Plaque Psoriasis

Updated: Nov 29, 2022
  • Author: Harvey Lui, MD, FRCPC; Chief Editor: Dirk M Elston, MD  more...
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Practice Essentials

Psoriasis, which manifests most often as plaque psoriasis, is a chronic, relapsing, inflammatory skin disorder with a strong genetic basis. Plaque psoriasis (see the image below) is rarely life threatening, but it often is intractable to treatment.

Plaque psoriasis. Courtesy of University of Britis Plaque psoriasis. Courtesy of University of British Columbia, Department of Dermatology and Skin Science.

See Psoriasis: Manifestations, Management Options, and Mimics, a Critical Images slideshow, to help recognize the major psoriasis subtypes and distinguish them from other skin lesions.

Signs and symptoms

Psoriatic plaques are characterized as follows:

  • Raised and easily palpable - Owing to the thickened epidermis, expanded dermal vascular compartment, as well as infiltrate of neutrophils and lymphocytes

  • Irregular to oval in shape

  • One to several centimeters in size

  • Well defined, with sharply demarcated boundaries

  • Very distinctive rich, full red color; lesions on the legs sometimes carry a blue or violaceous tint

  • Typically have a dry, thin, silvery-white or micaceous scale

  • Typically have a high degree of uniformity, with few morphologic differences between the 2 sides

  • Range in number from a few to many at any given time

  • Most often located on the scalp, trunk, and limbs, with a predilection for extensor surfaces, such as the elbows and knees

  • Symmetrically distributed over the body

  • May, in the case of smaller plaques, coalesce into larger lesions, especially on the legs and sacral regions

Other manifestations of plaque psoriasis include the following:

  • Pruritus - One of the main symptoms of plaque psoriasis

  • Nail psoriasis - Nails may exhibit pitting, onycholysis, subungual hyperkeratosis, or the oil-drop sign

  • Inverse psoriasis - A variant of psoriasis that spares the typical extensor surfaces and affects intertriginous areas (ie, axillae, inguinal folds, inframammary creases) with minimal scale

  • Psoriatic arthritis - Occurs in approximately 10-20% of all cases of plaque psoriasis

Manifestations of the psoriatic arthritis include the following:

  • Red, warm, tender, and inflamed joints

  • Joint deformity

  • Dactylitis

  • Sausage digits


In children with plaque psoriasis, plaques are not as thick, and the lesions are less scaly. Psoriasis often appears in the diaper region in infancy and in flexural areas in children. The disease more commonly affects the face in children than it does in adults.


Laboratory studies

The diagnosis of psoriasis is almost always made on the basis of clinical findings. Laboratory investigations are rarely indicated.

Skin biopsy

Skin biopsy can confirm the diagnosis of plaque psoriasis. This procedure, however, is usually reserved for the evaluation of atypical cases or for excluding other conditions in cases of diagnostic uncertainty.


Histologic epidermal findings include the following:

  • Mitotic activity of basal keratinocytes is increased almost 50-fold, with keratinocytes migrating from the basal to the cornified layers in only 3-5 days rather than the normal 28-30 days

  • The epidermis becomes thickened or acanthotic in appearance, and the rete ridges increase in size

  • Abnormal keratinocyte differentiation is noted throughout the psoriatic plaques, as manifested by the loss of the granular layer

  • Alternating collections of neutrophils are sandwiched between layers of parakeratotic stratum corneum, which is virtually pathognomonic for psoriasis

Histologic dermal findings include the following:

  • Signs of inflammation can be observed throughout the dermis

  • Marked hypervascularity and an increase in the size of the dermal papillae occur

  • An activated CD3+ lymphocytic infiltrate is noted around blood vessels

  • An aggregation of neutrophils in the dermis occurs that extends up into the epidermis


Topical therapy

Topical agents used (often concurrently) to treat plaque psoriasis include the following:


The two main forms of phototherapy are as follows:

  • Ultraviolet B (UVB) irradiation - UVB therapy is usually combined with one or more topical treatments

  • Psoralen plus ultraviolet A irradiation (PUVA) - This treatment uses the photosensitizing drug methoxsalen (8-methoxypsoralen) in combination with UVA irradiation to treat patients with more extensive disease

Systemic therapy

Systemic treatment is initiated only after topical treatments and phototherapy have proved unsuccessful. Systemic therapy should also be considered for patients with very active psoriatic arthritis, as well as for patients whose disease is physically, psychologically, socially, or economically disabling. [1, 2, 3, 4]

Biologic therapy

Biologic therapies provide selective, systemic, immunologically directed interventions, including the following, at key steps in the pathogenesis of plaque psoriasis [5] :

  • Inhibition of the initial cytokine release and Langerhans cell migration

  • Targeting of activated T cells, prevention of further T-cell activation, and elimination of pathologic T cells

  • Blockage of interactions that lead to T-cell activation or migration into tissue

  • Alteration of the balance of T-cell types

  • Inhibition of proinflammatory cytokines, such as tumor necrosis factor (TNF), [6] interleukin (IL)–12, IL-17, and IL-23 [7, 8, 9]



Psoriasis is a common, chronic, relapsing, inflammatory skin disorder with a strong genetic basis. The plaque type of psoriasis is the most common, although several other distinctive clinical variants of psoriasis are recognized (eg, Guttate Psoriasis; Psoriasis, Nails; Psoriasis, Pustular; Psoriatric Arthritis).

Plaque psoriasis is most typically characterized by circular-to-oval red plaques distributed over extensor body surfaces and the scalp. The plaques usually exhibit scaling as a result of epidermal hyperproliferation and dermal inflammation. The extent and duration of plaque psoriasis is highly variable from patient to patient. Acute flares or relapses of plaque psoriasis may also evolve into more severe disease, such as pustular or erythrodermic psoriasis.

Up to 10-20% of patients with plaque psoriasis also experience psoriatic arthritis. A population-based study by Wilson et al that spanned more than 30 years reported that less than 10% of psoriasis patients develop clinically recognized psoriatic arthritis. The clinical features that were associated with an increased chance of leading to psoriatic arthritis were reported as being scalp lesions, nail dystrophy, and intergluteal or perianal psoriasis. [10]

For more information, see Psoriasis.



The pathophysiology of psoriasis must be understood in terms of the prominent pathologies occurring in both major components of the skin—the epidermis and the dermis.

Psoriasis is fundamentally an inflammatory skin condition with reactive abnormal epidermal differentiation and hyperproliferation. Current research suggests that the inflammatory mechanisms are immune based and most likely initiated and maintained primarily by T cells in the dermis. [11]

In this model, antigen-presenting cells in the skin, such as Langerhans cells, are believed to migrate from the skin to regional lymph nodes, where they interact with T cells. Presentation of an as yet unidentified antigen to the T cells, as well as a number of co-stimulatory signals, triggers an immune response, leading to T-cell activation and the release of cytokines.

Co-stimulatory signals are initiated via the interaction of adhesion molecules on the antigen-presenting cells, such as lymphocyte function–associated antigen (LFA)–3 and intercellular adhesion molecule-1, with their respective receptors CD2 and LFA-1 on T cells. These T cells are released into the circulation and traffic back into the skin.

Reactivation of T cells in the dermis and epidermis and the local effects of cytokines such as tumor necrosis factor lead to the inflammation, cell-mediated immune responses, and epidermal hyperproliferation observed in persons with psoriasis.

An interleukin (IL)-12–related cytokine, IL-23, is involved in the establishment of chronic inflammation and in the development of a T helper (Th)–cell subset producing IL-17. These cells, which are designated Th17, are distinct from Th1 and Th2 populations. Th17 cells are now recognized as a third T-effector cell subset, and the IL-23/IL-17 pathway has been implicated in the induction and progression of a number of inflammatory diseases, including psoriasis. [12]

Environmental factors

Infection and a number of physical agents (eg, HIV infection, alcoholism, smoking, UV light) all can affect the course, duration, and clinical appearance of plaque psoriasis. See Etiology of Plaque Psoriasis, below, for more details on the role of environmental factors.



Genetic factors

HLA-B13, -B17, and -Cw6 are all associated with plaque psoriasis. Multifactorial inheritance mechanisms and etiologies without any genetic component have not yet been excluded, although many families appear to exhibit autosomal dominant patterns of inheritance with decreased penetrance. Studies of twin siblings have shown concordant disease in 73% of monozygotic twins compared with 20% in dizygotic twins.

Several putative genetic susceptibility loci have also been identified, including psoriasis susceptibility 1 (PSOR1) on chromosome 6, which is associated with up to 50% of cases. Six other psoriasis susceptibility loci (PSOR2, PSOR3, PSOR4, PSOR5, PSOR6, PSOR7) have been discovered, as well as the transcription factor RUNX1. While this certainly points to genetic mechanisms, the absence of 100% concordance among monozygotes suggests that environmental factors must play a role in the pathophysiology of this disease.


All types of trauma have been associated with the development of plaque psoriasis (eg, physical, chemical, electrical, surgical, infective, and inflammatory injury). Even excessive scratching can aggravate or precipitate localized psoriasis. The development of psoriatic plaques at a site of injury is known as the Koebner reaction.


Most patients consider sunlight to be beneficial for their psoriasis; they report a decrease in illness severity during the summer months or periods of increased sun exposure. However, a small minority of patients find that their symptoms are aggravated by strong sunlight, and these individuals actually experience a worsening of their disease in the summer. A severe sunburn can lead to an exacerbation of plaque psoriasis via the Koebner reaction.


Pharyngeal streptococcal infections have been shown to produce a clinically distinctive disease flare known as guttate psoriasis. Some evidence suggests that subclinical streptococcal colonization or overgrowth could be responsible for refractory plaque psoriasis.

HIV infection

An increase in psoriasis activity has been observed in patients who are infected, or become infected, with HIV. The extent and severity of skin disease initially appears to parallel the disease stage. Psoriasis often becomes less active in advanced HIV infection.


A number of medications have been shown to cause an exacerbation of psoriasis. Lithium and withdrawal from systemic corticosteroids are well known to cause flares of disease. Beta-blockers, antimalarials, and nonsteroidal anti-inflammatory drugs (NSAIDs) have also been implicated.

Psychogenic/emotional factors

Many patients report an increase in psoriasis severity with psychological stress. A clear cause-and-effect relationship between disease exacerbation and stress unfortunately has not been proven. Patients may show a decreased capacity to cope with their treatment regimen with higher levels of stress. Pruritus in the setting of increased anxiety or depression may promote scratching and a Koebner reaction.


An increased risk of chronic plaque psoriasis exists in persons who smoke cigarettes.

Alcohol consumption

Alcohol consumption is considered a risk factor for psoriasis, particularly in young to middle-aged men.

Endocrinologic factors

Psoriasis severity has been noted to fluctuate with hormonal changes. Disease incidence peaks at puberty and during menopause. During pregnancy, symptoms are more likely to improve than worsen, if any changes occur at all. In contrast, the disease is more likely to flare in the postpartum period, again if any changes occur at all.



Plaque psoriasis occurs worldwide, although its prevalence varies with race, geography, and environmental factors (eg, sun exposure). In the United States, 1-2% of the population has plaque psoriasis.

Family history has been shown to predict disease occurrence. When both parents are affected by psoriasis, the rate in siblings of probands is as high as 50%. When one parent is affected, the rate is 16.4%. When neither parent has psoriasis, only 7.8% of siblings of probands are affected.

Of patients with psoriasis, 36-71% have one relative who is also affected by psoriasis. For siblings of patients whose psoriasis appeared before age 15 years, a 3-fold higher risk exists of developing disease compared with siblings of patients who first presented after age 30 years.

Psoriasis affects adult males and females equally. Among children and adolescents, plaque psoriasis has been found to affect females more than males, but this observation may be due to the earlier age of onset in females.

Plaque psoriasis first appears during 2 peak age ranges. The first peak occurs in persons aged 16-22 years, and the second occurs in persons aged 57-60 years. Females develop plaque psoriasis earlier than males, and patients with a positive family history for psoriasis also tend to have an earlier age of onset.

Racial disparity in psoriasis

Psoriasis can affect persons of any race; however, epidemiologic studies have shown a higher prevalence in western European and Scandinavian populations. In these groups, 1.5-3% of the population is affected by the disease.

The highest documented disease prevalence is in Arctic Kasach'ye, with 12% of the population affected, followed by Norway, where 4.8% of the population has psoriasis. Lower prevalence rates for psoriasis have been reported among Japanese and Inuit populations.

Psoriasis is thought to be rare in West Africans and African Americans and is nearly absent in North American Indians. Psoriasis was undetected in the Samoan population and in a study that examined 26,000 South American Indians.



The course of plaque psoriasis is unpredictable. Predicting the duration of active disease, the time or the frequency of relapses, or the duration of a remission is impossible. The disease rarely is life threatening but often is intractable to treatment, with relapses occurring in most patients.

Both early onset and a family history of disease are considered poor prognostic indicators. Some suggest that stress is also associated with an unfavorable prognosis.

Environmental factors (particularly sunlight and warm weather) help alleviate the disease and are considered advantageous. Methotrexate, PUVA, cyclosporine, oral retinoids, and biologic therapies all have helped induce and maintain remission in severe cases of plaque psoriasis.

Mortality and morbidity

Disease-related mortality is exceedingly rare in psoriasis. Even then, mortality is related primarily to therapy: systemic corticosteroid therapy may provoke pustular flares of disease, which can be fatal; methotrexate therapy may result in hepatic fibrosis; and phototherapy (eg, psoralen plus UVA [PUVA]) may induce skin cancers, with subsequent metastasis.

Morbidity is a much greater problem in patients with psoriasis; it includes pruritus, dry and peeling skin, fissuring, self-consciousness and embarrassment about appearance, inconvenience, and the adverse effects and high cost of antipsoriatic treatment regimens. By far, reduced quality of life is the most significant morbidity. Studies have demonstrated that patients with psoriasis have deficiencies in quality of life similar to those for persons with congestive heart failure.

An association between psoriasis, obesity, and cardiovascular comorbidity was been recognized amongst patients with plaque psoriasis. This appears to be strongest in younger patients with severe disease. The association seems to be related to the metabolic syndrome, a state of chronic systemic inflammation characterized by at least 3 of the following:

  • Abdominal obesity

  • Impaired glucose regulation

  • Hypertriglyceridemia

  • Reduced high-density lipoprotein levels

  • Hypertension

Psoriasis and obesity are now believed to share similar mediators (eg, cytokines tumor necrosis factor [TNF]–alpha and IL-6) that drive the inflammatory process in these conditions. This finding, as it becomes further elucidated, may have future implications on health screening and treatment of patients with psoriasis. [13]


Patient Education

Patient education is one of the foundations for managing this chronic and typically relapsing disorder. Not only is psoriasis associated with morbidity, its treatment can also cause significant adverse effects (even death in rare instances). Patients should be familiar with these details in order to make proper and informed decisions about therapy.

The National Psoriasis Foundation is an excellent organization that provides support to patients with psoriasis.

For patient education information, see the Psoriasis Center, as well as What Is Psoriasis?, Plaque Psoriasis, Types of Psoriasis, Understanding Psoriasis Medications, and Nail Psoriasis.