When individuals hear the term acne, they generally visualize a condition that involves obviously noticeable lesions. In reality, acne is the name given to a complex process that may virtually be invisible in some individuals, or cause extreme gross disfigurement in others. Acne flourishes particularly in adolescence and almost no one endures their teenage years without a few lesions. In fact, medical studies show that there is an almost 100% incidence of acne and only the level of severity differs from person to person. Acne, especially in females, may persist well beyond the teen age years. Additionally, many women who were nearly acne free as adolescents find that they are plagued by the disease in their 20's, 30's and beyond.
Currently, there is no single known cause for acne. However, a number of factors may be present during the course of the disease. Such as:
1. Heredity. While it may be true that nearly everyone suffers from some form of acne, the more severe manifestations of the disease are believed to be strongly influenced by heredity. As an example, heredity is an important factor in determining the size and activity of sebaceous glands. Even though acne may skip certain family mem bers or even pass an entire generation, the presence of the disease is believed to be genetically based.
2. An increase in sebum (oil) production. Sebum is a critical factor in the develop ment of the disease of acne. Sebum production increases significantly at the on set of adolescence due to higher levels of hormones, and in particular androgens. While androgens are present in both females and males, they are primarily associated with the so-called "male" hormones.
The production of sebum itself may not be as important as the fact that sebum is "fed on" by Propionibacterium Acnes (P acne bacteria). The P acne bacteria then excretes certain highly inflammatory by-products which add to the process.
3. Bacteria. It is the Propionibacterium (P acne bacteria) that produce toxic sub stances that attack the follicle and eventually incite the follicle to rupture. For a long time, the medical profession considered acne to be a bacterial infection. This seemed like a logical conclusion since many of the features of acne (redness and tenderness) were in keeping with other infectious conditions. Not only that, antibiotics have generally proven to be beneficial in the control of the disease. However, physicians now know that bacteria only plays a role in the acne process. In fact, research studies in which P acne bacteria were injected directly into the dermis failed to induce acne. Further, colonies of P acne bacteria may exist in equal amounts in the follicles of individuals with or without acne. It appears that the presence of other factors such as increased sebum, hormonal changes, follicular retention, and inherited follicular characteristics, all contribute to the bacteria's ability to produce the by-products that accelerate and aggravate the disease.
4. Hormones. Acne, in and of itself, is not a hormonal disorder; normal hormone lev els need to be present for acne to occur. For example, acne does not occur in men who are castrated prior to the onset of puberty. In addition, individuals who have severe acne have normal hormonal levels in the same range as those who do not manifest acne. The rare exception is in people who have developed a specific abnormal hormonal condition in which acne may be one of a number of symptoms. More correctly, the individuals who are predisposed to develop acne have follicles with characteristics that make the follicle far more reactive to various otherwise normal hormonal changes.
5. Retention Hyperkeratosis. Simply stated, retention hyperkeratosis refers to the abnormal build-up and retention of cells in the follicles of individuals who are prone to acne. Microscopic cells line the inside of the follicles. As these cells are shed, they are normally pushed to the sur face by the various cellular secretions. It appears that individuals who develop more aggressive forms of acne may have a genetic "defect" that causes the intercellular ce ment to change in some manner. This results in a sort of nondegradable "glue" that causes the cells to stick together tightly, like bricks that form a solid mass. As the acne process continues, the mass expands to form a follicular blockage. It is also speculated that in these individuals, certain enzymes fail to be secreted into the inter cellular spaces in order to weaken the cement and assist in allowing the cells to come apart. In any case, this factor per haps more than any other sets the stage for conditions that enable other aspects of the disease to flourish. For example, P acne bacteria is known as anaerobic bacteria, meaning it cannot survive well when ex posed to oxygen. The blocking of the follicle is then a contributing factor in at least two essential components of the acne process. First, the anaerobic P acne bac teria has the perfect oxygen free environment. Secondly, oil that is now "trapped" in the follicle is fed on by the P acne bacteria, which then begins excret ing the by-products that play a primary role in the inflammatory process. If the abnormal cellular buildup did not occur, it is likely that much of the acne process could be diffused.
THE ACNE PROCESS
Anatomy of a Follicle
The layer of skin that we spend most of our time focusing on is the outer dead layer called the stratum corneum. The stratum corneum, or surface of the skin, (on the face, back, chest, and upper arms) is covered with pilosebaceous follicles. While there are other types of follicles over these areas, acne is strictly confined to hair follicles. There are three types of hair follicles that occur on the face: vellus, sebaceous and terminal. Acne only takes place in the sebaceous follicles. Sebaceous follicles are the largest and most numerous on the face, which is why acne is mostly evident in the facial region although severe cases of the disease can also be present on the back.
Sebaceous follicles have unique aspects that make them the appropriate target for the acne process. Such as:
- The oil glands in these follicles are extremely large
- The structure of the follicle is deep and cavernous
- Large masses of horny keratinized cells occupy the follicle
HOW ACNE LESIONS OCCUR
If we were to construct a flow chart detail ing the course of the acne process from onset to the appearance of a visible lesion, it would unfold something like this.
Stage one: Abnormal Keratinization The sebaceous follicle is a long hollow tube not much wider than the diameter of a hair. (Fig. 1)

The inside of the follicle is lined with microscopic dead cells very similar to those cells on the stratum corneum. Also, like the stratum corneum, these cells are constantly shedding. Normally, the cells shedding in the follicle are "flushed" to the surface via various lipid substances excreted in the follicle. In those individuals who are prone to developing acne, a pecu liar change occurs in the manner and pattern in which the dead cells line the fol licle. For example, the cells being produced are thicker and sturdier and thus more resistant to the normal "flushing" process of the follicle. Secondly, the cells begin to stick together forming a "kernel" of dead cells. This microscopic kernel is referred to as a microcomedone. The development of this abnormal cellular ad hesion is a key factor that enables the acne process to move forward. It also appears that the normal intercellular cement that we all produce, changes in some fashion and evolves into a glue that is nearly im possible to breakdown. As the cells stick together, they compact tightly like bricks and form a solid mass that steadily contin ues to expand into a formidable blockade within the follicle.
Stage Two: Sebum and Bacteria
The blockage, formed by the tightly com pacted cells, traps oil in the follicle. The bacteria involved in the acne process is called Propionibacterium Acnes or P acne bacteria. This bacteria thrives in conditions where oxygen is not present, such as a blocked follicular canal. The P acne bac teria feeds on the trapped oil and excretes various by-products and in particular certain highly inflammatory, toxic and corrosive fatty acids.
Stage Three: Expansion and Rupture of the Follicle
The average time for a microcomedone to mature is five months. (Fig. 2)

However, this maturation process can oc cur far more rapidly or much more slowly. Additionally, microcomedones can exist in a dormant state for long periods and then become active due to stress, hormonal fluc tuations or other variables.
As the acne process unfolds, the micro comedone can progress in one of two directions:
1) Non inflammatory lesions such as an open comedone (blackhead)
2) Inflammatory lesions such as papules, pustules, nodules and cysts
The process of the microcomedone into one direction or the other may be determined by where the blockage is located in the follicle.
Non-inflammatory Lesions:
Most acne lesions begin as what is referred to as a closed comedone. Closed comed ones may be invisible to the naked eye or they may resemble a small firm whitish bump under the skin. Closed comedones are the result of impacted material in the follicle that distends up toward the follicle opening. If the follicle opening dilates to accommodate the growing mass, then an open comedone occurs or what is com monly called a blackhead. It was once believed that the blackened appearance of the opening was caused by oil oxidizing. However, the color is actually melanin (pig ment) that is contained in the follicle matter. In general, when blackheads are squeezed, only the contents in the opening are elimi nated. Follicular matter then pushes forward and reappears in as soon as a few hours. This is why, for the most part, astringents, masks, scrubs, extractions, etc. only have very tem porary effects and do nothing to actually interrupt the acne process.
Inflammatory Lesions:
Inflammatory lesions also originate from a closed comedone. It is not entirely under stood why some closed comedones mature into blackheads and others progress into pustules, nodules and cysts. One reliable theory is that individuals who tend toward more severe forms of acne have follicle walls that are weaker and more likely to be affected by the toxic by-products in the follicle. Also, the position of the blockage in the follicle may play a role. Ultimately, inflammatory lesions are the result of the expansion of the follicle in order to accom modate the growing accumulation of dead cells, bacteria, oil and toxic fatty acid by products. As the follicles begin to bulge, they are often deservedly referred to as "time bombs" because this stage of devel opment is unpredictable. The corrosive toxic by-products can cause the follicle wall to rupture, releasing the contents of the follicle into the surrounding tissue. This in turn creates an inflammatory response that results in the actual lesion. Unpredictability is a factor because the fol licle can remain distended for extended periods of time. Or, the influence of stress, hormones and other aggravators can trig ger a more reactive state resulting in one or many lesions. Periods when the skin appears less involved and "calmer" can be deceiving. It is this "up and down" nature of the disease that is frustrating as well as psychologically damaging.
The severity of an inflammatory lesion usually depends on where the rupture occurs in the follicular wall. Ruptures or "blowouts" that are closer to the opening of the follicle produce less severe lesions than those that occur lower in the follicle.
Common Inflammatory Acne Lesions
In Order of Severity:
Papules: Ruptures occurring at the top of the follicle, just under the epidermis, pro duce a small solid red bump. (Fig. 3) Because the rupture is not very deep, these lesions usually clear rapidly.

Pustules: Pustules may start out as pap ules that then liquefy. As with papules, the rupture in the follicle wall is close to the top of the follicle. (Fig. 4) As a result, the lesion is usually not serious and generally heals without a scar.

Nodules: Nodules may appear as fairly large subsurface lesions that can initially be painful to the touch. Unlike papules and pustules, the follicle ruptures at a lower point which means that the inflammation is deeper and involves more tissue. (Fig. 5) In addition, the rupture in the fol licle wall is more like an explosion that causes so much toxic material to flow from the rupture that often nearby follicles are engulfed and become part of the inflam matory process. Nodules may take a considerable amount of time to resolve. (fig.5)

Cysts: Cysts and nodules are very similar. Technically, a cyst is a hollow cavity that is encapsulated by a shell like structure. Be cause of this shell like lining, cysts are unlikely to resolve without serious inter vention. Usually cysts slowly enlarge over time. As the cyst stretches, the wall be comes thinner and weaker and is extremely vulnerable to rupturing by most any trauma. When cysts rupture, they cause tremendous inflammation and because the inflammatory reaction is so deep and wide spread, the resulting destruction of underlying tissue will invariably leave a scar.
NON-PRESCRIPTION PRODUCT RECOMMENDATIONS
Benzoyl Peroxide:
Benzoyl peroxide is considered one of the most powerful antibacterial agents ever iden tified and is endorsed by the American Academy of Dermatology. Because of its abil ity to rapidly destroy P acne bacteria as well as yeast and other organisms, benzoyl perox ide is an important acne therapy.
Benzoyl peroxide's action takes place as the benzoyl forces peroxide into the follicle where it is released in the form of oxygen. Since P acne bacteria does not survive in oxygen, rapid depopulation takes place and, as a result, the toxic fatty acid by products also swiftly diminish. Unlike oral
or possibly topical antibiotics, the bacteria does not develop a resistance to benzoyl peroxide even after many continuous years of use.
Extensive medical studies have also dem onstrated that benzoyl peroxide is extremely safe.
Glycolic Acid:
In recent years glycolic acid has achieved significant medical respect as a tool to as sist in clearing acne. Studies indicate that glycolic acid appears to help in breaking down the "glue-like substance" in the fol licle that contributes to the formation of follicular blockage. This action is believed to then assist in clearing the follicle. In ad dition, research shows that glycolic acid acts as a delivery agent and may greatly enhance the effect of other topical medications. Other benefits include a reduction in the appearance of the size of the follicle. As the blockage in the follicle is reduced, the ca nal relaxes, making the opening look much smaller and more refined.
Salicylic Acid:
Salicylic acid is an acne medication that is endorsed by the American Academy of Der matology. Salicylic acid is categorized as a "comedolytic" agent. This refers to its abil ity to retard or reverse the formation of comedones. Salicylic acid is also mildly exfoliating, but its real value is that in combination with glycolic acid it may be able to prevent and resolve micro comedones, which are the basis of the eventual acne lesion. Salicylic acid has an excellent safety record and is well tolerated by most individuals.
Azelaic Acid: Azelaic acid (Heptadi carboxylic acid or AA) is rapidly emerging as a significant tool for the treatment of acne. While the mechanism whereby the agent produces its beneficial action on acne is not fully known, medical research shows that there is a marked reduction of horny keratinized cells that block the follicle. Azelaic acid also has an anti-bacterial effect against a variety of organisms including P acne bacteria. Follicular studies show the P acne bacterial numbers as well as yeast spores are dramatically decreased.
Numerous toxicology studies indicate that azelaic acid is a remarkably safe topical agent. No allergic reactions or complications have been reported after short or long term application.
When azelaic acid is combined with specially balanced combinations of glycolic acid and salicylic acid, the benefits may be greatly enhanced.
Factor-A and Factor-A Plus:
Factor-A and Factor-A Plus are cutting edge technologies that fall into the category known as Retinoids. Retinoids are a group of naturally occurring and synthetic compounds that have Vitamin A like biological activity. They play a critical role in skin growth, repair and epithelial cell differentiation. In the past 20 years tremendous research has focused on certain retinoids, particularly retinoic acid, for the purpose of treating various skin abnormalities including acne, actinic keratoses (pre-cancerous lesions) and skin changes due to photodamage and aging.
Retinoic acid has proven to be an extremely effective prescription medication, although in many cases the patient experiences mild to extreme redness and irritation. Because of the often difficult acclimation period and sometimes persistent continuing irritation, scientists have diligently searched for other
retinoids that would have equal or greater value without the potential side effects.
Recently numerous university medical and research facilities have reported that Retinol (ALL-Trans-Retinol or ROL) has the activity and efficacy of Retinoic acid without the majority of the side effects associated with products such as Retin-A
Jan Marini Skin Research has identified new stabilization and delivery components that enable Retinol to be delivered in a stable fashion where it is converted by certain enzymes into retinoic acid, while avoiding superficial redness, peeling and irritation. Some recent studies demonstrate that a stabilized Retinol may be more active in the skin than Retinoic acid.
Retinol has proven to be a potent tool in treating acne by preventing the cells that line the follicular canal from sticking together and creating the solid impactions that block the follicle. This comedolytic action is unequalled in addressing the underlying mechanisms that contribute to acne. While both preparations are excellent tools to address acne, Factor-A Plus is particularly aggressive in resolving acne lesions and improving the appearance of acne scars.
Additionally, when this new Retinol technology is formulated in combination with glycolic acid there is synergistic enhancement and the overall results are greatly intensified.
Factor-A and Factor-A Plus contain the highest percentages of Retinol (ALLTrans-Retinol) legally available. We have been able to provide this remarkable breakthrough by developing a proprietary, stabilized complex along with an unparalleled delivery system.