BACKGROUND

Hair exists within two domains: that which is above the skin surface (extracorporeal) and that which is embedded within the skin (intracorporeal). When considering the extracorporeal domain, the skin and hair are obviously distinct and independent entities. However, intracorporeal hair and skin have a much more intimate and inseparable relationship. The skin and hair are part of a complex interdependent system collectively called the integument (including nails, sebaceous and sweat glands, among other components). The hair fibre lengthens (i.e. ‘grows’) within the embedded structural unit of the hair follicle. When looking closely at the concentric multilamellar structures from which the follicle and the hair fibre are composed [1], clearly discerning hair from skin is much more difficult than in the extracorporeal domain.

The actual architecture of the scalp hair follicle is significantly different [2] (see Figure 1) than the idealized structure which is often portrayed in introductory texts. The base of the follicle (the ‘bulb’) is 4 mm deep in the skin and is the location of the cellular proliferation that initiates fibre elongation. The nascent hair fibre becomes biologically ‘dead’ soon after leaving the bulb zone [3, 4] and begins a two-week journey to the scalp surface.

Anatomically accurate human scalp follicle

This distal soft [5] pro-fibre initiates a maturation process (keratinization) and extension that eventually leads to the hard fibre familiar from post-emergent observation. This maturation process is analogous to that taken by basal epidermal cells which lead to the formation of the ‘dead’ stratum corneum. The coordinated series of physical-chemical changes enable the lengthening and strengthening of the hair fibre. This can be modelled as a mechanical process in which the physical forces due to hardening and water transport explain the resultant fibre progression towards the scalp surface [6].

Prior to complete keratinization, there is a complex interaction between what will eventually become the fibre surface (the cuticle layer) and the juxtaposed inner layers of the follicle to achieve the seemingly paradoxical results of fibre protrusion while simultaneously maintaining fibre anchorage. The closely apposed scalp–hair interface is likely the portal through which the condition of the scalp can impact the condition of, initially, the soft pre-emergent hair, resulting in impacts to the mature hardened post-emergent hair fibre. While the specific mechanism of how the surrounding scalp impacts the maturing hair fibre is not known, we review here the data supporting the cause-and-effect relationship between scalp skin condition and resultant hair condition as well as its normal retention.

METHODS

Keyword searches of PubMed were performed to identify all articles discussing human scalp conditions and their impact to hair growth and its properties. Search terms included “scalp psoriasis,” “dandruff,” “seborrheic dermatitis” and “tinea capitis” in combination with hair and its attributes. No language or time restrictions were used. Articles found were read and reviewed; they were judged appropriate for inclusion if they described hair impacts of the scalp condition. The references of these articles were reviewed to identify additional resources.

RESULTS

A total of 21 studies were found, and our results are summarized in Table 1. The studies date back over 50 years and are predominately epidemiological in nature, comparing hair from the scalps of diseased and normal populations. A single treatment study was conducted recently, which will be reviewed separately.

TABLE 1. Summary of epidemiological studies of various scalp conditions Skin condition Hair characterization methods Observed impacts to hair Refs. Scanning Electron Microscopy (SEM) Atomic Force Microscopy (AFM) Infrared Microscopy (FTIR) Nanoindentation Shine Evaluation GC/MS Quantitation of HODE ↓ Hair Diameter ↑ Surface Pitting, Roughness ↑ Cuticle Breakage and integrity ↑ Scale Thickness ↓ Protein (Amide A) ↑ Oxidative Stress (Cystine or HODE) ↓ Hair Shine ↑ Surface Hardness ↑ Altered Hair Fibre Morphology ↑ Hair Loss Psoriasis ● ● ● [7] ● ● [9] ● ● ● [10] ● ● [11] ● ● ● ● ● ● [13, 24] ● [8, 14-16] Dandruff and Seborrhoeic Dermatitis ● ● [18] ● ● ● [19] ● ● ● ● ● [17] ● ● [27] ● [15, 20-23] ● [30] Atopic Dermatitis ● ● ● [24] ● ● ● [19] Tinea Capitis ● [25] P. Versicolor ● [26] EPIDEMIOLOGICAL STUDIES EVALUATING IMPACT OF COMPROMISED SCALP CONDITIONS TO HAIR

The scalp conditions which have been studied for hair impacts include psoriasis, dandruff/seborrhoeic dermatitis (D/SD), atopic dermatitis (AD), pityriasis versicolor (PV) and tinea capitis.

Psoriasis

Psoriasis has been the most widely studied skin condition with respect to hair impacts and is the source of the earliest work evaluating the impact of scalp condition on hair condition. In the early 1970 's, scanning electron microscopy (SEM) was used to demonstrate [7] that hair from lesional psoriatic scalp sites showed significant morphological differences in comparison with hair obtained from a parallel group of normal individuals. Specifically, the psoriasis-derived hair was smaller in diameter and had more surface pitting. At approximately the same time, Shuster summarized [8] clinical observations of psoriasis sufferers in which there appeared unusual hair loss in lesional areas (the term psoriatic alopecia was proposed).

Headington [9] later also observed that hairs obtained from a scalp psoriasis group were thinner than those from a normal group. SEM was also used in two subsequent studies comparing hair from psoriasis and normal scalps. Both Plozzer [10] and Kumar [11] observed alterations to the cuticle of psoriatic hairs in the form of surface pitting, cuticle breakage and general wear.

Kim et al. used more sensitive atomic force microscopy (AFM) to study the surface morphology of psoriasis-derived hair samples compared to normal hair. These studies [12, 13] demonstrated that psoriatic hair had thicker cuticle edges, an overall rougher surface and more surface pitting.

The earlier observational work that suggested premature hair loss associated with psoriatic lesions was subsequently confirmed more definitively. Clinical evaluations of psoriasis using trichograms to quantify hair cycle stage showed increased telogen and decreased anagen [14, 15]. This has been extended to even include premature hair loss in non-scalp psoriatic sites as well [16].

Dandruff/seborrhoeic dermatitis

In comparing hair obtained from Dandruff/seborrhoeic dermatitis (D/SD) and a normal population, Sinclair [17] observed decreased shine of the hairs from D/SD sufferers. Kim, using similar techniques to those used for evaluation of psoriatic hairs, found very similar effects on D/SD-derived hairs [18]. While the overall magnitude of effects for D/SD was slightly less than psoriasis, the pattern of morphological impacts was similar: generally rougher, increased pitting and thicker cuticular edges. The rougher surface likely explains the decreased shine. The hair from D/SD was also observed to exhibit signs of experiencing higher oxidative stress, measured as cystine [19].

As with psoriasis, there has been a wide range of observational studies that indicate premature hair loss is also associated with D/SD [15, 20-23].

Atopic dermatitis

A single study was identified in which comparative evaluation of hairs from Atopic Dermatitis (AD) and a normal population using AFM [24] has led to similar observations as those seen for psoriasis and D/SD: increased roughness and thicker cuticular edges for the hairs from AD scalps.

Tinea capitis

The hair of those experiencing Tinea Capitis (TC) was evaluated using trichoscopy as an aid to help diagnose TC. It was frequently observed [25] that the appearance of individual hair fibres was altered yielding forms termed comma, corkscrew and zigzag hairs.

Pityriasis versicolor

Pityriasis Versicolor (PV) is a skin condition in which non-commensal Malassezia colonize non-scalp regions. While this review is intended to be focused on scalp conditions, PV is mentioned here from a broad mechanistic perspective since it was observed [26] to cause premature hair loss.

TREATMENT STUDY EVALUATING IMPACT OF COMPROMISED SCALP CONDITIONS TO HAIR

Only one treatment study has been conducted to evaluate the impact on associated hair of a scalp condition, in this case D/SD. The study was a 24-week (including 8-week pre-treatment) placebo-controlled clinical treatment of D/SD with a commercially available therapeutic product [27]. This study demonstrated, as expected, the improvement in typical scalp measures indicative of reduced dandruff and improved indicators of scalp health. A key element of this work was the quantitation of a lipid peroxidation product called HODE, which results from oxidation of linoleic acid [28, 29]. The scalp of D/SD sufferers demonstrated elevated levels of oxidative stress at baseline that was reduced significantly relative to placebo after 16 weeks of treatment. Critically, oxidative stress was also quantified and evident in hair sampled at baseline that was significantly reduced upon treatment, coincident with that seen in the scalp. This provides further support for a cause-and-effect relationship between scalp and resultant hair oxidative stress.

This unique treatment study also included evaluation of physical manifestations to the hair due to the oxidative stress [30]. Two attributes of cuticle condition were assessed: hair surface hydrophobicity due to the F-layer (surface energy, SE) and cuticular moisture barrier effectiveness (dynamic vapour sorption, DVS). Hair emerging from a compromised scalp health condition had decreased hydrophobicity and decreased ability to impede moisture vapour absorption. Both of these attributes were significantly improved relative to placebo upon scalp condition improvement. This treatment study has demonstrated that hair condition was improved (both chemically and physically) as a result of the underlying improvement in scalp condition.

DISCUSSION

Over 50 years, there have been more than 20 studies involving five different scalp conditions in which detrimental impacts to hair have been observed and associated with those scalp conditions. The scalp conditions involve a varied array of initiating stimuli as well as resultant scalp symptoms. They tend to have a common perturbation of the balance of pro-and antioxidant forces leading to oxidative stress.

Psoriasis is thought to be a chronic autoimmune condition initiated by allergic reaction and shows strong indications of oxidative stress: altered antioxidant enzymes [31], oxidized proteins [32, 33] and oxidized lipids [34]. Another chronic scalp condition is dandruff/seborrhoeic dermatitis (D/SD), which is thought to be initiated by the impact of microbial metabolism of commensal Malassezia yeast. D/SD also shows clear signs of oxidative stress: perturbed surface and systemic antioxidant enzyme levels [35-38] as well as elevated lipid peroxidation [27, 39]. Atopic dermatitis (AD) has a less clear aetiology, but is thought to be a cutaneous manifestation of a systemic disorder and also tends to be a chronic condition. AD is also associated with oxidative stress: quantitation of urinary indicators of stress is elevated [40-42] as are oxidized surface protein levels which may be exacerbated by environmental impacts [43]. Tinea capitis (TC) is likely more a manifestation of a follicular infection by Trichophyton and Microsporum, but also includes skin manifestations as a result. Oxidative stress in TC has not been studied. Finally, while pityriasis versicolor (PV) generally involves non-scalp areas, it is included here for completeness due to impacts to associated non-scalp hair as well as evidence of oxidative stress involvement: elevated antioxidant enzymes [44] as well as evidence of microbially mediated lipid oxidation [45].

In epidemiological studies of these scalp conditions, hair obtained from the specific compromised scalp health population was shown to have negative manifestations when compared to hair from a control group. Using a wide range of techniques, the most common impact to the hair is altered cuticular integrity. This is manifested as surface pitting, roughness, thicker cuticular edges and decreased shine. In addition to these physical perturbations, there were indications of oxidative chemical impacts as well. A substantial body of evidence suggests that premature loss of hair also accompanies the studied unhealthy scalp conditions.

While the epidemiological studies are of great scientific value, following the impact to the hair during intentional improvement of the scalp condition provides more direct cause-and-effect data. A treatment study demonstrated that hair growing from a D/SD population exhibited cuticular physical and functional modifications as well as chemical oxidative stress. After 16 weeks of improvement of scalp condition, the new hair emerging from the improved scalp was shown to have consequently improved cuticular chemical and physical attributes as well. The treatment study thus demonstrates the reversibility of the detrimental hair impacts upon normalization of the underlying scalp condition.

Between the epidemiological and treatment studies covering a wide range of scalp conditions, there is a substantial weight of evidence supporting the cause-and-effect association between scalp condition and resulting hair condition as well as its retention. These scalp conditions all have oxidative stress as a common aetiological element.

The association of scalp condition to resultant hair impacts may even be extended to the normal ageing process wherein the scalp is asymptomatic. The known impact of physiological ageing to exposed skin occurs to scalp skin as well, including increased oxidative stress. Although not as carefully studied as the above disease conditions yet, it is possible that the ageing follicular environment, via oxidative stress, has similar impacts to the emerging hair as has been observed for conditions such as psoriasis and D/SD [46].

The nature of these cuticular perturbations can provide both insights as to the possible mechanism leading to their formation in the pre-emergent hair as well as the consequences to the post-emergent hair (see Figure 2). The formation of the protective cuticle occurs via slow keratinization at the interface between the nascent hair fibre and the surrounding epidermis. The pro-fibre is quite soft [5] and vulnerable prior to hardening. While the exact details of the keratinization chemistry leading to cuticle hardening are not known, it is plausible that the oxidative stress in the surrounding scalp environment could alter the normal process. This may lead to cuticle cells in the pre-emergent hair fibre that are more brittle than normal and may impede normal fibre anchorage.

Model for pre- and post-emergent effects to hair due to a surrounding unhealthy scalp environment

Upon emerging from the scalp, the post-emergent fibre will be exposed to the normal mechanical manipulations associated with washing, combing, drying, etc. If the hair cuticle is more brittle than normal, such manipulations stress the physical integrity of individual cuticle cells. More brittle cells would increase the chance that small pieces of cuticle would break off. The cumulative impact of this fragmentation could explain many of the observations from both epidemiological and treatment studies. Such a brittle surface would yield enhanced roughness, uneven (pitted) micro-surfaces, thicker cuticle edges due to loss of the thin tapered cuticle edge, decreased shine and reduced effectiveness as a moisture vapour barrier.

These cuticle perturbations are very similar to those shown to occur from chronological ageing of the post-emergent hair fibre. Impact of time post-emergence on cuticular integrity has been studied using both SEM [47] and AFM [48] by evaluating morphological changes along the hair surface. A progressive deterioration in cuticle can be observed which includes chipping off cuticle edges, roughened cuticle surfaces and general surface irregularities. Many of these appear to have similar characteristics to those observed on hair from various scalp disease states as well as asymptomatic aged scalp. It appears that hair emerging from compromised scalp can be likened to that resulting from cumulative mechanical impacts associated with chronological ageing of the fibre. The hair produced from unhealthy scalps can be considered ‘prematurely aged’. This is important as the rougher the hair surface gets, increased fibre–fibre friction occurs resulting in accelerated wearing of the protective cuticular surface [49]. Thus, if the hair fibre surface as it emerges from the scalp is already compromised, the consequences with time will become accelerated leading to more rapid deterioration of hair quality.

CONCLUSIONS

A thorough review of technical literature results in strong support for concluding that the condition of the scalp can influence the quality of the hair which is produced. A possible explanation involves altered keratinization of the cuticles in the pre-emergent hair due to perturbations associated with a surrounding oxidative stress environment. The resultant cuticular cells are less flexible than normal which may impair both anchorage and subsequent fibre surface integrity. Once the fibre emerges from the scalp and experiences normal mechanical interactions, the more brittle cuticle breaks and chips off. This results in a rougher cuticle that is also less functionally effective. This leads to a prematurely accelerated wear process and deterioration of overall hair quality. Improvement in scalp health has been shown to be able to reverse these detrimental impacts to the hair by reducing oxidative stress thereby normalizing the environment from which it emerges.