The ‘Skinification’ Of Hair Care – HAPPI – happi.com

For years, I have been telling my patients your scalp is skin, so treat it well. Now, we are witness to a skinificaton of hair products and it is all because the scalp is a very important part of the hair growth process.

Healthy hair cannot be produced without a healthy scalp. The scalp skin is an extension of internal and external health. As I noted in a previous column (January 2020) the gut microbiome affects the skin microbiome which, in turn, affects the scalp microbiome, and therefore hair growth. Since 2020, we have witnessed the burgeoning of scalp care products with CBD formulations, products boasting microbiome benefits, and scalp serums and solutions for flaking, itching and tension. So, what is this all about? Lets dig into the science.

The surface of human skin is a site of microbial colonization. The commensal flora of the skin maintain a symbiotic relationship and shape the cutaneous immunity of the host. Several studies have characterized the cutaneous bacterial communities of healthy individuals and patients with inflammatory diseases, mostly in material collected using swabs. Sampling from hair follicle (HF) openings is challenging. Along their epithelium, HFs harbor a multitude of microorganisms able to reach deeper compartments, frequently organized in biofilms. The role of bacteria as disease-aggravating factors has been recognized for HF-associated inflammatory diseases such as acne vulgaris or folliculitis decalvans, an inflammatory, scarring hair loss.

Scalp hair follicles form large tubular invaginations, which extend deeply into the skin and harbor a variety of microorganisms. A single square centimeter of human skin, along with adnexal structures, such as sweat and oil glands, can be inhabited by up to one billion microorganisms including bacteria, fungi and viruses, forming a complex community known as the skin microbiome.

The scalp includes 100,000150,000 hair follicles (HFs); for comparison, the human body has about five million HFs. These follicles are formed during embryogenesis and ensure cyclic hair growth throughout ones lifetime. Those on the scalp contribute to a significant increase of skin surface area and, more importantly with regard to colonization, form pockets along the infundibulum, which extend into deeper scalp skin layers. The infundibulum is the upper portion of the hair follicle. It begins at the surface of the epidermis and extends to the opening of the sebaceous duct (where scalp oil is secreted). The infundibulum is typically filled with sebum, debris and microorganisms ranging from viruses to bacteria, as well as yeasts/fungi and even mites.

There is increasing proof of the presence of bacteria reaching below the skin surface and along the HFs, and evidence is emerging that the cross-talk between bacteria and the underlying tissue is a dynamic reciprocal process. External microbial stimuli create immunological responses across the HF epithelium, but events in the tissue also shape microbial composition. Along the infundibular HF epithelium, microorganisms find themselves in a highly immuno-active environment. In contrast to the massive exposure to microbial material in its upper part, immuneprivileged sites are found around the hair bulge and the anagen bulb. The bulge contains several epidermal stem cells. A collapse of the immune privilege is a key element in the pathogenesis of chronic scalp diseases. Numerous immune cells are deployed in the skin and around its appendages in close proximity to microbiota. Commensals are considered essential to maintain skin homoeostasis. They protect the skin from its colonization by pathogens, stimulate production of the complement system and cytokines involved in the initiation and maintenance of an immune response. Furthermore, microbiota help decrease the magnitude of inflammation and promote tissue repair.

Acne and primary scarring alopecias are good examples of how the local follicular microenvironment; e.g., hypoxic conditions and lipid substrates, resident microbes and their metabolic products, can influence inflammatory and antimicrobial processes in the skin.

The skin surface and follicular openings are recognized sites of rich microbial colonization and intense immune activation, with cross-talk across the skin barrier. The bacterial microbiome extends below the infundibulum, with the confirmed presence of various species and high abundance of Corynebacterium and Staphylococcus. It is in close proximity to structures of the immune privileged status, which are essential for the hair cycle.

Several preliminary studies suggest that external stimuli may affect the state of activation of the HF immune system. Lower sections of the HF are protected from immune cell infiltration under healthy conditions, the so-called immune-privileged areas. This includes the bulge, where a stem cell niche is found, and the bulb, where cells divide and grow to build the new hair. However, both regions are sites of intense inflammatory infiltrate in inflammatory hair diseases like primary cicatricial alopecia and alopecia areata. Alterations in the HF microbiome or the penetration depth of microbial material could be related to homeostasis, modulation of cutaneous immune reactions and inflammatory processes along the HF. The localization of this involvement with the immune system is critical, affecting the possibility of regrowth after subsidence of inflammation. When the stem cell niche is attacked, like in cicatricial alopecia, patients suffer permanent, scarring hair loss. On the other hand, AA pathogenesis involves inflammation of the peribulbar region, allowing a possible hair regrowth.

The strongest evidence supporting correlations with microorganisms colonizing the scalp has been found in seborrheic dermatitis/dandruff and in a type of inflammatory cicatricial alopecia named folliculitis decalvans (FD). An antimicrobial treatment administered in these diseases brings transient success in most cases. However, frequent recurrences, lack of efficacy in some patients and the additional need of antiinflammatory therapy in acute flareups, indicate the complexity of their pathogenesis.

Androgenetic alopecia (AGA) features shortening of the anagen phase and eventually, a slowly progressing miniaturization of the hair follicle. Infiltration of mononuclear cells and lymphocytes is detected in about 50% of skin samples. This microinflammation takes place in the upper third of the HF, where a great number of microorganisms are harbored. Moreover, the production of complement (inflammatory mediators), were identified in the pilosebaceous duct of 58% of patients with AGA compared to 12% of the control group. These arguments together with observed improvement after application of antimicrobial agents may suggest a possible connection with scalp microflora.

In scalp psoriasis, the rate of positive cultures of Malassezia species was higher in psoriatic scalp lesions compared to healthy controls. Changes of the scalp microbiome were found to depend on disease severity. GomezMoyano et al. identified M. restricta as the most frequent in mild scalp psoriasis, and M. globosa in moderate, and severe cases, and in patients with exacerbation in the last month. Cases of refractory scalp psoriasis successfully treated with imidazole, followed by reduction of yeasts, were presented and support the theory of a role of Malassezia as an exacerbating factor in scalp psoriasis. Furthermore, alterations in the composition of gut microbiome have been observed in patients with psoriasis.

A possible connection between colonization of the scalp by Alternaria spp. and Alopecia Areata (AA) development was postulated. Fungi of this genus were cultured from epidermal scrapings in 20% of patients compared to 13.3% of controls. Not only skin but also gut microbiome has recently been considered to be associated with AA. An increased intestinal permeability due to dysbiosis and/or inflammation may be an underlying stressor of the immune system in genetically susceptible individuals.

Low production of short chain fatty acids by intestinal bacteria as a result of insufficient intake of fibers in the Western diet is likely disadvantageous to the intestinal barrier and function of the colon. This further supports the idea that a healthy gut is important in maintaining healthy skin and hair.

There is a greater prevalence of atopic dermatitis in patients with AA compared to population prevalence. Atopic dermatitis is associated with more severe course of AA. The defective skin barrier in atopic dermatitis may ease microbial penetration to deeper follicular compartments, possibly aggravating or causing alopecia areata.

So why the skinification of hair care? The aforementioned diseases of the skin and the HFs are all due to dysfunctions of dysbiosisthe imbalance of the skin microbiome. Skin barrier dysfunction translates into scalp barrier dysfunction, leading to inflammation and hair loss as evidenced by the link between eczema and more severe alopecia areata.

Just as it is important to maintain the skin barrier with ceramides and lipids, it is important to maintain the scalp barrier as well with scalp and hair care products that mimic skin care products. It only makes sense, as the scalp is a continuation of the skin. There is no line of demarcation separating bodily skin from scalp, so why not care for your scalp as you do for your skin?

References

Dr. Sharleen St. Surin-Lord is a board-certified dermatologist who has been practicing for more than 13 years. She is in private practice at Visage Dermatology, Largo MD. She also practices at the University of Maryland Capital Regional Health System in Maryland and she is an assistant professor of dermatology at Howard University College of Medicine. Dr. Sharleen is a member of the American Hair Research Society and you can follow her on Twitter, Instagram, and Facebook as DermHairDoc.

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The 'Skinification' Of Hair Care - HAPPI - happi.com