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5. Other factors

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 CLASSIFICATION AND GRADING
1). Clinical Types of Acne(Pillsbury, Shelley and Kligman)

Grade I (Mild): Comedones, occasional papules

Grade II (Moderate): Comedones, many papules, few

pustules

Grade III (Severe): Predominantly pustules,

nodules, and abscesses(acne conglobata)

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Grade IV (Cystic): Mainly cysts or abscesses,
widespread scarring.
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 THE GLOBAL ACNE GRADING SYSTEM

Location Factor

Forehead 2

Right cheek 2

Left cheek 2

Nose 1

Chin 1

Chest and upper back 3 14

 Each type of lesion is given a value depending on severity : No
lesions = 0
Comedones = 1
Papules = 2
Pustules = 3
Nodules = 4

 The score for each area (Local score) is calculated using the formula :

Local score = Factor × Grade (0-4)

 Global score is the sum of local scores

Acne severity was graded using global score
 1-18 mild 31-38severe 15

19-30moderate >39very severe

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SYNDROMES ASSOCIATED WITH ACNE

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 APERT SYNDROME

 Autosomal dominant

 Synostoses of the cranium, vertebrae, hands, feet, and acneiform eruptions.

 Underlying problem is an abnormal sensitivity to normal circulating level of

androgens.

 Association of acne lesions with bone anomalies can be explained by the mutation of
fibroblast growth factor receptor 2.

 Rare presentations of polydactyly, syndactyly with nodulocystic acne, and 19

Klinefelter’s syndrome with acne conglobata have been reported.
 POLYCYSTIC OVARY SYNDROME AND ACNE
 Persistent, severe, acne of late onset in females

 Other associated features may be

 Hirsutism
 Acanthosis nigricans
 Patterned hair loss

 Key etiological feature of PCOS are increased androgen secretion and insulin
resistance

 Hormonal therapy along with lifestyle modifications (e.g. weight reduction) are
helpful treatment options
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 HAIR-AN syndrome(subset of PCOS)
Hyperandrogenism
Acne
Insulin resistance
Acanthosis nigricans

 SAHA syndrome:
Seborrhea
Acne
Hirsutism
Alopecia
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 CONSEQUENCES OF ACNE

SCARRING
 Consequence of abnormal
resolution or wound healing
following the inflammation.

 Atrophic scars
> Ice pick scars
> Rolling scars
> Boxcar scars

 Hypertrophic scars

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 Keloid
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 HYPERPIGMENTATION

 In patients particularly with type III/IV

skin.

 Hyperpigmented macules may persist

following the resolution of inflammatory
acne lesions

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OTHERS
 Wide range of psychological abnormalities including,
Depression
Suicidal ideation
Anxiety
Psychosomatic symptoms (pain and discomfort)
Embarrassment
Body dysmorphic disorder
Social inhibition
Obsessive-compulsiveness

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 DIFFERENTIAL DIAGNOSIS

Condition Feature
1. Rosacea When papules, pustules, and erythema are prominent on the flush areas of the face
and chin. Eye involvement may be seen.

2. Oil acne When comedones are predominant and history is suggestive.

3. Senile acne: In the older age group.

4. Drug-induced acne: When lesions involve uncommon areas and the onset is sudden.

5. LMDF If papules and nodules are predominant on the face.

6. Sycosis barbae.

7. Gram-negative When pustules are the predominant lesions

folliculitis

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8. Folliculitis due to Candida.

9. Demodex folliculitis.

10. Pseudofolliculitis When the hairs of beard are thick, curly, and penetrate back into the skin.

11. Trichostasis spinulosa When the predominant lesions are open comedones.

12. Metastatic Crohn’s disease on the A rare extraintestinal feature of Crohn’s disease, may be mistaken for
face severe treatment-resistant acne.

13. Atypical mycobacterial infection: Mycobacterium chelonae infection in an immunocompetent host

mimicking as acne conglobata.

14. Systemic lupus erythematosus The malar rash of SLE may resemble treatment resistant acne.

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MANAGEMENT

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 TREATMENT
General Measures

1. Education and counseling with emphasis on making the patient understand,

>Nature and course of the disease
>Different modalities of treatment available and their limitations
>Likely duration of treatment, outcome of therapy, and the importance of
adherence to a particular regimen.
>All wrong notions and myths about the disease, such as diet, hygiene or
bowel disturbances, should be dispelled.

2. To avoid the use of oils, pomades, and heavy cosmetics.

3. To eliminate emotional stress by reassurance.

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4. To educate regarding premenstrual flare and seasonal variation.

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 VARIANTS OF ACNE

 Drug induced acne/ acneiform eruption  Maskcne

 Acne excoriee  Occupational acne/chloracne

 Neonatal acne  Pyoderma faciale

 Infantile acne  Endocrine acne

 Post-adolescent acne  Cosmetic/pomade acne

 Acne mechanica  Acne fulminans

 Acne conglobata 35
 Gram negative folliculitis
 ACNE EXCORIEE
 More often in young women
 Acne excoriée des jeunes filles

 Typical comedones and inflammatory papules are

systematically excoriated in a ritualistic manner,
leaving crusted erosions that may scar.

 Linear erosions suggest self-manipulation, and an

underlying psychiatric component should be
considered.
 Individuals with an anxiety, obsessive compulsive,
or body dysmorphic disorder are particularly at
risk.
 Antidepressants or psychotherapy may be helpful. 36
 POST ADOLESCENT ACNE
 Inflammatory acne beyond 25 years of age is most common in women and may be
associated with a high level of psychological stress.

 Majority of affected women present with findings similar to those of adolescent acne,
with a mixture of inflammatory and comedonal lesions.

 Involving various facial sites and sometimes the trunk.

 Mandibular area is involved in 80% of women

 Half of women report persistence of their acne since its onset.

 Premenstrual flares are common but only 20% of women with acne have irregular 37
menses.
Post adolescent acne in 28yr female

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 NEONATAL ACNE
 Neonatal acne occurs in more than 20% of healthy newborns.

 Lesions usually appear at about 2 weeks of age and generally resolve within the first 3
months of life.

 Small papulopustules (not comedones) arise primarily on the cheeks, forehead, eyelids
and chin, although the neck and upper trunk can also be involved

 Pathogenesis of neonatal acne :

1. An inflammatory response to Malassezia spp. (e.g. sympodialis, furfur) has
been proposed, leading to renaming of the disorder as "neonatal cephalic pustulosis".
2. The active sebaceous glands and high sebum excretion rate in neonates .

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 Treatment: Parental reassurance alone is usually adequate.
Therapy with topical imidazoles can be effective.
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 INFANTILE ACNE
 Typically presents at 2-12 months of age.

 In contrast to neonatal acne, comedone formation is prominent and pitted scarring may
develop in up to half of patients .
 Deep, suppurative nodules are occasionally seen.

 Pathogenesis :
1. Elevated levels of LH stimulating testicular production of testosterone in male
infants during the first 6-12 months of life.
2. Elevated levels of DHEA produced by the infantile adrenal gland in both male
and female infants.

 Patients with infantile acne should be assessed for signs of hyperandrogenism,

precocious puberty, or abnormal growth 41
 Infantile acne usually resolves within 6-18
months and remains quiescent until around
puberty, with an increased risk of severe acne
during adolescence

 Treatment:
1. Topical retinoids (e.g. tretinoin, adapalene) and
benzoyl peroxide are first-line treatments.

2. Oral antibiotics (e.g. erythromycin, azithromycin)

in more severe inflammatory lesions.

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 CHLORACNE

 It is due to exposure to halogenated

aromatic hydrocarbons.

 Comedo like lesions with relatively little

associated inflammation mostly seen over
malar and retroauricular areas, as well as
axilla and scrotum.

 Hypertrichosis and grayish discolouration

of skin.

 Management:
Removal of source of exposure
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Topical / oral retinoids
 MASKCNE

 Long-time mask wearing could increase the flare of

acne.

 Higher temperature and humidity on the surface of

facial skin caused by expired air and the perspiration.

 Recently described entity during covid-19 pandemic.

 Itching and excessive seborrhea.

 Comedones, papules on cheek and nose.

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 DRUG INDUCED ACNE
 Acne or acneiform eruptions can be seen as a side effect of a number of medications.

 An abrupt, monomorphous eruption of inflammatory papules and pustules is often

observed in drug-induced acne.

 When a history of prescription medication use is not elicited, a comprehensive review

of all OTC medications and supplements, as well as recent medical procedures, may
reveal the responsible agent.

 Bodybuilders and athletes should be questioned about anabolic steroid use.

 Steroid-induced acne (and rosacea) can also result from the inappropriate use of
topical corticosteroids on the face.
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24yr/F with steroid-induced acne

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Acneiform eruptions with facial hypertrichosis 20 to topical steroid abuse

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 SEVERE FORMS OF ACNE

 Acne conglobate

 Acne fulminans

 Solid facial edema

 Gram negative folliculitis

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 ACNE FULMINANS
 Most severe form of acne
 Uncommon variant
 Characterized by the abrupt development of nodular and suppurative acne lesions in
association with systemic manifestations.

 Primarily affects boys 13–16 years of age.

 Face, neck, trunk, and arms are all affected.

 Microcomedones suddenly erupt and become markedly inflamed
 Rapidly coalescence into painful, oozing, friable plaques with hemorrhagic crusts.
 Lesions tend to ulcerate and can lead to significant scarring.

 Osteolytic bone lesions may accompany the cutaneous findings (clavicle and sternum)50
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 Fever, arthralgias, myalgias, hepatosplenomegaly, and severe malaise.

 Erythema nodosum may also arise in association with acne fulminans.

 Lab abnormalities: elevated ESR, proteinuria, leukocytosis, and anemia.
 Treatment:
Prednisone 0.5–1 mg/kg/day as monotherapy for at least 2–4 weeks
followed by
Low-dose isotretinoin (e.g. 0.1 mg/kg/day) (acute inflammation subsides)
after at least 4 weeks of this combination
Isotretinoin slowly increased and the prednisone tapered over 1–2 mo.
 Additional treatment: topical or intralesional corticosteroids, oral antibiotics
(generally of limited efficacy), TNF-α inhibitors, interleukin-1 antagonists, and
immunosuppressive agents (e.g. azathioprine, cyclosporine).
 Dapsone (acne fulminans associated with erythema nodosum) 52
 ACNE CONGLOBATA
 Rare but severe form of nodulocystic acne in young males.

 Presents with tender, disfiguring, double- or triple-interconnecting comedones, cysts,

inflammatory nodules, and deep burrowing abscesses.

 On face, shoulders, back, chest, upper arms, buttocks, and thighs.

 Eruptive onset but without systemic manifestations.

 This recalcitrant acne variant is part of the follicular occlusion tetrad.

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 FOLLICULAR OCCLUSION

1. Dissecting cellulitis of scalp

2. Hidradenitis suppurativa TRIAD
TETRAD
PENTAD
3. Acne conglobate
4. Pilonidal sinus
5. Sebaceous cyst

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ACNE CONGLOBATA

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 SOLID FACIAL EDEMA(MORBIHAN DISEASE)
 An unusual and disfiguring complication of acne
vulgaris.

 Clinically, there is a distortion of the midline face

and cheeks due to soft tissue swelling.

 Impaired lymphatic drainage and fibrosis in the

setting of chronic inflammation.

 Treatment :
Isotretinoin(0.2-1mg/kg/day) for 4-6 months
Isotretinoin + Ketotifen 1–2 mg/ day (or) Prednisone
10–30 mg/day may have additional benefit. 56
 GRAM NEGATIVE FOLLICULITIS
 Patients with preexisting acne vulgaris who have
been treated with long-term systemic antibiotics
(usually tetracyclines) may develop GNF.

 Exhibit an initial response to the oral antibiotic,

followed by apparent resistance to the treatment
and worsening of acne.

 Inflammatory papules, pustules, and nodules

typically appear on perinasal skin and the central
face.

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 Of all the Enterobacteriaceae spp., E. coli, Klebsiella spp., and Proteus spp. cause
majority of the cases of GNF.

 Although trimethoprim, cotrimoxazole, and ampicillin have been used in GNF, the
present MIC values do not favor their use.

 Mech. Of Resistance:
All strains of Klebsiella express a chromosomally encoded β-lactamase that confers
resistance to ampicillin.
Proteus vulgaris, Enterobacter, and Serratia frequently harbor plasmids.

 Quinolones are an ideal drug classLevofloxacin 750 mg is effective.

 Oral isotretinoin 0.5–1 mg/kg/day for 4–5 months is an option.

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LATEST UPDATES

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 ROSACEA
 Rosacea is a chronic inflammatory disease predominantly affecting the central
zones of the face, mainly the chin ,nose, cheeks and forehead.

 Common in adults ( predominantly between 45 and 60 years of age).

 No sex preponderance reported incontrast to common belief.

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MAJOR PATHOMECHANISM

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 CLINICAL PRESENTATION
 Transient to persistent facial erythema
 Telangiectasia
 Papules , pustules
 Edema
 Combination of any of the above

 NRSEC classication of subtypes of rosacea

• Erythematotelangiectatic
• Papulopustular a/k/a ADULT ACNE
• Phymatous
• Ocular
• Granulomatous rosacea ( new addition )
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 HISTOPATHOLOGY

 Erythematotelangiectatic subtype: Solar

elastosis, telangiectasia and edema.

 Papulopustular subtype: Perivascular and

perifollicular lymphohistiocytic infiltrate.

 Phymatous subtype: Hyperplasia of sebaceous

glands, fibrosis and dilation of hair follicles.

 Granulomatous rosacea: Non caseating

epithelioid granuloma formation.
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 DIAGNOSTIC CRITERIA
One of the following clinical presentations is considered diagnostic for rosacea:
1. Fixed centrofacial erythema in a characteristic pattern that may periodically intensify
2. Phymatous changes

Two of the following major criteria below are also diagnostic

3. Flushing
4. Papules and pustules
5. Telangiectasia
6. Occular manifestations: lid margin Telangiectasia, interpalpebral conjuctival injection ,
spade shaped corneal infiltrates , scleritis and sclerokeratitis.

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DIFFERENTIAL DIAGNOSIS OF ROSACEA

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 TREATMENT

General measures

 1st step: advise the patient to identify the possible triggers and avoid them ( “
triggers diary”)

 Gentle cleansers and broad spectrum sunscreens and moisturisers.

 There is an underlying barrier defect, hence irritant cosmetics should be avoided.

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IMPORTANT THINGS TO KEEP IN MIND WHILE TREATING
ROSACEA

 The choice of therapy is guided by the signs and symptoms present for the individual
patient.

 Though they have anti-inflammatory properties topical steroids should be avoided as

they are associated with rebound flaring or induction of rosacea like perioral
dermatitis.

 The persistent erythema and telangiectasia is not completely secondary to

inflammation, hence requires treatment targeting the skin vasculature.

 Phymatous changes result in irreversible damage to the skin necessitating surgical 77

intervention.
 TOPICAL TREATMENT

 ERYTHEMA
 Brimonidine tartrate (alpha-2 agonist) 0.33% gel (Daily application on the face)
 Oxymetazoline hydrochloride (alpha-1 agonist) 1% cream (Daily application on
face)

 INFLAMMATORY PAPULES AND PUSTULES

 Ivermectin 1% cream (daily application)
 Azelaic acid 15% gel, foam or 20% cream (daily 1 to 2 times application)
 Metronidazole 0.75% and 1% gel or cream (daily 1 to 2 times application)

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 OCCULAR INVOLVEMENT

 Artificial tears

 Fusidic acid gel (daily 1 to 2 times application on eyelids) limited data available
for efficacy.

 Metronidazole 0.75% gel (daily 1 to 2 times application on eyelids) limited data

available for efficacy.

 Cyclosporine 0.05% eyedrops, (one drop every 12 hours) limited data available
for efficacy
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 SYSTEMIC TREATMENT
 FLUSHING
 Propranolol (20 to 40 mg 2 to 3 times/day), carvedilol (6.25mg 2 to 3 times/day)
 Clonidine (50 mcg twice daily)

 INFLAMMATORY PAPULES AND PUSTULES

 Subantimicrobial-dose doxycycline, (modified-release 40 mg daily, 30 mg
Immediate-release and 10 mg delayed-release beads, for 8 to 12 weeks)
 Minocycline (50 to 100 mg twice daily for 8 to 12 weeks)
 Tetracycline (250 to 500 mg twice daily for 8 to 12 weeks)
 Azithromycin (250-500 mg 3 times weekly for 4 to 8 weeks)
 Isotretinoin (0.25 to 0.3 mg/kg/day for 12 to 16 weeks)
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 PHYMA (INFLAMED)
 Doxycycline (100 mg 1 to 2 times daily for 8 to 12 weeks)
 Tetracycline (250 to 500 mg twice daily for 8 to 12 weeks)
 Isotretinoin (0.25-0.3 mg/kg/day for 3 to 4 months)

 OCULAR INVOLVEMENT
 Subantimicrobial-dose doxycycline, modified-release (40 to 100 mg daily)

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PROCEDURES/INTERVENTIONS

 Erythema/telangiectasia
 Intense pulsed light therapy
 NdYAG laser
 pulsed dye laser 585 to 595 nm

 Phyma (non-inflamed)
 CO2 laser 10,600 nm
 Surgical resection
 Electrosurgery

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LATEST UPDATES

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 PERIORAL DERMATITIS
 Perioral dermatitis is a benign eruptions.

 Occurs most commonly in young females (20 to 45 years)

 Consisting of small inflammatory papules and pustules or pink, scaly patches around
the mouth.

 Although the perioral region is the most common area of distribution, this disease also
can affect the periocular and paranasal skin.
 For this reason, it is often referred to as periorificial dermatitis.

 Topical steroid use to the face can trigger this, and therefore, a primary
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recommendation for treatment would be discontinuation of steroid application by the
patient.
 PATHOPHYSIOLOGY
 DRUGS : topical steroids ( influence the microflora of the hair follicle and increased density of D.
Folliculorum)

 COSMETICS : fluorides , chewing gums, dental fillings, skin care ointments or creams with
petrolatum or paraffin base and vehicle isopropyl myristate
 Physical sunscreens act as causative agent in children

 PHYSICAL FACTORS : UV light ( Light sensitive seborrheid)

Heat and wind

 MICROBIAL FACTORS : fusiform spirilla bacteria , D.folliculorum , candida species.

 HORMONAL FACTORS : common in childbearing age group and premenstrual deterioration.

 IMPAIRED SKIN BARRIER and atopic diathesis

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 OTHER FACTORS : immunocompromised(leukemia), tobacco chewing, GIT disturbances ,

 CLINICAL PRESENTATION
 The classical presentation consists of discrete
and grouped erythematous papules,
papulovesicles and pustules.

 Present symmetrically
 Involving the perioral area with a distinct 5mm
clear zone at the vermilion edge.

 Background erythema and scaling may be

noted.

 Mild to moderate itching or burning is present

in most cases
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 MANAGEMENT :
TOPICAL TREATMENT:
 First-line treatment options are
- metronidazole cream or gel
- clindamycin lotion or gel
- erythromycin gel
- topical sulfur preparations
- azelaic acid gel
 Topical calcineurin inhibitors such as tacrolimus ointment/ pimecrolimus cream

 Topical adapalene

 Photodynamic therapy using 5-aminolevulinic acid as a photosensitizer

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 SYSTEMIC TREATMENT
 Tetracycline 250 to 500 mg twice a day, doxycycline 100 mg twice a day or once a
day, and minocycline 100 mg twice a day or once a day, for an 8-12 week tapering
course can be prescribed.

 When tetracycline antibiotics are contraindicated (children <8yr, nursing mothers, and
pregnant)
Erythromycin 250 mg to 500 mg daily can be substituted.

 The goal of oral antibiotic therapy is to provide rapid improvement, but topical
therapies should be used concurrently.

 In recalcitrant and severe cases, low-dose oral isotretinoin can be used, initially at 0.2
mg/kg per day, then tapering to 0.1 to 0.05 mg/kg per day. 90
 KEY TAKE HOME POINTS
 Do not use oral antibiotic monotherapy; combine oral antibiotic with a topical
non-antibiotic topical agent to treat acne.

 Use a step-wise approach when reviewing and treating patients with acne.

 Take note of any mental health issues caused by acne or scarring and refer to
psychiatrist if required.

 Because acne might be simple problem clinically, but malignant mentally.

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 REFERENCES

 Rook’s Textbook of Dermatology 9 th edition.

 Fitzpatrick's Dermatology, 9e Kang S, Amagai M, Bruckner AL, Enk AH, Margolis DJ, McMichael
AJ, Orringer JS. Kang S.

 Textbook of Dermatology 5th edition by Jean L. Bolognia, Julie V. Schaffer, Lorenzo Cerroni.

 IADVL Textbook of Dermatology 5th/2022 by S. Sacchidanand, Savitha A S, Shilpa K

 Dessinioti C, Katsambas A. Difficult and rare forms of acne. Clin Dermatol. 2017 Mar-
Apr;35(2):138-146.

 Sunita Keshari, Manish Kumar, Arun Balasubramaniam, Ting-Wei Chang, Yun Tong & Chun-Ming
Huang (2019) Prospects of acne vaccines targeting secreted virulence factors of Cutibacterium 92
acnes, Expert Review of Vaccines, 18:5, 433-437
Thankyou
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