Lichenoid Inflammatory Infiltrate Research Articles

CD14 Mouth ulcer mayhem secondary to dental fillings

Abstract Dental amalgam contains mercury, which may cause an uncommon lichenoid allergic contact dermatitis (ACD) affecting the oral mucosa in direct contact with the amalgam filling. Distinguishing a lichenoid amalgam reaction from oral lichen planus is challenging, both clinically and histopathologically. This case illustrates the important role that patch testing to dental materials can play in providing a simple answer in the management of resistant cases of mouth ulceration, protecting patients from exposure to potentially toxic immunosuppressive treatments. A 64-year-old woman presented with a 5-year history of oral ulceration affecting the buccal mucosa and tongue bilaterally. These ulcers were persistent, very painful and bled intermittently, causing a significant adverse effect on her quality of life. She worked as a manager at a local wildlife sanctuary, and hobbies included walking, writing and artwork. An incisional biopsy taken from an ulcer in the left buccal mucosa demonstrated a dense lichenoid inflammatory cell infiltrate. The oral surgical team treated her for presumed ulcerative oral lichen planus with multiple treatments, including topical steroids, high doses of oral prednisolone, hydroxychloroquine, mycophenolate mofetil and azathioprine. She gained only very minimal benefit. The oral surgeons then requested dermatological advice for the next potential treatment option, which was suggested to be rituximab. At this point, the surgeons noticed that the ulcers seemed to be most prominent at sites of the patient’s longstanding amalgam fillings and she was referred for patch testing. Patch tests were performed to the British Standard series, medicaments series and oral and dental series. Positive reactions were noted to both amalgam (D2+/D4+) and mercury (D2+/D4+). The patient had her amalgam fillings replaced with white acrylate fillings, and her oral ulceration completely healed without the need for any further immunosuppression. Clinically and histologically, lichenoid ACD secondary to dental fillings can be indistinguishable from idiopathic oral erosive lichen planus. However, the proximity of ulceration to dental filling materials should always raise the possibility of a lichenoid ACD and trigger referral for patch testing, preferably prior to systemic medications being tried. This case highlights the importance of patch testing in patients with localized, asymmetrical, difficult-to-treat oral ulcers adjacent to amalgam fillings, which could spare the patient from exposure to potentially harmful immunosuppressive treatments.

CPC07 Lupus comedonicus: a not so common entity

Abstract Lupus comedonicus (LC) is an exceedingly rare variant of chronic cutaneous lupus erythematosus (CCLE), with only 13 reported cases in the literature to date. While its aetiology remains unknown, hallmarks include the presence of comedones on erythematous plaques, particularly in seborrhoeic areas. We report a case of LC involving the scalp, concha bowl and upper back. A 53-year-old female smoker with a 20-pack-year history and previous unprovoked pulmonary embolism presented to dermatology with a 2-year history of alopecia and rash affecting her face and upper back. She was initially reviewed by oral medicine for ulcers, where erythematous buccal mucosal plaques with white striations were seen. The initial biopsy showed a patchy lichenoid inflammatory infiltrate, raising suspicions for lichen planus; however, repeat biopsy highlighted perivascular inflammation and keratin plugging suggestive of lupus. Full skin examination revealed patchy scarring alopecia with perifollicular scale and erythema. Erythematous infiltrated plaques were seen on the face with similar more indurated lesions on the upper back associated with open comedones. The eponymous Shuster sign was observed in the left conchal bowl, with associated follicular occlusion. Laboratory studies all returned within normal limits, including antinuclear antibody titres and complement levels. Differential diagnosis included lupus erythematosus tumidus, discoid lupus erythematosus and LC. Lesional biopsies taken from her back confirmed LC, highlighting lichenoid inflammation involving follicles and interfollicular skin, with superficial and deep perivascular infiltrate. We commenced oral hydroxychloroquine at 200 mg once daily for management, with topical mometasone furoate 0.1% to be used while awaiting its full effect. Smoking cessation has also been advised given the potentially antagonistic effect of smoking with lupus and hydroxychloroquine. Hypotheses of the pathogenesis of LC include the effect of sun exposure. Ultraviolet radiation is known to not only enhance the activity of CCLE but may also contribute to the formation of comedones. Actinic damage alters collagen of normal skin, promoting sebum retention and follicular plugging. Given its infrequency, LC could be mistaken for benign conditions, including acne vulgaris, naevus comedonicus and Favre–Racouchot disease. It is plausible that the small case numbers are due to current underdiagnoses. It is important for dermatologists to be aware of and accurately diagnose LC. Apart from its potentially destructive, scarring complications, especially in untreated and misdiagnosed cases, it is associated with systemic lupus in 30% of cases. Delay in diagnosis and therapeutic management can be associated with significant potential morbidity and even mortality.

CPC05 A case of extensive hypertrophic lupus erythematosus responsive to topical steroids

Abstract Hypertrophic lupus erythematosus (HLE) is a rare variant of lupus erythematosus, occurring in 2% of cases of chronic cutaneous lupus erythematosus (CCLE). It is an exaggerated proliferative epithelial response manifesting as verrucous-appearing hypertrophic indurated lesions occurring on sun-exposed sites. We present a case of the development of extensive HLE in a patient with subacute cutaneous lupus erythematosus (SCLE) with underlying pulmonary malignancy. A 74-year-old woman with Sjögren syndrome presented to dermatology with a 2-month history of a rash affecting her face and décolletage. Laboratory studies illustrated elevated antinuclear and anti-Ro antibodies. Biopsy from her chest confirmed SCLE. Malignancy screening revealed T1aN0 pulmonary lepidic adenocarcinoma, which was successfully managed with a lower lobectomy. Hydroxychloroquine was initially trialled but required discontinuation following intolerable side-effects. Mepacrine was then initiated, which allowed clearance of the rash, alongside yellow discoloration of the skin. Six months later, she developed a raised pruritic rash on her arms, legs and buttocks, resistant to current management alongside a trial of mycophenolate mofetil. Examination revealed violaceous hypertrophic plaques affecting 40% of her body-­surface area. The differential included hypertrophic lichen planus, nodular prurigo and HLE. Repeat lesional biopsies highlighted a lichenoid inflammatory infiltrate with overlying scale, favouring HLE. Owing to patient choice, topical mometasone furoate 0.1% was used to manage cutaneous disease, with a reduction in lesion size. HLE is a distinct subset of CCLE, regarded as a separate entity to SCLE. Twenty per cent of patients with SCLE also exhibit other types of cutaneous lupus erythematosus (CLE) lesions. No cases in the literature describe progression from SCLE to CCLE, or HLE, in particular. Hallmarks of HLE include verrucous lesions, chronicity and treatment resistance. Early recognition and follow-up are essential as malignancy may arise in long-standing lesions. Lung adenocarcinomas and hypertrophic lupus are both associated with p53 mutations and decreased granzyme B expression. Mutated p53 results in constitutive cell proliferation and DNA damage can accumulate in cells. Granzyme B is a protease in cytotoxic T cells involved in immune-mediated cell lysis. Both processes result in the potential to produce exaggerated hyperproliferative lesions, such as those observed in HLE and the lepidic adenocarcinomas. HLE is a rare clinical entity that can be easily misdiagnosed clinically and histopathologically. Increased awareness of this condition is essential to highlight the variety of clinical presentations of uncommon variants of CLE, to ensure they are considered while approaching clinical diagnosis.

Vulvar Lichen Planus Presenting as Chronic Vulvar Purpura

Background: There is a broad spectrum of vulvar pigmented lesions that differ based on their histopathological and clinical features. Chronic vulvar purpura is a rare entity, associated with a broad morphological spectrum, from lichen aureus, Zoon's vulvitis, pigmented purpuric dermatosis and with lichen planus as in our case. Case presentation: In this article we discuss a case of an 86-year-old white woman with hyperpigmentation on her upper vulva, next to the introitus, with complaints of urine incontinence. Biopsy revealed subepithelial stromal lichenoid inflammatory infiltrate containing plasma cells, lymphocytes and some neutrophilic granulocytes as well as dilated and congested vessels. Hemosiderin deposits and erythrocyte extravasation were found. There was evidence of hyperkeratosis with hyper granulosis and erosions. Spongiosis was also noted. Few melanocytes were identified with no sign of malignancy. These findings correlate with the diagnosis of vulvar lichen planus. Conclusions: Chronic vulvar purpura is a clinical term used for different chronic inflammatory dermatoses presenting as red bluish or violaceous discolorations on the vulva, often associated with cayenne-pepper-like speckling. Considering a great overlap of possible diseases, the final diagnosis could be challenging. It is important to exclude a melanocytic tumour in these cases.

IL-17 Expression in the Perifollicular Fibrosis in Biopsies From Lichen Planopilaris.

Lichen planopilaris (LPP) is a primary lymphocytic cicatricial alopecia for which therapy is often ineffective and there is no cure. Looking for a new targetable molecule in the treatment of LPP, we sought to verify whether IL-17 expression is increased in scalp biopsies from patients with active scalp lesions of LPP. Horizontal sections of hematoxylin and eosin-stained slides from 40 scalp biopsies of active LPP were retrospectively collected and stained with the monoclonal antibody against IL-17 (Abcam, Cambridge, MA; ab79056, dilution 1:100). Twenty biopsies from patients with chronic telogen effluvium served as controls because of their morphological resemblance to the normal scalp. Statistical analysis was performed using IBM SPSS Statistics for Windows (IBM Corporation, Armonk, NY). The main finding was the positive cytoplasmic expression of IL-17 in the perifollicular fibrosis of the affected follicles in LPP which was statistically significant compared with the controls ( P < 0.0001). The labeled cells were identified as fibroblasts based on their spindle shape and fascicular concentric arrangement in tight perifollicular distribution. Although most of the LPP specimens (n = 35; 87.5%) also revealed cytoplasmic IL-17 expression in the lichenoid inflammatory infiltrate, the results were not statistically significant ( P = 0.1351). Our immunohistochemistry results show that blocking the IL-17 inflammatory pathway may interfere with the progression of the perifollicular fibrosis and inflammation in LPP.

Histopathology oforallichen planus andorallichenoid lesions: An exploratory cross-sectional study.

To better characterize the histopathology of oral lichen planus and oral lichenoid lesions and to highlight the differences between them in order to support the clinician in the diagnostic and therapeutic management of such conditions. Fifty-five patients, clinically diagnosed with oral lichen planus (n = 25) or oral lichenoid lesions (n = 30), were consecutively enrolled in the present study. Subsequently, one blind pathologist reviewed all the biopsy specimens of enrolled subjects following a specific protocol to provide a detailed histopathological description. Demographic, anamnestic, and clinical data were also recorded from all the participants. Patients' data were analysed and compared using the chi-squared test, to provide distinguishing features between the studied conditions. We found a higher and statistically significant number of eosinophils in the oral lichenoid lesions compared with the oral lichen planus group (p < 0.01), an equally promising result was seen regarding plasma cells, which were more represented (p = 0.05) in the oral lichenoid lesions than in the oral lichen planus cases. No statistically significant differences were detected in demographic, anamnestic and clinical data. A mixed lichenoid inflammatory infiltrate, consisting of eosinophils and plasma cells, could be used as reliable histological features for the diagnosis of oral lichenoid lesions, as long as compared with findings obtained from the patients' history and clinical examination.

Established Genital and Extragenital Lichen Sclerosus:A Clinicopathological Analysis

Objective To investigate the clinicopathological characteristics of established genital and extragenital lichen sclerosus(LS)and compare the differences between them. Method The clinicopathological data of 55 patients with established genital and extragenital LS diagnosed by pathological examination in the Department of Dermatology of Beijing Hospital were retrospectively analyzed. Results The 55 patients included 11 males and 44 females.Among them,38,15,and 2 patients had genital lesions,extragenital lesions,and both genital and extragenital lesions,respectively.Extragenital LS mainly involved the back(14.55%)and extremities(7.27%).Among the patients,28.30% were asymptomatic,and 73.58% and 24.53% felt itchy and painful,respectively.The asymptomatic patients had a higher proportion in extragenital cases(χ2=31.224,P=0.000),and the itchy symptom was more common in genital LS cases than in extragenital LS cases(χ2=39.073,P=0.000).Vulvar pain only appeared in the patients with genital LS.A total of 57 biopsy specimens from the 55 patients were reviewed,of which 40 were from genital lesions and 17 were from extragenital lesions.In addition to papillary dermal homogenization (100%),the common pathological changes include hyperkeratosis(98.25%),atrophy(50.88%),basal cell liquefaction degeneration (52.63%),dilated blood vessels(64.91%),a perivascular lymphocytic infiltrate(100%),histiocytic infiltrate(85.96%),and lichenoid inflammatory infiltrate(54.39%).Higher proportions of acanthosis (χ2=4.402,P=0.036),dilated blood vessels (χ2=9.330,P=0.002),and eosinophilic infiltrate (χ2=4.162,P=0.041) were observed in genital LS cases.A higher proportion of follicular plugging appeared in extragenital LS cases (χ2=5.076,P=0.024). Conclusion The established genital LS and extragenital LS showed some differences in clinical symptoms and pathological changes including acanthosis,dilated blood vessels,eosinophilic infiltrate,and follicular plugging.

Lichen Planus.

Lichen planus (LP) is a T cell-mediated disease affecting the stratified squamous epithelia of the skin and/or mucus membrane. Histologically, the disease is characterized by a lichenoid inflammatory infiltrate and vacuolar degeneration of the basal layer of the epidermis. LP has three major subtypes: Cutaneous, mucosal and appendageal LP. Rarely, it may affect the nails in the absence of skin and/or mucosal changes. LP may also be induced by several drugs, typically anti-hypertensive medication or be associated with infections, particularly viral hepatitis. The diagnosis is based on the clinical presentation and characteristic histological findings. Although the disease is often self-limiting, the intractable pruritus and painful mucosal erosions result in significant morbidity. The current first-line treatment are topical and/or systemic corticosteroids. In addition, immunosuppressants may be used as corticosteroid-sparing agents. These, however are often not sufficient to control disease. Janus kinase inhibitors and biologics (anti-IL-12/23, anti-IL17) have emerged as novel future treatment options. Thus, one may expect a dramatic change of the treatment landscape of LP in the near future.

Intérêt des biopsies œsophagiennes au cours de la maladie du greffon contre l’hôte

Graft-versus-host disease (GVHD) is a complication of hematopoietic stem cell transplantation. It frequently affects the digestive tract. Oesophageal damage is not part of its typical clinical picture. The objective of this study was to determine whether oesophageal lesions could be found in this condition. Cases coded as GVH at the CHU of Amiens in anatomopathology were identified from 2004to 2019. Each patient who had an oesophageal biopsy was included. The slides were re-read by 2pathologists to assess the lesions. A total of 24patients were included. A total of 79.1% of the biopsies showed inflammatory lesions: 25% erosions, 37.5% a cleavage between the lamina propria and squamous epithelium, 41.7% a lichenoid inflammatory infiltrate, 54.1% apoptotic cells and 54.1% epithelial vacuolations. 25% of the biopsies were classified as Lerner's grade 4 (used in dermatopathology to assess cutaneous GVH lesions), 12.5% as grade 3, 25% as grade 2, 16.7% as grade 1, and 20.8% of the biopsies did not show oesophageal GVH lesions. None of the histological lesions observed were correlated with the prognosis, however erosions and epithelial cleavage were more frequently associated with death. Lesions evocative and probably specific for acute GVH can be found in the esophagus. They could help and be part of the diagnosis. A protocol for oesophageal biopsy sampling, and the exclusion of other causes of esophagitis, should be performed in the future during suspicion of acute GVH.

Immunohistochemical evaluation of Langerhans cells in oral lichen planus and oral lichenoid lesions

Objectivethe aim of this study was to evaluate the density of Langerhans cells in oral lichen planus (OLP) and oral lichenoid lesions (OLL). Design14 cases of OLP, 15 cases of OLL and 14 cases of oral inflammatory fibrous hyperplasia (OIFH), were selected for immunohistochemical analysis of CD1a, CD207 and S100 expression. The OIFH group was subdivided according to the presence (OIFHL n = 14) or absence (OIFHNL n = 14) of lichenoid inflammatory infiltrate. Positive cells were counted in intraepithelial and subepithelial areas. Results were analyzed by multivariate comparative analysis, correlation analysis, linear regression models and Student’s T-test. ResultsA significantly higher amount of CD207+ cells in OLL vs OLP was observed (p = 0.015). The prevailing reticular pattern observed was CD207high for OLP (p = 0.0329). A statistically significant difference in the expression of CD1a and CD207 was observed for intraepithelial vs subepithelial areas (p = 0.024 and p=0.015, for CD1a and CD207, respectively). Significant correlations were also observed between the expression of CD1a + and CD207+ cells in the pathogenesis of OLP and OLL. ConclusionHigh levels of CD207+cells in OLP compared with OLL may help explain the differences in the immunopathogenesis of both diseases. Additionally, CD1a + and CD207+ cells appear to be more essential to immunopathogenesis of OLL than to the pathogenesis of OLP.

Alopecia Fibrosante em Padrão de Distribuição Androgenética: Patogénese, Diagnóstico e Tratamento

Fibrosing alopecia in a pattern distribution is a recently recognized type of scarring alopecia, with hair loss in androgens- dependent area. Loss of follicular openings, perifollicular erythema, perifollicular hyperkeratosis and anisotriquia are the trichoscopic clues and follicular lichenoid inflammatory infiltrate the important finding in histopathology. It shares features of androgenetic alopecia and lichen planopilaris. Dermatologists should be familiarized with this entity in order to optimize the diagnosis and provide early treatment to prevent irreversible follicular damage.

Features of classic lichen planopilaris and frontal fibrosing alopecia in reflectance confocal microscopy: A preliminary study.

Classic lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) are primary lymphocytic cicatricial alopecia. In patients with ambiguous clinical presentation, reflectance confocal microscopy (RCM) a new noninvasive skin imaging technique, could be a helpful diagnostic tool. The aim of our study was to describe the characteristic features of classic LPP and FFA using RCM. Ten patients with classic lichen planopilaris and two with frontal fibrosing alopecia were examined with RCM. Lichenoid inflammatory infiltrate around the hair follicle was observed in three cases of classic LPP and FFA (3/12; 25.0%). Extensive perifollicular fibrosis was seen in nine patients (9/12; 75.0%) with classic LPP and FFA. An increased number of white, ill-defined, coarse dermal fibers at the level of the superficial dermis were visible in seven cases (7/12; 58.3%). Moreover, dilated blood vessels were present in seven patients with classic LPP and FFA (7/12; 58.3%). Summing up, reflectance confocal microscopy allows to visualize major key diagnostic features of classic lichen planopilaris and frontal fibrosing alopecia in the real time. The value of RCM examination in scarring alopecia needs to be further evaluated, but it appears to be a useful adjuvant tool for the initial diagnosis of classic LPP and FFA.

ALDH1 immunoexpression in epithelial and stromal cells of oral lichen planus and lesions with lichenoid inflammatory infiltrate.

Oral Lichen Planus is a potential malignant disorder and shares clinical and histopathological features with other similar lesions. ALDH1 is a specific biomarker for stem cells identification, however its role in stromal cells of immune inflammatory infiltrate has not been explored. The aim of this study was to investigate the ALDH1 immunoexpression in epithelial and stromal cells of Oral Lichen Planus and other lesions with lichenoid inflammatory infiltrate. 64 samples of Oral Lichen Planus, Oral Lichenoid Lesions, Oral Leukoplakia and Unspecific Chronic Inflammation were included. ALDH1 was evaluated in both epithelium and stromal cells. ALDH1+ cells ≥ 5% were considered positive in epithelium. Stromal cells were evaluated semi quantitatively. Fields were ranked in scores, according to criteria: 1 (0 to 10%); 2 (11 to 50%) and 3 (>50%). The mean value of the sum of the fields was the final score. Statistical differences among groups were investigated, considering p < 0.05. ALDH1 expression in epithelium was low in all groups without difference among them. ALDH1+ cells in the lamina propria were higher for Lichen Planus [2.0], followed by Leukoplakia [1.3], Lichenoid lesions [1.2] and control [1.1] (p<0.05). ALDH1 immunoexpression in epithelium of lichenoid potential malignant disorders did not show a contributory tool, however ALDH1 in stromal cells of lichen planus might be involved in the complex process of immune regulation associated with the pathogenesis of this disease.

IDENTIFICATION AND CHARACTERIZATION OF ORAL LESIONS WITH LICHENOID INFLAMMATORY INFILTRATE

Objective To review the cases diagnosed as oral lichen planus (OLP), oral lichenoid lesion (OLL), lichenoid reaction (LR), leukoplakia with lichenoid aspect (L), and proliferative verrucous leukoplakia with lichenoid aspect (PVL), in the period to 2014 to August 2017 and compare the clinical, demographic, histopathologic characteristics of the lesions. Study Design This is an observational, longitudinal and retrospective study. The histopathologic exam requisitions were recovered to collection of demographic data, clinical data and habits. Results A total of 1225 cases were diagnosed in that period, 46 (3.75%) had lichenoid inflammatory infiltrate (LII), with a mean age of 57 years old, 15 males and 31 females, and a greater number the white race (43.4%). There was a prevalence of clients with a no-smoking (45.6%) and no-alcohol–drinking history (39.1%). The most commonly type of biopsy performed was incisional (80.4%) on the buccal mucosa (50%). Clinically, the lesions described as plaque (52.2%), white (27.7%), and with the absence symptoms (41.3%). Conclusions The clinical-pathologic profile of LII found in this survey is similar to that described in the literature. For accurate diagnosis of LII, clinical information should be considered, as it is not possible to distinguish only the diagnosis of OLP and lesions with LII pattern by histopathologic evaluation

Oral lichenoid dysplasia and not oral lichen planus undergoes malignant transformation at high rates.

Oral potentially malignant disorders (OPMD) include a variety of mucosal lesions such as oral lichen planus (OLP), oral lichenoid lesions (OLL) and oral lichenoid dysplasia (OLD). Their rate of malignant transformation ranges from 0% to 34% and is dependent on OPMD type, lesion site and a range of risk factors. This study seeks to determine the proportion of oral lichenoid conditions that transform into oral squamous cell carcinoma (OSCC) in an Australian population. The study is a retrospective audit of patients from a private oral medicine clinic, diagnosed with OLP, OLL or OLD using clinical and histopathological data between 2006 and 2014. Patients were cross-matched with Cancer Registry data for OSCC, and the rate and time to malignant transformation determined. OLP and OLL patients displayed a low risk of malignant transformation; 0.49% (1/206) for OLP and 0% (0/31) for OLL. In contrast, OLD patients, all of whom presented clinically as OLP, were at much higher risk with 6.81% (3/44) developing OSCC over an average time of 4.6years (±2.4 SD). Rates of smoking and alcohol consumption were no higher in OLD patients compared to others. Compared with other oral lichenoid conditions, OLD lesions are at a particularly high risk of malignant transformation and should be managed based on the presence of dysplasia and not the lichenoid inflammatory infiltrate. OLP demonstrates a relativelylow rate of malignant transformation. Diagnostic histopathology is important for discriminating OLP from OLD.

10 YEAR REVIEW OF CHRONIC GRANULOMATOUS INflAMMATORY REACTIONS FOUND IN THE ORAL CAVITY: 2007-2016

Chronic granulomatous inflammatory reactions are uncommon in the oral cavity. These lesions are reactive in origin and are characterized by macrophages which fuse to form multinucleated giant cells or transform into epithelioid histiocytes. Multiple etiologies exist for CGIR and include foreign body reactions to endogenous and exogenous materials, allergic reactions, infectious diseases (fungal or bacterial), sarcoidosis, and Crohn's disease. Here we review CGIR seen over ten years and attempt to clarify their etiologies with the hope that this data will yield information which will allow us to better guide clinicians in the evaluation and treatment of their patients. A review of all cases of CGIR from New York Presbyterian/Queens between 2007-2016 was performed. After eliminating all lesions where foreign material or fungal organisms could be seen, 120 cases of CGIR were identified. Additionally, cases seen in conjunction with a lichenoid inflammatory infiltrate were excluded from the review as they warrant further, separate study. Using relevant clinical information submitted as well as responses to a ten-question survey sent to doctors which included questions regarding the etiology of the CGIR, medical work up, the presence of additional lesions, treatment, progression and recurrence, we identified the following information. Of the 120 cases, 56 were male and 64 were female. The age range was 3–88 years old. 122 sites were identified as some cases had multiple lesions. Only 13 of the 122 lesions were central in bone. The most striking findings was that 9 cases occurred under the age of 18 and all these were in males. Two of these patients had intrabony lesions. In this group, Crohn's disease was found to be the commonest etiology, seen in 5 patients. Therefore, the finding of granulomas, especially intrabony, in a young male warrants a gastrointestinal work up prior to an extensive medical evaluation.

Dermal changes in superficial basal cell carcinoma, melanoma in situ and actinic keratosis and their implications

Basal cell carcinoma (BCC) has a characteristic stroma, but less is known about the dermal characteristics associated with melanoma in situ (MIS) and actinic keratosis (AK). Dermal changes were studied in 301 specimens of AK, BCC and MIS. Subsequently, blinded images of dermal changes from 90 randomly selected cases of those entities were used to assess the predictive value of the dermal changes. Agreement with the final diagnosis was calculated using kappa coefficient (κ). Fibromyxoid stroma was present in 82% of BCC cases; fibrous stroma was seen in 25% of BCC, 58% of MIS and 35.6% of AK specimens (p < 0.05). A lichenoid inflammatory infiltrate was frequently associated with AK and a perifollicular infiltrate with periadnexal fibrosis with MIS. Blinded evaluation of images of the dermal changes associated with the tumors yielded the correct diagnosis in (54.4, 41.1 and 27.8%; average 41.2%) by the three appraisers. Coefficient of agreement in blinded imaged evaluation with the actual diagnosis was higher in the BCC and MIS compared with AK (κ = 0.37, p = 0.0001; κ = 0.2, p = 0.0005 and κ = -0.06, p = 0.84, respectively). Dermal features may be helpful in predicting the correct diagnosis when tumor is not visible.

Clinical and Histopathologic Study of Benign Lichenoid Keratosis on the Face

Benign lichenoid keratosis is a cutaneous entity that consists of a nonpruritic papule or slightly indurated plaque that is histologically characterized by a band-like inflammatory infiltrate with interface involvement. The purpose of this study was to investigate the clinical and histopathologic features of benign lichenoid keratosis localized on the face. Fourteen benign lichenoid keratosis patients diagnosed clinically and histopathologically in our clinic during the 10-year period from 2002 to 2012 were studied. Thirteen female and 1 male patients were included. The mean age at diagnosis was 46.5 years. The color of most of the lesions was brown (10 cases, 71%). The cheek was the most commonly involved area (10 cases, 71%). All of the lesions were single. There were 9 (64%) flat lesion cases and 5 (36%) raised lesion cases. Most patients denied having any symptoms; 3 had mild pruritus. The histopathological findings indicated that all the cases exhibited lichenoid inflammatory infiltrate obscuring the dermal-epidermal junction and vacuolar alteration of basal cell layer. The lesions showed focal parakeratosis (79%), melanophages (79%), hyperkeratosis (71%), and necrotic keratinocytes (71%). Solar elastosis (50%) and acanthosis (43%) were also seen frequently. Diagnosis of benign lichenoid keratosis should be made by a combination of clinical manifestations and histopathological findings. In particular, benign lichenoid keratosis should be considered if a middle-aged patient presents a solitary asymptomatic brown lesion on the face. We think benign lichenoid keratosis may be a specific disorder rather than the inflammatory stage of regressing solar lentigines, large cell acanthoma or reticulated seborrheic keratosis.

Placas anulares en grandes pliegues: cuatro casos de liquen plano pigmentoso-inverso

We report 4 patients with relatively asymptomatic, annular brownish plaques arising in the skin creases. The lesions had remained stable for months despite many topical treatments. Histological amination revealed an atrophic epidermis with a dermal lichenoid inflammatory infiltrate showing marked pigmentary incontinence. These clinical and pathological features were consistent with lichen planus pigmentosus-inversus, a rare, recently described variant of lichen planus, with only 10 cases reported to date. It has been suggested that the intensity and speed of onset of the inflammatory response could be modulated by keratinocyte surface markers, which could also determine the typical morphology of the lesions of this disease.

Annular Plaques in the Skin Folds: 4 Cases of Lichen Planus Pigmentosus-Inversus

We report 4 patients with relatively asymptomatic, annular brownish plaques arising in the skin creases. The lesions had remained stable for months despite many topical treatments. Histological examination revealed an atrophic epidermis with a dermal lichenoid inflammatory infiltrate showing marked pigmentary incontinence. These clinical and pathological features were consistent with lichen planus pigmentosus-inversus, a rare, recently described variant of lichen planus, with only 10 cases reported to date. It has been suggested that the intensity and speed of onset of the inflammatory response could be modulated by keratinocyte surface markers, which could also determine the typical morphology of the lesions of this disease.