What is causing psoriasis?

Genetic factors

Immunological factors

Environmental factors

Psoriasis is a condition with multiple causes, which may be genetic, immunological, environmental and psychological. These factors alter the functioning of skin cells, in particular keratinocytes and fibroblasts (1).

Genetic factors

There is a large amount of evidence suggesting that there is a genetic predisposition to psoriasis (2). However, there is no one specific psoriasis gene, but instead, there are a number of genetic characteristics which make a patient more likely to develop the condition (1).

Several studies have shown that there is a family history of psoriasis in 30% to 50% of psoriasis cases.

Research on monozygotic twins (identical twins) has however shown that in 70% of cases, both twins were subject to psoriasis (1). If heredity was the sole cause, there would be a 100% match. These findings therefore show that psoriasis depends on other factors.

Our knowledge of the genes associated with psoriasis is currently incomplete. However, studies of families of people with psoriasis have demonstrated that there are chromosome regions associated with the condition (1). These clusters of genes leading to skin inflammation vary from one family to another and from one patient to another.

Researchers think that in a few years they will be able to identify different treatments appropriate to the genetic characteristics of psoriasis patients (1).

Unaffected groups

Some groups, such as native Americans from the Andes and Eskimos, do not get psoriasis. This could possibly be explained by genetic differences coupled with environmental factors.

Read more about genetic factors. 

Immunological factors

The skin consists of the epidermis, dermis and hypodermis. The epidermis is chiefly made up of keratinocytes (cells which produce the horny layer that protects the skin); melanocytes (cells which produce the pigments responsible for tanning and protection from the skin); and Langherans cells (which play a key role in immune protection and in the nerve endings that are connected directly to the central nervous system and control the majority of skin functions).

Cells are renewed too quickly

We know that in psoriasis, the epidermis is renewed too quickly - at four to six times the rate of normal skin. This is because the keratinocytes in the epidermis multiply abnormally, and produce poor quality keratin that results in scales.

The main cells in the dermis, the fibroblasts, control the renewal of keratinocytes. However, this control is defective in psoriasis.

Inflammatory skin reaction

In addition to the fast turnover rate of keratinocytes, psoriasis is the result of inflammatory skin reactions. Two types of cells cause the inflammatory reaction: polymorphonuclear neutrophils, and T lymphocytes which play a key role in the immune response.

What happens to the skin?

Polymorphonuclear neutrophils are attracted to the stratum corneum (the horny outer layer of the epidermis). They detach the superficial layer of the skin and cause continual irritation which is more severe than that caused by scratching. As a result, the skin begins a permanent scarring process. These cells are hence involved in maintaining inflammation in the epidermis.

The skin is also attacked by T cells which keep the inflammatory response active. In psoriasis there is a chronically persisting response in the T cells (1) .

The T cells are involved in initiating and maintaining skin inflammation by releasing certain cytokines, which have a pro-inflammatory action.

Psoriasis resembles an auto-immune disorder; it is as if a skin molecule is mistaken for a foreign body and attacked by the immune system, which responds in an exaggerated manner to this "attack". However, the classification of psoriasis as an autoimmune disorder is controversial. It is clear that lesion-associated T cells are central to psoriasis but there is a lack of evidence for self-reactive T cells (2).

Environmental factors

In patients with a genetic predisposition to psoriasis, disease manifestations may be triggered by internal and external environmental factors. All these factors accelerate skin renewal.

External factors include a change in season and clothes rubbing on the skin.

Internal factors include emotional stress, certain medicines and infectious diseases.

Stress in a broad sense is often responsible to the outbreak of psoriasis, ranging from the stress caused by going back to school after the holidays to serious psychological trauma. It is a significant factor which can lead to the first flare of psoriasis and ensuing eruptions.

Beta-blockers, lithium and quinolines are among the medicines which are sometimes suspected of triggering the condition. Sudden withdrawal from corticotherapy can also exacerbate psoriasis.

In children, guttate psoriasis is most commonly triggered by streptococcal infections.

As with any condition affecting quality of life that is triggered by the environment, psoriasis cannot be managed unless multiple factors are taken into consideration.

Psoriasis is not a life-threatening condition, and the main objective of treatment is to improve the patient's quality of life. It is therefore up to the patient, in consultation with a dermatologist, to decide on the treatment which best suits him or her. The therapeutic strategy should be based on dialogue between the doctor and patient.

References:

1) Schon, N Engl J Med, 2005.

2) Bowcock & Krueger, Nat Rev Immunol, 2005.