Tropical Journal of Medical Research

: 2017  |  Volume : 20  |  Issue : 2  |  Page : 115--121

Nail changes in oral lesions: A clue to diagnosis

Tibin K Baby1, G Umesh Chandra Prasad2, S Sunil1,  
1 Department of Oral Maxillofacial Pathology, Pushpagiri College of Dental Sciences, Tiruvalla, Pathanamthitta, Kerala, India
2 Department of Oral Maxillofacial Pathology, K D Dental College, Mathura, Uttar Pradesh, India

Correspondence Address:
Tibin K Baby
Department of Oral Maxillofacial Pathology, Pushpagiri College of Dental Sciences, Tiruvalla, Pathanamthitta, Kerala


Although most nail abnormalities are reactional and nonspecific, some occurs in conjunction with single or multisystem disorders and drug insults which may have associated oral manifestations. Understanding nail changes in oral lesions aids prompt investigations and correct diagnosis. These nail changes are broadly classified into color, structural, and contour nail alterations. This review focuses mainly on oral lesions with clinical nail abnormalities along with brief pathogenesis that is readily recognizable by dental specialists.

How to cite this article:
Baby TK, Prasad G U, Sunil S. Nail changes in oral lesions: A clue to diagnosis.Trop J Med Res 2017;20:115-121

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Baby TK, Prasad G U, Sunil S. Nail changes in oral lesions: A clue to diagnosis. Trop J Med Res [serial online] 2017 [cited 2019 Aug 22 ];20:115-121
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Nail changes can occur in conjunction with or as a result of underlying systemic pathologies. These pathologies can be from single organ or multisystem diseases to drug-induced insults which may have associated oral manifestations. Understanding of these nail changes in association with oral lesions helps in prompt investigations and correct diagnosis.[1] Briefly, the nail unit is composed of nail matrix, nail plate, nail bed, cuticle, and nail folds. The nail plate lies on the nail bed and is surrounded by the proximal nail fold and the two lateral folds. The nail matrix is located just beneath the proximal nail fold. The proximal part of the nail plate is known as lunula. 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.[2] This review focuses mainly on oral lesions with clinical nail changes that are readily recognizable by dental specialists. These nail changes are broadly classified into color, structural, and contour nail alterations.

 Nail Color Alterations

Nail dyschromia or chromonychia is defined as any color alteration of the otherwise transparent nail and involves multiple nails.[3]


Leukonychia or “white nails” is classified on the basis of the anatomical location of the inciting pathology into true and apparent [Figure 1]. True leukonychia results from a disturbance in distal nail matrix keratinization, evidenced by opaque white nail plate which moves distally with nail growth and does not fade with pressure.[3] Apparent leukonychia is caused by compromised nail bed vasculature or substance deposition within the nail plate, both alter the translucency of the nail plate which fades with pressure and does not move distally with nail growth.[4] Drug toxicity results in true or apparent leukonychia.[3]{Figure 1}

True leukonychia has four clinical forms based on the distribution:[1],[3]

Leukonychia punctate - white spots due to minor traumaLeukonychia striata - transversely or longitudinally oriented white bands caused by microtrauma, congenital, or idiopathicLeukonychia totalis - complete white nails, for example, Hodgkin's lymphoma and ulcerative colitisLeukonychia partialis - incomplete white nails, for example, Hodgkin's lymphoma and tuberculosis.

There are three clinical forms of apparent leukonychia:[1]

Terry's nails present with ground-glass appearance and lunula are obliterated. All and entire nails are affected, except for a thin 1–2 mm at the distal free edge. Terry's nails are strongly associated with diabetes mellitus, chronic congestive heart failure, and hepatic cirrhosis.[5],[6] It may also arise in Reiter's syndrome and tuberculosis[5],[7]Muehrcke's nails are paired transverse white bands that span across the entire nail bed, parallel the shape of the distal lunula, and disappear temporarily on squeezing the distal digit.[8] These bands are most prominent on the second, third, and fourth fingernails, with the thumbnails often being spared. For example, nephrotic syndrome, AIDS, and Peutz Jeghers syndrome[9]Half-and-half nails or Lindsay's nails have a 20%–60% pink to brownish distal segment that sharply contrasts with the remaining proximal leukonychia that often obscures the lunula. For example, chronic renal disease, Behcet disease, and Crohn's disease.[1],[10]

Yellow chromonychia

Yellow chromonychia or “yellow nails” may occur normally in the elderly, or it may develop in association with oral lesions or medications. Pachyonychia congenita is characterized by thick, yellowish brown-colored nails present at birth or developed during neonatal period with or without natal teeth. Other systemic diseases associated with yellow chromonychia include inflammatory dermatoses (e.g., onychomycosis, psoriasis), jaundice and also related to the yellow nail syndrome.[11],[12]


Longitudinal erythronychia involves both the lunula and the nail bed, emerges from a defective nail matrix, and is characterized by a linear red band or streak that extends from the proximal nail fold to the distal tip of the nail plate. Polydactylous longitudinal erythronychia is most commonly associated with inflammatory dermatoses such as Darier's disease and lichen planus.[13],[14],[15]

Blue chromonychia

Blue chromonychia is seen limited to the lunula, commonly occurs due to drug insults especially cancer chemotherapy [Figure 1]. Blue lunula rarely indicates systemic disease, but they have been described with Wilson disease and hemoglobin M disease.[16],[17] Blue nails may be acquired in patients with HIV/AIDS.[18] The inheritance of blue nails may occur normally in persons with blue lips and blue areolae in families with hereditary acrolabial telangiectasias.[19] Purple nail bands in a child with progressive psychomotor retardation, coarse facies, and angiokeratoma on the skin and tongue are suggestive of fucosidosis.[20]


The melanin pigmentation typically appears as longitudinal brown to black band, is almost always monodactylous, and represents epithelial hyperplasia with only focal melanocytic activation [Figure 1]. A longitudinal gray band composed of homogenous, regularly spaced, thin gray lines may represent lichen planus, onychomycosis, psoriasis, scleroderma, and systemic lupus erythematosus.[20],[21],[22],[23] The nail plate discoloration often develops concurrently with mucocutaneous hyperpigmentation in pernicious or megaloblastic anemia and Peutz-Jeghers syndrome.[24],[25] Multiple nails pigmentation can be seen with HIV/AIDS in association with hyperpigmented macules on the palms, soles, and mucosa. It may be related to immunosuppression because most patients die within months after the pigmentation appears.[26] Laugier–Hunziker syndrome is characterized by acquired pigmentation on lips, oral mucosa, and acral area, frequently associated with longitudinal melanonychia.[27]

Subungual hemorrhages

Subungual (splinter) hemorrhages represent the extravasation of blood along the parallel longitudinal capillaries of the nail bed. Within days of their onset, they change from red to brown or black in color and move distally with the growth of the nail.[28] Splinter hemorrhages arise in Osler-Weber-Rendu syndrome, Langerhans cell histiocytosis, psoriasis, and internal malignancy.[14],[28],[29],[30] Subacute bacterial endocarditis is the most common systemic cause for splinter hemorrhage, also found in leukemia, bleeding diatheses, systemic lupus erythematosus, and systemic sclerosis.[20],[28],[31]

 Structural Nail Alterations


Onychodystrophy/nail dystrophy occurs due to systemic disorders affecting nail matrix or nail bed [Figure 2]. Onychodystrophy is a frequent feature of ectodermal dysplasia, Ellis van-Creveld syndrome, dyskeratosis congenita, progeria, and Rothmund–Thomson syndrome.[14],[20] Dystrophy of all the twenty nails is a feature common to all the three variants of pachyonychia congenita. Any nail dystrophy that develops in conjunction with an erythematous to violaceous hyperkeratotic psoriasiform eruption at acral sites warrants consideration of Bazex syndrome. Dystrophic nail plates and recurrent tender paronychia (periungual inflammation) in a child with associated oral thrush warrant screening for chronic mucocutaneous candidiasis.[14]{Figure 2}


Anonychia or permanent failure of the nail plate as well as micronychia (small nail) may be noted in ectodermal dysplasia, chondroectodermal dysplasia, and epidermolysis bullosa[14],[20],[32] [Figure 3].{Figure 3}

Beau's lines and onychomadesis

Beau's lines are transverse depressions in the nail plate that originate within the matrix and that progress distally as the nail grows. Beau's lines develop 4–11 weeks after a precipitating stressor temporarily halts the mitotic function of the proximal matrix.[32],[33],[34] Hence, the onset can be determined by measuring the length from the eponychium to the Beau's line, and the duration of the stressful state can be determined by measuring the width of the depressed line. Multiple lines indicate a recurrent stressor, such as Pel-Ebstein fevers related to Hodgkin's lymphoma or cyclical chemotherapeutic regimens.[32],[33],[34] When the stressor is particularly severe, classic Beau's lines deepen to cause actual shedding of the nail plate known as onychomadesis [Figure 1].[32] Some of the numerous pathologies associated with Beau's lines and onychomadesis are organized by system in [Table 1].[1],[32],[33],[34],[35],[36]{Table 1}

Nail pitting

Pitting develops in response to the foci of parakeratotic cells within the stratum corneum of the proximal nail matrix that shed as the dorsal nail plate keratinizes, thereby leaving discrete punctate areas within the nail plate. With psoriasis, the pits are numerous (20 per plate), irregularly distributed, and either shallow or deep. In patients with diabetes mellitus, the pits are typically small and crateriform. Pitting can also be seen in lichen planus, pemphigus vulgaris, systemic lupus erythematosus, etc.[35],[36],[37]


Onycholysis is caused by direct damage to the nail bed epithelium that results in the loss of adhesion between the nail bed and the nail plate [Figure 1]. Primary onycholysis is idiopathic while secondary may be hereditary or associated with systemic disease or drug toxicity [Table 2].[1],[14],[36],[37],[38],[39],[40]{Table 2}

Hyperthyroidism has been most commonly reported to induce onycholysis. When complicated by thyrotoxicosis, the onycholytic nails become undulated with central “scoop shovel” indentation into the nail bed. This progressive variant, known as “Plummer's nails,” usually affects the fourth then fifth fingers.[36],[37],[38]

Fragilitas unguium

Fragilitas unguium/brittle nails manifest as either longitudinal ridging of the nail plate (onychorrhexis) or bilayered lamellar splitting at the distal free edge of the nail plate (onychoschizia). The dysregulation of metrical keratinization causes onychorrhexis, whereas the dissolution of the cohesion between corneocytes within the nail plate results in onychoschizia.[41] Pathologies associated with brittle nails are listed in [Table 3].[1],[41],[42],[43]{Table 3}

Periungual tissue changes

Inflammatory conditions such as Langerhans cell histiocytosis, pemphigus vulgaris, and psoriasis may induce chronic paronychia, which progress with time into pyogenic granulomas [Figure 1]. Periungual fibromas along with hyperkeratotic nail tips and longitudinal midline depression on nail plate are characteristic of tuberous sclerosis.[14] Periungual warts lesions with underlying osteolysis points to incontinentia pigmenti during adolescence.[20]

 Nail Contour Alterations


Digital clubbing/Hippocratic finger/watch-glass nail presents as soft-tissue hypertrophy of the distal digit and bidirectional enlargement of the nail-plate curvature with the angle between the proximal nail fold and the nail plate, Lovibond angle, widens to more than 180°.[44] True clubbing is identified by Schamroth sign, the obliteration of the normal diamond-shaped window created by placing the dorsal surfaces of opposing terminal phalanges together.[45] Existing theories of clubbing implicate vasodilation, hypervascularization, neurocirculatory mechanisms, elevated plasma growth hormone levels, hypoxia, platelet-activated growth factor release from unfragmented megakaryocytes, and most recently, the immune-mediated activation of macrophages releasing profibrotic tissue repair factors that target sites of sensitive vasculature such as the nail bed.[1] Clubbing occurs in HIV infection, Crohn's disease, ulcerative colitis, systemic lupus erythematosus, sarcoidosis, and malignancies.[44],[45],[46],[47]


Koilonychia or “spoon nail” deformity presents as a concave nail plate with everted lateral edges; particularly thumbnails. Upward nail bed pressure from hyperkeratotic dermatoses (e.g., lichen planus, psoriasis, onychomycosis) causes koilonychias.[1] It is most commonly associated with iron-deficiency anemia and hemochromatosis.[1],[36] Other systemic pathologies associated with koilonychia include acromegaly, ectodermal dysplasias, porphyria, polycythemia vera, and thyroid disease.[1],[14],[48],[49]


Fusion of nails/synonychia between middle three fingers along with syndactyly is characteristic of Apert syndrome, helps to distinguish it from other craniosynostosis syndromes [Figure 3].[50]

Pincer nails

Pincer nails are characterized by increased transverse curvature along the longitudinal axis of the nail, which produces decreased width but increased height of the nail plate. The majority of cases are acquired during adulthood as a result of onychomycosis or psoriasis.[51] Pincer nails have rarely been reported in association with systemic diseases including diabetes mellitus and systemic lupus erythematosus.[52],[53],[54]

Growth alteration

Average growth rate is 3 mm/month for the fingernails and 1 mm/month for the toenails. Systemic conditions such as hyperpituitarism, hyperthyroidism, and pregnancy exhibit increased nail growth. A decreased growth rate may be seen with hypothyroidism, lichen planus, malnutrition, measles, mumps, onychomycosis, tobacco abuse, etc.[1],[54],[55]

Thus some oral lesions are associated with specific nail changes which help us diagnose and understand the underlying systemic pathologies. Nail abnormalities commonly seen in systemic disorders affecting oral cavity are listed in [Table 4].[50],[56]{Table 4}


Awareness in nail changes is essential for a dental specialist. It helps to diagnose the oral pathologies accurately and also to understand associated systemic disorders, which may alert special precautions in treatment delivery.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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