Oral Lichenoid Lesion following Dental Implant Placement and Successful Management with Free Gingival Graft: A Case Report with 10-Year Follow-Up.

Titanium and metal alloys are widely used in implants, crowns, and bridges in implant dentistry owing to their biocompatibility. In this case report of a 45-year-old female patient, multiple implants were placed in five different sextants at different time points. Notably, oral lichenoid lesions (OLL) occurred in three sextants following implant placement, strongly suggesting that the dental implants or prostheses were the causative factors for OLL. The lesion was of the reticular type with erythematous surroundings and was symptomatic. Although several conservative treatments, including repeated topical application of corticosteroids, were repeatedly continued, no discernible improvement or alleviation of symptoms was observed. Consequently, surgical excision and replacement of the lesion with a free gingival graft (FGG) harvested from the palatal soft tissue were performed. No clinical symptoms or recurrence of lesions were observed during 10 years of follow-up post-FGG.

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

Background: 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. Material and Methods: 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. Results: 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). Conclusions: 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. (AU)

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

BACKGROUND: 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. MATERIAL AND METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Lichenoid dermatitis following PD-1 inhibitor-induced toxic epidermal necrolysis: a case report and literature review.

Immune checkpoint inhibitors such as anti-PD-1 receptor antibodies have been shown to be effective in patients with advanced gastric cancer. However, there is a growing concern about immune-related adverse events. A case of a patient with gastric adenocarcinoma who developed toxic epidermal necrolysis (TEN) induced by sintilimab and subsequently developed lichenoid dermatitis is reported. TEN was diagnosed according to a history of sintilimab use, clinical symptoms and physical examination. During hospitalization, the patient developed recurrent fever caused by bacteremia and recovered from TEN after anti-infection and anti-inflammatory treatments. However, when TEN was controlled, the patient developed the lesional manifestations of lichenoid dermatitis. To date, no cases of lichenoid dermatitis after TEN have been reported following the use of PD-1 inhibitors.

PD-1 inhibitors are drugs that help fight stomach cancer but can sometimes cause skin problems. Most skin problems are minor and do not have a serious impact on the patient's health. However, life-threatening skin problems such as toxic epidermal necrolysis (TEN) can sometimes happen. This case report describes a patient with stomach cancer who had lichenoid dermatitis (another skin problem) after TEN, following the treatment of his cancer with PD-1 inhibitors. To the best of our knowledge, it is very rare to experience both skin problems after treating cancer with PD-1 inhibitors. This rare phenomenon is reported to bring more attention to it. More research is needed to determine how to treat this problem better.

Cytotoxic dermatitis: Review of the interface dermatitis pattern in veterinary skin diseases.

Interface dermatitis or lichenoid interface dermatitis refers to a cutaneous inflammatory pattern in which keratinocyte cell death is the essential feature. These terms have evolved from the originally described lichenoid tissue reaction. These lesions are the basis for an important group of skin diseases in animals and people where cytotoxic T-cell-mediated epidermal damage is a major pathomechanism. Yet, for largely historical reasons these commonly used morphological diagnostic terms do not reflect the essential nature of the lesion. An emphasis on subsidiary lesions, such as the presence of a lichenoid band, and definitions based on anatomical features, such as location at the dermo-epidermal location, may cause confusion and even misdiagnosis. This review covers historical aspects of the terminology, including the origin of terms such as "lichenoid." The types of cell death involved and the histopathologic lesions are described. Etiopathogenesis is discussed in terms of aberrations of immune/inflammatory mechanisms focusing on cutaneous lupus erythematosus, erythema multiforme, and Stevens-Johnson syndrome/toxic epidermal necrolysis. Mechanisms have most extensively been studied in humans and laboratory animals and the discussion is centered on these species. As interface dermatitis is firmly entrenched in dermatological parlance, rather than using "cytotoxic" as its substitute, the terminologies "interface cytotoxic dermatitis" and "panepidermal cytotoxic dermatitis" are recommended, based on location and extent of epithelium affected.

[Lichenoid drug eruption with unfavorable evolution. Difficulties in diagnosis]. / Erupción liquenoide medicamentosa con evolución desfavorable. Dificultades en el diagnóstico.

We report the case of a woman who started with a lichenoid eruption, unfavorable evolution, for which a drug reaction was suspected. The final diagnosis was paraneoplastic pemphigus. Multidisciplinary care and evaluation by an Allergist is important in patients with severe skin reactions, suspected of drug reactions, due to the difficulty in establishing the diagnosis.

Se reporta el caso de una mujer que inició con erupción liquenoide, con evolución desfavorable, por lo que se sospechó una reacción medicamentosa. El diagnóstico final fue pénfigo paraneoplásico. Es importante la atención multidisciplinaria y la evaluación de un alergólogo en pacientes con reacciones cutáneas graves, por sospecha de reacciones farmacológicas, debido a la dificultad para establecer el diagnóstico.

ADVERSE DRUG EVENTS: LICHEN PLANUS OF THE PENIS AFTER INTAKE OF NEBIVOLOL- FIRST REPORTED CASE IN THE WORLD LITERATURE.

The pathogenesis of lichen planus and lichenoid-type reactions remains shrouded in mystery to this day, precisely because of the inability to perform acute/specific tests for reproduction of a particular type of reaction (in this case lichenoid) in order to prove a causal relationship. Nevertheless, the concept of molecular mimicry/antigen mimicry as a possible important pathogenetic inducer for lichen planus and lichenoid-type reactions, is increasingly becoming a topic of discussion and remains more than relevant at present. Disturbances in the integrity of tissue homeostasis- in one form or another, in fact, become a powerful generator of cross-mediated immunity, possibly directed at tissue-localized structures/structural elements/proteins or amino acids. The observation and reporting of this kind of disorders (even in the absence of the mentioned tests), as well as their parallel manifestation with a disease such as lichen planus (or lichenoid-type reaction), has led over the years to the validation of the now universal belief that the disease is multifactorially determined. And the causes of disruption of this integrity can be both external- infectious, meicamentous as well as internal- tumoral, paraneoplastic, etc. Medication induction or triggering of lichen planus by beta blockers has been observed and reported frequently over the years, and the clinical picture can vary and be extremely heterogeneous. We describe the first case in the world literature of a lichen planus after nebivolol administration that developed in the strictly restricted area of the glans penis. According to a reference in the medical literature, this is also the second case in the world literature of penile localized lichen planus after beta blocker intake. The other analogous one was recorded and described back in 1991 after propranolol intake.

Immune checkpoint inhibitor lichenoid eruption due to pembrolizumab.

Pembrolizumab is an immune checkpoint inhibitor used in many cancer types, including genitourinary cancers. Although immunotherapies have dramatically changed the landscape of cancer treatment by providing an alternative to traditional chemotherapy, they have been associated with significant immune-related adverse events (IRAEs) with wide-ranging clinical manifestations. We present the case of an elderly woman on pembrolizumab for metastatic bladder cancer who developed cutaneous IRAE with lichenoid eruptions that responded to high-dose intravenous glucocorticoids.

Clinical and epidemiological profile of lichen striatus in children-Experience from a tertiary care hospital.

We analyzed records of 30 patients with lichen striatus (age < 18 years) in this retrospective study. Seventy percent were females and 30% were males with a mean age of diagnosis of 5.38 ± 4.22 years. The most common age group affected was 0-4 years. The mean duration of lichen striatus was 6.66 ± 4.22 months. Atopy was present in 9 (30%) patients. Although LS is a benign self-limited dermatosis, long-term prospective studies with a greater number of patients will help in better understanding of the disease including its etiopathogenesis and association with atopy.

Annular Lichenoid Dermatitis of Youth: Its Pathogenesis, Diagnosis, and Management.

Annular lichenoid dermatitis of youth (ALDY) is a newly described controversial benign lichenoid inflammatory cutaneous disorder often characterized by annular patches with hypopigmented center and surrounding erythematous border. Primarily, it affects the trunk and groin of young patients. Since its first description in 2003, additional patients have been reported, leading to better characterization of the entity; nevertheless, the pathogenesis is still unclear, and several hypotheses have been provided about possible triggering or causative factors. It tends to follow a chronic course, with some lesions spontaneously remitting, while others may be persistent or recur post-treatment. No standard validated treatment has been indicated so far for this disorder. Commonly prescribed topical treatment includes corticosteroids and calcineurin inhibitors with variable response.

Prevalence of and prognostic factors for Candida superinfection in oral lichen planus and lichenoid reactions: A retrospective cohort study.

BACKGROUND: Oral candidiasis occasionally occurs in patients with oral lichen planus (OLP) or lichenoid reaction (OLR). However, not all patients undergoing corticosteroid therapy develop Candida superinfection. Thus, the identification of prognostic risk factors may help to identify patients at risk of Candida superinfection. METHODS: A retrospective cohort study was conducted to review patients with OLP/OLR who received steroid therapy at a single dental hospital between January 2016 and December 2021. The prevalence of Candida superinfection and prognostic factors were assessed. RESULTS: Eighty-two eligible patients with OLP/OLR were retrospectively reviewed. The overall prevalence of Candida superinfection during the study period was 35.37%; the median time-to-event between initiation of corticosteroid therapy and diagnosis of superinfection was 60 days (interquartile range; 34-296). The ulcerative type of OLP/OLR, number of topical steroid applications, poor oral hygiene, and oral dryness were significantly associated with superinfection (p < 0.05; Fisher's Exact test) and were identified as prognostic factors in univariable risk ratio regression. Multivariable risk ratio regression revealed the ulcerative type of OLP/OLR and number of topical steroid applications were significant prognostic factors for Candida superinfection in patients with OLP/OLR. CONCLUSION: Candida superinfection occurs in approximately one-third of patients with OLP/OLR undergoing corticosteroid therapy. Patients with OLP/OLR should be closely monitored in the first 2 months (60 days; median time to infection) after steroid prescription. The ulcerative type of OLP/OLR and a higher number of topical steroid applications per day may represent prognostic factors to identify patients at risk of Candida superinfection.

PRAME immunohistochemistry can distinguish melanocytic pseudonests of lichenoid reactions from melanoma in situ.

BACKGROUND: Distinguishing melanocytic pseudonests encountered in lichenoid dermatoses or lichenoid keratoses from melanoma in situ (MIS) with brisk lichenoid inflammation can prove challenging. METHODS: We designed a case-control study to evaluate the accuracy metrics of PRAME immunohistochemistry to distinguish melanocytic pseudonests in lichenoid dermatoses or keratoses from inflamed MIS. Immunostaining for PRAME was performed on paraffin-embedded formalin-fixed diagnostic tissue using a rabbit monoclonal antibody to PRAME (Abcam), with a 1:3200 dilution on a Leica Bond detection system. RESULTS: Our search identified 21 cases of melanocytic pseudonests (n = 21, 46%) encountered in lichenoid dermatoses and 24 cases of inflamed MIS (n = 24, 53%). Each method of evaluating PRAME immunohistochemistry (PRAME+ clusters, PRAME % of melanocytes by four categories and PRAME+ melanocyte counts per linear mm of epidermal basal layer) showed statistically significant differences between the MIS and the pseudonest cohorts (respectively, p < 0.001; p < 0.001; and p < 0.001). Receiver operating characteristics analysis for PRAME+ melanocyte counts per linear mm of epidermal basal layer revealed an area under the curve of 0.9 ± 0.05 (95% confidence interval 0.9-1.0). When determining an optimal cut-off point for the best Youden index [sensitivity (%) + specificity (%) - 100], the cut-off of 1.0 PRAME+ melanocytes per linear mm showed a sensitivity of 79.2% and specificity of 85.7% (Youden index 0.65) to distinguish MIS from pseudonests. CONCLUSION: PRAME immunohistochemistry may constitute an additional tool for this challenging differential diagnosis.

Imatinib-induced lichen planus and lichenoid drug eruption: A report of three cases.

Cutaneous adverse effects of imatinib are common and well documented in the literature. However, imatinib-induced lichen planus is an uncommon side effect with only four reported cases. In addition, reactivation of hepatitis B is an extremely rare association. We report two cases of imatinib-induced lichen planus, one of which is associated with hepatitis B reactivation, and one case of lichenoid eruption caused by imatinib. The aim of our report is to make physicians aware of this rare association between lichen planus and imatinib. We also recommend screening for hepatitis B virus before starting treatment with imatinib to avoid serious complications.

Pustular Lichenoid Eruptions Induced by Immune Checkpoint Inhibitors: Two Case Reports and a Review of the Literature.

Immune checkpoint inhibitors (ICIs) have become the standard treatment for many types of cancer. After several years of using these therapies, many adverse events related to ICIs have been observed. Dermatologic toxicities such as nonspecific morbilliform rash, vitiligo, Stevens-Johnson syndrome/toxic epidermal necrolysis, and more rarely, lichenoid eruptions have been described in the literature. We report 2 cases of pustular lichenoid eruptions, 1 in a patient with nonsmall cell lung carcinoma and 1 in a patient with metastatic melanoma, induced by pembrolizumab and nivolumab, respectively. The 2 patients were treated with topical corticosteroids, and complete healing of lesions was slowly obtained. Due to the severity of the cutaneous eruptions, pembrolizumab and nivolumab were discontinued. We identified 6 cases of pustular lichenoid eruptions induced by ICIs in the published literature and in the French Pharmacovigilance Database and reviewed their main clinical features and courses.

Senescence in oral lichen planus as assessed by the immunohistochemical evaluation of senescence marker protein-30 (Regucalcin).

Background: Oral lichen planus is a T-cell-mediated chronic inflammatory disease affecting approximately 1% to 2% of the population, the etiology of which is currently unknown. The objectives of this study were to observe if senescence occurs in oral lichen planus, through the assessment of the immunohistochemical expression of a novel marker for senescence called Senescence marker protein-30 or regucalcin, and compare the expression to that in oral lichenoid reaction and non-specific inflammation. Subjects and Methods: The study material consisted of 30 cases of oral lichen planus, 15 cases of oral lichenoid reaction and 15 cases of non-specific inflammation. The number of positive cells in ten randomly selected high power fields were counted in the epithelium and the connective tissue separately and the mean was determined. Results: Mann-Whitney U test was used to statistically analyze if there was any significant difference in the expression of Senescence marker protein-30 between oral lichen planus, oral lichenoid reaction and non-specific inflammation. Even though a greater expression was seen in the oral lichen planus cases than oral lichenoid reaction, the difference in both the epithelium and connective tissue was not statistically significant. Conclusion: This study shows that in addition to the already known mechanisms like apoptosis and increased cell proliferation rates, the activated T-lymphocytes may also trigger a senescent change in the cells of oral lichen planus. As with the other mechanisms, this is also seen only in a small proportion of the cases.

Cutaneous lichenoid drug eruptions: A narrative review evaluating demographics, clinical features and culprit medications.

Cutaneous lichenoid drug eruptions (LDE) are adverse drug reactions (ADR) characterized by symmetric, erythematous, violaceous papules reminiscent but rarely fully characteristic of lichen planus (LP). We aimed to analyse the literature describing cases of LDE within the last 20 years to provide additional insight into culprit drugs, typical latency to onset of the eruption, the spectrum of clinical presentations, severity and management. A literature search was conducted in MEDLINE between January 2000 and 27 January 2021. The keywords 'lichenoid drug rash' and 'lichenoid drug eruption' were used. Cases were included if LDE diagnosis was made, and culprit drugs were identified. A total of 323 cases with LDE were identified from 163 published case reports and studies. The mean patient age was 58.5 years (1 month to 92 years), and 135 patients (41.8%) were female. Checkpoint inhibitors (CKI) were the most frequently reported culprit drugs (136 cases; 42.1%), followed by tyrosine kinase inhibitors (TKI) (39 cases; 12.0%) and anti-TNF-α-monoclonal antibodies (13 cases; 4.0%). The latency between initiation of the drug and manifestation was 15.7 weeks (range: 0.1-208 weeks). After discontinuing the culprit drug, the median time to resolution was 14.2 weeks (range: 0.71-416 weeks). One hundred thirty-six patients (42.1%) were treated with topical, and 54 patients (16.7%) with systemic glucocorticoids. Overall, we conclude that, albeit rare, LDE is challenging to diagnose ADR induced by mostly CKI, TKI, and biologics. Treatment modalities resemble that of lichen planus, and the culprit drugs had to be discontinued in only 26%, which is low compared with other types of adverse drug reactions. This is probably due to the low risk of aggravation (e.g. toxic epidermal necrolysis) if the drug is continued and the benefit/risk ratio favouring the drug, as is often the case in cancer therapy.