Tuesday, 23 February 2021 11:40

Cystic Acne Considerations: Pathology & Treatment

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Defined as acne grades four and five, cystic acne is a skin condition centered on the pilosebaceous unit that may exhibit intense erythema, inflammation, nodules, cysts, and scarring. It is considered a rare and serious form of acne vulgaris. Acne vulgaris affects approximately 80of adolescents and young adults. Several clinical types of acne also include less inflamed comedones and pseudocysts that may occur at the same time as the more severe lesions. Inflamed lesion results in the rupture of a closed comedone.Acne can affect the face or spread to the neck, chest, and back. The onset of debilitating acne lesions can interfere with the quality of life and self-esteem. 

 

 

REVIEW OF ACNE

Acne is a disease of the sebaceous follicle, primarily affecting the face, back, and chest. It is an inflammatory disorder of the pilosebaceous unit (hair follicle), a very active apparatus residing within the dermis and epidermis. There are four main interrelated pathogenic factors involved with this apparatus, including excess and altered sebum production under the control of androgens, abnormal follicular hyperkeratinization and differentiation, follicular canal colonization with cutibacterium acnes, (c. acnes), and chronic inflammation (controlled by a complex innate and acquired immunological mechanisms.)

 

Nodular Acne

Nodules appear as raised and solid lesions and are located deeper into the dermis as subcutaneous tissue. 

 

Cystic Acne

Cystic acne is similar to nodules; however, they are filled with pus, appearing large and swollen.

 

ANATOMY AND FUNCTION OF THE HAIR FOLLICLE

To understand acne, the structure and function of the pilosebaceous unit are importantThe hair follicle is an active apparatus residing within the dermis and epidermis. There are two kinds of folliclesa hair, and a sebaceous follicleBoth follicles have sebaceous glands attached. There may be microscopic hair in the follicle called rudimentary hair. When acne develops, this hair usually coils up, gets lost in the rest of the debris, and never gets to the surface.

Sebum inside the follicle plays an important role in the building of the acid mantle. The environment within the follicle normally contains anaerobic bacteria (grows without oxygen). Bacteria feed off the triglycerides produced by the sebaceous glands, leaving fatty acid by-products. The sebum moves from the sebaceous gland interior and flows up the hair shaft to the surface of the skin.

The stratum corneum curves into the top of the follicle where the opening serves as an exit or entrance to the pilosebaceous duct. Epithelial cells inside the follicle are an extension of the stratum corneum. They are interspersed with melanocytes and line the entire pilosebaceous unit. At the base of the follicle is the papilla that supports the various stages of the hair growth cycle. Also known as the bulge, the papilla houses several types of stem cells that supply the follicle with new cells.

Just as cells desquamate off the stratum corneum, the same process occurs inside the follicle where the movement of sebum washes cellular debris upward to the opening of the follicle, spilling its contents onto the surface of the skin. The hair then acts as a wick inside the follicle.

 

Role of Cutibacterium

Cutibacteriumor c.acnes (formerly propionibacterium acnes) is a slow-growing, anaerobic bacteria that naturally colonize within the duct of the sebaceous follicle.C. acnes secretes numerous proteins including digestive enzymes. These enzymes are involved with the digestion of sebum and the acquisition of other nutrients. In healthy skin, the bacterium resides within the fatty acids in the sebum secreted by sebaceous glands within the follicle. Sebum lubricates the skin and hair and acts as a seal in the hair follicle, protecting it from the outside. As the sebum rises upwards towards the follicle opening, it moves onto the skin’s surface transforming a moreacidic stateWhen the sebum amalgamates with the epidermal lipids, the skin flora and microbiome at the stratum corneum and acid mantle meet.

The onset of acne causes an innate immune response that initially develops as a microcomedoneHowever, the combination of increased sebum with abnormal hyperproliferation of keratinocytes can easily escalate into enlarged and inflamed lesions as bacteria becomes entrapped within the follicular cavity. The acidic nature of the free fatty acids now becomes pro-inflammatory and comedogenic. Due to the arrival of the cells from the immune system to combat the inflammation and infection, irritation soon causes pustules. The immune system looks at the bacteria components of the c.acnes as adversary molecules. Immune cells also release large amounts of inflammatory cytokines that induce more white blood cells to release destructive enzymes and free radicals at the infection site. The follicle and surrounding tissue become red and swollen with the increased immune response that vigorously combats trapped bacteria. The presence of white blood cells (pus) causes the lesion to expand and finally rupture. The skin’s surface becomes a field of inflammation with swollen lesions and compromised tissue.

 

Table 1 - Clinical features of acne

There are numerous grades based on severity  mild, moderate, or severe. Comedones and inflammatory lesions are normally considered separately.

Superficial lesions

  • Open and closed comedones (blackheads and whiteheads)
  • Papules (small, tender red bumps)
  • Pustules (white or yellow “squeezable” spots)

Deeper lesions

  • Nodules (large painful red lumps)
  • Pseudocysts (cyst-like fluctuant swellings)

Secondary lesions

  • Excoriations (picked or scratched spots)
  • Erythematous macules (red marks from recently healed spots – best seen in fair skin)
  • Pigmented macules (dark marks from old spots, mostly affecting those with dark skin)
  • Scars or various types.

 

 

Recent research confirms that inflammation exists throughout the lifecycle of an acne lesion and even prior to a comedone formation. This statement is significant because skin care professionals must carefully examine their approach for treatment, taking into consideration the inflammatory factor, age, environment and lifestyle, and the overall health profile of thclient. Inflammation is a vigorous indicator that the immune system is involved. Moreover, it is an indicator as to how the skin care professional is going to manage a long-term care pathway.

 

ADOLESCENT & ADULT ACNE

Hormones are linked to acne from adolescent to adult life. They are responsible for the development of the sebaceous glands that produce sebum. During puberty, the body produces an excess of male hormones (androgens) stimulating an overproduction of sebum. Adolescent acne occurs during early adolescence years during which time hormonal fluctuations accompany puberty transformation into teenage years to adulthood. Normally, acne improves after puberty, but severe cases may leave pitted scarsWhile in other cases, it can linger on into the client’s early 20s. The appearance of these acne lesions accompanies the active life of approximately 70% of teenagers. 

Adult acne may occur due to hormonal changes during a women’s menstrual cycle, pregnancy, and menopause. Drug-induced acne is an adverse effect of a series of systemic drugs such as corticosteroids, thyroid hormones, antibiotics, lithium, halogen compounds, antibiotics, and during chemotherapy treatments. Acne can also become a red flag of an underlying disease, especially if there is no prior history of acne. Examples are polycystic ovarian syndrome or other endocrine disorders.

 

 

THE ROLE OF CUTIBACTERIUM ACNES

The role of c.acnesbacteria is a gram-positive, non-spore-formingand normal skin bacterium typical to human skin. It contributes to the formation of the acid mantle and skin barrier. They have evolved to be both anaerobic and aero-tolerant and reside deep within the follicleThey are found at the top of the pilosebaceous duct and on the skin surface near the exit. As sebum moves up the follicle, the triglycerides are transformed into free fatty acids. C.acnes use sebum, cellular debris, and metabolic byproducts as an energy source. They ingest the abundant triglycerides in the sebum and excrete specialized enzymes (lipases) required to create the free fatty acids. 

During normal functioning, c. acnes do not directly cause significant damage to the follicle and surrounding skin. Most of the damage caused by acne is due to an inflammatory process of the immune system.9Whenever there is an impairment of the acid mantle compounded with follicular imbalance the c.acnes moves away from their normal environment and seeks the next highest source of triglycerides – the sebaceous gland interior down inside the follicle. It is here where the bacteria continue to breakdown triglycerides into free fatty acids. Unfortunately, this location is very close to the dermis that has a pH of around seven. The acidic nature of the free fatty acids now becomes pro-inflammatory and comedogenic. Due to the arrival of the cells from the immune system to combat the inflammation and infection, the irritation soon causes nodules or pustules. The immune system looks at the bacteria components of the c. acnes as adversary molecules. Immune cells release large amounts of inflammatory cytokines that induce more white blood cells to release destructive enzymes and free radicals at the infection site.

Some individuals with acne vulgaris have a faulty and oversensitive immune response that causes the arrival of more inflammatory cytokines to induce additional white blood cells that continue to fight infection. This vicious cycle begins to affect the surrounding tissue with more injury, continuing the propagation of bacteria. Furthermore, it is not uncommon to have ruptured glands that form fibrotic tissue. They can be shallow or deep, creating permanent pitting and scarring.

 

GENETIC TRAITS LEADING TO POOR FOLLICULAR FUNCTION

A genetic predisposition in the makeup of the follicle structure may occur during embryonic development. Some individuals may inherit more sebaceous glands on the face and other areas or have inherited a higher sensitivity to circulating androgens. A hereditary factor called retention hyperkeratosis may be present, whereby the keratinocytes do not shed off the surface on the stratum corneum and out of the follicle as in normal skin.

 

ANDROGENS & THEIR ROLE IN SEBUM PRODUCTION

Androgens are hormones that are important for normal male sexual development during embryonic development and during puberty. The AR gene provides instructions for making a protein called the androgen receptor. Androgens and their receptors direct the development of male sexual characteristics. They also have important functions in both males and females such as hair growth and sex drive.10

Androgen receptors located within the sebaceous follicle stimulate an upsurge of sebum production. At the onset of puberty, androgen hormones are produced, beginning with testosterone. An enzyme called 5-alpha-reductase converts testosterone to dihydrotestosterone. Dihydrotestosterone stimulates the sebaceous glands to begin the production of sebum.

Retention hyperkeratosis is a result of the buildup of epithelial cells. Continuous overproduction of sebum causes distention of the gland and a notable enlargement of the follicle. Essentially, the process of pimple formation is a result of an obstruction in the follicle. Cellular debris mixes with sebum dry out and creates a plug that obstructs the drainage of the sebum.

Other circumstances that affect and modulate sebum production include pregnancythe use of oral contraceptiveslow levels of circulating androgens in womenhormonal changes during menopause, and drugs.

 

REMEDY AND TREATMENT

Acne is an inflammatory condition involving the activity of the hair follicle, the immune system, as well as fluctuating hormone activity. Moreover, the skin barrier has been compromised due to breakout, pustules, and over-activity of bacteria. The stratum corneum is a biologically active cellular tissue and requires a pathway of restoration based on corneotherapy principles for the correction of skin conditionsThe improper choice of treatment and products may irritate, cause more inflammation, and prevent the restoration of the skin. A significant objective is to obtain a clear understanding of the nature of acne and what stimulates its onset and what calms it. Age, health profile, diet, and lifestyle are fundamental when determining a treatment pathway.

There are effective options for remedying acne, including supporting the skin barrier through in-clinic and homecare intervention using formulations that provide a balancing, restorative, and anti-inflammatory effect to the skin. Lymphatic drainage, photo modulation, microcurrent, and other less invasive interventions may become necessary to support a reduction in inflammation and gradual correction. It is highly recommended to reduce stress, modify lifestyle habits that may not be supportive, like smoking, and poor diet and health care.

During acute inflammation, a primary focus is to reduce the swelling and infection and support the well-being of the client. Improvement of the health of the acid mantle is essential. A multi-faceted approach may be recommended, especially when it comes to conditions beyond the scope of practice for the skin care professional. Teaming with a medical professional may be necessary to add a medical component that addresses the severity of the condition. There also may be nutritional deficiencies such as vitamin D, essential fatty acids, and other nutrients that can be evaluated and adjusted by a licensed professional.

Skin care ingredients for improving acne may contain active agents with attributes that are sebum-liquefying, sebum-suppressive, keratosis-impeding, antimicrobial, anti-inflammatory immune-suppressive, and regenerativeFor example, studies with the application of liposomal phosphatidylcholine showed improvement of acne vulgaris comedones after 14 to 28 days. Use caution when choosing the appropriate composition of base creams and cosmetic products in order to avoid counterproductive effects. Cleansers and active ingredients should not dry out, stripor irritate.Skin care regimens require review throughout the course of correction and should be adjusted when necessary.

 

Examples of Active Agents: Selection is dependent upon the acne type.

Keratolytic effects

Salicylic acid and willow bark extracts, urea, alpha hydroxy fruit acids (only to be used if required and not as a routine), enzyme peelings, and azelaic acid

Anti-inflammatory effects

Boswellia acids are protease inhibitors. The dermal 15-liposygenase transfers of essential fatty acids of herbal oils, such as linoleic acids, alpha-gamma-linoleic acids can transfer into anti-inflammatory metabolites.

Phosphatidyl-choline, buckhorn extract, chamomile, hamamelis (witch hazel), green teaand zinc

Antimicrobial

Azelaic acid (5-alpha-reductase inhibitor, algae extract, betulinic acid (from the bark of the Betula alba, (white birch), and benzoyl peroxide

Regenerative - supporting

Vitamin A and derivatives, niacinamide (Vitamin B3), yeast extracts (B vitamins), D-panthenol (provitamin B5), sodium ascorbyl phosphate (vitamin C), vitamin E and esters, echinacea (coneflower, sunbonnet) extract, and phytohormones (soya, red clover) with their high content of isoflavonoids.

 

References

 

  1. Marissa D. Newman, et al. Therapeutic considerations for severe nodular acne. Am J Clin Dermatology, Feb. 2011;12(1) https://pubmed.ncbi.nlm.nih.gov/21062102/
  2. What is Cystic Acne? Retrieved fromhttps://www.usdermatologypartners.com/blog/caring-for-cystic-acne/
  3. Tanghetti, Emil A., MD.The Role of Inflammation in the Pathology of Acne.Clinical and Aesthetic Dermatology.Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3780801/
  4. What are inflammatory lesions in acne? Dr. Amanda Oakley, Dermatologist.Retrieved from https://dermnetnz.org/topics/inflammatory-lesions-in-acne/
  5. McLaughlin, Joseph, et al.Propionibacterium acnes and Acne Vulgaris: New Insights from the Integration of Population Genetic, Multi-Omic, Biochemical, and Host-Microbe Studies.Https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6560440/pdf/microorganisms-07-00128.pdf
  6. Zani, A. (June 2015). The Pathogenesis of Acne.Retrieved fromhttps://www.dermascope.com/acne/the-pathogenesis-of-acne?tmpl=component
  7. Grice, E.A., The skin microbiome.Retrieved fromhttps://pubmed.ncbi.nlm.nih.gov/21407241/
  8. What are Propionibacterium acnes?Retrieved fromhttps://healthjade.net/propionibacterium-acnes/
  9. Acne vulgaris.Reviewed and updated by Dr. Amanda Oakley Dermatologist, Hamilton, New Zealand, June 2014https://www.dermnetnz.org/topics/acne-vulgaris/
  10. IBID See Ref. 3
  11. Harvard Blog.Adult acne: Understanding underlying causes and banishing breakouts.Retrieve from https://www.health.harvard.edu/blog/adult-acne-understanding-underlying-causes-and-banishing-breakouts-2019092117816

1 What is Corneotherapy.https://corneotherapy.org/about-corneotherapy/what-is-corneotherapy

  1. Lautenschlager, Dr. Hans, Elke Klein.KosmetikInternational 2003 (5), 27-31. Retrieved from https://dermaviduals.de/cms/upload/Publikationen_english/KI-05-03-Akne-engl.pdf
  2. IBID See Ref 3
  3. Lautenschlager, Dr. Hans.Hormones control puberty, pregnancy, and menopause - can we control their impact? Retrieved from https://dermaviduals.de/cms/upload/Publikationen_english/KI-10-18-hormones-engl.pdf

 

 

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