Genesis of Acne

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Genesis of Acne

• Michael Q. Pugliese
• Circadia by Dr. Pugliese
• Reading, Pa

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What we will discuss in this lecture

• What is Acne?
• What causes Acne?
• How is Acne classified?
• What are some of the lasting effects?
• How can we treat it?
• What we should not do.
• Addressing some myths about Acne.

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What is Acne?

• Acne is the term used for a plugged pore, usually
  manifested in the form of a blackhead (open
  comedones), or whitehead (closed comedones).
• It is primarily an abnormality of the sebaceous
  follicle.

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Opening of hair shaft on to skin
Stratum corneum
Basal layer
Capillaries
Sebaceous gland
Hair bulb
Fat Tissue
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Open comedones (blackheads)
Open comedo
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Closed Comedones
Histological cross section of a closed comedo.
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Anatomy of the an Acne Lesion
Impacted follicle
Normal Skin
Infundibulum

• Comedo

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What causes acne?

• There are five main factors that play a part in
  the formation of Acne
• 1.Hormones
• 2.Excess sebum
• 3.Follicle fallout
• 4.Bacteria
• 5.Inflammation

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Factor 1 Hormones

• Most Acne sufferers experience the onset during
  puberty, when the body begins to produce hormones
  called androgens. These hormones cause the
  sebaceous glands to enlarge, a natural part of
  the bodys development. In acne sufferers,
  however, the sebaceous glands are over-stimulated
  by androgens, sometimes well into adulthood.
  Androgens are also responsible for acne flare-ups
  associated with the menstrual cycle, and
  occasionally, pregnancy.

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Factor 2 Excess Sebum

• When the sebaceous gland is stimulated by
  androgens, excess sebum is produced. In its
  journey up the follicle, the sebum mixes with
  skin bacteria and dead cells that have been shed
  from the lining of the follicle. While this
  process is normal, the presence of extra sebum
  increases the chance of clogging and can cause
  acne.

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Factor 3 Follicle Fallout

• Normally, dead cells within the follicle shed
  gradually and are expelled onto the skins
  surface. In patients with overactive sebaceous
  glands--and nearly everyone during pubertythese
  cells are shed more rapidly. Mixed with a surplus
  of sebum, the dead skin cells form a plug in the
  follicle, preventing the skin from finishing its
  natural process of renewal.

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Factor 4 Bacteria

• The bacterium Propionibacterium acnes (P. acnes)
  is a regular resident of all skin types, and is
  part of the skins natural sebum maintenance
  system. Once a follicle is plugged, however,
  P.acnes bacteria multiply rapidly, creating
  inflammation in the follicle and surrounding
  skin.

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Factor 5 Inflammation

• When the body encounters unwanted bacteria, white
  blood cells are sent to attack the intruders.
  This is called the inflammatory response, or
  chemotaxis. This is what causes pimples to get
  red, swollen and painful. This response is
  different for everyone, but can be especially
  strong in adult women.

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Anatomy of the an Acne Lesion
Impacted follicle
Normal Skin
Infundibulum

• Comedo

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Who gets Acne?

• 80 of young teenagers, adolescents and young
  adults ages 11-30 experience some degree of acne.
• Some adults report breakouts into their 40s and
  50s.
• Guarantees a large pool of potential customers.

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How do we classify Acne?

• Dermatologists generally classify acne into four
  grades
• Grade I Blackheads and milia
• Grade II Papules and pustules
• Grade III Nodules
• Grade IV Cysts

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Acne Grade I

• The mildest form of acne. There may be one or
  two minor, small pimples. Blackheads and milia
  may be found but no inflammation.
• Grade I acne is commonly seen in early
  adolescence, especially on the nose and forehead.
  Adults also experience Grade I acne as blackheads
  on the nose and forehead. Milia are found in the
  eye area, and on the chin.

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Acne Grade II

• Considered Moderate acne. Greater numbers of
  blackheads and milia. More papules appear along
  with the formation of pustules.
• General breakout activity is more obvious. Slight
  inflammation is now apparent. In teens, acne
  progresses to chest and shoulders. Adult women
  see breakouts on cheeks and jawline.

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Acne Grade III

• Considered Severe acne, with the main difference
  being the presence of increased and obvious
  inflammation. Papules and pustules increase and
  nodules will be present.
• Grade III involves other areas of the body as
  well as the face, and chance of scarring from the
  spread of infection is higher.

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Acne Grade IV

• The most serious form of acne, often referred to
  as cystic acne. The skin displays numerous
  papules, pustules and nodules, and is very
  painful. The back, shoulders, chest and neck are
  usually affected. Infection is deep and nearly
  all cystic acne sufferers will develop scarring.
  Usually requires systemic medication in addition
  to topical treatments.

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Cystic Acne Grade 4
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So How Do We Treat Acne?

• Benzoyl peroxide
• Salycylic acid (and other AHA and BHAs)
• Retinoids (Vitamin A)
• Anti-inflammitory Agents
• Oral antibiotics

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Benzoyl Peroxide

• One of the most proven substances used to combat
  acne.
• It is used in a concentration anywhere for 2-10
• Potent antibacterial agent effective at
  controling P. Acnes.
• May cause erythema and flaking.

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Salicylic Acid

• Has anti-inflammatory and comedolytic effects
• Used mainly at 2 concentrations in cleansers,
  creams, and lotions.
• Higher percentages (10-30) are used in
  proffessional chemical peels

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Retinoids (Vitamin A)

• Strong comedolytic agent
• Retinol mainly prescribed by non physician
  skincare professionals.
• Retin-A or retinoic acid must be prescribed by a
  physician
• Studies show it also helps to normalize
  follicular desquamation.
• Accutane- contriversial oral form

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Oral antibiotics

• Tetracycline
• Doxycycline
• Erythromycin

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What to Avoid

• Excessive washing
• Comedogenic agents
• Squeezing or poping
• Tanning beds or sun exposure

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ACNE MYTHS

• FOR GENERATIONS, acne sufferers have been plagued
  by the ignorance --and therefore the judgment--
  of a handful of unfounded myths which, even in
  our enlightened world, endure to this day.
• EDUCATION IS, AS ALWAYS, THE SOLUTION.

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ACNE MYTH 1

• Acne is caused by poor hygiene.
• This myth led previous generations to vigorously
  scrub with harsh or abrasive cleansers, and thus
  irritate and worsen the condition. We now know
  that acne is not caused by dirt or surface oils,
  and must be treated gently.

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ACNE MYTH 2

• Acne is caused by a poor diet.
• No scientific study has found a relationship
  between foods and the onset or worsening of acne.
  
• Eating a balanced diet with adequate nutritional
  supplements is always a good idea, in any case.

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ACNE MYTH 3

• Acne is caused by stress.
• Not true. The day- to- day stress of living does
  not directly influence acne.
• Some medications used to treat severe depression
  may cause acne as a side effect.

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ACNE MYTH 4

• Acne is just a cosmetic problem.
• Hardly. Although systemic infection from acne is
  not a serious threat, permanent physical scarring
  is likely without treatment.
• Active acne and its scars can cause social and
  emotional distress to a degree that impacts the
  well-being and health of the individual over a
  lifetime.

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MYTH 5

• Acne will just run its course.
• The truth is, acne can be cleared by a qualified
  practitioner, the right products, and a
  cooperative client willing to participate in her
  own ongoing program of skin health and wellness.

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Traditional Concepts

• The pathogenesis involves four processes.
• 1. Abnormal follicular keratinization.
• 2. Overproduction of sebum.
• 3.Proliferation of P. acnes.
• 4. Inflammation.

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Current Concepts of the Genesis of Acne
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Abnormal follicular keratinization

• The earliest physical change seen in acne is that
  which occurs in the horny cells lining the
  sebaceous follicle. A disturbance in the
  differentiation of these cells leads to abnormal
  shedding of the cells. Either decreased shedding
  and excess shedding and subsequent Impaction of
  the follicle occurs as these horny cells stick
  together.

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Overproduction of sebum.

• The sebaceous gland responses to hormonal
  stimulation by androgens. Hypertrophy of the
  sebaceous gland occurs with increased production
  of sebum. This increase in sebum is blocked by
  the follicular keratosis sebum content increases
  in the follicle.

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Proliferation of P. acnes.

• The retention of sebum in the follicle provides
  ideal conditions for the proliferation of P.
  acnes, which is an anaerobic diphteroid, a normal
  part of the microflora of the sebaceous follicle.
  P. acnes is able to break down sebum
  triglycerides by converting them to free fatty
  acids. It is believed that the acids irritate the
  follicular wall causing inflammation.

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Inflammation.

• Dumping of sebum into the dermal layer of the
  skin occurs with the rupture of the pilosebaceous
  follicle. This results in an inflammatory process
  that produces lesions such as pustules and cysts.
  P. acnes produces materials which increase the
  permeability of the follicular epithelium, as
  well as chemotactic factors that attract
  inflammatory cells to the area.
• Chemotactic means chemicals that are able to
  attract cells to a certain area.

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The New Concept of the Pathogenesis of Acne
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The Keratinocyte

• The key cellular components of the
  pathophysiologic processes of the skin are the
  keratinocytes.
• These cells are in a unique position between the
  interface of the environment and the skin.

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Cytokine Secretion

• By the secretion of soluble factors such as
  cytokines and antimicrobial peptides,
  keratinocytes are able to maintain the immune
  response of the skin.

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Introduction to Toll-Like Receptors

• Acne lesions, Toll-like receptors
  (TLR)2-expressing macrophages, surround the
  pilosebaceous follicles and that P. acnes induced
  cytokine production of monocytes via TLR2.

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First, look at the macrophage.
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Second, look at the antigens
Antigens are the bacteria, or parts of the
bacteria.
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Third, look at the Toll Receptor
Toll rcp activates IL-12 and CDs 28 and
80-86 along with MHCII. Result T cell is
activated.
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Fourth, Interleukens (cytokines) are produced.
Interferons (IFNs) are natural proteins produced
by the cells of the immune system of most
vertebrates in response to challenges by foreign
agents such as viruses, bacteria, parasites and
tumor cells. Interferons are cytokines
IL-4 involved in proliferation of B cells and the
development of T cells and mast cells. IL-5 role
in differentiation of B cells 1L-10 inhibits Th1
cytokine production
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Fifth, Inflammation is the net result.

• Remember this cascade
• Bacteria sensed by Toll receptors
• Toll receptors activate naïve T-Cell
• T-Cell is activated activates Helper Ts
• TH1 produces interferon gamma
• TH2 produces interleukens
• Inflammation results.