Melanocytic and pseudomelanocytic nests coexist in interface dermatitis from head-neck sun-exposed skin: A report of three cases.

Discrete junctional cellular aggregates ("nests"), partially staining with melanocytic markers, are described in lichenoid tissue reaction, mainly from chronically sun-exposed skin. The concomitant epidermal flattening and papillary dermal fibrosis with melanophages, may raise the differential diagnosis to that of a regressing melanoma. We describe three cases of interface dermatitis of the head/neck area with clinicopathological features of melanotic discoid lupus erythematosus. These cases showed junctional aggregates, a few composed of inflammatory cells and colloid bodies ("pseudomelanocytic nests"), while others composed of S100- but MART-1+, MITF+, and SOX-10+ cells ("true melanocytic nests"); negativity of the melanocytic component for PRAME was a clue to benignity. True junctional melanocytic nesting may be induced by lichenoid dermatoses on chronically sun-damaged skin. The presence of colloid bodies and of the double negativity for S100 (within nests) and PRAME (both within nests and single melanocytes), together with clinicopathological correlation, avoids misdiagnosis.

Lichen planus and lichenoid dermatoses: Clinical overview and molecular basis.

Deriving from the Greek word λειχήν for "tree moss" and the Latin word planus for "planar," lichen planus is a relatively uncommon and heterogeneous cutaneous disorder that typically develops in middle-aged adults. Despite the significant clinical burden associated with the disorder, little well-conducted molecular research has been undertaken, possibly because of heterogeneity impeding consistent and confident phenotyping. The multiple variants of lichenoid disease bear overlapping clinical and pathologic features despite manifesting as distinct clinical disorders. The first article in this 2-part continuing medical education series provides a comprehensive overview of the clinical and pathologic characteristics of cutaneous lichenoid dermatoses and links these manifestations to recent advances in our understanding of the underlying pathobiology of such diseases.

Lichen planus and lichenoid dermatoses: Conventional and emerging therapeutic strategies.

Having reviewed the diverse clinical subtypes of lichenoid disease and the postulated molecular basis thereof in the first article in this 2-part continuing medical education series, we discuss herein the existing and emerging treatment strategies in the most common clinical forms of lichenoid inflammation and provide an overview of their pharmacodynamics and evidence base. The scope of this review is not to exhaustively discuss treatment modalities for all lichenoid variants discussed in the previous article of this series. Instead, the focus will be on frequently encountered subtypes of lichen planus and on linking mechanisms of disease with mechanisms of drug action. Future directions and potential avenues for translational research will also be discussed.

PD-1 inhibitor-associated lichenoid inflammation with incidental suprabasilar acantholysis or vesiculation-Report of 4 cases.

BACKGROUND: Immune checkpoint agents targeting programmed cell death-1 protein (PD1) or cytotoxic T-lymphocyte-associated protein-4 (CTLA-4) receptors are increasingly utilized in treatment of advanced malignancies. However, these immunotherapies are commonly associated with idiosyncratic cutaneous adverse reactions. Thus, recognition and awareness of these reactions are necessary. METHODS: We reviewed the skin biopsies of all patients on anti-PD1 therapy with or without ipilimumab who developed lichenoid inflammation and included those with microscopic suprabasal or intraepidermal clefts. RESULTS: Four patients presented with interface dermatitis with microscopic intraepidermal clefts. In 2 patients, the clefts were well developed and had some acantholytic cells while the other 2 appeared to be spongiosis or inflammation related. Immunofluorescence was negative in 1 patient. None of them had clinical findings in keeping with paraneoplastic pemphigus (PP) and the symptoms improved with either topical corticosteroid or withdrawal of immunotherapy. CONCLUSIONS: Lichenoid drug reaction occurring in patients receiving anti-PD1 therapy may be associated with microscopic suprabasal or intraepidermal clefting. The clinical course was similar to lichenoid drug reactions without clefting even though some lesions may resemble PP microscopically.

Intraoral features and considerations in face transplantation.

Face transplantation (FT) is a unique and novel addition to the field of reconstructive surgery, which offers new hope to facially disfigured individuals. This review provides an overview of FT, including clinical indications, immunological principles, and functional outcomes, as well as an in-depth characterization of the intraoral hard and soft tissue findings in the six patients transplanted to date at Brigham and Women's Hospital in Boston, MA, USA. Six FT recipients underwent comprehensive clinical and radiographic evaluation to assess their intraoral status, function, and overall health. The extra- and intraoral soft tissue was assessed via quantitative sensory testing. The vitality of the transplanted dental hard tissue was evaluated with clinically available testing methods. Native teeth and prostheses were also assessed. Sensation of transplanted oral mucosa varied based on time elapsed from FT, ranging from minimal at 3 months post-FT, to nearly complete recovery by approximately 24 months. There was mixed success with the integration of donor teeth (Patients 1, 4 and 6), including associated occlusal discrepancies. Mucosal complications included constriction at the donor/recipient interface (Patients 2 and 5) and solitary episodes of mucosal rejection presenting as lichenoid inflammation (Patients 2 and 4). Face transplantation represents a pivotal moment in the history of reconstructive surgery and transplant medicine, providing new optimism to patients with gross facial deformities. This report highlights the successes of FT, but also the challenges of transplanting hard and soft tissues to restore complex stomatognathic function. Further attention directed toward comprehensive oral rehabilitation in FT will contribute to improved outcomes, with the ultimate goal of restoring and optimizing patient quality of life.

Histopathological findings of oral epithelial dysplasias and their relation to malignant transformation.

OBJECTIVES: Oral squamous cell carcinomas (OSCCs) are often diagnosed late. This study aimed to determine how frequently oral epithelial dysplasia (OED) transforms to OSCC and to identify histological features that could influence the rate of malignant transformation. MATERIALS AND METHODS: The study was a retrospective analysis of OED over 29 years at the Institute of Dentistry, University of Turku, Finland. OEDs with co-existing carcinomas were excluded from the data (5.8%). OED patients who developed carcinoma were identified from the Finnish Cancer Registry database. RESULTS: Altogether 681 OED patients had a mean age of 59.0 years, and the male:female ratio was 0.67. Of all OED samples, 21.8% were on the tongue, followed by lining mucosa (21.3%), lip (5.3%), and masticatory mucosa (4.85%). In addition, 46.7% had no location cited. The prevalence of mild dysplasia was 62.4%, moderate dysplasia 29.1%, and severe dysplasia 3.2%. Of the patients, 94.7% had an additional histological diagnosis alongside OED. Candidiasis, lichenoid inflammation, and ulcer were found in 18.2%, 0.0%, and 22.7% of severe dysplasias, in 12.1%, 12.2%, and 22.7% of moderate dysplasias, and in 6.6%, 12.2%, and 15.8% of mild dysplasias, respectively. An additional histopathological diagnosis did not increase the risk for OED to transform to OSCC. In a mean time of 5.2 (range 0.7-29.0) years, 7.5% of OED patients developed OSCC. CONCLUSIONS: Location on the tongue and the more severe OED grades increased the risk of malignant transformation of OED. These patients may benefit from an intensified follow-up schedule to ensure early diagnosis of OSCC.

Segmental and generalized vitiligo: both forms demonstrate inflammatory histopathological features and clinical mosaicism.

BACKGROUND: Segmental vitiligo (SV) and generalized vitiligo (GV) are perceived to evolve by different mechanisms, the former with unspecified neural mechanisms and the latter by melanocyte specific autoimmune mechanisms. However, the two diverse mechanisms are difficult to reconcile in cases of "mixed vitiligo". To test the possibility of a common pathogenesis, we reviewed clinical and histopathological features of SV and GV. MATERIALS AND METHODS: As part of an ongoing histopathological study on vitiligo and vitiligo like lesions, over a 10 year period from 2002 to 2011, biopsies were taken routinely from evolving or recently evolved lesions. 50 cases of SV with quasi-dermatomal distribution and 154 cases of GV were identified and the clinical and histopathological features were compared. RESULTS: Mild clinical inflammation was recorded in 33 of 154 GV cases but, none among 50 SV had such features. In addition to bilateral symmetrical involvement, mirror image lesions with unusual segmentation were observed in nine cases of GV. SV with a few bilateral lesions (4) and GV with quasi-dermatomal lesions (3), i.e., mixed vitiligo, were included in their corresponding groups for analytical purposes. Focal lichenoid inflammation of varying degrees around epidermal/adnexal melanocytes was identified as a common feature in evolving lesions of both SV (78%) and GV (70%). CONCLUSIONS: SV and GV demonstrated a similar inflammatory histopathological spectrum. "Segmentation/mosaicism", identified for the first time in GV is another unifying factor. Cutaneous mosaicism harboring fragile melanocyte populations, which are susceptible to external as well as auto-inflammatory mechanisms, is an attractive hypothesis to pursue in the causation of vitiligo.