**1. Introduction and short history**

Psoriasis is defined as chronic inflammatory systemic ailment, affecting the teguments foremost, and characterized by important genetic and immune constituents. The most common form is represented by psoriasis vulgaris, affecting every race and all ages, most often between the ages of 50 and 69 years, concerning at least 100 million individuals worldwide [1, 2]. It is a potentially devastating disorder with a progressive natural course, associated with multiple comorbidities and typified by underlying immunologic and inflammatory elements [3]. Despite it being a convoluted pathology with an incompletely elucidated pathogenesis, it has been shown that the environment, immune system and genetic predisposition all play a decisive role in triggering the psoriasis cascade [4]. As of today, treating psoriasis remains a demanding endeavour, merely attending the symptoms and ignoring the principal cause. Medical management is satiated by a wide variety of choices with fluctuating efficiency, for example, topical therapies, phototherapy, systemic drugs and biological agents [5]. It is fathomable that choosing the most appropriate treatment scheme for each individual can oftentimes be perplexing or even disheartening. Nevertheless, the treatment involved should imply a multidisciplinary course

of action, with psychologists, rheumatologists and dermatologists collaborating in order to deliver the best possible care, with the most satisfactory outcome.

To properly understand the breakthroughs of modern treatment of psoriasis, it might be worthwhile to glance over the history of this complicated disease. The first reported cases were identified in ancient Greece, many of the description written by Hippocrates (460–377 BC) himself [6, 7]. Portrayals of psoriasis can also be traced back to the times of the Old Testament, wherein people suffering from such skin disorders were publicly ostracized since they were considered punished by divinity. Numerous historians acknowledge Celsus (ca. 25 BC–45 AD) as documenting the first clinical description of papulosquamous diseases, whereas Galen (133–200 AD) first utilized the term psoriasis [6, 8, 9]. However, his depiction was inconsistent regarding the disorder that we now know as psoriasis. He described it as a pruritic, scaly skin illness of the eyelids and scrotum, probably referred to as today as seborrheic dermatitis. Nevertheless, the unselective grouping together of all inflammatory skin disorders contributed to the stigmatization of psoriasis patients. During the Middle Ages, when it was believed that psoriasis was as contagious as leprosy, these patients were mandated to carry a chime or clapper that would announce their approach. Furthermore, they had to wear a special garment and could only eat or come into physical contact with others considered lepers.

In the dawn of the nineteenth century, Willan expanded on Celsus's explanations of papulosquamous afflictions by describing characteristics we know considered compatible with psoriasis. Even so, he labelled modern psoriasis as 'lepra vulgaris', which maintained the confusion between these two distinct diseases [6, 7, 10]. Afterwards, there was an incongruity when referring to these pathologies, as authors could not properly agree on which term to use. Ultimately, Gibert corroborated Willan's description with the term psoriasis, putting an end to some of the perplexity and guiding to an improved awareness and understanding of psoriatic patients. Heinrich Auspitz (1835–1886) noticed the papillary bleeding that appeared after removing the scale of psoriatic lesions, currently referred to as the Auspitz sign (or bloody dew phenomenon) [6, 7, 11, 12]. In 1877, Heinrich Köbner (1838–1904) defined the sign that carries his name, specifically the occurrence of a psoriatic lesion within the location of a physical injury. After two more decades, in 1898, William Munro (1863–1908) described the microabscesses that appear in psoriasis, otherwise known as Munro's abscesses. The beginning of the twentieth century led to further advancements in the understanding of psoriatic lesions. In 1910, Leo von Zumbusch (1874–1940) was the first to note generalized pustular psoriasis, now called the von Zumbusch disease [6, 13]. Among other descriptions was also the one of the Russian dermatologist D.L. Woronoff in 1926 regarding a pale halo now known as the 'Woronoff ring' enclosing a plaque of psoriasis [7, 14]. The characterization of the Auspitz sign, Köbner's phenomenon, Munro's abscess, and pustular psoriasis, as well as the Woronoff ring made it possible for practitioners to more easily identify patients with psoriasis.

The next discoveries furthered our understanding of pathophysiology, especially concerning epidermal hyperplasia and keratinocytes' cell cycle shortening by van Scott and Ekel in 1963, followed by the role of the immune system by Gubner in 1951 and Muller in 1979 [6, 7]. However, there is still much to be learned about this complex disease and its intricate mechanisms.

The treatment of psoriasis also varied across the ages, from arsenic and ammoniated mercury in the nineteenth century (which both had a comparable toxic potential), to chrysarobin, anthralin and coal tars in the late nineteenth and early twentieth centuries, reaching to corticosteroids, methotrexate and PUVA in the middle of the last century [6, 7, 10, 15]. In what follows, we describe the modern forms of therapy which have been scientifically proven to ameliorate the symptoms in psoriasis.

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*Medical Management of Chronic Plaque Psoriasis in the Modern Age*

psoriasis is the utmost step in offering the best available therapy.

In the past few years, countless achievements have been made in grasping the intricate physiopathological contrivances of psoriasis. Studies repeatedly demonstrated that it is a chronic, systemic immune-mediated ailment, the dermatologic manifestation representing its most debilitating aspect, usually followed by joint involvement. However, the explicit mechanisms of this process have not been untangled. Even so, it appears that the myeloid dendritic cells begin producing interleukins such as IL-12, IL-23 and TNF-α prior to a minor traumatic injury that perform as chemoattractants for the T helper Th-1 and Th-17 cells [16, 17]. In the next step, these cells will raise the production of psoriatic cytokines such as IL-17 within the site of injury, hence increasing the keratinocytes' turnover and eventually piloting towards the cutaneous symptoms of psoriasis [18–21]. Also, the proinflammatory substances may extend into the bloodstream with a significant influence on insulin signalling, angiogenesis, lipogenesis or adipogenesis, which will ultimately lead to comorbidities such as obesity and dyslipidaemia, hypertension, depression and type 2 diabetes mellitus [3, 22]. Grasping the mechanisms of

Topical therapy as the only form of treatment has demonstrated a mediocre rate of improvement, with patients often describing ongoing clinical symptoms, for instance, redness, pruritus or scales [23]. One survey targeted to such patients showed that 40% of cases with a mild disease, circa 50% of those with moderate psoriasis and well above 40% with the severe form were discontented with the recommended topical therapies. The lowermost treatment satisfaction quotients were found in the topical medications versus systemic and phototherapy group [24]. Should topical therapy in itself fail to achieve the expected outcome, practitioners have to be ready for alternative strategies, such as systemic and biological therapies.

Topical therapies are recommended in mild psoriasis, when the affected body

Anthralin via mitochondrial dysfunction might reduce the proliferation of keratinocytes and re-establish cell differentiation. As such, it is used to treat the localized plaques that are covered with thick scales localized either on body or the scalp that have failed to clear with other treatments. It is applied on the affected areas in concentration of 1%, and it is left between 20 min and 1 h before removal [26]. Among the adverse effects, the common is skin irritation or staining of the

Coal tar seems to reduce hyperproliferation of keratinocytes by supressing DNA synthesis, and it has exhibited efficacy on chronic plaque psoriasis, palmoplantar psoriasis or scalp psoriasis, improving the general aspect of the psoriasis plaque after 1 month of treatment. It appears as though the remission period of the lesions

Adverse effects number odour, staining, contact dermatitis, erythema and

It can be used during pregnancy, but in children caution is advertised [27].

persists longer than that with other topical treatments [25].

*DOI: http://dx.doi.org/10.5772/intechopen.90626*

**2. Management of psoriasis**

**2.1 Topical therapy**

*2.1.1 Anthralin*

adjoining skin [25].

*2.1.2 Coal tar*

folliculitis.

surface area is below 10% [25].
