The “Dry Skin Cycle”
Paul J. Matts, Ph.D1; Anthony V. Rawlings, Ph.D2 ;
1The Procter & Gamble Company, Rusham Park Technical Centre, Egham, Surrey, UK; 2AVR Consulting Ltd, Northwich, Cheshire, UK
Dry body skin continues to be the number one unmet cosmetic body skincare consumer need in geographies around the world (taken from a P&G Skin Care Market Segmentation Study conducted in 2003 / 2004 amongst 4000 women aged 18-65 in multiple geographies). Fundamental to trying to address this need, therefore, are two prerequisites:
(a) the development of a coherent, holistic model that explains the induction and propagation of the dry skin condition in otherwise normal human skin
(b) a product with excellent consumer acceptance that addresses the mechanistic principles underlying the dry skin model
It is the first need that concerns this current poster. Classically, cosmetic xerosis (interpreted by the consumer as flaky, dry skin) has been described in two ways - (a) as a condition that is simply either present or absent or (b) as a linear progression of sequelae, resulting in the concomitant development of clinical tools such as linear visual grading scales, etc. Whilst not refuting the validity of the above dry skin models, it is proposed that the induction and propagation of dry skin conditions may be best and most intuitively expressed as a cyclical model, dependent on stratum corneum integrity and particularly upon barrier function and homeostasis, essential for controlling stratum corneum water flux / content and enzymatic reactions within the SC. A cyclical model implies a spiralling deterioration in outcome that, without intervention, would lead to a progressive worsening in model endpoints. Additionally, it is implicit that intervention at one, or preferably multiple, points within this cycle is necessary to arrest the progression of this continuing downward spiral. This is indeed the case with most dry skin conditions and, moreover, reflects extremely well consumer perception of dry skin - the seeming repetitive cycle of product usage, re-usage, disappointment with treatment outcome and, often, a corresponding loss of compliance. This poster, therefore, describes a new cyclical model for dry skin that attempts to draw together previous disparate models and knowledge into one coherent hypothesis. The model describes several phases within this cycle and, therefore, possible targets against which treatments could be directed. Several model phases are described; reference may be made to the diagram shown, to facilitate the relationship of these, one to another.
The induction phase can be mediated by a variety of different factors:
- Low environmental temperature and humidity (consistent with seasonal variation) have a strong association with barrier dysfunction and dryness1,2.
- Abrupt changes in environmental condition have recently been shown to be critical in influencing basal skin barrier function and overall condition1,3,4,6.
- Modern indoor climate-controlled environments are also becoming recognised as drivers of dry skin conditions, probably due to the low relative humidity of the air re-circulated3,5,6.
- Surfactant dissolution of stratum corneum lipid and consequent Natural Moisturizing Factor (NMF) loss, occurring as a consequence of everyday cleansing or occupational exposure7,8,9.
- In general, chronological ageing results in a reduction in stratum corneum ceramide levels and progressive impairment of barrier function, concurrent with an increase in dry skin expression2,10,11.
- Psychological stress has recently been shown to result in reduced stratum corneum ceramide levels, reduced NMF levels and smaller corneocytes and consequent barrier dysfunction12,13.
- Genetics can also be involved in the expression of dry skin conditions, expressed in extremis within atopic skin14.
Once the skin has been provoked by one or more of the mechanisms above, there is an inevitable sequence of events
1. A mini-cycle of barrier deterioration (Steps A & B)
An initial dehydration of the SC surface can quickly lead, without intervention, to a steeper SC internal hydration gradient, a decrease in net re-condensation on the SC surface, a corresponding increase in evaporative water loss from the SC surface, a consequent further drop in SC water content and so on. Surface SC lipid bilayer disruption and NMF loss rapidly ensue, propagating further these events. Due to the cyclical nature of these processes, therefore, it becomes virtually impossible to distinguish between dry skin conditions that are provoked initially by barrier disruption or by dehydration of the SC itself7,16,17,18. Once the barrier has been disrupted, even superficially, a new cascade of events is initiated:
2. Induction of a hyper-proliferative state (Step C)
Acute and chronic insults to the SC barrier will lead to enhanced keratinocyte proliferation, consequent hyperkeratosis and mild inflammatory changes (one of the hall-marks of dry skin conditions), as the skin attempts to repair itself. This response is mediated via production and secretion of cytokines and growth factors. The induction of this inflammatory hyperproliferative state is absolutely key in the dry skin cycle as it leads fundamentally to aberrant differentiation and the over-hasty production of a variety of poor quality materials and structures vital to the proper functioning of the SC barrier and normal healthy skin19,20, described in the next phase.
3. Development of abnormal, dysfunctional stratum corneum components (Steps D,E)
(a) Immature corneocyte envelopes: In dry skin, there is a significant increase in the ratio of fragile, immature cornified envelopes displaying reduced hydrophobicity and consequent impairment of covalent-bonding to ceramide lipids, essential for barrier integrity21.
(b) Abnormal ceramides: Although up-regulated in dry skin overall, there is an accumulation of sphingosine-containing ceramides at the expense of phyto-sphingosine ceramides, apparently contributing to, rather than ameliorating, barrier dysfunction22.
(c) Reduction in desquamatory enzyme activity at the surface: It is known that stratum corneum desquamatory enzyme (SCCE / SCTE) specific activity within the stratum corneum is reduced in superficial dry skin conditions due to either changes in stratum corneum lipid architecture, reduced stratum corneum water activity of the stratum corneum can further reduce enzyme activity and desquamation which thereby contributes significantly to all stages of the dry skin cycle7,23.
(d) Immature smaller corneocytes: Finally, the barrier of the SC is also dependent upon the highly convoluted, tortuous path around corneocytes. In hyper-proliferative states, the projected size of the corneocytes decreases, reducing the tortuous pathway and, thus, compromising further the SC barrier24.
4. Loss in efficiency of desquamation and ensuing scaling, thickening and loss of hygroscopicity of the SC (Step F)
Impaired activity of desquamatory enzymes automatically leads to a dramatic increase in scaling and a compaction of multiple layers of sheets of un-separated corneocytes7,25. Marked scaling, is, of course, one of the obvious consumer-noticeable expressions of "dry skin". Importantly, the water gradient across the thicker SC becomes steeper, further increasing evaporative water loss, reducing further water concentration in the outer SC, propagating directly the dry skin cycle. Corneocytes that should have already been shed via desquamation remain adhered to the SC surface for significantly longer periods of time. The corneocytes of dry SC are, therefore, subject to exaggerated environmental insult as a direct result of their increased residence time at the surface. The dry skin cycle, thus, is propagated further by an increased loss of NMF relative to normal skin and a corresponding loss in SC hygroscopicity. Finally, the development of an increasingly thick, dry SC results in a layer characterised, from a biomechanical viewpoint, by a dramatic increase in hardness and brittleness26. These properties create a SC barrier inherently susceptible to mechanical stress and fracture, another factor driving the impairment in barrier function and the cyclical nature of the dry skin cycle.
A cyclical model of dry skin has been described that appears to bring together all current knowledge relating to the induction and propagation of xerosis in normal human skin. As such, we propose that treatment modalities addressing multiple aspects of this model, to repair / augment the pivotal endpoint of SC barrier function, would offer the best solution to this universal consumer skin condition.