**1. Introduction**

As a common and complex skin condition (Section 1.1), the root causes of psoriasis begin inside our body [1], making it far more than just skin deep. The fact that psoriasis affects the skin's hydration, barrier structure, function and integrity (Section 1.2) [2] means that a combination of several management strategies (Section 1.3) is usually required in order to alleviate associated symptoms [3, 4]. Topical moisturisers (Section 1.4) represent *the* first-line defence strategy that forms the backbone of psoriasis management by reducing and relieving both dryness and the associated itch-scratch cycle, enhancing skin hydration, and strengthening barrier function by influencing its subsequent repair and recovery [5–7] and thus, improving underlying psoriatic symptoms and overall quality of life (QoL) [2].

### **1.1 Psoriasis at a glance**

Psoriasis is a chronic, inflammatory, non-contagious and relapsing skin condition with a strong genetic predisposition and autoimmune pathogenic traits [8]. While psoriasis can present at any age, it most commonly appears for the first time between the ages of 15 and 25 years, and then again between ages of 57 to 60 years [9], affecting both men and women equally [3, 10]. The worldwide prevalence is about 2–5% on average, but varies according to regions and ethnicities [3, 10]. In general, the higher or lower the latitude, the higher the prevalence; people from Asian and African countries are less prone to psoriasis than people from regions further from the equator such as Northern Europe, North America and Australia [10, 11].

The term 'psoriasis' encompasses several distinct clinical forms of the disease, the most common and well-known of which is psoriasis vulgaris, also known as plaque psoriasis. Given the ubiquity of psoriasis vulgaris relative to other forms of the disease, our focus in this chapter will be on this particular form.

The pathogenesis of psoriasis is multifactorial, with genetics being a primary contributor, especially in those with early onset of the disease. Many of the candidate genes are either involved in antigen presentation, immune cell signalling and activation, or skin barrier function, suggesting an intricate interplay between dendritic cells, T cells and the main skin cell type, known as keratinocytes [12, 13]. Several other factors can either initiate and/or exacerbate psoriasis flare-ups. These include: (a) trauma induced by various physical, chemical and inflammatory skin disruptions (e.g., abrasions, incisions, rubbing); (b) bacterial (e.g., *Staphylococcus aureus*) and viral infections; (c) the use of certain medications or drugs (e.g., lithium, blood pressure reducing medications); (d) poor lifestyle habits such as excessive alcohol consumption and smoking; and (e) stress [10, 13, 14].

Psoriasis manifests in several distinct clinical forms according to appearance and the body part affected but predominantly presents as well-demarcated salmon pink plaques (dry and piled up skin cells) and/or lesions with silvery-white scale, accompanied by skin tightness, itchiness, a burning sensation and, in severe cases, even bleeding [1, 3, 10, 13, 15]. These plaques typically appear in a symmetrical distribution and affect extensor areas such as the elbows, knees, lower back, limbs, the scalp, tips of the fingers and toes, palms and soles, the fingernails and toenails, and occasionally, the genitals [3, 10, 13–15]. Patients suffering from psoriasis are frequently categorised into two main groups: (1) mild or moderate psoriasis (most common category; affecting 3–10% of total body area) and (2) severe psoriasis (rare; affecting more than 10% of total body area). Such categorisation primarily depends on the following three aspects: (1) the clinical severity score (also known as Psoriasis Area Severity Index—PASI) of the plaques, which is an assessment tool based on the degree of plaque redness, thickness, itchiness and scaling; (2) the percentage of affected body surface area (BSA); and (3) patient QoL [13, 14, 16].

As alluded to in the introduction, psoriasis is not only a skin condition, it also involves multiple organ systems (e.g., cardiovascular, hepatic, respiratory and haematological) and people with psoriasis regularly display a broad spectrum of symptoms and significant co-existing conditions such as obesity, cardiovascular disease, nonalcoholic fatty liver disease, cancer, diabetes and metabolic syndrome, with rates being especially elevated in those with more severe psoriasis [1, 13]. For example, diabetic patients with psoriasis appear to be more likely to require pharmacological management and suffer from micro- and macrovascular diabetes complications than diabetic patients without psoriasis [17].

#### **1.2 Skin barrier alterations in psoriasis**

The barrier function of the skin resides in the outermost layer of the epidermis, known as the stratum corneum (SC) and is linked to the protein enriched corneocyte

#### *Topical Moisturisers for the Management of Psoriasis Vulgaris DOI: http://dx.doi.org/10.5772/intechopen.101964*

(dead keratinocytes lacking vital cellular organelles) layers and the intercellular membrane lipid matrix mostly composed of ceramides, cholesterol and free fatty acids [18–21]. Corneocytes are continually and efficiently replaced to maintain skin hydration, flexibility and structural integrity, and to repair any perturbation and damage [21]. Continuous exposure to environmental insults such as harsh climatic conditions (e.g., extreme temperatures, wind) and chemicals (e.g., harsh detergents and soaps) can significantly impact the skin's structural and functional properties, which in turn can cause acute or chronic damage of the skin barrier resulting in unfavourable changes in skin morphology and physiology over time [19, 20, 22–24].

Skin dryness is a major underlying problem of the dysfunctional psoriatic skin barrier as it reflects an abnormal and defective desquamation (shedding) process, where corneocytes are shed as visible scales, causing the cosmetically unattractive rough texture associated with dry skin and excessive transepidermal water loss (TEWL), ultimately leading to discomfort and itchiness. Such compromised, dry and fragile skin that is unable to efficiently bind and hold water is also susceptible to the penetration of irritants, allergens and microorganisms that can result in irritation, inflammation and infection [3, 10, 13–15, 19, 20, 22–24].

Normally, healthy skin cells mature and are shed from the skin's surface every 28 to 30 days [25]. However, when psoriasis develops, these skin cells mature much faster, usually in 3 to 6 days, and subsequently move to the skin surface. Due to such a rapid turnover of skin cells, it is possible that even live and healthy cells can reach the surface and accumulate with the dead cells. Instead of being shed, the skin cells pile up, causing the development of thick plaques that are characteristic of psoriasis [14]. There are two main schools of thought as to the exact pathological process that leads to the development of such psoriatic plaques, however, neither of these can stand independently from each other. The first considers psoriasis primarily as an unregulated condition of excessive growth and regeneration of skin cells, characterised by abnormal keratinocyte differentiation and hyperproliferation. Such a problem is simply seen as a 'fault' of the epidermis and its keratinocytes [3, 14, 26]. The second considers psoriasis as an immune-mediated skin condition in which the excessive regeneration of skin cells is secondary to factors produced by the immune system, suggesting that the inflammatory mechanisms are immune-based and most likely initiated and maintained primarily by T cells found within the deeper layer of the skin, the dermis [14, 27, 28]. Given that keratinocytes, dendritic cells and activated T cells are all crucial to the development and persistence of psoriatic plaques, the pathophysiology of psoriasis cannot be explained by the role of a single cell type exclusively – it is likely a dynamic and complex interplay between those cell types. Furthermore, the contribution of each cell type is equally essential in different phases (e.g., initiation, formation, maintenance) of psoriatic alterations. Therefore, the exact sequence of events that lead to the development of psoriatic plaques remains unknown [28].

#### **1.3 Management of psoriasis**

Choosing the best management strategy for psoriasis can often be problematic and frustrating for both patients and healthcare professionals, and usually there are several factors to consider: the type, severity and localisation of the condition; the patient's age and medical history; the impact the disease has on QoL; and the patient's expected goals [1]. Before embarking on a management strategy, it is absolutely crucial to establish expectations and goals. The 'ideal' goal would be complete clearance of psoriatic plaques but this is currently not achievable in most patients. Thus, it is necessary to set

a minimal target to allow modification of the management strategy if the target is not achieved within a set time [29]. In very basic terms, management for 'generalised' psoriasis follows a 1-2-3 step-ladder approach (**Figure 1**), starting with topical therapies (e.g., topical moisturisers) (Section 1.4) followed by phototherapy and then systemic medications that can include a range of oral drugs and small biologicals [1, 10, 30].

Topical therapy as monotherapy is useful in psoriasis patients with a mild to moderate condition. Topical moisturisers are also used as an adjuvant strategy for moderate to severe psoriasis that is concurrently treated with either phototherapy or systemic medications [10].

Phototherapy represents a second-line defence strategy in the management of psoriasis (**Figure 1**). It involves exposure of the psoriatic skin to ultraviolet (UV) radiation, which can decrease the appearance of plaques on the skin [10, 31]. Many types of phototherapy have been developed and used for the treatment of psoriasis over the last few decades. Broadband ultraviolet B light (BB-UVB, 290–320 nm) was the first such therapy developed, but was later replaced by narrowband ultraviolet B light (NB-UVB, 311 nm) as the latter is more effective than the former. The excimer laser/ lamp of 308 nm was next invented and used as a monochromatic (single wavelength) UVB source for psoriasis treatment. The advantage of using excimer is its targeting ability that can spare unaffected skin while providing high doses targeted directly at psoriatic skin [32]. In short, phototherapy acts by causing cutaneous immuno-suppression, slowing down excessive growth of skin cells and altering cytokine expression [10, 31]. The drawbacks to phototherapy include the extensive time investment that is required; usually, three to five therapy sessions per week are needed, with the total therapy period ranging from approximately 2–3 months. Additionally, the response to phototherapy can vary from individual to individual, and there can be health implications to consider, such as the risk of skin cancer [10].

**Figure 1.** *Schematic of psoriasis 1-2-3 step-ladder management approach [1, 10, 30].*

*Topical Moisturisers for the Management of Psoriasis Vulgaris DOI: http://dx.doi.org/10.5772/intechopen.101964*

The decision to progress to systemic therapy (**Figure 1**) should be based not only on objective disease severity (where PASI ≥10% or QoL index ≥10% or BSA ≥10%; indicating more than 10% of involvement of the skin) [33], but also on social and psychological factors. The patient should understand the risks (e.g., higher risk and more adverse effects) (**Figure 2**) associated with systemic medications and should be allowed to determine whether the risk of therapy outweighs the benefit [10]. Indications for systemic therapy include widespread plaque psoriasis, erythrodermic (potentially life-threatening inflammation) psoriasis, or the need for repeated hospitalisation for topical therapy. The therapies for extensive and severe forms of psoriasis usually have long-term side effects [34].

The order in which these management strategies are employed should progress in a stepwise fashion from lowest to highest risk (**Figure 2**), hence, the concept of a management ladder (**Figure 1**). The management strategy with the fewest side-effects (e.g., topical moisturisers) should be employed first. If this strategy proves ineffective or if the psoriasis is more severe, strategies with greater toxicity (e.g., phototherapy and systemic medications) may be initiated (**Figure 2**) [10, 34].

#### **1.4 Topical moisturisers are the backbone of psoriasis management**

Most topical moisturisers are specifically formulated to promote and maintain healthy skin, but may also serve to manage dry and itchy skin conditions such as psoriasis. Moisturisers are crucial to achieving a reduction in clinical signs of irritation and dryness, scaling and roughness, and a decrease in perceived feelings of tightness and itching [6, 20, 35, 36]. There are no specific rules on what is the best or 'correct' type of topical moisturiser to use. Since topical moisturisers are effectively used either as cosmetics (providing basic skin moisturisation) or therapeutics (e.g., managing psoriasis and preventing its exacerbation), the patients' considerations will be mainly influenced by their personal preferences and lifestyle, and the nature and severity of their skin condition. Individual patient preferences and history may have an impact on the choice of moisturiser or moisturising base to use. A psoriasis patient presenting with severe dryness may benefit most from an occlusive ointment, yet their distaste for this particular base may dissuade them from using the product consistently, which could lead to increased morbidity. Conversely, while a lotion or

**Figure 2.**

*The order in which management strategies for psoriasis should be implemented [10, 34].*

cream may not provide as much hydration as an ointment, the patient's preference for such ingredient base may improve compliance and, therefore, outcome. Patient expectation can also impact the choice or use of moisturiser. Despite wide management options being available, psoriasis is still an incurable disease, so expectation needs to be carefully managed. Complete psoriatic plaque clearance and relief from symptoms is often very difficult, if not impossible, a fact that can lead to patient dissatisfaction, as well as poor adherence and compliance with the current management options [10, 37].

The 'ideal' topical moisturiser (**Figure 3**) is one that the user prefers and will use regularly and liberally, keeping in mind that it should be: (a) cosmetically acceptable and elegant; (b) absorbed rapidly providing immediate skin moisturisation and achieve the intended cosmetic and/or therapeutic effect(s); (c) free from common irritants and allergens such as fragrance, colour and soap to minimise irritation and aggravation of the skin or underlying skin condition; and (d) non-sensitising, noncomedogenic (will not block pores), long-lasting [36, 38] and pH-balanced [39].

The efficacy of topical moisturisers is related to its basic skin moisturisation and 'conditioning' benefits, as well as its therapeutic effects. This is achieved most commonly through a well-designed combination of fundamental and specialty ingredients and actives, formulated and delivered in a range of topical formulations (Section 3) [20, 40, 41].

**Figure 3.** *The 'ideal' topical moisturiser characteristics [36, 38–41].*
