In addition to these substances, a more commonly known culprit, “oil”, is the igniting fuel for the acne flare-up along with these other resident perpetrator’s of bacteria and dead skin cells.
Acne flourishes in adolescence, beginning in pre-puberty and subsides in most cases when the threshold of early adulthood is entered. Acne behaves differently in females than in males. It is more common and more severe in boys, subsiding in the great majority below the level of clinical significance by age 25. The “fact” of acne is millions of women face off with this “adult” skin disease daily. The “truth” of acne is many women are battling the complications of the aging clock along with the ugly on-set of either new or old black heads, whiteheads, papules, pustules, and cysts daily.
Acne is not, however, an endocrine disorder. The general belief is that there are usually neither deficiencies, excesses, nor imbalances. However, normal circulating levels of androgens from the gonads and adrenals are absolute requirements. The fact remains that without a source of androgens, the sebaceous glands will remain small.In addition, adrenal glucocoricosteriods play a collaborative role. They potentate the effects of androgens and have an “influence” over the end organ sensitivity where they influence the capacity of the follicle to form comedones.
There is, however, a clear, positive correlation between the occurrence and severity of acne and the sebum secretion rate. Human sebum from isolated sebaceous glands consists mainly of squalenes, wax esters, and triglycerides with small proportions of cholesterol and cholesterol esters. As this viscous liquid flows outward through the follicle, lipases of both microbial and epithelial origin hydrolyze some of the triglycerides.
The development of an inflammatory acne lesion is a multistep process. The initiating event is the formation of a keratinous plug, or comedo, that blocks the pore of the follicle. Even the most innocent comedo can evolve into a nasty cyst with life long consequences. It begins its journey with resident bacteria living within the follicle as it grows, becoming distended. The follicular epithelium becomes thin, and an inflammatory response is induced as bacterial products diffuse into the surrounding tissue. This action discharges a flood of microorganisms into the surrounding tissue releasing sebum and skin cells resulting in thr inflammation action previously discussed.
Inflammation is also caused by a bacterium called Propionobacterium acnes (P-acnes) that live normally on the skin, but can thrive within the blocked follicle. This infection causes inflammation, which is responsible for the redness and swelling of a lesion. In chronic and more severe cases, the pocket of inflammation within a follicle can rupture, causing damage to the surrounding skin triggering inflammatory response, resulting in potential deep scarring if left untreated.
Heredity and skin type plays a central role in determining the size and activity of the sebaceous gland. Understanding the differences of ethnic skin dynamics can be your point of difference between success and failure when treating African skin clinically and recommending professional home care acne products.
Juxtaposing Acne and African Skin
Acne is a common skin condition that afflicts most people of all races and ages to a varying degree during different stages of their lives. Acne vulgaris is a wearisome condition plaguing people of color who live in the Americas, Europe, Africa, and Asia with additional challenges. Although there are many similarities in acne between people of color and European (white) skin, there are significant differences in the presentation of the skin complaint; clinical appearance, cultural skin and hair care practices, treatment selection, and adverse events surrounding the acne grade.
The clinical lesion characteristics in skin of color acne vulgaris include inflammatory papules, pustules, nodules, and cysts in addition to non-inflammatory lesions of open and closed comedones. The inflammation in black skin is far in excess than what appears clinically than what is visible for white skin.
Black skin is understood to have more oil glands than white skin and these are larger and the follicle more prone to lesion formation. The inflammatory reaction to acne is more aggressive and violent in black skin than in white skin. However, the relative frequency of comedonal and noncomedonal lesions may differ between various racial and ethnic groups and there is no data that conclusively supports the notion that the pathogenesis of acne vulgaris in individuals with skin of color is different from that in European (Caucasian, white) skin.
Halder et al. examining the biopsies of 30 African American women with acne have reported noteworthy histologic acne vulgaris differences in black skin with a study. This study found marked histologic inflammation linking their fierce reaction to this disease in contrast to white skin. An inflammatory reaction also has grave secondary consequences that involve skin scarring that can lead to a keloid scar.
A keloid scar is an overgrowth of a fibrous tissue on the skin following a trauma, in this case acne. The tissue response is abnormal to the normal process of wound healing, resulting in the overproduction of collagen or a deficiency of metalloproteases (MMP). The outcome is a raised, firm thickened red-brown scar that may grow for a prolonged period and develop claw-like projections. Genetics and age play a role in keloid development. This is a process where larger scars are produced and can lead to additional pigmentation injury. The Inflammation leads to increased melanin formation as the white blood cells pick up the pigment and migrate deep into the dermis. These factors greatly affect the pigment morbidity in black skin.
Also notable, significant polymorph nuclear cell infiltration was observed even in clinical noninflammatory lesions (e.g. comedones). Furthermore, in defiant papules and pustules, the inflammatory infiltrate was extensive and located at a substantial distance from the actual papule or pustule. Response to this injury creates a pigment reaction, more commonly known as a “dark spot”. This finding might explain why the propensity toward post-inflammatory hyperpigmentation (PIH) is universal in dark-skinned individuals suffering with acne. PIH is often the primary complaint. This is because a typical acne lesion resolves within two weeks, but the hyperpigmentation that results from acne may remain for months, or even years in African skin types. Lesions of PIH are often of greater concern to African skin care clients than the actual acne and therefore treatment of acne in conjunction with the pigment injury is recommended for both clinical and home care acne remedy.
The prevalence of acne and rebounding pigmentation disorders in black skin can also be a result of the use of topical products not suited for the skin type. Many hair pomades and conditioners, popular with individuals of the African, African-Caribbean, and African American communities, contain various mixtures of unknown sources of petrolatum, lanolin, vegetable, animal, and low-grade comedogenic oils. When used on the hair, these agents can “creep” to other areas of the facial skin irritating the follicular residents, thus producing an inflammatory response resulting into a papular and comedonal acne war inside the follicle resulting in post-inflammatory hyperpigmentation.
Pomade spreads to the forehead and inflames the pores, causing pimples called ‘pomade acne.’ Pomade can also contribute to a bacterial infection of the scalp called folliculitis producing pus, bumps, and a redness around the hair also resulting in hair loss and spreading infection. In addition, this can also be true of many skin care products that do more harm than good. African skin is very sensitive and must be approached with caution. Know your skin care company and the ingredients they use and never recommend a product blindly or foolishly.
A common ‘dark spot’ resulting in a hyperpigmentation injury for African skin is a condition often mistaken for acne called ‘Pseudofolliculitis Barbae’ (PFB), a.k.a. ‘in-grown hair’, or ‘razor bump’. PFB is a chronic inflammatory disorder with hair growing in areas of the face that can be a potentially disfiguring condition. Both men and women suffer from PFB. The hair follicles of African skin are curved and after shaving the sharp point of the hair curves and grows back into the skin. The condition is given the name ‘pseudo’ follicultis because it is caused not by a bacterial infection, as associated with common acne, but by the re-growth of hair back into the skin. Red or hyperpigmentated papules, or both, indicate the hallmark of this condition. It is common for pustules to form if the papule acquires a secondary infection, however not all bumps are inflammatory. The bumps may be small or large and commonly occur on the cheeks, chin, jaw-line, and neck areas.
In human color assessment, skin is mainly derived from the interplay of two pigments, hemoglobin, and melanin. Melanin is the major source of skin color increased by exposure to ultraviolet radiation, UVR. The protection afforded by a black epidermis against sunburn is on the average equivalent to an SPF of 13.40; however, a wide inter-individual variation exists due to differences in pigmentation and the influences of other races. Natural UV protection is established with a thorough skin analysis and should influence your course of professional treatment and home skin care maintenance. Always incorporate an SPF of full spectrum 15 or higher, as an integral function of the acne treatment program. African skin must be protected from UVR.
Treating African skin for acne can include a myriad of home care and clinical remedies. Most agents used to address the acne condition are antibacterial, comedolytic agents that target the various pathogens responsible for the development of acne vulgaris. However, many of the ingredients needed to manage acne can cause rebound hyperpigmentation if not properly administered and supervised due to their ‘peeling’ agent nature. Always conduct appropriate clinical skin investigation prior to any treatment and home care remedy recommended and re-evaluate treatment needs of the skin frequently.
There is evidence that black skin is extremely susceptible to dryness compared to white skin, suggesting racial differences in the Stratum Corneum (SC) lipid content. Acne therapy targets to dry up the ‘oil’ and in the same context, dehydrates and depletes the skin of essential water elements indigenous to the SC environment. Studies by Reed et al suggested that there might be lipid differences in the dark versus light skin with an increase of spontaneous desquamation in blacks compared to other races. This was attributed to a difference in the composition of the innercellular cement of the SC where blacks were found to have the lowest levels of ceramides as compared to white skin. Ceramides, make up almost 50 percent of the lipid content in this region and play a critical role in cell recovery and hydration of the SC. When treating acne, skin responds more favorably in an aqueous (water) wound-healing environment, thus reducing inflammation (free radical activity) and expediting recovery.
When it comes to acne and African skin, further complications can arise resulting in additional challenges the aesthetician should always be prepared the handle. For instance, treating acne skin from ethnic combinations requires you to take additional precaution. Knowing the genetic history of your clients skin and what makes it tick will enable you to be more effective in your judgment and treatment selection, directly affecting positive results.
Keeping this in mind, also note inadequate duration is the usual suspect that underlies acne’s non-response to treatment. This unfortunate therapy sabotage is due to lack of client compliance and is generally linked to insufficient education disseminated by the aesthetician. Clients can never be ‘over-educated’ regarding their skin condition. It takes time and patience and there are never ‘short cuts’.
When treating African skin affected by acne, it is always prudent to measure your success on a conservative scale and expect only moderate improvement in 30 days, 40 percent at three months and 80 percent at six months. Fifteen percent of patients will need more time, some more resistive skins up to 12 months. Although this is the general consensus to the overall African acne condition, I personally exceeded these expectations and know of many other aestheticians who have done the same using their knowledge of ingredients and thoroughly understanding the histology, anatomy, and physiology of African skin.