Cath Lab Digest

   As all those who specialize in the treatment of lower extremity ailments will acknowledge, there is nothing uncommon about nail unit pathology. Though pristine appearing nail units are commonplace in children, advancing age may bring a combination of acute and chronic trauma, neoplastic processes, non-infectious dermatological diseases, and bona-fide mycotic and non-mycotic infections that take their toll. These stressors manifest as alterations in nail color, shape and/or texture.

   Too often in mainstream medicine, there is a tendency to attribute such changes within the nail unit solely to onychomycosis, leading clinicians to rely on oral or topical antifungal medications as “silver bullets” in their management. Such ill-fated reliance may lead to presumed drug inefficacy as even a perfect antifungal can only eradicate the organism if it is there. Often fungal infections are indeed present but represent a secondary phenomenon affecting a nail unit that was originally altered by a different pathologic process. In these cases, the best that one can hope for is a mycotic cure but a clinical failure.

   To fine tune our management of patients with nail unit dystrophy, we might benefit by viewing the problem as a constellation of several factors as opposed to equating nail unit dystrophy with onychomycosis. By assessing all the possible contributors to the nail unit abnormality, we will recognize the various processes that must be addressed in addition to, or in lieu of, antifungal therapy.

A Guide To The Pathogenesis Of Nail Unit Dystrophy And Onychomycosis

   Abnormal epithelial keratinization is the single most important process in the development of an overwhelming majority of nail unit dystrophy cases. The body’s outer surface, oral cavity, anus and vagina are covered by stratified squamous epithelium. The principal feature that distinguishes the skin of the body from the mucosa of the genital tract or oral cavity is surface keratinization or a stratum corneum. The surface skin requires keratin to protect us from water loss but the mucosa has no such requirement.

   This does not mean that the mucosa cannot become keratinized. In fact, stimuli such as persistent trauma, inflammation and exposure to the external elements routinely lead to mucosal keratinization as might various neoplastic processes. Classic examples of such abnormal keratinization include: that which occurs in the oral cavity in people who perpetually bite their inner cheeks or routinely dip tobacco; that which might occur in association with severe vaginal or uterine prolapse; or that which occurs naturally in circumcised men.

   Discourse on the topic of abnormal epithelial keratinization is pertinent to the subject of nail unit dystrophy for several reasons. Foremost, in the overwhelming majority of cases, nail unit dystrophy is the product of abnormal nail bed and matrical keratinization. It does not arise as the result of an abnormality in the nail plate itself. Unlike when keratinization occurs at exposed sites, when a stimulus leads to keratinization of the nail bed, the overlying (and usually unremarkable) nail plate serves as a barrier that prevents keratin from being sloughed and leads to its accumulation.

   Whether the stimulus is microtrauma, psoriasis, onycholysis, lichen planus or squamous cell carcinoma, nail bed keratinization may result in “dystrophic nails” that are clinically indistinguishable. It is only with some superficial patterns of onychomycosis not associated with nail bed keratinization and some cases of late stage total dystrophic onychomycosis (with florid infiltration of the nail plate itself) that one can make a diagnosis of “onychomycosis” with reasonable surety based on clinical findings alone.