Literatura académica sobre el tema "Oral lichen planu"
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Artículos de revistas sobre el tema "Oral lichen planu"
Hasan Zeynalova, Jala, Gulnara Salam Mammedova, Gunel Mammad Sultanova, İrada Arif Mammedxanova, Sevda Tariyel Huseynova y Shahla Rafael Yusubova. "TREATMENT OF ORAL LICHEN PLANUS LICHEN PLANUS WITH PHOTODYNAMIC THERAPY". NATURE AND SCIENCE 14, n.º 09 (23 de noviembre de 2021): 10–13. http://dx.doi.org/10.36719/2707-1146/14/10-13.
Texto completoKoneru, Dr Jyothirmai, Dr Mallika Mahalakshmi P y Dr Ravindra Naik. "Management of Oral lichen Planus – A Review". Indian Journal of Applied Research 3, n.º 3 (1 de octubre de 2011): 289–90. http://dx.doi.org/10.15373/2249555x/mar2013/95.
Texto completoTimková, S., J. Minčík, M. Riznič, E. Ďurovič y A. Konečná. "Lichen planus of the Oral Mucosa". Česká stomatologie/Praktické zubní lékařství 118, n.º 1 (1 de marzo de 2018): 3–7. http://dx.doi.org/10.51479/cspzl.2018.015.
Texto completoTimková, S., J. Minčík, M. Riznič, E. Ďurovič y A. Konečná. "Lichen planus of the Oral Mucosa". Česká stomatologie/Praktické zubní lékařství 118, n.º 1 (1 de marzo de 2018): 3–7. http://dx.doi.org/10.51479/cspzl.2018.015.
Texto completoDermawan, I. G. N. Putra y I. Nyoman Gede Juwita Putra. "MANAGEMENT OF ORAL LICHEN PLANUS TRIGGERED BY STRESS". Interdental Jurnal Kedokteran Gigi (IJKG) 17, n.º 1 (22 de junio de 2021): 27–33. http://dx.doi.org/10.46862/interdental.v17i1.1949.
Texto completoJanovská, M. y Š. Podzimek. "ORAL LICHEN PLANUS - CURRENT POINT OF VIEW". Česká stomatologie/Praktické zubní lékařství 119, n.º 4 (1 de diciembre de 2019): 100–111. http://dx.doi.org/10.51479/cspzl.2019.026.
Texto completoJanovská, M. y Š. Podzimek. "ORAL LICHEN PLANUS - CURRENT POINT OF VIEW". Česká stomatologie/Praktické zubní lékařství 119, n.º 4 (1 de diciembre de 2019): 100–111. http://dx.doi.org/10.51479/cspzl.2019.026.
Texto completoPadmapriya, N. y K. Karthikeyan. "Oral lichen planus with linear lichen planus: a rare association". International Journal of Research in Dermatology 5, n.º 2 (26 de abril de 2019): 429. http://dx.doi.org/10.18203/issn.2455-4529.intjresdermatol20191776.
Texto completoBradić-Vasić, Marija, Ana Pejčić, Milena Kostić, Ivan Minić, Radmila Obradović y Ivana Stanković. "Lichen planus: Oral manifestations, differential diagnosis and treatment". Acta stomatologica Naissi 36, n.º 81 (2020): 1980–94. http://dx.doi.org/10.5937/asn2081980b.
Texto completoIon, Daniela I. y Jane F. Setterfield. "Oral Lichen Planus". Primary Dental Journal 5, n.º 1 (febrero de 2016): 40–44. http://dx.doi.org/10.1177/205016841600500104.
Texto completoTesis sobre el tema "Oral lichen planu"
Siponen, M. (Maria). "Oral lichen planus – etiopathogenesis and management". Doctoral thesis, Oulun yliopisto, 2017. http://urn.fi/urn:isbn:9789526214702.
Texto completoTiivistelmä Suun punajäkälä on krooninen immuunivälitteinen limakalvotauti, jonka etiologia on tuntematon. Taudin syntymekanismiin liittyy tämän hetkisen näkemyksen mukaan T-soluvälitteisen immuniteetin aktivoituminen epiteelin keratinosyyttejä vastaan. Suun punajäkälä aiheuttaa osalle potilaista kivuliaita oireita ja lisää suusyövän riskiä. Parantavaa hoitoa tautiin ei ole. Yleisimmin suun punajäkälän oireiden hoidossa käytetään paikallisia kortikosteroidivalmisteita. Kuitenkin eri hoitomuotojen tehosta on vain heikkoa näyttöä. Tämän väitöskirjatyön tarkoituksena oli tutkia uusia näkökohtia liittyen suun punajäkälän etiopatogeneesiin ja hoitoon. Epidemiologisessa tapaus-verrokkitutkimuksessa selvitettiin, liittyvätkö yleissairaudet, erityisesti kilpirauhassairaudet, suun punajäkälään. Lisäksi satunnaistetussa kontrolloidussa tutkimuksessa verrattiin paikallisen takrolimuusin, triamsinoloniasetonidin ja lumelääkkeen tehoa oireisesta suun punajäkälästä kärsivillä potilailla. Tutkimuksessa selvitettiin myös tollin kaltaisten reseptorien 4 ja 9, hyaluronaanin ja sen pääasiallisen reseptorin CD44-antigeenin, hyaluronaanisyntaasien 1–3, hyaluronidaasien 1–2 sekä katepsiini K:n immunohistokemiallista ilmentymistä suun punajäkälänäytteissä ja terveessä suun limakalvossa. Lisäksi tutkittiin takrolimuusihoidon vaikutusta näiden molekyylien ilmentymiseen suun punajäkälässä. Tämän tutkimuksen tulokset osoittivat, että kilpirauhasen vajaatoimintaan liittyi noin kaksinkertainen riski sairastaa suun punajäkälää. Lisäksi havaittiin, että suun punajäkälässä sekä takrolimuusi että triamsinoloniasetonidi ovat tehokkaampia kuin lumelääke oireiden ja kliinisen taudinkuvan lievittämisessä. Takrolimuusin ja triamsinoloniasetonidin tehossa ei todettu tilastollisesti merkitseviä eroja. Lisäksi suun punajäkälänäytteissä tutkittujen molekyylien ilmentyminen oli muuttunut joko epiteelissä tai stroomassa verrattuna terveeseen limakalvoon. Takrolimuusihoito vähensi CD44-antigeenin ilmentymistä stroomassa ja katepsiini K:n ilmentymistä epiteelissä suun punajäkälässä. Yhteenvetona voidaan todeta, että tämä tutkimus lisää tietoa suun punajäkälään liittyvistä systeemisistä tekijöistä ja suun punajäkälän hoidosta. Lisäksi löydökset lisäävät ymmärtämystä suun punajäkälässä tapahtuvista molekyylitason muutoksista
Marshall, Alison Shona. "The role of chemokines in oral lichen planus". Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413748.
Texto completoZhao, Zhen Zhen. "Mast cell-related mechanisms in oral lichen planus /". [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16304.pdf.
Texto completoJungell, Peter. "Oral lichen planus an ultrastructural and immunohistochemical study /". Helsinki : [s.n.], 1989. http://catalog.hathitrust.org/api/volumes/oclc/21180820.html.
Texto completoAt head of title: Department of Oral Surgery, Institute of Electron Microscopy, University of Helsinki, and Fourth Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. Includes bibliographical references (p. 58-71).
Lage, Denise 1979. "Doenças liquenoides da pele e mucosa oral = análise histológica e imuno-histoquímica = Lichenoid diseases of the skin and oral mucosa : histological and immunohistochemical analysis". [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312892.
Texto completoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-24T06:34:44Z (GMT). No. of bitstreams: 1 Lage_Denise_D.pdf: 12121159 bytes, checksum: f93ebe72b9dc8acf40f7ff2245de6a21 (MD5) Previous issue date: 2014
Resumo: O líquen plano (LP) pode afetar a pele e/ou as mucosas. Histologicamente apresenta infiltrado linfo-histiocitário na junção epitélio-tecido conjuntivo e apoptose de células epiteliais basais. No LP oral (LPO), ocorre erosão frequente pela maior intensidade da necrose. O LP cutâneo (LPC) e o LPO apresentam características histopatológicas similares, mas o curso clínico é diverso. O LPC costuma ter seu curso limitado, enquanto o LPO é frequentemente recidivante. A erupção liquenoide a droga (ELD) desenvolve-se após semanas da ingestão do medicamento e a resolução do quadro é lenta após a interrupção, dificultando o diagnóstico diferencial com o LP idiopático. Os achados clínicos e histológicos podem ser indistinguíveis daqueles do LP, mas a patogênese da ELD não é conhecida. Diferenças locais no sistema imune da mucosa oral e pele poderiam explicar a diversidade no comportamento clínico do LP. Quanto à ELD, há poucas publicações sobre as alterações imunes que atuam no seu desenvolvimento. A citotoxidade celular é mediada, dentre outros mecanismos, por grânulos contendo granzima B e perforina, produzidos por linfócitos T citotóxicos e células natural killers. Com o objetivo de estudar a citotoxicidade celular na patogênese destas doenças, foram analisadas 29 amostras de LPO, 16 de LPC e 6 de ELD. Os cortes foram corados pela H&E e técnica de imuno-histoquímica, para a demonstração de linfócitos CD4 e CD8, macrófagos HAM 56+ e MAC 387+, granzima B, perforina e ICAM-1. As amostras de LPO apresentaram maior densidade de células granzima B+ e perforina+, em comparação às do LPC. Nos dois grupos de doenças, quanto maior era o número de células perforina+, maior era o de células granzima B+. Maior número de células CD4-positivas foi encontrado nas lesões ativas, quando comparado com o das regressivas, no LPO, mas não no LPC. À comparação entre o LPC e a ELD, quanto maior o número de células CD8-positivas, maior era o número de células que expressavam a perforina no grupo LPC. Quanto maiores eram os valores da granzima B, maiores os da perforina, no grupo LPC. Quanto maiores eram os valores da granzima B, maiores os de células apoptóticas agregadas, no grupo da ELD. Nas amostras do LPC, quanto maiores os valores das células T, maiores os dos macrófagos HAM56-positivos e vice-versa. Nas amostras da ELD, foi encontrada correlação negativa entre o número de células T e o de histiocitos jovens (MAC 387+). Havia correlação positiva entre o número de células T e o de células CD8, no grupo da ELD. O mesmo não ocorreu, no grupo do LPC. Concluindo, a expressão aumentada dos grânulos citotóxicos no LPO pode estar associada à maior gravidade da doença na mucosa. Os resultados favorecem um papel mais importante da granzima B e linfócitos TCD8+, no mecanismo patogenético da ELD, comparativamente com o da perforina, de maior importância no LPC. É possível que a ação da granzima B esteja ligada ao número abundante de clusters encontrado na ELD. Embora o LPC e a ELD apresentem semelhanças clínicas e histológicas, a etiopatogênese parece ser distinta
Abstract: Lichen planus (LP) can affect the skin and/or mucous membranes. Histologically it presents lymphohistiocytic infiltrate in the epithelium-connective tissue junction and apoptosis of basal epithelial cells. In oral LP (OLP), erosion occurs frequently by higher intensity of necrosis. Cutaneous LP (CLP) and OLP present similar histopathological features, but the clinical course is diverse. Spontaneous remission is common in CLP, but OLP follows a prolonged course, with periods of remission and relapse. Lichenoid drug eruption (LDE) develops after weeks of drug intake and the resolution of lesions is slow after drug discontinuation, hampering the differential diagnosis with (idiopathic) LP. Clinical and histological findings of LDE may be indistinguishable from those of LP, but LDE pathogenesis is poorly understood Local differences in the immune system of the skin and oral mucosa could explain the diversity in the clinical behavior of CLP and OLP. Regarding LDE, there are few publications on the immune changes that act in its development. Cellular cytotoxicity is mediated, among other mechanisms, by granules containing perforin and granzyme B, produced by cytotoxic T lymphocytes and NK cells. In order to study cellular cytotoxicity in the pathogenesis of these diseases, we analyzed 29 samples of OLP, 16 of CLP and 6 of LDE. The sections were stained for H&E and immunohistochemically targeted with CD4, CD8, HAM 56, MAC387, granzyme B, perforin and ICAM-1. OLP specimens exhibited higher density of cytotoxic granules (perforin and granzyme B) when compared with CLP. In both groups of diseases, the greater the number of perforin+ cells, the greater was the number of granzyme B+ cells. Increased number of CD4+ cells was found in active lesions as compared with the regressive ones in OLP but not in the CLP. The comparison between CLP and LDE revealed that the greater the number of CD8+ cells, the greater the number of cells expressing perforin in CLP group. The higher were the values of granzyme B, the higher the perforin values in the CLP group; the higher were the values of granzyme B, the higher the number of clusters of apoptotic cells in the LDE group. Within CLP group, the higher were the values of T cells, the greater the number of HAM56+ macrophages and vice versa. In LDE samples, negative correlation was found between the number of T cells and young histiocytes (MAC 387+). There was a positive correlation between the number of T cells and CD8 cells in LDE group, but not in CLP group. Concluding, increased expression of cytotoxic granules in OLP may be associated with greater mucosa severity. The results favor a greater role of granzyme B and CD8+ lymphocytes in the pathogenic mechanism of LDE, when compared with perforin, of greater importance in CLP. It is possible that the action of granzyme B is connected to the abundant number of clusters found in LDE. Although CLP and LDE present clinical and histological similarities, the etiopathogenesis appears to be distinct
Doutorado
Anatomia Patologica
Doutora em Ciências Médicas
Erfanian, Nima y Kaiser Ghodbeni. "Clinical Description of Patients Diagnosed with Oral and Genital Lichen Planus, a Register Study". Thesis, Umeå universitet, Institutionen för odontologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-143876.
Texto completoOlivieri, Charles-Vivien. "Inflammations orales et infection par le virus d’Epstein-Barr : vers un nouveau paradigme en pathogenèse orale". Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4201/document.
Texto completoThe oral cavity is a major entry point and reservoir site for a variety of viruses. Apart from herpesvirus simplex, few virological studies detail the role of oral pathogenic viruses, including Epstein-Barr virus. The consensus is that oral inflammation occurs mainly in response to bacterial and fungal infections causing dysbiosis of the oral biofilm. However, this model is not perfect and does not explain well the recurrences observed after decontamination, the decoupling between dysbiosis and inflammatory outbreaks, the proximity of affected and healthy teeth in a similar bacterial environment. The hypothesis of a synergistic mechanism combining viruses and bacteria has been proposed for periodontitis. According to this model, the complementary action of the 2 types of infectious agents on the immune microenvironment would promote inflammatory chronicity and disease progression. Our work focuses on the study of oral cavity infection with EBV. EBV is a ubiquitous virus that persistently infects humans. The oral cavity is the preferred site for its replication with almost constant saliva production. In addition to a major transformative role, EBV's involvement is also suspected for several inflammatory diseases. First, we focused on oral plan lichen (OPL), an autoimmune disease whose etiopathogeny is not clearly established. On biopsies of patients with OPL (n=99), we demonstrated by in situ hybridization that OPL is frequently infected with EBV (74%), particularly in erosive clinical forms. We show that the degree of infiltration of lesions by EBV-infected cells (EBV+) is correlated with inflammatory parameters and that the infiltrated EBV+ cells are plasma cells. This brings a new element to the extent that plasma cells are recognized as major regulatory immune cells. We describe different cytokinic profiles between infected and uninfected OPL, although it is not possible at this stage to directly involve plasma cells. We confirm by electron microscopy that plasma cells host the late stages of the EBV cycle and produce virions in the OPL, suggesting a local amplification mechanism of infection. Then, we focused on periodontitis, a common chronic inflammatory disease that destroys the periodontal structure and causes tooth loosening. This disease is clearly identified as an aggravating factor in many systemic diseases. Our studies had already shown a direct link between EBV infection and the severity of periodontitis. My work has shown that the inflammatory periodontium is infiltrated by EBV+ cells, which appear to be predominantly plasma cells. The presence of virus-producing plasma cells within the inflammatory lesion may explain the infection of adjacent epithelia. In addition, a clinical study conducted on a small cohort of patients treated for periodontitis showed a correlation between the decrease in salivary EBV load and the clinical improvement of patients after treatment. If this result is confirmed, it would be an additional argument in favour of a contribution of periodontal EBV infection to the overall salivary EBV burden. In conclusion, our data show the almost constant presence of EBV in two types of inflammatory oral lesions. This viral infection contributes to worsening a local inflammatory situation associated or not with bacterial dysbiosis. The main observation concerns the presence, often massive, of infected plasma cells whose role remains to be identified. These observations represent significant advances that support a new model of oral pathogenesis combining viruses and bacteria
Camargo, Alessandra Rodrigues de. "Líquen plano oral associado a Hepatite C". Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/23/23139/tde-20032015-154058/.
Texto completoThe objective of the present study was to verify the association between oral lichen planus (OLP) and chronic hepatitis C virus infection (HCV) in two distinct populations in the municipality of São Paulo. A total of 308 patients were evaluated distributed in two study groups: group HCV, comprising 275 patients (132 men and 143 women; average age = 49.8 years old) with chronic HCV infection; and group OLP, comprising 33 patients (10 men and 23 women; average age = 52.9 years old) with OLP. In group HCV, the diagnosis of chronic infection was established through serology for anti-HCV (MEIA, kit AxSYM® HCV version 3.0, Abbott Laboratories, North Chicago, Illinois) confirmed by RNA-HCV research through qualitative PCR testing (Cobas Amplicor HCV MonitorTM test, version 2.0, Roche Diagnostic Systems, NJ, USA). In group OLP, the diagnosis of oral lesions followed the criteria established by the World Health Organization (WHO) in 1978 and later modified by van der Meij and van der Waal in 2003. As exclusion criteria for group HCV, patients that made use of interferon and/or ribavirin for a period below 6 months were excluded from the study, as well patients that were under antiviral treatment for HCV. In this group the presence of co-infections - HIV, HBV, HTLV - was also discarded. In group OLP, patients with clinical diagnosis suggestive of drug-induced lichenoid reactions (DLR) and oral lichenoid lesions related to dental materials (LLDM) were excluded from the sample, as well as patients treated locally or systemically for OLP for a period below 6 months. Cases with histopathological findings of lichenoid dysplasia were also discarded. For result analysis, two comparisons were conducted: (1) in group HCV, OLP prevalence was determined and compared to OLP prevalence in our institution (control group); (2) in group OLP, the prevalence of HCV infection was determined and compared to the prevalence of HCV infection in the São Paulo population. OLP prevalence in patients with Chronic HCV (group HCV) was 2.18% and 1.54% in the control group (P = 0.39). Chronic HCV prevalence in patients with a diagnosis of OLP (group OLP) was 3.03% and 1.42% in the general population (P = 0.39). No statistically significant difference was verified when groups were compared. Our study did not verify an association between OLP and chronic HCV infection in the two populations assessed in the municipality of São Paulo.
Zwet, Marwa. "The extent of the role of apoptosis in oral lichen planus – a morphometric study". University of the Western Cape, 2016. http://hdl.handle.net/11394/5491.
Texto completoOral lichen planus (OLP) is a T-cell mediated chronic inflammatory disease with different clinical types that remains inscrutable in respect of its pathogenetic mechanisms and effective therapy. Increased apoptosis may influence the histopathological criteria of oral lichen planus (decrease in thickness of the epithelium and band of inflammatory infiltrate). Null hypothesis: The apoptotic rate does not correlate with a decrease in the epithelial thickness as well as the thickness of the band of inflammatory infiltrate in OLP. Aim: The present study aims to quantify apoptotic activity and to correlate the apoptotic rate with epithelial thickness as well as thickness of the inflammatory infiltrate of OLP cases diagnosed at Tygerberg Hospital from 2006 – 2015. Further, the epithelial thickness and thickness of the inflammatory infiltrate were also assessed for their association, if any. Materials and Methods: The study sample comprised 17 diagnostically verified cases of OLP. Sections stained with Haematoxylin and Eosin (H&E) were used to identify and count the number of apoptotic cells as well as measure the thickness of epithelium and the thickness of the lymphocytic inflammatory infiltrate by using software morphometric analysis (Zen Blue lite 2012). Statistical analysis was applied to analyse the correlation between apoptotic cells and histopathological features of OLP. Results: The present study's results showed no statistically significant association between the apoptotic rate, the epithelial thickness and the thickness of the lymphocytic inflammatory infiltrate.
Altersved, Karin y Agneta Wallén. "Patienters upplevelse av oral hälsa vid diagnosen erosiv oral lichen planus : En kvalitativ studie". Thesis, Karlstads universitet, Fakulteten för hälsa, natur- och teknikvetenskap (from 2013), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-26876.
Texto completoLibros sobre el tema "Oral lichen planu"
Migliari, Dante Antonio. Critical Thoughts on Oral Lichen Planus. Nova Science Publishers, Incorporated, 2020.
Buscar texto completoAgrawal, Rahul, Akhilesh Chandra y Romi Agrawal. Oral Lichen Planus: Past and Present. LAP LAMBERT Academic Publishing, 2013.
Buscar texto completoUpadhyay, Ram Ballabh, Juhi Upadhyay y Sunitha Carnelio. oxidatve stress in oral lichen planus and oral lichenoid reactions: Oxidative stress and antioxidant defence in oral lichen planus and oral lichenoid reactions. LAP Lambert Academic Publishing, 2012.
Buscar texto completoTaghipour, Kathy. Mucosal disease. Editado por Patrick Davey y David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0255.
Texto completoDudhia, Sonal, Bhavin Dudhia y Jigna Shah. Oral Lichen Planus: An Etiopathologic Study With Various Therapies. LAP Lambert Academic Publishing, 2013.
Buscar texto completoGrover, Vishakha y Anoop Kapoor. Erosive oral lichen planus: Surgical therapy with bio-resorbable membrane. LAP Lambert Academic Publishing, 2012.
Buscar texto completoCapítulos de libros sobre el tema "Oral lichen planu"
Herman, Bjorn y Zoukaa B. Sargi. "Oral Lichen Planus". En Encyclopedia of Otolaryngology, Head and Neck Surgery, 1903–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23499-6_66.
Texto completovan der Wal, Jacqueline E. "Oral Lichen Planus". En Encyclopedia of Pathology, 1–4. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-28845-1_736-1.
Texto completoMcCullough, Michael J., Mohammad S. Alrashdan y Nicola Cirillo. "Oral Lichen Planus". En Contemporary Oral Medicine, 1043–82. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-72303-7_14.
Texto completoMcCullough, Michael J., Mohammad S. Alrashdan y Nicola Cirillo. "Oral Lichen Planus". En Contemporary Oral Medicine, 1–40. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28100-1_14-1.
Texto completoNayee, Shalini, Cameron Herbert y Jane F. Setterfield. "Oral Lichen Planus". En Diseases of the Oral Mucosa, 111–24. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-82804-2_11.
Texto completovan der Wal, Jacqueline E. "Oral Lichen Planus". En Encyclopedia of Soil Science, 290–93. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-3-319-28085-1_736.
Texto completoBragazzi, Nicola Luigi y Claudio Nicolini. "Lichen Planus". En Genomics, Personalized Medicine and Oral Disease, 185–217. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17942-1_9.
Texto completoLaeijendecker, R. "Orale lichen planus". En Praktijkboek tandheelkunde, 594–601. Houten: Bohn Stafleu van Loghum, 2008. http://dx.doi.org/10.1007/978-90-313-7318-5_47.
Texto completoLi, Yan, Kun Wang, Bo Zhang, Qichao Tu, Yufei Yao, Bomiao Cui, Biao Ren et al. "Mycobiome Dysbiosis in Oral Lichen Planus". En Atlas of Oral Microbiology: From Healthy Microflora to Disease, 315–32. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7899-1_9.
Texto completoDe Carli, João Paulo, Soluete Oliveira da Silva, Bethânia Molin Giaretta De Carli, Angélica Zanata, Micheline Sandini Trentin, Maria Salete Sandini Linden y Daniela Cristina Miyagaki. "Clinical Correlation of Oral Candidosis and Oral Lichen Planus". En Oral Candidosis, 75–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-47194-4_11.
Texto completoActas de conferencias sobre el tema "Oral lichen planu"
Ganesha, Raziv y Priyo Hadi. "Management of Oral Lichen Planus Due to Stress". En The 7th International Meeting and The 4th Joint Scientific Meeting in Dentistry. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007293601300134.
Texto completoTaranu, Tatiana, Magda Constantin, Didona Ungureanu, Irina Mihaela Esanu y Mihaela Paula Toader. "IL6 is correlated with metabolic syndrome parameters in oral lichen planus". En 2015 E-Health and Bioengineering Conference (EHB). IEEE, 2015. http://dx.doi.org/10.1109/ehb.2015.7391410.
Texto completoPrasetyaningtyas, Neken, Ayu Fresno Argadianti y Iwan Hernawan. "Management of Oral Lichen Planus Due to Stress In Post-Menopausal Women". En The 7th International Meeting and The 4th Joint Scientific Meeting in Dentistry. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007295302200226.
Texto completoKistenev, Yury, Alexey Borisov, Alexander Shapovalov, Olga Baydik y Maria Titarenko. "Diagnostics of oral lichen planus based on analysis of volatile organic compounds in saliva". En SPIE BiOS, editado por Valery V. Tuchin, Kirill V. Larin, Martin J. Leahy y Ruikang K. Wang. SPIE, 2017. http://dx.doi.org/10.1117/12.2252131.
Texto completoTabeti-Bentahar, CF, F. F Bouzouina y F. F. Bénali. "Lichen plan buccal et transformation maligne : dix ans de suivi au Service de Pathologie et Chirurgie Buccales CHU Oran". En 62ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2014. http://dx.doi.org/10.1051/sfco/20146203004.
Texto completoInformes sobre el tema "Oral lichen planu"
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