Papulosquamous Disorders — Psoriasis, Lichen Planus, Pityriasis Rosea and PRP

Papulosquamous disorders are skin diseases in which raised lesions (papules and plaques) carry scale (squame). The group is a classic spotter and differential-diagnosis theme in dermatology. The exam-relevant members are psoriasis, lichen planus, pityriasis rosea and pityriasis rubra pilaris (PRP); guttate psoriasis also has to be separated from secondary syphilis, tinea corporis and pityriasis lichenoides chronica.

The practical approach is to anchor each disease on one sign that no other member shares: Auspitz sign for psoriasis, Wickham striae for lichen planus, the herald patch for pityriasis rosea and islands of sparing for PRP.

Psoriasis is an immune-mediated inflammatory disorder in which keratinocytes hyperproliferate and differentiate abnormally. Antigen-presenting cells such as Langerhans cells activate T cells in regional lymph nodes; the T cells return to the skin and release cytokines centred on the IL-23/IL-17 axis and TNF-α, driving chronic inflammation. Genetic susceptibility includes the HLA-Cw6 allele, strongly associated with early-onset and more severe disease.

• Trauma — Koebner (isomorphic) phenomenon: new lesions appear at sites of skin injury.
• Infection — streptococcal infection is the classic trigger (especially for guttate psoriasis).
• Drugs — lithium, beta-blockers and abrupt withdrawal of systemic corticosteroids.
• Lifestyle — emotional stress, heavy alcohol use and smoking.

Plaque psoriasis is the commonest type. Well-demarcated erythematous plaques covered by micaceous, silvery-white scale appear most often on the extensor surfaces of the elbows and knees, the scalp, trunk and lumbosacral region; nails and intertriginous areas can also be involved.

Systemic associations matter in clinical questions: psoriatic arthritis, cardiovascular disease, metabolic syndrome and depression. Severity is quantified by body surface area (BSA) involvement and the Psoriasis Area and Severity Index (PASI), with the Dermatology Life Quality Index (DLQI) for quality of life.

Histology shows acanthosis, parakeratosis (nuclei retained in the stratum corneum), near-absence of the granular layer, elongated clubbed rete ridges and thinning of the epidermis over the dermal papillae (suprapapillary thinning). Munro microabscesses (neutrophils in the stratum corneum) and dilated papillary vessels are characteristic.

• Methotrexate — give with folate; monitor CBC, liver and renal function; hepatotoxicity and myelosuppression; check pregnancy status.
• Cyclosporine — nephrotoxicity and hypertension.
• Acitretin — teratogenic, so pregnancy must be avoided for up to three years after treatment.
• Vitamin D analogues reduce keratinocyte proliferation and promote differentiation.

Lichen planus is an inflammatory disease of skin, mucosae, nails and hair. The classic cutaneous picture is pruritic, violaceous papules and plaques on the wrists, lower back and ankles. The textbook summary is the 6 Ps: purple, polygonal, planar, pruritic, papules and plaques. The surface is shiny and firm, overlaid with a lattice of fine white lines called Wickham striae, best seen on the buccal mucosa.

• Oral lichen planus — six subtypes (reticular, erosive, papular, plaque-like, atrophic, bullous); reticular is the commonest, with asymptomatic white lacy lines on the buccal mucosa. Erosive disease is painful and carries a risk of malignant transformation to oral squamous cell carcinoma.
• Nail involvement — about 10% of patients: thinning and longitudinal ridging, then scarring, dorsal pterygium, sandpaper nails (trachyonychia) and nail loss; 20-nail dystrophy is a variant.
• Koebner phenomenon — new lesions along scratch lines, as in psoriasis.
• Associations — hepatitis C virus infection is the infection most emphasised; lichenoid drug eruptions can mimic idiopathic disease and are often photo-distributed.
• Course — most cutaneous disease clears spontaneously within 1 to 2 years; drug-induced lichen planus resolves after stopping the drug.

Histology shows hyperkeratosis without parakeratosis, irregular thickening of the granular layer (hypergranulosis), destruction of the basal layer, loss of rete ridges giving a sawtooth appearance and a dense band-like lymphocytic infiltrate along the dermo-epidermal junction (interface dermatitis). Colloid (Civatte) bodies are apoptotic keratinocytes near the basal layer. Direct immunofluorescence helps separate lichen planus from lupus erythematosus.

For limited disease, the first-line treatment is superpotent topical steroid (clobetasol). Other options include isotretinoin, acitretin, phototherapy (PUVA or UVB), topical calcineurin inhibitors and methotrexate. Because oral erosive disease and esophageal involvement can lead to squamous cell carcinoma, follow-up matters.

Pityriasis rosea is an acute, self-limiting papulosquamous disorder. It begins with a slightly raised, oval, scaly herald patch (mother patch), followed within about 2 weeks by clusters of similar oval scaly patches on the trunk and proximal limbs along the Langer lines of cleavage, giving a Christmas-tree pattern. Reactivation of human herpesvirus 6 and 7 is the proposed cause. It must be separated from secondary syphilis, guttate psoriasis, tinea, nummular eczema and pityriasis lichenoides chronica; the acral variant can mimic erythema multiforme or syphilis (see syphilis stages and serology).

Pityriasis rubra pilaris (PRP) features follicular papules that coalesce into well-demarcated reddish-orange plaques with non-adherent scale and palmoplantar keratoderma. Generalised forms classically show islands of sparing. StatPearls records methotrexate and acitretin as historical first-line systemic treatments, with oral retinoids and methotrexate each giving a good response in roughly a third or more of patients.

• Auspitz sign = psoriasis (not lichen planus).
• Wickham striae = lichen planus; herald patch = pityriasis rosea.
• Koebner is positive in both psoriasis and lichen planus.
• Psoriasis histology = parakeratosis, absent granular layer, Munro microabscess; lichen planus = hyperkeratosis without parakeratosis, hypergranulosis, sawtooth, Civatte bodies.
• Methotrexate needs folate; acitretin is teratogenic; cyclosporine is nephrotoxic; PUVA is carcinogenic with cumulative dose.
• Drugs that trigger or worsen psoriasis: lithium, beta-blockers, abrupt steroid withdrawal.
• Hepatitis C is the infection associated with lichen planus.
• Guttate psoriasis vs secondary syphilis: check serology and palm-sole and mucosal involvement.

For related skin topics see vesiculobullous disorders, SJS and TEN and the structure of the epidermis layers.