Since treatment of nail psoriasis is always disappointing, before treatment is started the
individual problems of every patient should be carefully considered, and in particular the
degree of discomfort that results from the nail lesions. Reassuring the patient is probably
the best approach for isolated nail pitting, oily patches, mild onycholysis and splinter
haemorrhages. However, diffuse onycholysis, subungual hyperkeratosis and severe nail
plate surface abnormalities may require a positive therapeutic approach.

Local therapies of nail psoriasis only rarely induce complete
remission of the disease

When the nail folds are affected, regular application of topical emollients is useful to
reduce scaling and prevent self-induced trauma.
Topical steroids, or combinations of topical steroids with salicylic acid and/or retinoic
acid, are widely prescribed. Their efficacy is poor, even when applied with occlusive
dressing after chemical or mechanical avulsion of the onycholytic nail plate. Long-term
application of topical steroids may result in marked atrophy of the soft tissues of the
digits or even in focal resorption of the distal phalanges.
A nail lacquer containing 8% clobetasol propionate, formulated to optimize
penetration of the drug through the nail plate, has been developed for use in this
condition. This topical treatment, which is effective and well tolerated, produces
improvement in most cases of nail psoriasis, with effects directly related to the duration
of treatment.
Topical calcipotriol is effective when onycholysis and subungual hyperkeratosis are
prominent symptoms. Topical tazarotene 0.1 % gel has also been used with good results
and tolerability in psoriasis. The latter drug is especially effective in reducing
onycholysis (in occluded and non-occluded nails) and pitting (in occluded nails).
Topical psoralens followed by exposure to ultraviolet-A (PUVA) are not very effective
owing to poor penetration of the UVA through the nail plate, especially when the plate is
thickened. However, this treatment may be useful in pustular psoriasis when recurrent
pustular lesions have destroyed the nail plate. Intralesional injections of triamcinolone
acetonide 10 mg/ml, at a dose of 0.2–0.5 ml per nail, have proved effective in some cases
of nail matrix psoriasis. In patients with nail-plate surface abnormalities the steroids
should be injected in the nail matrix, whereas in patients with subungual hyperkeratosis
the site of injection should be the nail bed. Injections should be repeated monthly for 6
months, then every 6 weeks for the next 6 months and finally every 2 months for 6–12
months. A digital block is sometimes useful to make the treatment less painful, but when
several digits are involved, a wrist block may be the appropriate anaesthesia. However,
routine use of this treatment is not recommended because of the pain caused by the
injections, the local side-effects and recurrence of the nail abnormalities after
discontinuation of the therapy. In addition, the efficacy of intralesional steroids in nail
matrix psoriasis is limited, with only 50% success in treating nail pits.
Systemic treatment with methotrexate or cyclosporin can clear the nail changes, but
this can be recommended only when nail psoriasis is associated with widespread disease
or psoriatic arthritis.
Retinoids are of little value in the treatment of nail psoriasis except for hyperkeratotic
nails and pustular psoriasis. Oral administration of etretinate or acitretin can even worsen
the nail changes owing to the development of nail brittleness, pyogenic granuloma-like
lesions and chronic paronychia. Oral photochemotherapy can improve crumbling of the
nail plate and psoriatic involvement of the proximal nail fold, but is less effective in nail
pitting or subungual hyperkeratosis. Superficial radiotherapy can have a beneficial effect
on psoriatic nails but is not recommended because the benefits are short-lived.
Pustular psoriasis of the nail unit usually fails to respond to conventional topical
treatments. Local treatment with topical anti-metabolites (mechlorethamine, 1 %
fluorouracil) is an option, even though results are variable. Systemic steroids, PUVA and
cyclosporin can arrest the development of pustular lesions and avoid permanent scarring
of the nail apparatus. A study of 46 patients with pustular psoriasis of the nails indicates
that systemic retinoids at low dosage (less than 0.5 mg of acitretin per day) are the
treatment of choice in patients with multiple nail involvement, whereas topical
calcipotriol is the best option for pustular psoriasis limited to one or two nails. Topical
calcipotriol is also useful as maintenance therapy in patients who responded to retinoids,
in order to prevent recurrence.

Onycholysis (detachment of the nail plate from the nail bed) starts in the central or lateral
portion of the nail plate free margin, progresses proximally and can even involve the
whole nail. The onycholytic area looks whitish because of the presence of air under the
detached nail plate. It may occasionally show a greenish or brown discoloration due to
colonization of the onycholytic space by chromogenic bacteria    (Pseudomonas
aeruginosa), moulds or yeasts. Onycholysis may be idiopathic or represent a symptom of
numerous diseases (such as psoriasis, onychomycosis or contact dermatitis) or drug
reactions.
Depending on the cause of the complaint (e.g. disease or impaired peripheral
circulation), appropriate local treatment, systemic treatment or both is prescribed. The
detached nail should be clipped away and a mild antibacterial solution (thymol 4% in
chloroform) should be applied on the exposed nail bed at night. Pseudomonas infection
is easily treated by using sodium hypochlorite solution or 2% acetic acid. Accurate
drying of the fingers after hand washing is necessary. A hair dryer may be useful for this
purpose.

Chronic paronychia represents an inflammatory reaction of the proximal nail fold to
irritants or allergens. It affects hands that are continually exposed to a wet environment
and to multiple microtrauma, favouring cuticle damage. Secondary colonization with
Candida albicans and/or bacteria occurs in most cases.
Patients with chronic paronychia should avoid a wet environment, chronic
microtrauma and contact with irritants or allergens. Application of high-potency topical
steroids (clobetasol propionate 0.05%) once a day at bedtime is an effective first-line
therapy. If    Candida is present a topical imidazole derivative should be applied in the
morning. Topical antifungal agents alone and systemic antifungal therapy are not useful.
In severe cases, intralesional or even systemic steroids (prednisone 20 mg/day) can be
used for a few days to obtain a prompt reduction of inflammation and pain. Acute
exacerbations of chronic paronychia do not necessitate antibiotic treatment since they
subside spontaneously in a short time. Pseudomonas colonization can be treated with
sodium hypochlorite solution or 2% acetic acid. Complete recovery of the condition
usually requires several weeks and treatment should be continued until the cuticle has
regrown. Recurrences are frequent since the barrier function of the proximal nail fold
may be impaired for months or even years after an episode of chronic paronychia. In rare
cases, foreign bodies such as hair or fibreglass spicules can be responsible for chronic
paronychia. These patients should be treated by the excision of a crescent-shaped, full-
thickness piece of the proximal nail fold, including its swollen portion. Complete healing
by granulation takes about 4 weeks.

Blistering distal dactylitis is a childhood disease usually caused by    ? hemolytic
streptococcus infection, characterized by bullous lesions with purulent content localized
at the tip of the digits. Treatment includes surgical drainage of the blisters, topical
medication with antiseptics and systemic antibiotics (oral erythromycin or amoxicillin).

Chemical avulsion of the overgrowing nail plate with urea ointment is useful and
provides considerable relief of the patient’s discomfort. Different formulations can be
used, ranging from a simple 40% urea in 60% white petrolatum preparation, to the South
and Farber’s ointment, which has the following formulation: urea 40%, white beeswax
5%, anhydrous lanolin 20%, white petrolatum 25%, micronized silica gel 10%. Before
the ointment is applied to the nail plate surface, it is mandatory to cover the periungual
skin with plastic tape in order to protect the skin from maceration. The urea ointment is
then applied to the nail and covered with a plastic wrap; the medication is fixed to the
digit with a plastic tape and maintained in place for 7–10 days. Finally, the medication is
wiped off and the softened nail plate is removed using nail clippers.
Chemical nail avulsion is only effective when the nail plate is partially or totally
detached from the nail bed. It is not useful on normal nails, but can be successful in
removing onychomycotic nails as well as thickened psoriatic nails.

Cosmetics available for nail treatment include:
• nail varnish and stick-on nail dressing
• preformed artificial nails
• sculptured artificial nails
• nail wrapping
• adaptable nail prostheses
• abrader.

Nail varnish
Nail varnish may hide any type of chromonychia in women (or even girls) if the surface
of the nail plate is smooth, or if it can be rendered so by fine sandpaper. The hue
resulting from Pseudomonas nail infection is often hidden by nail varnish, which may be
kept on during the treatment with sodium hypochlorite and is a helpful therapy for this
condition. Psoriasis may benefit from the use of nail varnish under some circumstances.

Stick-on nail dressing
Also known as ‘press-on nails’, this consists of a very thin, coloured synthetic film with
an adhesive which fixes it firmly to the nail.
Press-on nails may be used to hide nail discolouration or mild dystrophies. They may
cause side effects that vary considerably in intensity from patient to patient: flaking,
roughness, ridging, onycholysis, disappearance of the lunula and disorganization of the
nail plate which may be delaminated and broken off. Mild paronychial inflammation
with loss of the cuticle may be seen.
In some instances 9–12 months will pass before the nails entirely return to normal. The
effect on the nail is simply traumatic, not allergic, a combination of the impermeability
of the adhering film and the cumulative trauma to the nail plate when the film is
repeatedly pulled off.

Preformed artificial nails
Any dystrophy may be hidden by preformed artificial nails, providing that some natural
nail plate surface is still present to allow adequate adhesion. It is obvious that a severe
dystrophy will prevent this and the usefulness of such a prosthetic nail is then limited.
Local complications may appear when preformed artificial nails remain on for 3–4 days.
Distant allergic eczematous contact dermatitis may occur, more often due to the glue
than to the prosthetic nail itself.

Sculptured artificial nails
Some natural nail keratin must be present for sculptured artificial nails to be used. The
natural nail is first roughened with a burr, then painted with the acrylic resins which
harden at room temperature and become moulded on to the nail. The prosthesis can be
filed and manicured to shape. As the nail grows out, further applications of the self-
curing acrylic resins can be made to maintain a regular contour.
Allergic contact dermatitis may appear, generally after 2–4 months of application, as
distant sensitization (face, eyelids) or local reactions (onychial and paronychial tissues).
On patch testing, the patient may react strongly to the acrylic liquid monomer.

Nail wrapping
In nail wrapping the free edge of each nail is splinted with layers of a fibrous substance
such as cotton wool, paper or plastic film affixed with a variety of glues; after drying, the
edge is fashioned to requirements and the nail is coated with enamel. The entire
procedure is repeated every 2 weeks. Nail wrapping is useful but can do significant harm
if the entire nail is covered because of the occlusive nature of the material used. Allergic
reactions to cyanoacrylate nail preparations (painful paronychia, onychodystrophy,
discoloration and even exceptional permanent nail loss) are rare, but may persist for
more than a year.

Adaptable nail prosthesis
In a wide variety of conditions, ranging from deformed nails to complete loss of the
distal phalanx, and in women particularly, a silicone rubber thimble-shaped finger cover
may be employed. The fixation is excellent. The device is easy to clean (plain soap),
flame-resistant, and the formed nail takes varnish well.

Nail abrasion
Thick nails caused by diseases such as psoriasis, pityriasis rubra pilaris and
pachyonychia congenita can be abraded. Hyperkeratosis is prone to be associated with
onychomycosis of the toes. Nail abrasion helps to expose the nail bed to antifungal
chemicals, especially in elderly people in whom systemic treatment is not advisable.
Abrasion is a good way to improve the contour of an abnormal nail, for example in
onychogryphosis. In selected cases of ingrowing toe nail, repeated thinning of the nail
plate may be a useful conservative method in association with appropriate definitive
treatment.
There are many products, implements and devices for maintaining clean, well-
groomed nails to satisfy individual needs. These benefits are obtained with small risk.
The physician can and should be well versed in nail care and adornment to aid patients in
achieving an improved, positive self-image: when specific medical cure is shown to be
impossible, the physician will then be in a good position to judge the value of cosmetic,
chiropody or podiatry treatments.

Nail brittleness causes several clinical symptoms including splitting, softening, lamellar
exfoliation and onychorrhexis. Brittle nails are a common complaint. It is often an
idiopathic condition, but can also be a symptom of a large number of dermatological nail
disorders. Although brittle nails have been linked with many internal diseases, the high
frequency of nail fragility in the general population makes it difficult to prove the
validity of any such association. Environmental and occupational factors that produce a
progressive dehydration of the nail plate play an important part in the development of
idiopathic nail brittleness. The lipid content of the nail is influenced by sexual hormones
and decreases after menopause. This explains the high prevalence of brittle nails in
postmenopausal women.
Management of brittle nails requires preventive and protective measures to avoid nail
plate dehydration. Affected individuals should wear cotton gloves under rubber gloves
during household tasks, avoid repeated immersion of the hands in soap and water, and
keep their nails short. Nail varnishes may be protective, but the use of nail varnish
remover should be limited since it exacerbates brittleness. Local therapies are useful in
the treatment of nail brittleness. Application of a petroleum jelly preparation on wet nails
at bedtime helps to retain the moisture in the nail plate. Frequent topical application of
preparations containing hydrophilic substances such as phospholipids, hyaluronic acid,
alpha-hydroxy acids and proteoglycans may favour nail plate rehydration.
Nail wrapping limited to the distal portion of the nail may afford protection and
camouflage in recalcitrant fragility of the nail keratin. Oral treatment with biotin 2.5 mg
per day for several months or even all year round can be useful as it may improve the
synthesis of the lipid molecules that produce binding between nail plate corneocytes.

Nail fold
The proximal nail fold is similar in structure to the adjacent skin but is normally devoid
of dermatoglyphic markings and sebaceous glands. From the distal area of the proximal
nail fold the cuticle reflects on to the surface of the nail plate. The cuticle is composed of
modified stratum corneum and serves to protect the structures at the base of the nail,
particularly the germinative matrix, from environmental insults such as irritants, allergens
and bacterial and fungal pathogens.

Nail matrix
The proximal (dorsal) and distal (intermediate) nail matrix produces the major part of the
nail plate. Like the epidermis of the skin, the matrix possesses a dividing basal layer
producing keratinocytes; these differentiate, harden, die and contribute to the nail plate,
which is thus analogous to the epidermal stratum corneum. The nail matrix keratinocytes
mature and keratinize without keratohyalin (granular layer) formation. Apart from this,
the detailed cytological changes seen in the matrix epithelium under the electron
microscope are essentially the same as in the epidermis.
The nail matrix contains melanocytes in the lowest two cell layers and these donate
pigment to keratinocytes. Under normal circumstances pigment is not visible in the nail
plate of white individuals, but many black people show patchy melanogenesis as linear
longitudinal pigmented bands.

On the great toes, the nail matrix sits like a saddle on the distal
phalanx

Nail bed
The nail bed consists of an epidermal part and an underlying dermal part closely apposed
to the periosteum of the distal phalanx. There is no subcutaneous fat layer in the nail bed,
although scattered dermal fat cells may be visible microscopically. The epidermal layer is
usually no more than two or three cells thick, and the transitional zone from living
keratinocyte to dead ventral nail plate cell is abrupt, occurring in the space of one
horizontal cell layer. As the cells differentiate they are incorporated into the ventral
surface of the nail plate and move distally with this layer.
The nail bed dermal fibrous tissue network is mainly oriented vertically, being directly
attached to phalangeal periosteum and the epidermal basal lamina. Within the connective
tissue network lie blood vessels, lymphatics, a fine network of elastic fibres and scattered
fat cells; at the distal margin, eccrine sweat glands have been seen.

Nail plate
The nail plate is composed of three horizontal layers: a thin dorsal lamina, the thicker
intermediate lamina and a ventral layer from the nail bed. Microscopically it consists of
flattened, dead squamous cells closely apposed to each other. In older people acidophilic
masses are occasionally seen, called ‘pertinax bodies’.
The nail plate is rich in calcium, found as the phosphate in hydroxyapatite crystals; it is
bound to phospholipids intracellularly. The relevance of other elements which are present
in smaller amounts, such as copper, manganese, zinc and iron, is not exactly known.
Calcium exists in a concentration of 0.1% by weight, 10 times greater than in hair.
Calcium does not significantly contribute to the hardness of the nail. Nail hardness is
mainly due to dense sulphur protein from the matrix, which contrasts with the relatively
soft keratin of the epidermis. The normal curvature of the nail relates to the shape of the
underlying phalangeal bone to which the nail plate is directly bonded via the vertical
connective tissue attachment between the subungual epithelium and the periosteum.

The component parts of the nail apparatus are shown in Figure 1.1. The
rectangular nail plate is the largest structure, resting on and firmly attached to
the nail bed and the underlying bones; it is less firmly attached proximally, apart
from the posterolateral corners. Approximately one-quarter of the nail is covered
by the proximal nail fold, while a narrow margin of the sides of the nail plate is
often occluded by the lateral nail folds. Underlying the proximal part of the nail
is the white lunula (‘half-moon’ or lunule); this area represents the most distal
region of the matrix. The natural shape of the free margin of the nail is the same
as the contour of the distal border of the lunula. The nail plate distal to the
lunula is usually pink owing to its translucency, which allows the redness of the
vascular nail bed to be seen through it. The proximal nail fold has two epithelial
surfaces, dorsal and ventral; at the junction of the two the cuticle projects
distally on to the nail surface. The lateral nail folds are in continuity with the
skin on the sides of the digit laterally, and medially they are joined by the nail
bed.
The nail matrix can be subdivided into proximal (or dorsal) and distal (or
intermediate) sections, the latter underlying the nail plate to the distal border of
the lunula. It is now generally considered that the nail bed contributes to the
deep surface of the nail plate (ventral matrix), although this thin, soft, deep
component plays little part in the functional integrity of the nail plate in its distal
part. At the point of separation of the nail plate from the nail bed, the proximal
part of the hyponychium may be modified as the solehorn. In hooved animals
this is the site of hard keratin hoof formation—it may also be the source of hard,
distal subungual hyperkeratosis in diseases such as psoriasis and pachyonychia
congenita. Beyond the solehorn region the hyponychium terminates at the distal
nail groove; the tip of the digit beyond this ridge assumes the structure of the
epidermis elsewhere.
When the attached nail plate is viewed from above, several distinct areas may
be visible, such as the proximal lunula and the larger pink zone. On close
examination two further distal zones can often be identified: the distal
yellowish-white margin, and immediately proximal to this the onychodermal
band. The latter is a barely perceptible, narrow transverse band 0.5–1.5 mm
wide. The exact anatomical basis for the onychodermal (onychocorneal) band is
not known but it appears to have a separate blood supply from that of the main
body of the nail bed; if the tip of the finger is pressed firmly, the band and an
area just proximal to it blanch, and if the pressure is repeated several times the
band reddens.

Figure 1.1

(a), (b) Nail apparatus structures; (c) longitudinal nail biopsy
section, oriented to equate with (b).