Fingernails and toenails are evolved claws that protect the distal digits of the hands and feet. The nail is formed from hard keratin created by modified matrix epithelial cells. Each fingernail matrix has cells under the skin surface that extend from halfway between the distal interphalangeal joint and the proximal nail fold to the proximal aspect of the nail, creating the visible white lunula. The translucent lunula is the only part of the nail plate with living cells. Once the keratinizing cells leave the lunula, a transparent hard keratin is extracted and grows to the distal free edge of the nail plate.
Keratin in normal fingernails takes approximately 6 months to grow from the proximal nail fold to the distal free edge; toenails take approximately 12 to 18 months. Nails grow faster in the summer months, probably because of improved vascular perfusion in the warm weather; they also grow more slowly as we age. This growth creates the perfect window into the body’s internal milieu.
In this month’s CE/CME article on dermatophyte infections, a case-based approach is used to describe and illustrate the various sites on the body where fungal infections may be found. Besides the nails, other body sites commonly involved are the scalp (especially in children), as well as the torso, face, neck inguinal area, and feet. The authors’ clinical examples are helpful in pointing out the “fungus among us.” However, only about half of nail disorders are caused by a pathogenic dermatophyte and other fungal or yeast-based organisms. The other half are attributable to more than 20 inflammatory and traumatic disorders.
Psoriasis is a good example of how inflammatory diseases can cause nail changes. In indivdiuals with psoriasis, cells that typically take 4 weeks to travel from the basal area of the epidermis to the stratum corneum take only 14 days. This acceleration results in immature stratum corneum cells with retained nuclei that form a white plug of immature keratin on the surface of the nail as it migrates distally. The immature keratin does not have the attachment to the surrounding cells and the plug falls out, leaving a pit on the nail surface (surface change). The keratinization process can also be incomplete, and the nail keratin can stay in the translucent immature stage, leading to a thickened nail plate often with distal separation of the nail plate (onycholysis). This process destroys the hyponychial attachment of the nail plate to the nail bed that partially protects the nail from fungal invasion. For this reason, secondary fungus can be present in abnormal psoriatic nails more frequently than in those with a normal nail plate (some studies describe an incidence of up to 20%).1
Increased psoriatic epidermal turnover is now known to be an autoimmune process; several cytokines are responsible for up-regulating psoriatic skin inflammation, including interleukin and tumor necrosis factors, all of which are targets of successful biologic treatment of psoriasis.2 Psoriatic skin disease often occurs prior to involvement of the joints with psoriatic arthritis. The arthritis involves deeper inflammation with the bones and joints. There are five subtypes of psoriatic arthritis, but the three peripheral patterns are more commonly involved with fingernail changes:3
- asymmetric oligoarthritis
- symmetric polyarthritis
- arthritis mutilans
Psoriatic nail changes are more common with psoriatic arthritis, and clinicians should explore this potential connection in every case in which fingernail changes are observed. Because toenails are thicker and prone to trauma, the changes are less likely to reflect an inflammatory process. In addition, toenails are more commonly involved with fungal infections compared with fingernails. Providers should check the fourth and fifth toe web space, as well as dry skin on the plantar surface that extends around the sides of the feet in a pattern (like a moccasin would cover the sides of the foot).
Based on the information in this month’s CE/CME and this editorial, we recommend practitioners view the nails as an external reflection of internal inflammation. As Dr Ayello often quotes, “The eye sees only what the mind is prepared to comprehend.”4
Elizabeth A. Ayello, PhD, RN, CWON, ETN, MAPWCA, FAAN
R. Gary Sibbald, MD, DSc (Hons), MEd, BSc, FRCPC (Med Derm), FAAD, MAPWCA, JM
1. Gupta AK, Lynde CW, Jain HC, et al. A higher prevalence of onychomycosis in psoriatics compared with non-psoriatics: a multicentre study. Br J Dermatol 1997;136(5):786–9.
2. Brandon A, Mufti A, Sibbald RG. Diagnosis and management of cutaneous psoriasis. Adv Skin Wound Care 2019;32:58–69.
4. Davies R. Tempest-Tost. Toronto, ON, Canada: Clarke, Irwin & Company; 1951.