P-Acne Bacteria & Acne Biofilms

In my last post we talked about retention hyperkeratosis being the cause for acne. Read here: Retention Hyperkeratosis 

 P-Acnes Bacteria

For the longest time it was believed that the Propionibacterium acnes (p-acnes bacteria) were the cause of acne. We know now that these bacteria exist in the pores of every human being, and do not dwell in greater numbers in acne-prone people. P- acne bacteria are anaerobic bacteria, which means they thrive without the presence of oxygen. So when the follicle swells and dead skin cells cover the opening of the follicle, the bacteria start to party.  The party starts by  the bacteria feeding off of triglycerides produced by our sebaceous glands.  They then excrete an enzyme called lipase to split the oil into fatty acids and glycerol.  They devour the glycerol portion, the part that they like, and discard the fatty acid byproducts.  The problem with the bacterial action is that the fatty acids, which the bacteria create and then discard as garbage, are quite irritating to the pores and aggravate acne.

These digestive enzymes also destabilize the layers of cells that form the wall of the follicle. The cellular damage, metabolic by-products, and bacterial debris produced by the rapid growth of p.acnes trigger inflammation.  When these digestive enzymes spiral out of control for too long, they destroy the follicle so much that it breaks, and leaks out infection into the other areas of the skin.  This is shown by the presence of cysts and nodules.  

There Are Two Forms of P-Acnes Bacteria

1) Gram-Positive Bacteria
2) Gram-Negative Bactera

The damage caused by P-acnes and the associated inflammation make the affected tissue more susceptible to colonization by opportunistic bacteria such as Staphylococcus Aureus.
Research shows that only healthy pores are colonized by P-acnes, while unhealthy ones universally include the nonpore-resistant Staphylococcus Epidermidis.

There are types of acne caused by gram negative bacteria.  Gram negative bacteria have the potential to secrete toxic byproducts which can cause intense inflammation and infection. Gram negative folliculitis is a bacterial infection present in pustules, cysts, and nodules. Unfortunately, gram-negative bacteria are resistant to most antibiotics. If you take antibiotics for too long, it causes bacterial interference.  The gram positive bacteria that proliferates in your nasal cavities and mucous membranes can turn into gram negative bacteria.

Tea tree oil only kills gram positive bacteria.  Mandelic acid kills gram negative bacteria along with licorice root, black cumin oil, and manuka oil.  Mangolia extract and mandelic acid kill both p acnes bacteria.

Symptomes & Appearance of Gram- Negative Folliculitis

 Sudden increase in the number and severity of acne lesions despite antibacterial treatment.  Sufferers who previously had whiteheads and blackheads will start developing numerous cysts, pustules, and nodules.  They will develop large clusters of nodules, cystic lesions that burrow and interconnect. Skin appears red, inflamed, irregular, and painful to touch.

Acne Biofilm

Part of the reason why cells stick together in the follicle is due to p-acne biofilm. Biofilms produce irritant fatty acids that promote inflammation and enhance p.acnes adhesion to the sebaceous follicle.

P- acne bacteria reside in the pilosebaceous unit in a biofilm, which means they live in a community that encases itself in an extra cellular lining to survive. Research is showing that the biofilm may explain the development of retention hyperkeratosis as they cause the keratinocytes to be very sticky. It may also explain the immunogenicity of the organism as well as the clinical course of the disease.  The biofilm is a new discovery.  We are not sure if it has always been there or is something that happened to resist antibiotics and other treatments. 

What Causes Retention Hyperkeratosis ?

In my last post we talked about What Is Acne
This is where I discussed that acne was a inflammatory skin disease and not a skin condition.

What Happens Differently In Acne

As I have discussed Retention hyperkeratosis is at the very heart and soul of acne, and it is the process you must interfere with in order to outfox the disease. The stratum corneum sloughs off a layer of cells each day very easily, but not very well inside the pore.  The dead cells begin to stick together and form a mass (impaction) down inside the follicle. The chemical compisition of our sebum is not sticky, the sticky part is the dead skin cells in the follicle brought on by Acne Bio-Film (we will get to that in the next article).  So acne is the renention of dead skin cells and the mad proliferation of additional cells to make matters worse in the pores of acne-susceptible families.

What Cause Retention Hyperkeratosis?

There are lamellar granules present in the the skin which produce an enzyme to break down the ‘glue’ between skin cells in order for them to be sloughed off in a normal manner.  This leads to congestion in the follicles.  There are many of these granules down in a healthy pore where the layer is normal and thin, but if you look onto an acne-affected follicle with it's thicker layer, there are few granules.

A popular misconception about acne is that the oil hardens and plugs up the pore opening.  This in not true. The oil plays only a minor part in the acne impaction. It is the retained cells, not sebum, that produces the mass itself. In fact, as the lesion develops, the sebaceous glands become smaller, and whatever oil they continue to produce is not actually trapped. Studies show that a clear channel is always maintained between the sebaceous gland and the surface. The channel appears to be kept open by protein- digestive enzymes that gradually digest the dead skin cells in the center of a lesion.  This explains why an acne impaction often reaches a certain size then appears to stop growing. Even though more cells are rapidly being produced by the follicular wall, the lesion does not enlarge because the cells next to the bacteria on the inside are being digested about as rapidly as new cells are being dumped into the impaction. This happens in the mildest form of acne Grade 1.  The white heads and blackheads reach a certain size but do not burst into inflamed acne.

Stay tuned for my next post where we will talk about P-acne bacteria and Acne Bio Film

What Is Acne?

My quest to understand acne started with questioning extraction procedures.  My Journey
But then quickly changed to what actually goes on in the body when a person suffers from acne?
What are the bacteria cells doing?
What chemical breakdowns are happening?
What is the chain reaction of events?

We were are all taught in school

Acne is caused by dead skin cell accumulation in the follicle (hyperkeratinization) mixed with p- acne bacteria and sebum, combined with a lack of oxygen.  This creates a pimple. Simply put, that is true, but there is much more that goes on. This is not for the client that has breakouts here and there during menstruation.  This research is for clients that suffer from chronic acne.

ACNE IS A DISEASE

Acne is not a skin condition, but rather an inflammatory skin disease. Acne is a disease just like any other genetic disease.  Take diabetes, for instance.  As yet, there is no known cure for diabetes.  There is insulin that helps control it, but no known cure. Acne is not as serious as diabetes, but the comparison is important. Acne also knows no cure.  We have treatments and products that keep it under control, but no known cure.

SO WHAT GOES WRONG? The chain of events that lead to acne.

1) At puberty the body starts producing testosterone
2) An enzyme in the skin changes testosterone to dihydrotestosterone
3) Dihydrotestosterone stimulates the sebaceous glands to begin producing sebum
4) In the acne-defective follicle, sebum sets off retention hyperkeratosis (acne).

The first three processes occur in everyone.  We all begin producing hormones at puberty.  Everyone's pores begin to flow with sebum in adolescence.  But it is only in the individuals with a special vulnerability to the fourth that a reaction occurs- retention hyperkeratosis, which produces the acne explosion.

HORMONES THEMSELVES DO NOT CAUSE ACNE! 

"Acne sufferers do not necessarily produce more testosterone.  Hormones merely trigger the process in genetically acne-prone skin.  Oily skin does not cause acne. True, most acne sufferers do have oily skin, but you can possess very oily skin and still never sprout a pimple.  Oily skin is just the triggering component, once again affecting only those with the genetic defect. In those individuals, sebum provides the match that ignites the acne fire."  Dr Fulton: Acne RX

Genetic Connection

Acne is often inherited as a dominant characteristic, which means that if both parents had acne approximately three out of four offspring will develop acne.  If one parent had acne, one or two offspring out of four will develop it. In addition to genetics, cultural and environmental factors could affect the entire population.

Stay tuned for my next article.  An inside look at the chemical reactions, and breakdowns that cause acne.