Damage to the nail as a result of trauma or specific disease results in nail dystrophy. Nail dystrophy is defined as the presence of misshapen or partially destroyed nail plates. Soft, yellow keratin often accumulates between the dystrophic nail plate and nail bed, resulting in elevation of the former. Various aspects of nail dystrophy are discussed below.
Trauma Trauma to the tips of the digits occasionally results in the formation of a subungual hematoma. The severe pain that accompanies this problem can be relieved by piercing the nail plate with a heated needle or paper clip. Large subungual hematomas result in sloughing of the nail plate weeks to months later. Permanent scarring with nail plate thickening and ridging sometimes accompanies trauma. Scarred nails seem particularly predisposed to the subsequent development of Onychomycosis. Unfortunately, surgical removal of the scarred nail plate is simply followed by regrowth of an equally dystrophic nail.
Onychomycosis Fungal infection is a very common cause of nail dystrophy. The great toenail, in particular, seems prone to infection. Infection of the fingernails occurs only in nails previously traumatized or in tinea manum with subsequent involvement of the nail. The likelihood of Onychomycosis increases with age; children are rarely if ever affected.
The first sign of Onychomycosis is the development of a small area of Onycholysis (separation of the nail plate from the nail bed) at the distal tip of the nail. Shortly thereafter, a buildup of soft yellow keratin occurs in the space created by the onycholysis. This is accompanied by further lifting of the proximal nail. Eventually, the process results in a partially destroyed, heaped up, misshapen yellow nail. The entire process is asymptomatic unless a thickened toenail begins to press against the top of the shoe.
Most Onychomycosis is due to infection with Trichophyton rubrum, but in a few cases Epidermophyton flocwsum and Trichophyton mentagrophytes may be recovered. Infection with mentagrophytes is usually associated with a mild form of Onychomycosis in which portions of the superficial nail plate whiten. Treatment is the same regardless of which organism causes the disease. Orally administered griseofulvin (or rarely ketoconazole) is required if treatment is desired. For all practical purposes, topical therapy with currently available agents is never curative.
Most fingernail infections will clear after 3 to 6 months of continuous therapy. Toenails, because of their slower growth rate, will require 9 to 12 months of treatment. Nearly all fingernail infections respond to therapy, but the response rate for toenail infections is considerably lower. Moreover, the recurrence rate, once treatment is stopped, is extremely high. Consequently, many clinicians discourage treatment of toenail Onychomycosis.
PsoriasisNail dystrophy occurs in a considerable proportion of patients with psoriasis. Most often, nail changes follow the development of cutaneous lesions, but on rare occasions they may precede any other clinical evidence of the disease. Several types of nail dystrophy are recognized. The specific clinical appearance depends on whether the pathology occurs in the nail matrix or nail bed.
Onycholysis occurs as the result of nail bed involvement. In early lesions the normally smooth, curvilinear distal junction of the nail plate with the nail bed becomes irregular; later, deeper levels of separation occur. In advanced disease, soft yellow keratin accumulates between the nail plate and nail bed in a manner clinically indistinguishable from that which occurs in onychomycosis.
Another type of psoriatic lesion occurs between the plate and bed. This results in the appearance of sharply marginated, yellow-brown, nonpalpable color changes in the nail plate. These changes have been likened to “oil spots.”
The earliest reflection of nail matrix disease is the development of ice pic stippling or pitting on the surface of the nail plate. This type of pitting occurs primarily in patients with psoriasis, but it can also be seen with eczematous disease of the hand and in alopecia areata. More advanced involvement of the nail matrix, in concert with nail bed disease, leads to the development of grossly misshapen nails. These more serious nail dystrophies are often accompanied by inflammatory, arthritic changes in the distal interphalangeal joint.
There is no widely acceptable, effective treatment for psoriatic nail dystrophy. Topical steroid therapy used under finger cot occlusion can be tried, but the degree of improvement is usually disappointing. Steroids injected into the nail matrix are more efficacious, but the considerable discomfort associated with multiple injections discourages most patients. Improvement following the long-term use of topically applied fluorouracil has been reported in a few patients. Systemic therapy with methotrexate and etretinate usually leads to clearing of the nails, but the benefits of these agents must be balanced against their toxicity. Concomitant improvement in nail dystrophy often occurs during spontaneous or therapeutically induced remission of the accompanying cutaneous lesions.
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