Onychocytic matricoma (OCM) is an acquired benign onychogenic tumor producing a localized thickening of the nail plate that usually presents as longitudinal pachymelanonychia. However, longitudinal pachyleukonychia as the presenting sign of OCM is increasingly recognized in clinical practice. To our knowledge, polydactylous OCM has not previously been reported in the literature. This study aims to describe a new nail genodermatosis presenting as polydactylous longitudinal leukonychia with histology typical of OCM. Four cases were identified. The previously unreported familial nail abnormality occurred in at least 2 first-degree relatives. Longitudinal white bands located exclusively on the fingernails were the only characteristic of this disease. The longitudinal bands varied in number from 2 to 4 per nail. Nail changes may appear during childhood, but most cases were observed between the ages of 20 and 50 years. The multiple longitudinal bands corresponded histologically to multiple OCM. Three cases in this series had no relevant personal of family history of neoplasm, but only 2 generations were analyzed. In 1 family, polydactylous OCM was associated with a family history of melanoma and renal cell carcinoma. The genomic profile of this single family allowed a diagnosis of OCM associated with BRCA1-associated protein ( BAP1 ) tumor predisposition syndrome (TPDS). Our results are limited by incomplete follow-up and the small size of this retrospective case series. As such tumors are rare, additional cases need to be collected to clarify the role of onychocytic hamartoma as an early indicator of BAP1 TPDS.

Recent studies have proposed the use of the polydactyly nail unit model as a tool for the study of the molecular basis of onychogenesis. However, the histological and immunohistochemical description of this model is still a matter of debate in the literature, and the validity of the concept of the onychodermis used in the histological interpretation of both polydactyly and the adult nail unit has been challenged on the basis of detailed histological studies of adult fingernail units. The aim of this study was to provide new histological and immunohistochemical data on both the adult toenail unit and polydactyly nail unit to test the onychodermis/onychofibroblasts hypothesis. A histological study was performed on a series of 20 normal adult toenails from 10 cadavers and 10 polydactyly nail units. This study supported a strong analogy between the finger and toe dermis of the adult nail. The telocyte population is relatively sparse compared with the fibroblast (fibrocyte) population of the nail mesenchyme as a whole. The dynamic immunohistochemical profile of the nail telocytes was present in both fingers and toes, with the CD34+/CD10+ profile correlating with the onychogenic epithelial region, and the CD34−/CD10+ profile correlating with the spatial rearrangement of the epidermal ridges of the nail bed that are aligned longitudinally and almost parallel to each other. The main differences resulted from more consistently well-formed adipose tissue, a more discrete mucinous component at the level of the distal hypodermis of the hallux, and a thicker nail bed dermis. Previous studies of polydactyly have not taken into account the stage of development of the distal phalanx. Morphological variations of the developing phalanx have been classified into 2 types with 4 subtypes. In all but 1 type, the nail mesenchyme had 2 compartments: a matrical dermis devoid of onychofibroblasts and a CD10+ loose connective tissue with onychofibroblasts. In all cases, the onychofibroblasts interact closely with the thick periosteal/perichondrial layer of the developing bone. By contrast, in the adult nail unit, the matrix apex is independent of the distal interphalangeal (DIP) joint synovioentheseal complex and has only focal and lateral connection to the periosteum through a lateral fenestrated fascia. Moving proximally to distally the quiescent periosteum is separated from the matrix epithelium by a thick matrical dermis and its hypodermis, whereas the nail bed dermis shows a definite and stable anchorage to the periosteum. The oversimplified concept of onychodermis does not allow us to analyze the complex microanatomy of the adult nail unit with major misunderstanding of the matrical hypodermis and the hypodermal channel of the nail bed. The polydactyly nail unit is a good model for studying early nail morphogenesis and hereditary and congenital nail disorders, but not a histological model for analyzing the normal nail unit, in particular the role of telocytes versus onychofibroblasts as nail mesenchymal stem cells. The classification of morphological variations of the polydactyly nail unit is essential for the future interpretation of molecular studies using this model.

ABSTRACT:Onychopapilloma (OP) is a benign tumor of the nail. In all studies of the literature including the World Health Organization new classification of nail tumor, OP is proposed as a tumor originating in the distal matrix and defined histologically by its onychogenic property as "matrix metaplasia of the nail bed."The aim of this study is to clarify the origin and type of keratinization of OP, to emphasize the application of clear histological criteria according to the type of surgical procedure, to present new clinical and histological subtypes of OP, and to discuss the differential diagnosis.Eighty-six cases were available for clinicopathologic review. Detailed clinicopathological analysis could be performed on 56 cases.In addition to the classic clinical presentations of longitudinal erythronychia, longitudinal leukonychia, longitudinal melanonychia, 2 cases presented an unusual band pattern in the form of xanthonychia. Histological interpretation was more difficult for samples obtained by tangential longitudinal excision than for those obtained by longitudinal monobloc excision. The superficial eosinophilic layer of the nail bed was either clearly identified by its round to oval nuclei or showed features simulating a keratogenous zone by foci of irregularly contoured pycnotic nuclei. In all cases, the so-called matrix metaplasia of the nail bed corresponded to an onycholemmal keratinization with 2 types of cornified cells: clear cells either parakeratotic or orthokeratotic, and eosinophilic cells. The clear orthokeratotic cornified cells sometimes simulated abnormal enlarged onychocytes. The onychogenic marker including hair related keratin (HK) 31, HK85, HK86, LEF-1, and beta-catenin were not expressed in the nail bed. The samples obtained by tangential longitudinal excision frequently showed incomplete or complete deepithelialization. In incomplete deepithelialization, 2 clues suggested a diagnosis of OP: numerous filiform superficial papillae and remnants of nail bed epithelium with a superficial eosinophilic layer. In complete deepithelialization, only examination of the nail plate allowed the diagnosis to be established. Loss of the organization of the suprabasal layers, dyskeratosis, and keratinocytes with clear cytoplasm were occasionally observed. However, the absence of nuclear atypia confirmed by the normal expression of Ki67 and p53 ruled out in situ onycholemmal carcinoma/malignant OP. Two new histological subtypes have been observed. OP with lesions resembling seborrheic keratosis. OP with an overexpression of CD10 simulating the stroma of OM. Nail clipping has proven to be potentially useful in the differential diagnosis between OP with seborrheic keratosis-like lesions and onychogenic tumor such as onychocytic matricoma and onychomatricoma. In contrast to the thick nail plate perforated by cavities of onychogenic tumors, OP was characterized by a focal thin nail plate with longitudinal groove. On excised lesion, the negativity of the onychogenic markers such as LEF-1 or beta-catenin led to a definitive diagnosis of OP.OP is a nail bed onycholemmal papilloma. Numerous whorls of fusiform eosinophilic cells and true dyskeratotic cells could raise concern for the possibility of a low-grade in situ onycholemmal carcinoma. Awareness of this distinctive pattern of OP along with supplemental immunostaining will assist in enabling the correct diagnosis to be made. The KS-like variant could cause a diagnostic pitfall with onychocytic matricoma. The lack of white dots and rounded white clods on clinical examination and the focal thinning of the nail plate, on histological examination of nail clipping, provide clues for the diagnosis.

ABSTRACT:Some authors have suggested that the fibroblasts of the nail mesenchyme (onychofibroblasts) can be distinguished from skin fibroblasts by their high expression of CD10. My 2015 study documented the presence of a relatively sparse CD34 + /CD10 + dendritic subpopulation in the dermis and hypodermis of the matrix. For some time now, my hypothesis has been that these interstitial dendritic mesenchymal cells of the matrix correspond to telocytes. Telocytes have been described as peculiar interstitial dendritic cells present in the mesenchymal tissue of numerous organs, including the skin, but their presence and characteristics in the nail unit have not been explored. This study was undertaken to more comprehensively investigate the existence and characteristics of nail telocytes. A series of 20 normal adult nail units were examined with a combination of morphological and immunohistochemical analyses. The matrix dermis contained a sparse subpopulation of CD34 + /CD10 + elongated telocytes with a higher density in the lunular region and, at this distal level, a change in their immunohistochemical profile, resulting in a progressive loss of CD34 expression. The matrix hypodermis showed CD34 + /CD10 + telocytes in their classical elongated aspect, which acquired, especially in the distal fibromyxoid area of the thumb, an oval to round morphology with multiple intracytoplasmic vacuoles. The characteristic dynamic immunophenotypic profile of the dermal telocytes with a progressive distal loss of the defining molecule CD34 was equally observed in the distal hypodermis. The nail bed dermis was thick with a dense fibrous connective tissue. A reticular network of CD34 - /CD10 + telocytes was present in the superficial dermis of the proximal nail bed. The mesenchymal cells of the deep part of the proximal nail bed dermis and the entire distal nail bed dermis were CD34 - /CD10 - . The adult nail mesenchyme is composed of 3 microanatomically distinct regions. Only the thumb has a distal hypodermis rich in mucinous material. The population of telocytes is relatively sparse compared with the fibroblastic population of the entire nail mesenchyme. The concept of onychodermis/onychofibroblasts is not valid. Nail telocytes have a dynamic immunohistochemical profile depending on whether they are located proximally or distally. The CD34 + /CD10 + profile correlates with the onychogenic epithelial region, while the CD34 - /CD10 + profile correlates with a spatial rearrangement of the nail epidermal bed.

Onychocytic matricoma (OCM) is a benign neoplasm of the nail matrix. Only 18 cases of this tumor have been reported in the literature to date. We retrospectively analyzed the clinical features of 14 patients with OCM. The most common clinical feature was longitudinal xanthopachyonychia (n = 9), followed by longitudinal leukopachyonychia (=3) and longitudinal pachymelanonychia (n = 2). The most common clinical findings identified following dermoscopy and analysis at high magnification of classical photographs were free-edge thickening of the nail plate without pitting (n = 14), longitudinal ridging (n = 7), round white clods (n = 7), white dots (n = 7), and filiform hemorrhages (n = 7), followed by oval and linear white clods (n = 5), fuzzy lateral border (n = 5), and red-purple blood clods (n = 3). Nail clipping histopathology showed a thickened nail plate with multiple, small, round-to-oval spaces. The tumor expressed immunopositivity for LEF-1. Dermoscopy of the nail plate and nail clipping histology provides useful information with regards to the differential diagnosis with subungual squamous cell carcinoma and nail melanoma. Ex vivo-in vivo correlation facilitates a better dermoscopic assessment of this unique underrecognized disease. However, the differential diagnosis between OCM and onychocytic carcinoma requires biopsy of the tumor. LEF-1 as an onychogenic marker can be used to resolve the differential diagnosis between OCM and subungual longitudinal acanthoma/seborrheic keratosis.

AimsThe distinction between the benign subungual melanocytic lesions and an early lesion of subungual melanoma (SUM) remains a diagnostic challenge. We evaluated the routine diagnostic utility of array Comparative Genomic Hybridization (aCGH) to detect whole‐genome copy number variations (CNV) as well as targeted next‐generation sequencing (NGS) in SUM.Methods and ResultsThis retrospective study included 20 cases of in situ SUM and 11 cases of invasive SUM. Analysis by aCGH detected common oncogene amplifications in all but one case of invasive SUM (n = 10) and in all cases of in situ SUM with a melanocyte count (MC) >45/mm (n = 4 true positive) and the average number of CNV was 8.5. Thirteen remaining cases of in situ SUM gave false negative results (n = 13), owing to a lack of sufficient melanocytes to analyse (median MC of 35.35; range: 10.16–39.5). Molecular analysis failed in four cases (three in situ SUM and one invasive SUM) due to insufficient amounts of DNA. Across the whole cohort, the sensitivity of aCGH was 52%, but when adjusting the cutoff to MC >45/mm, the sensitivity was 93%. Targeted NGS was less informative than aCGH analyses in our series of SUM.ConclusionTo distinguish malignant from benign lesions, especially in situ SUM versus atypical lentiginous melanocytic proliferations, aCGH analysis should be performed when the MC is above 45 melanocytes per linear millimetre. This pangenomic method can detect oncogene amplifications, as well as a number of CNV >3, which strongly support the diagnosis of malignancy.

Abstract: The concept of nail psoriasis as an entheseal-driven disease has essentially been formulated on the basis of radiological findings because it is usually not possible to obtain the tissue directly from the joints. The aim of this retrospective study was to evaluate the histological features of isolated nail psoriasis with and without distal interphalangeal psoriatic arthritis (PsA), focusing on the question as to whether the fascia and adipose tissue surrounding the apex of the nail unit genuinely show an inflammatory infiltrate. In support of the nail-enthesitis theory, an ongoing inflammatory infiltrate could be expected. An immunohistochemical study was performed to evaluate the distribution and phenotype of the inflammatory infiltrate in nail psoriasis with and without PsA. This study did not show an inflammatory infiltrate in the fascia connecting the nail to the extensor tendon. CD8 and CD4 subsets were present in equal number in the nail dermis of nail psoriasis with or without PsA, which is a similar distribution to that seen in psoriatic synovium while skin psoriasis is characterized by a dermal predominance of CD4 T lymphocytes. Because of this study and recent microanatomic studies of the normal nail unit, it is possible to move away from a purely anatomic explanation of the strong association between nail psoriasis and PsA and to propose immunological factors as contributory. This study provides support for the hypothesis that CD8+ T cells play a crucial role in the pathogenesis of nail psoriasis through a pathogenic pathway similar to that of PsA and contrasting with that of the skin.

Onychomatricoma (OM), an uncommon benign fibroepithelial neoplasm of the nail unit, is sometimes diagnostically challenging for clinicians and pathologists. OM consistently expresses CD34, but no specific immunohistohemical markers or recurrent genetic alterations have been identified to date. Recent studies have suggested that Wnt signalling is a key molecular characteristic of OM.

HistopathologyAccepted Articles Correspondence Tinea corporis with misleading clinical and histologic features of lymphomatoid papulosis Christophe Perrin, Corresponding Author Christophe Perrin xst.perrin@bbox.fr orcid.org/0000-0002-6214-3416 Laboratoire Central d’Anatomie Pathologique, Hôpital Pasteur, University of Nice, France Nail’s Dermatology Consultations, Cannes, FranceAddress for correspondence: Christophe Perrin, MD, Laboratoire Central d’Anatomie Pathologique, Hôpital L Pasteur, 30, Avenue Voie Romaine- CS 51069,06001 Nice, Cedex 1. France. e-mail: xst.perrin@bbox.frSearch for more papers by this authorToni Giorgio, Toni Giorgio Laboratoire Central d’Anatomie Pathologique, Hôpital Pasteur, University of Nice, FranceSearch for more papers by this authorMichael Coutts, Michael Coutts Department of Cellular Pathology, Maidstone Hospital, Kent, UKSearch for more papers by this authorDamien Ambrosetti, Damien Ambrosetti Laboratoire Central d’Anatomie Pathologique, Hôpital Pasteur, University of Nice, FranceSearch for more papers by this author Christophe Perrin, Corresponding Author Christophe Perrin xst.perrin@bbox.fr orcid.org/0000-0002-6214-3416 Laboratoire Central d’Anatomie Pathologique, Hôpital Pasteur, University of Nice, France Nail’s Dermatology Consultations, Cannes, FranceAddress for correspondence: Christophe Perrin, MD, Laboratoire Central d’Anatomie Pathologique, Hôpital L Pasteur, 30, Avenue Voie Romaine- CS 51069,06001 Nice, Cedex 1. France. e-mail: xst.perrin@bbox.frSearch for more papers by this authorToni Giorgio, Toni Giorgio Laboratoire Central d’Anatomie Pathologique, Hôpital Pasteur, University of Nice, FranceSearch for more papers by this authorMichael Coutts, Michael Coutts Department of Cellular Pathology, Maidstone Hospital, Kent, UKSearch for more papers by this authorDamien Ambrosetti, Damien Ambrosetti Laboratoire Central d’Anatomie Pathologique, Hôpital Pasteur, University of Nice, FranceSearch for more papers by this author First published: 08 July 2022 https://doi.org/10.1111/his.14723 This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.1111/his.14723 AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Accepted ArticlesAccepted, unedited articles published online and citable. The final edited and typeset version of record will appear in the future. RelatedInformation

Abstract: Recent studies have argued that melanocyte preferentially expressed nuclear antigen in melanoma (PRAME) is a sensitive and specific immunohistochemical marker of melanoma, including acral melanoma. In addition, loss of p16 expression has recently been suggested to have diagnostic utility in acral melanocytic tumors. The purpose of this study was to report PRAME expression in 3 cases of melanocytic activation (MAN). There were 2 men and 1 woman ranging in age at diagnosis from 46 years to 78 years (mean 61, 6 years). All cases involved a single digit. One lesion was in the fingernail (fifth finger), whereas the remaining 2 lesions were in the toenails (hallux). All the patient presented with a longitudinal melanonychia. The width of the lesions varied from 3 mm (2 cases) to 4 mm (1 case). The duration of the lesions before diagnosis varied from 12 to 24 months. Distinction of MAN from melanoma in situ is not always easy. Some morphological misleading features are illustrated in this study: (1) the suprabasal location of matrix melanocytes with long and thick dendrites within the 2–4 germinative cell layers; (2) the microconfluence of 2 melanocytes and rare melanocytes with a relatively large nucleus, however in a general context of melanocyte scarcity; and (3) the occasional nonspecific nuclear microphtalmia-associated transcription factor (MITF) staining of keratogeneous cells. Such staining could suggest a pagetoid spread of melanocytes in the keratogenous zone. PRAME antibody revealed a strong and diffuse staining in all cases. In addition, all cases were p16 negative. In this study, the melanocyte count inferior to 9 melanocytes/mm and the lack of nuclear atypia or confluence of melanocytes permitted a confident diagnosis of MAN. Limitations of our study lie largely in the small number of cases. Despite this, the expression of PRAME in some MAN seems to hamper its diagnostic value in differentiating benign from malignant lesion.

ABSTRACT:The aim of this analysis was to re-examine the classical concept of distal interphalangeal joint (DIP) psoriatic arthritis (PsA) as an entheseal-driven disease. Two cadaveric fingers with severe psoriatic arthritis were analyzed. Our results demonstrate that inflammation of DIP PsA is multifocal without interconnection between entheses and articular cartilage of the DIP. We found a clear association between synovitis and focal loss of articular cartilage at the head of the intermediate phalanx. By contrast, the articular cartilage adjacent to the zone of severe enthesitis did not show notable damage. Fibrocartilaginous destructions of enthesis were characterized by either a multifocal lymphocytic inflammation, accompanied by osteoclastic resorption, beginning on the interface between the uncalcified and calcified fibrocartilage and then extending into the bone or a subchondral bone inflammation which insidiously destroyed first the bone and then the fibrocartilage. Some sections well showed an inflammation either mild or prominent starting at the level of vascular foramina of flexor enthesis, with secondary invading into the interface between bone and enthesis. The different anatomic sites examined showed a slight predominance of CD8+ T cells over CD4+ T cells: 52% up to 63% for CD8+ T cells vs. to 36% up to 48% for CD4+ T cells. Sparse interspersed CD1a+cells and PS100+cells were also seen with a predominance of PS100+ cells on CD1a+ cells. CD20+ B cells, plasmocytes, neutrophils, and mastocytes were absent or rare. CD123 positive cells were not observed. In DIP PsA, 3 findings predominate: (1) cartilage invasion by the thin pannus offers a more rational explanation for the focal joint destruction than does inflammation of the enthesis which is independent from articular cartilage, (2) the thick ventral plate and to a lesser extend the thin dorsal plate constitute a barrier between the inflamed entheses and the articular cartilage, and (3) an unusual form of minute vascular foramen contributes to the early stage of enthesitis. This small study suggests that DIP PsA is a complex disease. It affects anatomical micro sites which, although close, are in fact relatively independent of each other. Further studies are needed to test this hypothesis.

Society for Publication of Acta Dermato-Venereologica Superficial CD34+ fibroblastic tumour (SCFT) is an uncommon low-grade mesenchymal tumour of intermediate (borderline) malignancy. It occurs in middle-aged adults, with a slight male predilection, most frequently on the lower limbs, particularly the thighs (1–8). To the best of our knowledge, there has been no report of this tumour occurring in the subungual or periungual region. We report here the first case of SCFT of subungual region of the finger with a misleading clinical feature. Immunohistochemical features and RNA sequencing analysis using a panel dedicated to sarcomas ruled out more aggressive neoplasms, such dermatofibrosarcoma protuberans (DFSP).

### Summary box A secured supply of quality-assured medicines and other medical products is an essential prerequisite for universal health coverage. Unfortunately, on average one in 10 medicines do not meet acceptable quality standards in low-income and middle-income countries (LMICs).1 2 The high prevalence of poor-quality medicines in LMICs greatly depends on the globalisation of pharmaceutical production and distribution, combined with the weakness of many national medicines regulatory authorities (NMRAs).3 4 The use of non-quality-assured medicines, often undetected, causes poor case management and unfavourable medical outcomes in individual patients, while at population level, it is translated in poor control of communicable diseases, emergence of resistance to medicines and loss of trust in health systems.2 4–6 Risks are magnified by the COVID-19 pandemic, which triggered disruption of supply chains, stockouts, substandard production, falsification of repurposed medicines and irrational use of medicines.7 8 European taxpayers’ money is used to fund medical programmes in LMICs in the context of humanitarian aid and development. Medicines for these programmes are purchased either …

This is a report of a previously undescribed type of onychomatricoma (OM) with an unusual clinical presentation as a thickened free edge of the nail plate without discernible cavities and distinguished histologically from the ordinary OM by 3 features: (1) the lack of cavitation at the proximal border of the nail plate and the small sizes of the cavities at the free edge of the distal nail plate; (2) a papillated epithelial hyperplasia pattern very different from the digitate pattern of the ordinary OM; and (3) a special pattern of matrical keratinization with pseudohorn cysts that mirror closely those found in onychocytic matricoma (OCM). Furthermore, the sex ratio and sites of the lesion seem different than those of conventional OM with the caveat that the numbers in this series are small. A practical approach to the diagnosis of onychogenic tumor mainly involves consideration of tumors that clinically present as localized longitudinal pachyonychia including melanoma and Bowen disease. Whether pachyonychia is caused by a thickened nail plate or by a localized band of subungual hyperkeratosis may not be clinically and dermoscopically obvious, and leucoxanthonychia or melanonychia is observed in OCM, OM, and onychocytic carcinoma. Therefore, the definitive diagnosis of these 3 onychogenic tumors is made by histopathology on nail clipping specimen or nail biopsy. OM is easily diagnosed as a fibroepithelial tumor keeping in mind its micropapilliferum variant which can simulate trichoblastoma or basal cell carcinoma on biopsies without nail plate. In these biopsies, the fibroepithelial portion of OM micropapilleferum resembles trichoblastoma including trichoepithelioma, or keratotic basal cell carcinoma, whereas the pseudohorn cysts may be mistaken for seborrheic keratosis. As previously indicated in the seminal report of OCM and perfectly demonstrated in this series, the pseudohorn cysts of both OCM and OM micropapilleferum have 2 distinct layers with a ring pattern, the prekeratogenous and keratogenous zone, and the transitional eosinophilic onychocytes become progressively clear with shadow cells. By contrast, horn cysts with hyaline and trichilemmal keratinization have rounded or irregular shapes, a thin inner layer of eosinophilic cells with large, oval, pale, vesicular nuclei, and are filled with compact keratinous masses without transition to onychocytic shadow cells. The squamous eddies of irritated seborrheic keratosis are easily differentiated from the pseudohorn cysts of OM by their inner layer of eosinophilic flattened squamous cells, and their loose or compact eosinophilic keratinous masses without transition to onychocytic shadow cells. To avoid confusion with the pseudohorn cysts of seborrheic keratosis which present a thin granular layer and laminated cornified cells, we propose to designate the pseudohorn cysts of both OM and OCM as keratogenous spheres. The papillae of the latter end as a tip without keratogenous zone explaining the microcavities. The microcavities getting in touch with the surface of the nail plate are responsible for the white dots (the so-called milia cysts) observed by dermoscopy both in OCM and OM micropapilliferum. The low, projecting ridges separated by the irregular longitudinal furrows explain the clinically irregular white line. The evenly thickened free edge of the distal nail plate is explained either by the small size of the cavities or the presence of a keratogenous zone at the tip of the papillae which manufacture a homogeneous thick nail plate. This free edge nail wall-like pattern (with or without a pitted wall) is in stark contrast to the usual honeycomb-like cavity pattern seen in conventional OM. It is inferred that these dermatoscopic findings could be clinical clues to differentiate both OCM and OM micropapilliferum from conventional OM. In the initial description of OCM, this entity was clearly differentiated from seborrheic keratosis. From time to time, these 2 lesions continue to pose problems in the histological differential diagnosis, and OCM with its various clinical presentations as leucoxanthonychia or melanonychia has been described using different names as subungual seborrheic keratosis, nail unit acanthoma, or longitudinal subungual acanthoma. These new superfluous synonymies add confusion in nail tumors. In the estimation of the author, these so-called new entities are OCM, if the histologic criteria of keratogenous spheres defined in this article are used. In sum, there are 2 clinicopathological variants of OM: macropapilliferum and micropapillerum. As OM micropapillerum has small cavities, the main differential diagnosis on nail clipping is onychocytic carcinoma.