Plaque psoriasis or Psoriasis vulgaris (common type) – affects between 58% and 97% of all psoriasis cases. The difference in prevalence can be explained by race and geographical placement.1
It is characterized by sharply demarcated erythematous (red), silvery (whitish/yellowish), scaling plaques which most commonly occur on the elbows, knees, scalp, chest, back, and groin regions. The lesions are well-defined round or oval plaques that differ in size and in chronic plaque psoriasis often coalesce to form very large lesions covering large areas of the body. Other involved areas include the ears, glans penis, perianal region, and sites of repeated trauma.
The lesions vary in size from 0.5 cm in diameter to large confluent areas on the trunk and limbs. There is a sharp line of demarcation between a plaque and clinically normal, uninvolved skin. Longitudinal studies of individual plaques have demonstrated that plaques are dynamic with an active and expanding edge, sometimes to the extent that the advancing edge may become annular leaving clinically normal skin in the centre of the original plaque.2,3
Plaque psoriasis can present in several different ways.
Figure 1. Plaque Psoriasis – colour varies from pinkish red to deep red, shiny with minimal silvery scale. Multiple lesions often coalesce forming larger plaques. This patient would be classified has having sever psoriasis
Figure 2. Plaque Psoriasis – Rupioid subtype Deep violaceous annular (round) lesions with distinctive, thickened, silvery scale. Multiple small lesions can be seen to be coalescing.
The term rupioid relates to distinct morphological subtype of plaque psoriasis. Rupioid plaques are small (2–5 cm in diameter) and highly hyperkeratotic, resembling limpet shells (see Figure 2).
A white blanching ring, known as Woronoff’s ring, may be observed in the skin surrounding a psoriatic plaque.
Other morphological subtypes of plaque psoriasis:-
Psoriasis gyrate — Figure 3 – in which curved linear patterns predominate annular psoriasis (psoriasis annularis – see figure 7 & 8) )—in which ring-like lesions develop secondary to central clearing
Psoriasis follicularis — Figure 4 – in which minute scaly papules are present at the openings of pilosebaceous (hair) follicles.
Ostraceous psoriasis (see Figures 5 & 6 below) refers to hyperkeratotic plaques – extremely thick scaled plaques often resembling an oyster shell.
Figure 5 Figure 6
Plaque psoriasis (see Figures 7 & 8 below) with a discoid (circular or oval) appearance is called psoriasis annularis or annular psoriasis.
Figure 7 Figure 8
Scale is typically present in plaque psoriasis, is characteristically silvery white, but may appear a yellowish colour and can vary in thickness.
Removal of scale may reveal tiny bleeding points (Auspitz sign – See Figure 9). The amount of scaling varies among patients and even at different sites on a given patient. In acute inflammatory or exanthematic psoriasis, scaling can be minimal and erythema may be the predominant clinical sign.4
Lichenified psoriasis (Figure 10 and 11) – thickened psoriasis caused by chronic scratching (eczematized)
Figure 10 Figure 11
Elephantine psoriasis (Figure 12 and 13) – large persistent, leathery plaques
Psoriasis is one of the most common immune-mediated diseases world-wide. It is a chronic condition that waxes and wanes. Importantly it is not contagious but it can be an extremely painful, disfiguring and disabling condition for which there is no cure.
The exact causes of psoriasis have yet to be determined, however impairment of the immune system and genetics are known to play major roles in its development. When the immune system is somehow triggered it speeds up the growth cycle of skin cells among other immune reactions leading to a thickening of the skin, inflammation and excessive scaling.1
The prevalence of psoriasis in different populations varies between 0 and 12%, with estimates between 2 – 3% in most western populations. The prevalence in the northern most regions of the Russia and Norway ranges between 5–10% of the population and the highest 12% prevalence is found in the arctic population.2 In the U.S., prevalence ranges from 2.2% to 3.15% and the prevalence among African Americans is 1.3%. There is a low prevalence among North American Indians, Asians and Western Africans (0.3%). In Japan it is 0.1-0.2% of the population, in China 0.3% and is virtually undetected in Native South American Indians.3, 4, 5 Estimates of the prevalence of psoriasis in Australia ranges from 2.3% to 6.6% and in the U.K., the range was 1.3% to 2.6%.4,6 In Australia in the indigenous population it occur rarely, with two recent Australian studies reporting small numbers of Indigenous patients in both the urban and rural environment presenting with psoriasis.7
What triggers psoriasis is a complex question and a large number of factors are involved. Genes are important: numerous family studies have provided compelling evidence of a genetic predisposition to psoriasis, although the inheritance pattern remains unclear. The condition will develop in up to 50% of the siblings of persons with psoriasis when both parents are affected, but prevalence falls to 16% when only one parent has psoriasis and falls further to only 8% percent if neither parent is affected.8 Environmental risk factors also play a role: bacterial and viral infections, stress, skin trauma, smoking and obesity have all been associated with the onset and exacerbation of psoriasis.9
The classification of severity is based on several dermatological markers. It often is a combination of a PASI (Psoriasis Area and Severity Index) score and a BSA (Body Surface Area) coverage factor.
A PASI score is used by dermatologist to measure the dermatological markers to determine the severity and extent of psoriasis, especially during a clinical trial. Four body areas, the head, the arms, the torso and the legs, are measured according to redness (erythema), thickness (Induration/Infiltration) and scaling (Desquamation) from 0 to 4. (See Chart)
% coverage of the body affected is also involved in the classification of the severity of psoriasis. The classification of mild psoriasis is made when symptoms affect less than 3% of the body surface. Moderate psoriasis covers 3% – 10% and the classification of severe indicates that symptoms affects more than 10% of the body, also the involvement of the hands, feet, facial, or genital regions, by which, despite involvement of a smaller BSA, the disease may interfere significantly with activities of daily life. This of course does not take into account the emotional impact that the condition has on the sufferer.9
Redness / Erythema
Psoriasis can have a devastating impact on psychological well-being and social functioning, similar to that of cancer, arthritis, hypertension, heart disease, diabetes or depression. Most people with psoriasis suffer feelings of stigmatization because of their highly visible symptoms. This leads to feelings of social discrimination and alienation which compounds the feelings of anxiety and depression.9
Almost 90% of psoriasis sufferers have feelings of shame and embarrassment, 62% feel depressed, 58% suffer from anxiety, 44% feel that they have problems at work with most feeling that they are rejected for promotions, not accepted as part of the work group etc., 42% suffer from a lack of self-confidence due to their self-consciousness and 40% have difficulties in sexual relationships.10
TYPES OF PSORIASIS
Psoriasis has been classified into several different types10, depending upon presentation, including:-
Plaque psoriasis or Psoriasis vulgaris (common type) – comprises approximately 90 percent of cases. Characterized by sharply demarcated erythematous silvery scaling plaques which most commonly occur on the extensor surface of the elbows, knees, scalp, sacral, and groin regions. The lesions are well-defined round or oval plaques that differ in size and in chronic plaque psoriasis that often coalesce to form very large, oddly shaped lesions covering large areas of the body. Other involved areas include the ears, glans penis, perianal region, and sites of repeated trauma.
Scalp psoriasis is plaque psoriasis that is confined to the scalp, nape, forehead, sideburns, ears) the scalp lesions rarely extend > 2 cm beyond the hairline. Compared with plaque psoriasis elsewhere on the body, scalp involvement is frequently asymmetrical.
Guttate psoriasis – numerous small, red or salmon pink, drop-like spots which cover a large portion of the skin. Spots have fine, slivery scale. Lesions are usually located on the trunk, arms and legs. Usually proceeded by a bacterial streptococcal infection (strep throat, chronic tonsillitis) or a viral respiratory infection.
Flexural/intertriginous (Inverse psoriasis) – is located in the skin folds: i.e. armpits, under the breasts, skin folds around the groin and between the buttocks and in the skin fold of the obese. It is particularly subject to irritation from rubbing and sweating because of its location in the skin folds and tender areas. The plaques are thin, have minimal scale and a shiny surface commonly accompanied by secondary fissuring and/or maceration (the softening and breaking down of skin resulting from prolonged exposure to moisture). It is also prone to secondary infections such as tinea and candida.
Palmoplantar psoriasis – presenting as hyperkeratotic (thickened), red or yellowish, scaly plaques on the central palm or weight-bearing areas of the soles. The lesions are well demarcated and often accompanied by painful cracking and fissuring.
Palmoplantar pustulosis (PPP): is characterized by hyperkeratosis and clusters of pustules over the palms, and soles of hands and/or feet. These sterile pustules can remain as discrete pustules or may become confluent, producing lakes of pus which dry out, and the skin subsequently peels off, leaving a glazed, smooth erythematous surface. Quite often new crops of pustules will then appear.
Pustular psoriasis or Generalized Pustular psoriasis (von Zumbusch type) – Pustular psoriasis may be localized clusters of pinhead sized sterile pustules or as in the Generalized presentation – the skin becomes very red and tender and within hours, pinhead-sized pustules appear studding the erythematous back? These painful, sterile pustules may become confluent, producing lakes of pus. Subsequently, the pustules dry out, and the skin peels off, leaving a glazed, smooth erythematous surface on which new crops of pustules may appear. This is usually accompanied by a fever and systemic symptoms e.g. nausea, and may require the patient to be hospitalized.
Erythrodermic psoriasis – characterized by erythema, severe scaling, itching, and pain. This unstable psoriasis may some? times evolve to whole-body involvement that can lead to the inability to maintain homeostatic functions and often requires the patient to be hospitalized.
Nail psoriasis – affecting the nails of the fingers and/or toes, may affect only one or several nails. The most frequent signs of nail psoriasis are pitting and distal onycholysis. Clinical manifestations range from pitting, yellowish discoloration, and paronychia, to subungual hyperkeratosis, onycholysis, and severe onychodystrophy.
Psoriatic arthritis (PsA) a chronic inflammatory joint disease occurs in up to 39 % of patients with psoriasis. This type of arthritis can be slow to develop, with only mild symptoms or it can develop rapidly with extreme pain and characterized by focal bone erosions. PsA can be a severe form of arthritis with prognosis similar to that of rheumatoid arthritis
For more information on each classification of psoriasis refer to posts on each individual type.
Višnja Milavec-Pureti? et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat 2011;19(1):39-42
Bhalerao A., Bowcock A. M. ; The Genetics of Psoriasis: A Complex Disorder of the Skin and Immune System; Mol. Genet. (1998) 7 (10): 1537-1545 doi:10.1093/hmg/7.10.1537
Kuchekar A.B. et al.; Psoriasis: A comprehensive review; Int. J. of Pharm. & Life Sci. (IJPLS), Vol. 2, Issue 6: June: 2011, 857-877 857
Parisi R et al. Global epidemiology of psoriasis: A systemic review of incidence and prevalence. J Invest Dermatol 2012 Sep 27; [e-pub ahead of print]. (http://dx.doi.org/10.1038/jid.2012.339)
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Parisi R. et al. Global Epidemiology of Psoriasis; Journal of Investigative Dermatology (2013), Volume 133
Heyes C. et al.; Non-infectious skin disease in Indigenous Australians; Australasian Journal of Dermatology (2014) 55, 176–184
Farber, E.M., Nall, L. and Watson, W. (1974) Natural history of psoriasis in 61 twin pairs. Arch. Dermatol., 109, 207–211.
Pelle Stolt, Maglia Rotta; Bringing Psoriasis into the Light; International Federation of Pharmaceutical Manufacturers & Associations; http://www.ifpma.org/fileadmin/content/Publication/2014/Psoriasis_Publication-Web.pdf
Several viral infections have been associated with the provocation or exacerbation of psoriasis such as strep infections. Psoriasis preceded by herpes simplex virus (HSV) infection has also been reported in the past whilst other less well documented cases of viral induced psoriasis have been reported with Hepatitis B and C. Recently a case of human papilloma virus (HPV) and late onset of psoriasis has been reported. Chikungunya infection, HIV/AIDS, persistent Cytomegalovirus (CMV) infection and varicella zoster virus (VZV) have all been reported as causal and/or aggravating factors. 1,2,3,4,5,6
The relationship between bacterial infection and the exacerbation of psoriasis is perhaps most clearly demonstrated in guttate psoriasis where there are multiple reports demonstrating that acute exacerbation of guttate psoriasis, in the majority of patients, is preceded by an infection with group A streptococci. Streptococcus pyogenes infection has also been implicated.
Guttate psoriasis is a distinctive acute form of psoriasis that generally occurs in children and young adults. The association between guttate psoriasis and Streptococcus pyogenes is medically well recognized; however, the exact mechanism remains unknown. The streptococcal trigger and genetic background of psoriasis suggest that psoriasis patients may display a particular, genetically determined sensitivity to streptococcal infection. Streptococcal infection has been found exclusively in type I psoriasis patients. (Please refer to our Blog PSORIASIS – Is it all in the family?) In up to 45% of guttate psoriasis cases, Pharyngitis and upper respiratory infections are the most common trigger recorded. Recent studies suggest that continuing, subclinical streptococcal and staphylococcal infections might be responsible not only for the relapse of acute guttate psoriasis but also for a guttate flare of a new episode of chronic plaque psoriasis as 70%of patients with guttate psoriasis go on to develop chronic plaque psoriasis. 7,8.9,10
Activation of T-cells is considered as an important factor in the pathogenesis of psoriasis, since the laboratory studies have shown that the population of T-cells isolated from the skin of patients with psoriasis is capable of stimulating keratinocytes proliferation. Super antigens, including a group of viral or bacterial proteins, can directly bind to major histocompatibility complex (MHC) class II and the V? component of T-cell receptors, and cause T-cells activation. Recently, much attention has been paid to the role of super antigens as triggering factors in the pathogenesis of psoriasis. Super antigens produced by Staphylococcus aureus are among the most lethal toxins. Toxins of this large family trigger an excessive cellular immune response leading to toxic shock. Some examples of staphylococcal super antigens are staphylococcus enterotoxin A, B, and C (SEA, SEB, SEC), toxic shock syndrome toxin-1 (TSST-I) and exfoliative toxin (ET). Staphylococcal super antigens (SAg’s) play role in the pathogenesis of inflammatory skin diseases. Severity of PS is significantly correlated to enterotoxin production of the isolated S. aureus strains.11
Infectious perianal dermatitis is in fact a group of diverse diseases that are characterised by anal and/or peri-anal inflammation in children and rarely in adults. Perianal streptococcal dermatitis (PSD) generally occurs in children between six months and ten years of age and affects boys more often than girls. Although uncommon, PSD has also been reported as being caused by Staphylococcus aureus. In one study, the incidence was reported to range from one in 218 to one in 2000 pediatric outpatient visits.14Signs and symptoms in this study included perianal dermatitis (90%), perianal itching (78%), rectal pain (52%), and blood-streaked stools (35%). Intra-family spread has been reported in 50% of possible cases. Children with streptococcal pharyngitis have a 6% anal carriage rate. PSD develops 24 to 48 hours after acute afebrile pharyngitis. Some cases of perianal streptococcal dermatitis in children may be linked to guttate psoriasis.
A study published in 2014, concluded superantigens and toxins from Candida “…may play various roles in the exacerbation and the persistence of psoriasis.” 60% of the psoriasis patients tested positive for Candida versus 20% of the control group in oral tests and 15% of the psoriasis patients tested positive verses 4% of the control group in skin tests. The link between the exacerbation of psoriasis, and skin and/or gut colonization by Candida albicans was further confirmed in another study in 2015.12,15
The role of Malassezia species in psoriasis is still undetermined, but several reports have associated the lipophilic yeasts with the development of skin lesions in psoriasis, the lipophilic yeast Malassezia furfur has been implicated in the exacerbation of scalp psoriasis.15
It was found that when cell fragments of Malassezia were topically applied to the skin of psoriatic patients, new psoriatic plaques were induced.15 Research has also reported that there is a significant correlation between the presence of Malassezia yeast and the severity of skin irritation in existing psoriatic plaques.16 These findings suggest that there are several mechanisms by which Malassezia yeasts may contribute to exacerbate psoriasis, but still remains unclear whether these microorganisms are able to initiate the development of psoriasis lesions. Psoriasis is also known to have a strong genetic component. Therefore, research has investigated immune reactions in patients with psoriasis. It has been shown that these individuals have immunological responses to both Malassezia yeasts and to proteins derived from them. T cells reactive to the yeasts have been isolated from lesional skin and it has been demonstrated that antibodies to the yeasts are present in serum taken from patients with psoriasis, but not from control subjects.17
Jain SP, Gulhane S, Pandey N, Bisne E. Human papilloma virus infection and psoriasis: Did human papilloma virus infection trigger psoriasis?. Indian J Sex Transm Dis 2015;36:201-3
Shinichi Imafuku, Reiko Naito, Juichiro Nakayama; Possible association of hepatitis C virus infection with late-onset psoriasis: a hospital-based observational study. ; J Dermatol 2013 Oct 21;40(10):813-8. Epub 2013 Aug 21.
Mohamed A.E. et al.; Psoriasis; a new marker for Hepatitis C among Egyptian Patients; Int.J.Curr.Microbiol.App.Sci (2015) 4(6): 761-767
Ahmad QM, Sameem F, Shah IH. Prevalence of hepatotrophic viruses b&c in psoriasis -A study from kashmir. Indian J Dermatol 2005;50:200-2
Zakaria Mahran and Tarek M. Emran. Prevalence of hepatitis C virus infection in patients with chronic plaque Psoriasis in Damietta Governorate. J Am Sci 2015;11(7):130-133
Failla V. et al; Childhood Herpes Zoster-Triggered Guttate Psoriasis; The Open Dermatology Journal, 2012, Volume 6
Sigurdardottir S. L. et al.; The association of sore throat and psoriasis might be explained by histologically distinctive tonsils and increased expression of skin-homing molecules by tonsil T cells; British Society for Immunology, Clinical and Experimental Immunology, 174: 139–151
Bartenjev I. et al.; Subclinical Microbial Infection in Patients with Chronic Plaque Psoriasis; Acta Derm Venereol 2000; Suppl 211: 17-18.
Leung D.Y.M., et al; Evidence for a Streptococcal Superantigen-driven Process in Acute Guttate Psoriasis; The Journal of Clinical Investigation, Inc. Volume 96, November 1995, 2106-2112
Weisenseel P. et al.; Streptococcal infection distinguishes different types of psoriasis; Downloaded from http://jmg.bmj.com/ on February 7, 2016 – Published by group.bmj.com
Atefi et al.; The Rise of Staphylococcal Super Antigens in Psoriatic Patients: A Case-Control Study; Jundishapur J Microbiol. 2014 May; 7(5): e9912.
Taheri Sarvtin,et al.; Evaluation of candidal colonization and specific humoral responses against Candida albicans in patients with International Journal of Dermatology. Dec2014,Vol.53Issue12, pe555-e560. 6p.
Fakhrozaman Pezeshkpoor et al.; Prevalence of Candida in saliva and skin lesions of Psoriasis Vulgaris patients; Journal of Mycology Research. Vol 2, No 1, March 2015, Page 9-14
Abbas Rasi, Nargess Pour-Heidari; Association between Plaque-Type Psoriasis and Perianal Streptococcal Cellulitis and Review of the Literature – Case Report; Arch Iran Med 2009; 12 (6): 591 – 594
Prohi? A.; Psoriasis and Malassezia Yeasts; www.interechopen.com; http://cdn.intechopen.com/pdfs-wm/32471.pdf
Baroni A. et al.; Possible role of Malassezia furfur in psoriasis: modulation of TGF-b1, integrin, and HSP70 expression in human keratinocytes and in the skin of psoriasis-affected patients; J Cutan Pathol 2004: 31: 35–42
Zomorodian et al.; Malassezia isolated from psoriasis patients; J Cutan Pathol 2008 doi: 10.1111/j.1600-0560.2007.00968.x
Gomez-Moyano E, et al. Do Malassezia species play a role in exacerbation of scalp psoriasis?. Journal De Mycologie Médicale (2014), http://dx.doi.org/10.1016/j.mycmed.2013.10.007