Acne Types and Pathogenesis.

Acne - Types and
Pathogenesis
INTRODUCTION ABOUT ACNE
Acne is a chronic inflammatory skin disease that

is the most common skin disorder
Potential outcomes include

physical scars,
persistent hyperpigmentation
psychological sequelae
Titus and Hodge J. Am Fam Physician. 2012;86:734–740.
Content developed by Magna Health Solutions for Abbott Healthcare Private Limited. © 2016 Abbott. All rights reserved. 16P91-049F
INTRODUCTION ABOUT ACNE
• One of the most common skin diseases presenting to

family physicians
• Considerable psychological impact on the quality of life
• No cure, but the disease can be controlled through

medications
Leyden JJ. New understandings of the pathogenesis of acne J Am Acad Dermatol 1995;32:S15-25
ACNE VULGARIS
A cutaneous pleomorphic disorder of the pilo sebaceous unit
Non-inflammatory Inflammatory
(comedones, open and (papules, pustules and

closed) nodules)
Propionibacterium acnes and Staphylococcus epidermidis

are common pus-forming microbes responsible for the
development of various forms of acne vulgaris
Ray, et al. Int J Res Pharmaceut Biosci. 2013;3: 1-16.
SEBACEOUS GLANDS
• Distributed most densely on face, chest, back, upper

arms.
• Positioned around the infundibulum (main tube) of the
pore, each having a single duct communicating with it.
• Secrete sebum (oil) into the duct. Sebum is rich in
triglycerides.
• Highly sensitive to hormonal stimulation by androgens.
• Circulating testosterone reaches the skin, where it is
changed into dihydrotestosterone (DHT.)
• DHT acts on the sebaceous glands causing increase in
size and oil production.
OTHER STRUCTURES IN THE PILOSEBACEOUS
UNIT
• Apocrine sweat glands – have a duct communicating
with infundibulum of PS unit which secretes apocrine
sweat (clear sweat mixed with cytoplasmic components
of the gland which add odor, pheromones, etc.)
• Eccrine sweat glands – positioned alongside the PS unit
in the skin, but has its own vertically-oriented duct
communicating directly with the skin surface. As you
might expect, they secrete eccrine (clear) sweat.
• Arrector pili muscle – tiny muscle connecting
infundibulum with skin surface. Cause of “goose bumps”
COMEDONAL ACNE (NON-INFLAMMATORY)
Closed
comedones
(white heads)
Open comedones
(Black heads)
Mancini AJ. Adv Stud Med. 2008;8:100–105.
INFLAMMATORY ACNE
Papules Pustules
Nodules
Mancini. Adv Stud Med. 2008;8:100–105.
EPIDEMIOLOGY
Most commonly presents between ages of 12-24,

which estimates an 85% of population affected 1
In India, 50.6% of boys and 38.13% of girls in the age group 12-17
yeas are having acne.
It is believed that there are no gender differences in

acne prevalence, although such differences are often
reported
In clinics in the urban areas, there is a clear

preponderance of girls seeking treatment2
Ray et al. Int J Res Pharmaceut Biosci. 2013;3: 1-16

Kubba et al. Ind J Derma Venerol Lepro. 2009; 75:52-53.
STAGES OF ACNE
 Comedonal (non-inflammatory) – mild
 Papular (inflammatory) – mild-to-moderate
 Pustular (inflammatory) – moderate
 Nodulocystic – severe
Ray et al. Int J Res Pharmaceut Biosci. 2013;3: 1-16
STAGES OF DEVELOPMENT
STAGES OF ACNE
Acne vulgaris. http://www.dermnetnz.org/acne/acne-vulgaris.html. Accessed on 8.1.2016
PATHOGENESIS
• A disease of the pilosebaceous unit

• Anatomy of this structure is key to full understanding of
the disease.
• Each PS unit built around a long, narrow tube (a.k.a. –
“pore”) vertically oriented in the skin, which houses a
single hair follicle.
• Epithelial lining at entrance of pore is stratum corneum,
prone to over keratinization (“clogging”) if the right
etiological factors are present.
• Sebaceous gland activity is the biggest player in
instigating the disease.
PILOSEBACEOUS UNIT WITH APOCRINE AND
ECCRINE SWEAT GLANDS
Available at www.dermattext.com..Accessed on 25/5/2016.
FOUR MAIN FACTORS LEAD TO THE FORMATION
OF ACNE LESIONS:
1. Increased sebum production
2. Hyperkeratinization
All forms of acne involve 3. Colonization of the follicle by the
one or more of these anaerobe Propionibacterium
pathophysiologic factors acnes
4. An inflammatory reaction1,2
1. Titus and Hodge. J Am Fam Physician. 2012;86:734-740.

2. Ray, et al. Int J Res Pharmaceut Biosci. 2013;3: 1-16.
PATHOGENESIS OF ACNE STARTS WITH
FORMATION OF MICROCOMEDOS
• In predisposed individuals, starts with increased sebum
production from sebaceous glands and overgrowth of
keratin-producing cells lining the pore walls. Excess
keratinization leads to the formation of a sticky plug
which blocks the superficial aspect of the pore.
• This is a microcomedo – the precursor lesion to acne.
• At this stage the sebaceous glands are still producing

sebum, which is now unable to drain out to the skin
surface, causing the formation of a comedo.
PATHOGENESIS OF ACNE
Elsevier ebooks. Available at www.dermtext.com..Accessed on 25/5/2016.
A COMEDO IS THE BASIC LESION OF ACNE
VULGARIS. IT HAS TWO SUBTYPES:
• Open comedone – a “blackhead.” Forms when the pore
wall is able to dilate in response to the increased pressure
created by the trapped sebum, creating a non-inflamed
lesion.
• Closed comedone – a “whitehead.” A semi-firm, white,

dome-shaped papule, which is also non-inflamed. Forms
when trapped sebum pushes up against the non-dilated
opening of the pore.
• All the acne you see starts with one or both of these
lesions.
PATHOGENESIS OF ACNE – WHAT HAPPENS NEXT?
INFLAMMATION AND BACTERIAL OVERGROWTH
• Propionibacterium Acnes: Anaerobic bacteria which is
normal flora within PS unit. Has ability to digest sebum.
• Large plug of sebum stimulates p. acnes to produce lipase,

which breaks down (hydrolyzes) the triglycerides in the sebum
to free fatty acids.
• Free fatty acids highly irritating to PS unit and surrounding

tissues, causing inflammation and further comedo formation.
• Neutrophils are attracted to inflamed site, attach to follicular
wall, and release hydrolases which further weaken it. Wall
eventually ruptures, spilling out highly irritating FFA’s into
surrounding tissue.
PILOSEBACEOUS UNIT: RESIDENT MICROFLORA
WHAT HAPPENS AFTER COMEDOGENESIS
• Pustule formation – Inflamed comedo starts to fill

with purulent material which pools at the surface.
• Papule formation – Inflamed comedo enlarges into a
red papule without pooling of purulent material at top.
• Nodule formation – Follicular walls of
papules/pustules rupture and spill inflamed contents
into surrounding tissue. Lesion increases in size and
becomes a nodule (>5mm diameter.) At this point level
of skin involvement creates risk for later scarring.
Nodules can become hemorrhagic, secondarily infected,
or form communications between multiple draining
lesions (sinus tracks.)
PATHOGENESIS OF ACNE
INITIAL PATHOGENESIS (REASON UNKNOWN):
follicular hyper keratinization
proliferation +
decreased desquamation of keratinocytes
hyperkeratotic plug
(micro comedone)
PATHOGENESIS
Sebaceous glands enlarge
Sebum production increases
Growth medium for P. Acnes
plugs provide anaerobic

Lipid-rich environment
PATHOGENESIS
Bacteria thrive
Inflammation results
Chemotactic factors attract neutrophils
Depending on conditions
Non-inflammatory Inflammatory papule/

open/closed comedones pustule/nodule
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• The scientific content of this publication has been developed and designed by Magna Health
Solutions -India for educational purpose through monetary assistance of Abbott Healthcare
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based on their own clinical judgment. The content herein has been developed by clinicians
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Acne - Types and

Acne is a chronic inflammatory skin disease that

Potential outcomes include

Titus and Hodge J. Am Fam Physician. 2012;86:734–740.

• One of the most common skin diseases presenting to

• Considerable psychological impact on the quality of life

• No cure, but the disease can be controlled through

A cutaneous pleomorphic disorder of the pilo sebaceous unit

(comedones, open and (papules, pustules and

Propionibacterium acnes and Staphylococcus epidermidis

• Distributed most densely on face, chest, back, upper

Mancini AJ. Adv Stud Med. 2008;8:100–105.

Mancini. Adv Stud Med. 2008;8:100–105.

Most commonly presents between ages of 12-24,

It is believed that there are no gender differences in

In clinics in the urban areas, there is a clear

Ray et al. Int J Res Pharmaceut Biosci. 2013;3: 1-16

 Comedonal (non-inflammatory) – mild

 Papular (inflammatory) – mild-to-moderate

 Pustular (inflammatory) – moderate

Ray et al. Int J Res Pharmaceut Biosci. 2013;3: 1-16

Acne vulgaris. http://www.dermnetnz.org/acne/acne-vulgaris.html. Accessed on 8.1.2016

• A disease of the pilosebaceous unit

Available at www.dermattext.com..Accessed on 25/5/2016.

1. Titus and Hodge. J Am Fam Physician. 2012;86:734-740.

• This is a microcomedo – the precursor lesion to acne.

• At this stage the sebaceous glands are still producing

Elsevier ebooks. Available at www.dermtext.com..Accessed on 25/5/2016.

• Closed comedone – a “whitehead.” A semi-firm, white,

• Large plug of sebum stimulates p. acnes to produce lipase,

• Free fatty acids highly irritating to PS unit and surrounding

Elsevier ebooks. Available at www.dermtext.com..Accessed on 25/5/2016.

• Pustule formation – Inflamed comedo starts to fill

Elsevier ebooks. Available at www.dermtext.com..Accessed on 25/5/2016.

follicular hyper keratinization

Sebaceous glands enlarge

Sebum production increases

Growth medium for P. Acnes

plugs provide anaerobic

Chemotactic factors attract neutrophils

Non-inflammatory Inflammatory papule/

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