Psoriatic nail disease has many clinical signs. Most psoriatic nail disease occurs in patients with clinically evident psoriasis; it only occurs in less than 5% of patients with no other cutaneous findings of psoriasis.
An estimated 10-55% of all patients with psoriasis have psoriatic nail disease, and approximately 7 million people in the United States have psoriasis. About 150,000-260,000 new cases of psoriasis are diagnosed each year. US physicians see 1.5 million patients with psoriasis per year.
See the images of psoriatic nail disease below.
See 15 Fingernail Abnormalities: Nail the Diagnosis, a Critical Images slideshow, to help identify conditions associated with various nail abnormalities.
The pathogenesis of the psoriatic nail disorder is not completely known. Nail psoriasis may be due to a combination of genetic, environmental, and immune factors. A well-known fact is that a familial aggregation of psoriasis exists. Studies have linked psoriasis with certain human leukocyte antigen subtypes (eg, Cw6, B13, Bw57, Cw2, Cw11, B27). A T-cell–mediated inflammatory process is being investigated as part of the pathogenesis of psoriasis.
Psoriatic nail disease occurs in 10-55% of all patients with psoriasis, and approximately 7 million people in the United States have psoriasis (psoriasis affects 2-3% of the US population). Less than 5% of psoriatic nail disease cases occur in patients without other cutaneous findings of psoriasis. About 10-20% of people with psoriasis also have psoriatic arthritis, and nail changes are seen in 53-86% of patients with psoriatic arthritis.
Psoriasis tends to run in families. In Farber’s questionnaire study of 2100 patients,  36% of patients reported the presence of psoriasis in at least 1 relative. Among siblings, 8% are affected if neither parent has psoriasis. This percentage increases to 16-25% if 1 parent or sibling has the disease, and it reaches up to 75% if both parents are affected. If 1 twin has psoriasis, the other twin is at an increased risk of having psoriasis (25% for fraternal twins, 65% for identical twins).
In Scandinavia, the prevalence rate of nail psoriasis for adults with psoriasis approaches 5%. The prevalence increases with the age of the population studied.
Psoriatic nail disease is not associated with mortality. In severe cases, patients may have functional and psychosocial impairments.
Males and females are affected equally by nail psoriasis, and the prevalence of nail psoriasis increases with the age of the population studied.
Most psoriatic nail disease occurs in people with clinically evident psoriasis. The diagnosis of psoriatic nail disease without cutaneous psoriasis can be challenging because of the low index of suspicion and the lack of personal/family history of psoriasis.
A retrospective study from 2014 reports that nail involvement in psoriasis is a significant predictor of the patient also having psoriatic arthritis.  The study looked at retrospective data from three German cross-sectional independent national studies on patients with psoriasis and psoriatic arthritis. Data on the patient’s history of psoriasis and psoriatic arthritis, clinical findings, nail involvement, and patient- and practitioner-reported outcomes were collected from standardized questionnaires. In the results, the regression model of 4146 patients indicated one of the strongest predictors of concomitant psoriatic arthritis was nail involvement. Balestri et al also suggest nail psoriasis as a risk factor for subclinical psoriatic arthritis, reporting that 50% of subjects with nail psoriasis had interphalangeal stiffness, pain, and swelling. 
Choi et al sought to determine whether psoriatic nail features were associated with nail psoriasis or cutaneous psoriasis disease severity.  Studies results indicated nail fold psoriasis and subungual hyperkeratosis were significantly associated with disease severity in both cutaneous psoriasis and nail psoriasis.
The clinical findings associated with psoriatic nail disease correlate with the anatomical location of the nail unit that is affected by the disease. The nail unit is composed of the nail plate, the nail bed, the hyponychium, the nail matrix, the nail folds, the cuticle, the anchoring portion of the nail bed, and the distal phalangeal bones (see the images below). The nail plate is the largest component of the nail unit. The nail matrix gives rise to the nail plate.
Any defect to the matrix results in onychodystrophy of the growing nail plate. The proximal nail matrix forms the dorsal portion of the nail plate, whereas the distal matrix forms the ventral part of the nail plate. The clinical presentation may vary depending on the location and the severity of inflammation of the affected nail unit.  See the images below.
This lesion is a translucent, yellow-red discoloration in the nail bed resembling a drop of oil beneath the nail plate. This patch is the most diagnostic sign of nail psoriasis. 
Pitting is a result of the loss of parakeratotic cells from the surface of the nail plate.
These lines are transverse lines in the nails due to intermittent inflammation causing growth arrest lines.
Leukonychia consists of areas of white nail plate due to foci of parakeratosis within the body of the nail plate.
Subungual hyperkeratosis affects the nail bed and the hyponychium. Excessive proliferation of the nail bed can lead to onycholysis.
Onycholysis is a white area of the nail plate due to a functional separation of the nail plate from its underlying attachment to the nail bed. It usually starts distally and progresses proximally, causing a traumatic uplifting of the distal nail plate. Secondary microbial colonization may occur.
Nail plate weakening due to disease of the underlying structures causes this condition.
Splinter hemorrhages are longitudinal black lines due to minute foci of capillary hemorrhage between the nail bed and the nail plate. This is analogous to the Auspitz sign of cutaneous psoriasis, which is the pinpoint bleeding seen beneath the psoriatic plaques.
This is an erythematous patch of the lunula.
Most people with psoriatic arthritis have nail changes that can be classified as follows (see the images below):
Type I – Classic distal interphalangeal joint involvement (5% of patients)
Type II – Arthritis mutilans
Type III – Symmetric polyarthritis
Type IV – Asymmetric oligoarthritis (the most common type of psoriatic arthritis, occurring in 70% of patients)
Type V – Ankylosing spondylitis
See the images below.
Psoriatic nail disease may be due to a combination of genetic, environmental, and immune factors. A well-known fact is that a familial aggregation of psoriasis exists. Recent studies have linked psoriasis with certain human leukocyte antigen subtypes (eg, Cw6, B13, Bw57, Cw2, Cw11, B27). A T-cell–mediated inflammatory processing is being investigated as part of the pathogenesis of psoriasis.
The differential diagnosis of nail psoriasis includes the following:
Other problems to be considered include idiopathic trachyonychia and punctate keratoderma.
A nail biopsy is needed to confirm the diagnosis of nail psoriasis in some cases and is usually taken from the nail bed.
Psoriasis can affect any part of the nail unit. Most changes occur in the nail plate. Histologic findings of nail psoriasis include mild-to-moderate hyperkeratosis, hypergranulosis, serum globules and hemorrhage in the corneum layer, papillomatous epidermal hyperplasia, and spongiosis.
Many treatment options are available after the diagnosis of nail psoriasis is made. The treatments focus on improvement of the functional and psychosocial aspects of psoriatic nail disease.
The treatment options for nail psoriasis include topical corticosteroids, intralesional corticosteroids, psoralen plus ultraviolet light A (PUVA),  topical fluorouracil,  topical calcipotriol,  topical anthralin,  topical tazarotene, [13, 14] topical cyclosporine,  avulsion therapy,  and systemic therapy for severe cases. Onychomycosis (if present) requires antifungal therapy for improvement. Laser and light therapies have emerged as possible cost-efficient, in-office treatments; however, large-scale trials are needed, particularly in consideration for the effects in combination with other current therapies. 
For preventive care, keep the nails dry and protect them from trauma to avoid the Koebner effect and possible secondary microbial colonization. In areas of onycholysis, the nail plate should be trimmed to the point of separation for medications to be effective.
At present, no definitive and curative treatment has been agreed upon by medical experts. Discuss all treatment options for psoriatic nail disease with the patient, and choose the best individually tailored regimen.
Topical treatment with high-potency corticosteroid solution or ointment under occlusion with cellophane wrap at bedtime can improve nail psoriasis. Avoid long, continuous therapy with corticosteroids to avoid tachyphylaxis. Also, avoid prolonged occlusion (not to exceed 2 wk). A topical preparation of a combination of high-potency corticosteroid and calcipotriol may benefit some patients. 
Topical 1% 5-fluorouracil solution or 5% cream applied twice daily to the matrix area for 6 months without occlusion improves pitting and subungual hyperkeratosis.
Psoralen plus ultraviolet light A (PUVA) is very effective for cutaneous psoriasis and can improve nail psoriasis. Both oral and topical PUVA therapies have improved nail psoriasis in 3-6 months. A possible adverse effect of PUVA may be nail discoloration.
Intralesional triamcinolone acetonide suspension of 2.5 mg/mL into the proximal nail fold is very helpful for nail matrix psoriasis (eg, pitting, ridging, leukonychia). This medication may be administered every 4-6 weeks. The proximal nail fold is sprayed first with a refrigerant spray for anesthesia, and the injection is given with a 30-gauge needle.
Systemic therapies have been used in patients with severe cutaneous psoriasis. Few studies have shown significant improvement in nail psoriasis with long-term results.
Three systemic medications are most commonly used for psoriasis and nail psoriasis: methotrexate, retinoids,  and cyclosporine.  All three agents have potential serious adverse effects and toxicities. In most cases, the psoriatic nail disease recurs after the systemic therapy is stopped. Carefully weigh the risk-to-benefit ratio in the treatment of nail psoriasis. Systemic therapies are seldom a first-line therapy for nail psoriasis. Topical treatment with calcipotriol can be used as adjunctive therapy and maintenance therapy with systemic treatment. Biological therapy for psoriasis and psoriatic arthritis may have a significant benefit for some patients with psoriatic nail disease. 
In 2017, the US Food and Drug Administration (FDA) approved the addition of moderate-to-severe fingernail psoriasis data to the adalimumab prescribing information, based on results from a phase 3, multicenter, randomized, double-blind, parallel-arm, placebo-controlled clinical trial. 
Avulsion therapy by chemical or surgical means can be used as an alternative therapy for psoriatic nail disease. Chemical avulsion therapy includes the use of urea ointment in a special compound to the affected nail under occlusion for 7 days, and the nail is removed atraumatically. Chemical avulsion therapy is painless, involves no blood loss, and is less expensive than surgical avulsion.
Surgical avulsion therapy can be performed for psoriatic nail disease when other treatments have failed. During surgery, the matrix can be electively ablated to prevent regrowth of the nail. This procedure is performed under local anesthesia. Inform patients of postoperative discomfort, limitations, and possible physical nail disfigurement.
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Cindy Li, DO Dermatologist and Cosmetic Surgeon, Department of Dermatology, Kaiser Permanente Medical Group
Cindy Li, DO is a member of the following medical societies: American Academy of Cosmetic Surgery
Disclosure: Nothing to disclose.
Richard K Scher, MD Adjunct Professor of Dermatology, University of North Carolina at Chapel Hill School of Medicine; Professor Emeritus of Dermatology, Columbia University College of Physicians and Surgeons
Richard K Scher, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American Medical Association, Association of Military Surgeons of the US, International Society for Dermatologic Surgery, Noah Worcester Dermatological Society, Society for Investigative Dermatology
Disclosure: Nothing to disclose.
David F Butler, MD Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, Phi Beta Kappa
Disclosure: Nothing to disclose.
William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Mark G Lebwohl, MD Chairman, Department of Dermatology, Mount Sinai School of Medicine
Mark G Lebwohl, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Received none from Amgen for consultant & investigator; Received none from Novartis for consultant & investigator; Received none from Pfizer for consultant & investigator; Received none from Celgene Corporation for consultant & investigator; Received none from Clinuvel for consultant & investigator; Received none from Eli Lilly & Co. for consultant & investigator; Received none from Janssen Ortho Biotech for consultant & investigator; Received none from LEO Pharmaceuticals for consultant & inves.
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