Clinics in Dermatology (2013) 31, 578–586

Common nail disorders

Avner Shemer, MD a,⁎, C. Ralph Daniel III, MD b,c
a
The Chaim Sheba Medical Center, Affiliated with Tel-Aviv University, Sackler School of Medicine, Tel-Hashomer 52621, Israel
b
Department of Dermatology, University of Mississippi School of Medicine, Jackson, Mississippi
c
Department of Dermatology, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama

Abstract Brittle nail, simple chronic paronychia, and onycholysis represent three of the most prevalent
nail disorders. Brittle nails are characterized by increased fragility of the nail plate due to damage to the
nail matrix or changes to nail plate cohesion, caused by internal and/or external factors. Simple chronic
paronychia represents an inflammatory process of the lateral and/or proximal nail folds of the fingernails
or toenails often preceded by damage to the cuticle. Onycholysis describes the detachment of the nail
plate from its nail bed, often attributable to dermatologic conditions, infections, drug therapy, or trauma.
© 2013 Published by Elsevier Inc.

Introduction Brittle nails

Although they are often judged as minor aesthetic
concerns or irritations, common nail disorders, such as
brittle nails, simple chronic paronychia, and onycholysis, can
be indications of trauma, infection, or systemic issues.
Determining the cause is useful not only to prevent future
damage and but also to rule out serious underlying disorders.
Briefly, the nail unit is composed of the nail matrix, nail
plate, nail bed, cuticle, and nail folds. The nail plate lies on
the nail bed and is surrounded by the proximal fold and the
two lateral folds. The distal part of the proximal fold,
the eponychium, gives rise to the cuticle at the surface of
the proximal nail plate. Together, the eponychium and the
cuticle form a protective seal surrounding the nail plate. The
nail matrix (located just beneath the proximal nail fold),
the proximal part of the nail plate (lunula), and the nail bed
represent the nail plate.
⁎ Corresponding author. Tel.: +972-52-4575677; fax: +972-9-8853110.
E-mail address: ashemer1@gmail.com (A. Shemer).
The nail plate is a coherent structure composed of three
horizontal layers: a thin dorsal layer produced by the
proximal portion of the nail matrix, providing hardness,
smooth texture, and sharpness to the nail; the thicker
intermediate layer, produced by the distal matrix, provides
flexibility and elasticity; while the ventral layer produced
by the nail bed, supports the adhesion of the nail plate to
the nail bed and represents an anatomical barrier. Brittle
nails consists of alterations of the nails’ consistency and is
characterized by weakness, inelasticity, flaking, splitting,
crumbling, and overall fragility of the nail plate.1 Brittle
nail is associated with several comorbidities, such as
painful nails and can result in an unpleasant cosmetic
appearance. This can significantly impair daily activities,
occupational abilities, and furthermore result in major
psychosocial impact on people’s lives.2 Nail brittleness is
often an idiopathic condition but can also be caused by
factors that alter nail plate production and/or damage the
existing nail plate; thus, the condition can be classified as
secondary1 (Figure 1).

0738-081X/$ – see front matter © 2013 Published by Elsevier Inc.

http://dx.doi.org/10.1016/j.clindermatol.2013.06.015
Common nail disorders
Fig. 1 Brittle nails.
Idiopathic brittle nail
Idiopathic brittle nail occurs almost exclusively in
fingernails with a diverse clinical presentation. Patients
may present with a variety of longitudinal ridging, transverse
splitting, horizontal lamellar separation, and fissuring of the
distal nail plate.1 Idiopathic brittle nail is associated with an
intrinsic or extrinsic (acquired) defect in the intercellular
cement responsible for the adherence of the nail plate
corneocytes.3-5 Adhesion between cells is facilitated by
lipids and the cross-linking of keratin filaments via
disulphide bonds between cysteine residues. These keratin
filaments are normally oriented parallel or perpendicular to
the growth axis.1,2,6 Thus, sulfur and lipids play important
roles in the nail plate structure. The normal nail plate
contains up to 10% sulfur by weight, 10–18% water, and less
than 5% lipids.1,6-9 Brittle nails are characterized by a loss of
organization and/or changes in chemical composition e.g.
dehydration or changes in lipid concentrations.1,6
579
Environmental and occupational factors (excessive con-
tact with water or chemicals, recurrent manicure, recurrent
minor trauma to the distal nail plate, etc.) can disrupt cell
adhesion and/or composition of the nail plate.2 Dehydration
of the nail plate of less than 15%, can lead to brittle nail.8
However, some authors feel that nail plate cohesion is not
related to water content.10,11 The normal plate contains 5%
lipids, which are located at the dorsal and ventral parts of the
nail plate and are organized in a bilayer structure parallel to
the nail surface, and function at least partially to prevent nail
dehydration. Unfortunately, this arrangement of lipids can
also minimize environmental rehydration. Low lipid content
leads to low ability to retain water in the nail plate. With age,
there is a decrease in cholesterol in the nail plate, especially
in woman12; moreover, women and the elderly are prone to
weak intercellular keratinocyte bridges, which in turn results
in brittle nails.13 Indeed, up to 30% of women aged 50 years
and older are affected by brittle nails.1 Women are affected
twice as frequently as men.14
Other primary factors are genetic predisposition and nail
matrix or corneocyte abnormalities.2 Because epithelial
growth and keratinization occur in the nail matrix, as well as
in the nail bed, both components are responsible for creating a
normal healthy nail plate. If the abnormality in the nail matrix
is reversible, then the nail plate may revert to a normal state of
flexibility. Longitudinal ridges and longitudinal splits or
canaliculi (as occurring in lichen planus) may be caused by
local increases and focal decreases in nail production in the
matrix, respectively. Transient slowing down of nail produc-
tion during severe illness can produce structures such as
Beau’s lines. It should be stressed that vascularization and
oxygenation of the nail matrix is very important for normal
keratinization. Permanent abnormalities in the vascularization
in the nail matrix/bed may result in keratinization defects.
Secondary nail brittleness
Secondary nail brittleness may be caused by dermatologic
and/or systemic diseases, nutritional deficiencies (vitamins A–
E and H, zinc, or selenium, and eating disorders, such
as anorexia and bulimia) and after drug intake (antimetabolite
agents, penicillamine, retinoids, antiretroviral agents, and
iron).1,15 The clinical presentation of secondary nail brittleness
depends on the severity and the location of the nail matrix
damage. An example of secondary nail brittleness is nail plate
thinning combined with abnormality in the superficial nail
plate resulting from proximal nail matrix damage.
Dermatologic conditions may produce nail brittleness
directly by causing nail plate damage or indirectly by affecting
the nail matrix.1 In superficial white onychomycosis (usually
caused by Trichophyton mentagrophytes), degradation of the
most superficial area of the nail plate permits white, opaque,
friable spots to be seen, along with brittleness. The diseases
involving the nail matrix include psoriasis, lichen planus,
lichen striatus, alopecia areata, Darier’s disease, and derma-
titis. In psoriasis, if the proximal part of the nail matrix is
580 A. Shemer, C.R. Daniel III

involved, the result is deep pitting in the nail plate. In lichen
planus, the inflammatory process causes destruction in the nail
matrix and as a result deformation of the nail plate; a mild
effect results in nail thinning, while a more severe effect
causes a pterigium. If a severe inflammatory process is
localized at the nail matrix, the result is longitudinal grooving.
Eczema of the finger tips may affect the nail matrix, resulting
in nail brittleness and lamellar exfoliation.
There are many systemic disorders that may affect the nail
matrix/bed and result in nail plate deformation.1,2,15 Oxygen-
ation and vascularization of the nail matrix directly affect
normal keratinization and epidermal growth. Vascular diseases
or diseases affecting oxygenation such as peripheral arterial
disease, arteriosclerosis, microangiopathy, Raynaud’s disease,
polycythemia vera, Dyserythropoietic anemia, and chronic
infections can lead to the production of a thin nail plate. The
pathologic nail formation of brittle nails has been associated
with a number of endocrine and metabolic disorders. These
include, hypo- and hyper-thyroidism, hypopituitarism, ca-
chexia, gout, osteoporosis, diabetes, malnutrition, osteomala-
cia, and acromegaly. These disorders may result in brittle nails
and nails that exhibit slow growth, longitudinal riding, and/or
fissuring. Direct evidence that these disorders affect keratini-
zation or decrease nail growth has not been demonstrated.
Previous irradiation and arsenic exposure may also decrease
nail growth and result in abnormal keratinization. Chronic
infectious diseases such as pulmonary tuberculosis, empyema,
bronchiectasis, and sarcoidosis can also impair nail formation.
Systemic amyloidosis may cause onycholysis, with increased
fragility, crumbling, and longitudinal ridging of the nail plate.
Brittle nail, transverse grooving, and softening of the nail plate
may be seen in pregnant women.
As mentioned, systemic medication, such as retinoids or
antiretroviral agents, may cause distal lamellar splitting
(onychoschizia). In avitaminosis, different types and severity
of nail plate thinning may occur, as supported by increased
incidence of nail plate changes in hemodialysis patients who
develop micronutrient imbalances.16
minor trauma is a common and well-known reason for brittle
nails/distal nail splitting (onychoschizia) in the US.
Cosmetic treatment may give some temporary reduction
of nail abnormalities. Cosmetic treatments include nail
hardeners, nail lacquers, nail strengthening agents, and
fortifying nail builders. For example, a new, FDA-approved
product for brittle nails called Genadur (distributed by
Medimetriks Pharmaceuticals) is a hydrosoluble lacquer
containing hydroxypropyl chitosan, Equisetum arvense
extract, and methylsulfonylmethane.19,20
After treating the basic cause(s) of brittle nail, preventive
measures may reduce the risk of relapse. Reducing contact as
much as possible with water, chemicals, and detergents may
be efficacious. The use of nail polish removers should also be
minimized as much as possible. Management of brittle nails
requires preventative and protective measures to avoid nail
plate dehydration. Affected individuals should be advised to
wear cotton gloves under rubber gloves during household
tasks and avoid repeated immersions in soapy water.
Keeping the nails short decreases the area available for
dehydration. Patients should ensure that they hydrate their
nails with topical moisturizers. Application of hydrophilic
petrolatum on wet nails enhances retention of moisture in the
nail plate. Finally, the use of artificial nails and manicuring
of the cuticles should be avoided. Treatment of brittle nails is
not easy and multiple approaches are essential.

Treatment
Nail change correlates with the severity of damage of the
nail matrix. For example, patients with similar background
cause of brittle nail may present with diverse clinical
manifestations. Therapeutic approaches to brittle nails can
be targeted first on eliciting factors that need to be eliminated,
and second on general principles of nail care and prevention,
and last on more specific therapies that can be applied.
Treatment should aim to determine and treat the cause of
the brittle nail. Directly treating the underlying cause may
improve or even cure the nail brittleness; however, most
patients with brittle nails have idiopathic nail fragility. Biotin,
oligo elements, and amino acids may diminish nail brittleness
and enhance nail strength.17 In cases of iron deficiency (b 10
ng/ml) with accompanying brittle nails, iron supplements may
also be effective for the nail plate abnormalities.18 Repeated Fig. 2 Paronychia.
Common nail disorders
Simple chronic paronychia
Paronychia is an inflammation of the skin that surrounds
the fingernails and/or the toenails that can be associated with
infection. Paronychia can be categorized as an acute or
chronic condition depending on the nature of the inflamma-
tion. In acute paronychia, minor trauma commonly precedes
the infection. Direct or indirect trauma to the cuticle or nail
fold enables pathogens to invade the nail and cause infection.
A common pathogen is Staphylococcus aureus, although
other bacteria and herpes simplex may occasionally be
responsible. Simple chronic paronychia (SCP) can be caused
by improper treatment of acute paronychia or by a
multifactorial inflammatory reaction to irritants and/or
allergens.21 Secondary colonization may be caused by
bacterial and/or fungal (usually Candida spp.) agents. SCP
has a duration of more than 6 weeks and involves one or
more of the three nail folds22 (Figure 2).
The nail plate may present with a grey-green discoloration
as a result of Pseudomonas aeruginosa colonization
(Figure 3).
Etiology and risk factors
Improper treatment of acute paronychia may lead to
chronic paronychia.23,24 By fusing the skin of the digit and
the nail, the cuticle normally acts as a waterproof barrier to
external pathogens, irritants, or allergens. Many conditions
such as excessive hand washing, obsessive nail biting or
picking, obsessive cuticle removal, finger sucking, frequent
contact with chemicals, and the application of artificial nails
involving the use of chemicals can result in damage to the
cuticle.25-35 Frequent contact with water makes swimmers,
laundry workers, cleaners, dishwashers, food handlers,
bakers, chefs, etc. more prone to SCP.21,28,36,37 Elimination
of the cuticle leads to separation of the nail plate from the
Fig. 3 Paronychia with Pseudomonas.
581
folds, potentially allowing access beneath the nail folds by
various fungi and bacteria.35,36,38
The role of the Candida spp. in chronic paronychia is
controversial.24,36,39,40 Regardless, in chronic paronychia
attributed to Candida spp. infection, topical and/or systemic
anti-Candida treatment alone usually does not resolve the
disease.41 In this instance, in the absence of antifungal
therapy, restoration of the normal physiology of the nail unit
by whatever means is usually associated with cure of the
Candida fungal infection as well.28 The more effective
treatment of SCP with topical steroids, compared to systemic
antifungals, suggests that SCP is not a type of onychomy-
cosis but a variety of hand dermatitis caused by environ-
mental exposure.36 Similar to other dermatoses such as
onychomycosis, chronic paronychia is observed more often
in patients with diabetes mellitus.25
SCP can also be induced by drug treatments. Indeed,
different types of retinoids such as etretinate and/or
isotretinoin and protease inhibitors including lamivudine
and indinavir may also cause paronychia. Indinavir is the
most common cause of chronic paronychia in patients
infected with human immunodeficiency virus (HIV).
Cetuximab, an anti-epidermal growth factor receptor (anti-
EGFR) antibody used to treat solid tumors, can also cause
paronychia of the fingernails and/or toenails.41,42
Clinical manifestation
The classical clinical manifestation of SCP is erythema,
swelling of the proximal and/or lateral nail folds with
retraction of the proximal nail fold, and absence of the
adjacent cuticle. Discoloration and thickness of the nail plate
with transverse superficial depression of the nail plate
(Beau's lines) and/or proximal separation of the nail plate
from the nail matrix, possibly as a result of nail matrix
damage (onychomadesis), are also observed. The nails and
skin surrounding the nails are often painful and tender as pus
may form below the nail fold.22,29,38,40
Clinical manifestations of SCP are similar to those of
acute paronychia, but SCP symptoms need to have been
present for at least 6 weeks at the time of diagnosis. One or
several fingernails are usually affected, typically the thumb
and the second and third fingers of the dominant hand. The
condition has prolonged course with recurrent, self-limited
episodes of acute exacerbation.
The severity of the SCP can vary; the following grading
system was proposed by Daniel et al.43:
Stage I: some redness and swelling of the proximal and/or lateral
nail folds causing disruption of the cuticle.
Stage II: pronounced redness and swelling of the proximal and/
or lateral nail folds with disruption of the cuticle seal.
Stage III: redness, swelling of the proximal nail fold, no cuticle,
some discomfort, some nail plate changes.
Stage IV: redness and swelling of the proximal nail fold, no
cuticle, tender/painful, extensive nail plate changes.
582
Stage V: worsening of stage IV involving acute exacerbation
(acute paronychia) of chronic paronychia.
It is apparent that significant variability exists between the
individual stages.43 It should be stressed that due to this
variability, many manifestations of chronic paronychia could
be described. This staging system is very useful for choosing
the correct treatment to yield the best possible treatment
outcome. Usually one or several fingernails are affected, with
the nails of the thumb, second, and third fingers of the
dominant hand frequently involved.29
Diagnosis and differential diagnosis
The classical manifestation of SCP can be diagnosed by
clinical observation. Variants of the clinical manifestation
coupled with the diverse grading systems may sometimes
make diagnosis more difficult. The diagnosis of SCP is based
on: 1) patient history such as working habits with water,
manicure, contact with soaps or other chemicals, or
treatments with drugs known to induce SCP such as systemic
retinoids, anti EGFR antibodies, and antiretroviral agents; 2)
physical examination of the nail folds; and 3) disease
duration. At least 6 weeks is needed for definition of chronic
simple paronychia. The differential diagnosis is ingrown
toenail or fingernail, psoriasis or chronic eczema affecting
the distal digits, Reiter syndrome, squamous cell carcinoma,
and malignant melanoma.44-46 If treatment of classical SCP
is not successful, the possibility of neoplastic processes
should be considered and should prompt a biopsy.
Treatment and prevention
The treatment strategies for SCP depend on its cause(s),
its severity, and appropriate management of underlying
pathogenic fungi and/or bacteria. First, patients must avoid
all the predisposing factors, such as exposure to excessive
water and irritant and allergic ingredients.24,28 Treatment of
drug-induced paronychia depends on the culprit drug.
Paronychia caused by EGFR inhibitors should be treated
with systemic antibiotics such as doxycycline (Vibramy-
cin),41 whereas paronychia due to Indinavir should be treated
through cessation of Indinavir therapy and substitution of an
alternative antiretroviral agent.47 If pathogenic Candida
spp., especially Candida albicans, are present, topical and/or
systemic anti-Candida agents may cure the infection.22
Whether therapy will lead to a cure of the paronychia or just
eradicate the infection underlying the paronychia itself
remains controversial. Combination of a high potency topical
steroid and an antifungal agent is an effective first-line
therapy for patients with SCP. Systemic steroids are
prescribed for a limited period to patients with severe or
refractory SCP to prompt reduction of inflammation and
pain. Intralesional steroids should also be considered as an
alternative treatment option in recalcitrant cases of SCP.
Cases of SCP refractory to most therapies may be treated
A. Shemer, C.R. Daniel III
surgically through excision of the involved fold. En block
excision of the proximal nail fold should be attempted.35,38
After elimination of any clinical manifestation is
achieved, prevention of recurrence is accomplished through
avoidance of specific causes. Patients should avoid trimming
the cuticles and, when relevant, maintain substantial
glycemic control in cases of comorbid diabetes mellitus.
They should reduce activities leading to excessive exposure
to water. They should maintain normal physiological
conditions of the nail and its surroundings through the use
of moisturizers, in addition to avoiding contact with irritants
playing a role in paronychia. They should use proper nail
hygiene practices including proper nail cutting. Mechanical
trauma should also be reduced by avoiding finger sucking or
the removal of the cuticle by pushing back the proximal and/
or the lateral nail folds. Prompt treatment of future infections
will also assist in maintaining a healthy nail unit.
SCP usually responds slowly to treatment, and resolution
with drug therapies can take up to several weeks. Successful
treatment outcome also depends on the preventative
measures taken by the patient. If the condition remains
untreated, painful, recurrent episodes of acute inflammation
occur due to repeated penetration by various pathogens.
Onycholysis
Onycholysis describes the detachment of the nail plate
from its nail bed. Usually starting from the distal portion of
the nail bed, it progresses proximally and can involve the
whole nail. Separation of the nail plate from the matrix and
proximal nail bed is called onychomadesis. The presence of
air under the detached nail plate gives the affected nail an
opaque appearance. Onycholysis is a commonly encountered
phenomenon and is more prevalent in women48 (Figure 4).
Causes
Possible etiologies of onycholysis vary from physical
trauma to hereditary diseases.24,49,50 Idiopathic onycholysis
can result from a variety of mechanical injuries. Repeated
trauma to the ventral and distal sides of the nail plate, such as
daily typing with long fingernails on a keyboard or wearing
poorly fitting shoes, may result in onycholysis. Additionally,
prolonged nail immersion in water, detergents, or other
substances may result in detachment of the nail plate from its
nail bed and is a common cause of occupational onycholysis.
Also, overly aggressive "self-cleaning" under the nail plate
or excessive manicuring may also be detrimental to the
adhesion of the nail plate to the nail bed.
Onycholysis may represent a symptom of numerous skin
diseases including psoriasis of the distal nail bed; porphyria
cutanea tarda, pemphigus vulgaris, and Darier’s disease may
lead to nail plate detachment. Fungal (dermatophytes, molds,
or yeasts), bacterial (Pseudomonas spp.) (Figure 5), or viral
Common nail disorders 583

(herpes simplex) infections can result in detached nail plates.

Ungual lichen planus usually affects the proximal nail matrix
but it may also primarily affect the distal nail bed. Rarely,
alopecia areata may present with onycholysis that resolves
when the scalp condition improves.
Drug-induced onycholysis may arise from the action of
the drug itself or in combination with sunlight. Drugs may
cause onycholysis through an inflammatory process, but the
exact mechanism of action still remains unknown. Some of
these drugs include β-blockers, oral contraceptives, tetracy- Fig. 5 Onycholysis with Pseudomonas.
cline, psoralens, fluoroquinolones, antibiotics, and chemo-
therapy agents.47,50,51 Examples of these drugs are given in
Table 1. Photo-onycholysis after ingestion of a photosensi- Several systemic diseases such as systemic lupus
tizing drug is uncommon. Drugs implicated in photo- erythematosus (SLE), iron deficiency anemia, diabetes
onycholysis are doxycycline, fluoroquinolones, after photo- mellitus, hyperhidrosis, hyper- or hypo-thyroidism, impaired
therapy with psoralen, paclitaxel, and sparfloxacin. peripheral arterial circulation, erythropoietic porphyria,
sarcoidosis, pellagra, leprosy, Reiter’s syndrome, scleroder-
ma, and yellow nail syndrome can also result in onycholysis.
Congenital causes such as hereditary partial onycholysis,
congenital onycholysis, and hereditary distal onycholysis,
and irreversible nail bed injuries have also been associated
with onycholysis.

Diagnosis

Diagnosis is based on close inspection of the nails in

addition to patient history. On clinical examination,
separation of the nail plate from the nail bed starting from
the hyponychium and extending proximally without primary
matrix involvement can be easily observed. Whether it is

Table 1 Pharmacotherapeutics that may cause onycholysis

Antibiotics Cephaloridine
Cloxacillin
Chloramphenicol
Fluoroquinolones
Sulfa-based antibiotics
Tetracyclines:
Chlortetracycline
Demethylchlortetracycline
Doxycycline
Minocycline
Tetracycline hydrochloride
Chemotherapeutic agents Adriamycin
Bleomycin
Mitoxantrone
5–fluorouracil
Oral Contraceptives Norethindrone and mestranol
Anti-hypertensives Captopril
Practolol (discontinued)
Thiazides
Dermatologic Drugs Psoralen
Retinoids
Miscellaneous Acridine
Phenothiazine
Fig. 4 Simple onycholysis.
584
distal or lateral, the detachment can be seen easily because
the onycholytic part becomes opaque, loses its transparency,
and its color (white, yellow, brown, or green) is different
than that of the attached nail plate. 48 The signs of
onycholysis are varied, but generally irregular borders are
observed between the pink borders of the normal nail plate
attached to the nail bed and the white outside edge of the
affected part. The junction between the ventral surface of the
nail plate and the dorsal surface of the nail bed may be dry.
The ventral part of the nail plate may collect skin debris just
beneath the free end of the nail plate and pits may appear on
the surface of the nail plate. Onycholysis is usually painless
as the separation occurs gradually; however, pain may occur
due to acute trauma.52 If the onycholysis is prolonged for
more than 6 weeks, the resulting defect in the structure of the
nail bed may be irreversible. Chronic onycholysis may lead
to nail bed keratinization with subsequent disappearance of
the nail bed and irreversible onycholysis.53
When systemic diseases or drugs are the cause of the
onycholysis, it is common that all fingernails are involved
and to a lesser degree the toenails at the time of the diagnosis.
This mainly occurs because of the slower growth rate of the
toenails. Asymmetrical involvement is more suggestive of a
local cause.
Because onychomycosis and psoriasis are very common
causes of onycholysis (Figures 6 and 7), mycological
analysis should be performed to assess whether an infection
is causing the onycholysis. In cases of dermatophyte
infection, it should be considered as onychomycosis. It
should be noted that the finding in one laboratory analysis of
yeasts and/or molds should not be routinely considered as an
onychomycosis since these types of fungi could be
considered as pathogens or saprophytes. Indeed, in cases
with onycholysis in several fingernails, treatment of a non-
dermatophyte infection with topical/systemic antifungal
agents may improve the appearance of the nail such that
the classical presentation of onychomycosis is absent, but it
Fig. 6 Onycholysis due to onychomycosis.
A. Shemer, C.R. Daniel III
Fig. 7 Onycholysis due to psoriasis.
usually does not achieve total cure. At least three repeat
mycological analyses should be performed. If the same
molds or yeasts are identified on each occasion, regardless of
the presence of a dermatophyte, it should be considered a
pathogenic organism.52,54 In case of psoriasis and onycho-
mycosis in the nails, histological evaluation may be helpful
in diagnosis, but not always. Treatment with a systemic
antifungal agent may directly help the onychomycotic
component, and indirectly help by canceling the Köbner
phenomenon caused by the fungus and aggravating the nail
psoriasis. 55 The role of the Candida spp. in simple
onycholysis is unclear.22,24
A greenish color present just beneath the free edges of the
onycholytic part of the nail plate might be due to
contamination by Pseudomonas.22 In the case of onycho-
mycosis combined with Pseudomonas infection, both in-
fections may cause onycholysis. The Pseudomonas infection
should be treated first and then, after mycological analysis,
the onychomycosis should be treated.56
The progression of onycholysis can be graded and
standardized into stages.49
Stage I – Early in the disease development, initial separation of
1–2 mm of the distal nail plate from the hyponychium occurs.
Stage II – Progression of the disease with separation of the distal
one-third of the nail plate.
Stage III – Further progression of the separation: totaling one- to
two-thirds of the nail plate.
Stage IV – Total onycholysis extending from the proximal nail
fold (onychomadesis) to the distal end of the nail.
Stage V – Disappearance of the nail bed due to the cornification
of the nail bed/hyponychium and developing dermatoglyphics
such as the tip of the digit through this process.
Treatment
Depending on the cause, appropriate local or systemic
treatment is prescribed. Avoidance of known predisposing
factors leading to onycholysis is advocated and should be
promptly identified and eliminated. To minimize the risk of
developing onycholysis, injury of the nail plates should be
avoided and the nail bed should be kept as dry as possible,
considering that chronic exposure to damp conditions
predisposes to disease. In addition, when possible, patients
should be advised to avoid direct contact with irritants such
Common nail disorders
as formaldehyde, nail polish remover, or other detergents. If
contact with irritants is necessary, use vinyl gloves worn over
a pair of inner cotton gloves.24,48,50
A dermatophyte infection should be treated to allow
normal regrowth of the nail plate. Fingernails can take up to
4–6 months to achieve complete regrowth, while the toenails
may take twice as long; however, this period is increased
with older age. In the event that a clinically normal nail does
not re-grow, it is highly likely that another problem causing
onycholysis exists in conjunction with onychomycosis.
Conclusions
Treatment of these three common nail diseases should
focus on their cause. Because their causes are often
multifactorial, careful examination of the patient history is
crucial for the identification of these causes.
References
1. Iorizzo M, Pazzaglia M, Piraccini M, et al. Brittle nails. J Cosmet
Dermatol. 2004;3:138-144.
2. Van de Kerkhof PCM, Pasch MC, Scher RK, et al. Brittle nail
syndrome: a pathogenesis-based approach with a proposed grading
system. J Am Acad Dermatol. 2005;53:644-651.
3. Shelley WB, Shelley ED. Onychoschizia: scanning electron microsco-
py. J Am Acad Dermatol. 1984;10:623-627.
4. Colombo VE, Gerber F, Bronhofer M, et al. Treatment of brittle
fingernails and onychoschizia with biotin: scanning electron microsco-
py. J Am Acad Dermatol. 1990;23:1127-1132.
5. Wallis MS, Bowen WR, Guin JD. Pathogenesis of onychoschizia
(lamellar dystrophy). J Am Acad Dermatol. 1991;24:44-48.
6. Garson JC, Baltenneck F, Leroy F, et al. Histological structure of
human nail as studied by synchrotron X-ray microdiffraction. Cell Mol
Biol. 2000;46:1025-1034.
7. Forslind B, Wroblewski R, Afzelius BA. Calcium and sulfur location in
human nail. J Invest Dermatol. 1976;67:273-275.
8. Samman P. Nail dosorders caused by external influences. J Soc Cosmet
Chem. 1977;28:351-356.
9. Turek BA, Vieu M, Leduc M, et al. Water content and moisture-binding
capacity of some types of human soft and hard horn. Curr Med Res
Opin. 1982;7:87-90.
10. Duarte AF, Correia O, Baran R. Nail plate cohesion seems to be water
independent. Int J Dermatol. 2009;48:193-195.
11. Stern DK, Diamantis S, Smith E, et al. Water content and other aspects of
brittle versus normal fingernails. J Am Acad Dermatol. 2007;57:31-36.
12. Brosche T, Dressler S, Platt D. Age-associated changes in integral
cholesterol and cholesterol sulfate concentrations in human scalp hair
and finger nail clippings. Aging. 2001;13:131-138.
13. Helmdach M, Thielitz A, Röpke EM, et al. Age and sex variation in
lipid composition of human fingernail plates. Skin Pharmacol Appl Skin
Physiol. 2000;13:111-119.
14. Lubach D, Cohrs W, Wurzinger R. Incidence of brittle nails. Derma-
tologica. 1986;172:144-147.
15. Dimitris R, Ralph D. Management of simple brittle nails. Dermatol
Ther. 2012;25:569-573.
16. Scheinfeld N, Dahdah MJ, Scher R. Vitamins and minerals: their role in
nail health and disease. J Drugs Dermatol. 2007;6:782-787.
17. Hochman LG, Scher RK, Meyerson MS. Brittle nails: response to daily
biotin supplementation. Cutis. 1993;51:303-305.
585
18. Norton LA. Incorporation of thymidine-methyl-H3 and glycine-2-H3
in the nail matrix and bed of humans. J Invest Dermatol. 1971;56:
61-68.
19. Iorrizo M, Maill M. Use of the Hydroxypropyl-chitosan based medical
device. Chicago, IL: Poster, American Academy of Dermatology. 2009.
20. Sparavigna A, Setaro M, Genet M. Equisetum arvense in a Transungual
Technology Improves Nail Structure and appearance. J Plast Dermatol.
2006;2:31-38.
21. Rigopoulos D, Larios G, Gregoriou S, et al. Acute and chronic
paronychia. Am Fam Physician. 2008;77:339-346.
22. Daniel 3rd CR, Daniel MP, Daniel J, et al. Managing simple chronic
paronychia and onycholysis with ciclopirox 0.77% and an irritant-
avoidance regimen. Cutis. 2004;73:81-85.
23. Wollina U. Acute paronychia: comparative treatment with topical
antibiotic alone or in combination with corticosteroid. J Eur Acad
Dermatol Venereol. 2001;15:82-84.
24. Daniel 3rd CR, Daniel MP, Daniel CM, et al. Chronic paronychia and
onycholysis: a thirteen-year experience. Cutis. 1996;58:397-401.
25. Rockwell PG. Acute and chronic paronychia. Am Fam Physician.
2001;63:1113-1116.
26. Roberge RJ, Weinstein D, Thimons MM. Perionychial infections
associated with sculptured nails. Am J Emerg Med. 1999;17:581-582.
27. Hochman LG. Paronychia: more than just an abscess. Int J Dermatol.
1995;34:385-386.
28. Habif T. Nail diseases. Clinical dermatology: A color guide to diangosis
and therapy. Edinburgh: Mosby; 2004871-872.
29. Tosti A, Piraccini B. Nail disorders. In: Bolognia JL, Jorizzo JL, Rapini
RP, eds. Dermatology. London: Mosby; 20031072-1073.
30. Turkmen A, Warner RM, Page RE. Digital pressure test for paronychia.
Br J Plast Surg. 2004;57:93-94.
31. Bowling JCR, Saha M, Bunker CB. Herpetic whitlow: a forgotten
diagnosis. Clin Exp Dermatol. 2005;30:609-610.
32. Kall S, Vogt PM. Surgical therapy for hand infections. Part I. Chirurg.
2005;76:615-625.
33. Keyser JJ, Littler JW, Eaton RG. Surgical treatment of infections and
lesions of the perionychium. Hand Clin. 1990;6:137-153.
34. Journeau P. Hand infections in children. Arch Pediatr. 2000;7:779-783.
35. Baran R. Common-sense advice for the treatment of selected nail
disorders. J Eur Acad Dermatol Venereol. 2001;15:97-102.
36. Tosti A, Piraccini BM, Ghetti E, et al. Topical steroids versus systemic
antifungals in the treatment of chronic paronychia: an open, randomized
double-blind and double dummy study. J Am Acad Dermatol. 2002;47:
73-76.
37. Brook I. Paronychia: a Mixed Infection Microbiology and Manage-
ment. J Hand Surg [Br]. 1993;18:358-359.
38. De Berker D, Baran R, Dawber RPR. Disorders of Nails. In: Burns T,
Breathnach S, Cox N, Griffiths S, eds. Rook’s Textbook of
Dermatology [Internet]. Oxford, UK: Blackwell Publishing;
20083137-3198. Available from: http://onlinelibrary.wiley.com/doi/
10.1002/9780470750520.ch62/summary.
39. Daniel 3rd CR, Gupta AK, Daniel MP, et al. Candida infection of the nail:
role of Candida as a primary or secondary pathogen. Int J Dermatol.
1998;37:904-907.
40. Baran R, Barth J, Dawber R. Nail Disorders: Common Presenting
Signs, Differential Diagnosis, and Treatment. New York: Churchill
Livingston; 199193-100.
41. Shu K-Y, Kindler HL, Medenica M, et al. Doxycycline for the treatment
of paronychia induced by the epidermal growth factor receptor inhibitor
cetuximab. Br J Dermatol. 2006;154:191-192.
42. Boucher KW, Davidson K, Mirakhur B, et al. Paronychia induced by
cetuximab, an antiepidermal growth factor receptor antibody. J Am
Acad Dermatol. 2002;47:632-633.
43. Daniel 3rd CR, Iorizzo M, Piraccini BM, et al. Grading simple chronic
paronychia and onycholysis. Int J Dermatol. 2006;45:1447-1448.
44. Gorva AD, Mohil R, Srinivasan MS. Aggressive digital papillary
adenocarcinoma presenting as a paronychia of the finger. J Hand Surg
Br. 2005;30:534.
586
45. High WA, Tyring SK, Taylor RS. Rapidly enlarging growth of the
proximal nail fold. Dermatol Surg. 2003;29:984-986.
46. Kuschner SH, Lane CS. Squamous cell carcinoma of the perionychium.
Bull Hosp Jt Dis. 1997;56:111-112.
47. Baran R, Juhlin L. Drug-induced photo-onycholysis. Three subtypes
identified in a study of 15 cases. J Am Acad Dermatol. 1987;17:
1012-1016.
48. Daniel 3rd CR, Iorizzo M, Piraccini BM, et al. Simple onycholysis.
Cutis. 2011;87:226-228.
49. Kechijian P. Onycholysis of the fingernails: evaluation and manage-
ment. J Am Acad Dermatol. 1985;12:552-560.
50. Daniel 3rd CR. Onycholysis: an overview. Semin Dermatol. 1991;10:
34-40.
51. Hussain S, Anderson DN, Salvatti ME, et al. Onycholysis as a
complication of systemic chemotherapy: report of five cases associated
A. Shemer, C.R. Daniel III
with prolonged weekly paclitaxel therapy and review of the literature.
Cancer. 2000;88:2367-2371.
52. Baran R, Badillet G. Primary onycholysis of the big toenails: a review
of 113 cases. Br J Dermatol. 1982;106:529-534.
53. Daniel 3rd CR, Tosti A, Iorizzo M, et al. The disappearing nail bed: a
possible outcome of onycholysis. Cutis. 2005;76:325-327.
54. Shemer A, Davidovici B, Grunwald MH, et al. New criteria for the
laboratory diagnosis of nondermatophyte moulds in onychomycosis.
Br J Dermatol. 2009;160:37-39.
55. Shemer A, Trau H, Davidovici B, et al. Onychomycosis in psoriatic
patients - rationalization of systemic treatment. Mycoses. 2010;53:
340-343.
56. Foster KW, Thomas L, Warner J, et al. A bipartite interaction between
Pseudomonas aeruginosa and fungi in onychomycosis. Arch Dermatol.
2005;141:1467-1468.