Prevalence and risk factors associated with leukoplakia, hairy leukoplakia, erythematous candidiasis, and gingival hyperplasia in renal transplant recipients

King, Gaston N.; Healy, Claire M.; Glover, Mary; Kwan, Jonathan; Williams, David M.; Leigh, Irene M.; Thornhill, Martin H.

doi:10.1016/0030-4220(94)90086-8

Cited by 89 publications

(90 citation statements)

References 50 publications

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“…promised persons (9,17,20). This result suggests that the conversion of a focus of EBV replication in normal oral epithelium into an oral hairy leukoplakia lesion depends more upon local epithelial immune deficiencies (18), EBV mechanisms of immune evasion (46), and specific EBV gene expression patterns (48,50) than upon the frequency with which one or more EBV strains enter and reactivate within the oral epithelium (44,47).…”

Section: Vol 81 2007 Ebv In Pre-lc Transitions From Blood To Epithementioning

confidence: 97%

Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation

Walling

Ray²,

Nichols

et al. 2007

J Virol

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Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with many malignant and nonmalignant human diseases. Life-long latent EBV persistence occurs in blood-borne B lymphocytes, while EBV intermittently productively replicates in mucosal epithelia. Although several models have previously been proposed, the mechanism of EBV transition between these two reservoirs of infection has not been determined. In this study, we present the first evidence demonstrating that EBV latently infects a unique subset of blood-borne mononuclear cells that are direct precursors to Langerhans cells and that EBV both latently and productively infects oral epithelium-resident cells that are likely Langerhans cells. These data form the basis of a proposed new model of EBV transition from blood to oral epithelium in which EBV-infected Langerhans cell precursors serve to transport EBV to the oral epithelium as they migrate and differentiate into oral Langerhans cells. This new model contributes fresh insight into the natural history of EBV infection and the pathogenesis of EBV-associated epithelial disease. Epstein-Barr virus (EBV) is a human herpesvirus that ultimately infects 95% of adults worldwide. EBV is transmitted via mucosal fluids and establishes life-long persistent infection.Although persistent infection is asymptomatic in most people, EBV is associated with benign syndromes, including infectious mononucleosis and oral hairy leukoplakia, and a wide variety of both lymphoid and mucosal epithelial malignancies. Persistent latent EBV infection occurs in memory B lymphocytes that circulate in blood (22). While latent EBV infection also occurs in some epithelial malignancies (29), EBV infection of epithelial cells typically results in productive replication, as demonstrated in oral hairy leukoplakia (9) and in normal oral epithelium (8,10,48).Three different models have previously been proposed to explain the transition of EBV from the latent reservoir of infection in blood-borne B lymphocytes to sites of productive replication in oral epithelium. Model 1 proposes that B lymphocytes carrying latent EBV infection migrate from the blood to the epithelium, where the EBV reactivates and infects adjacent epithelial cells (12), but evidence of intraepithelial B lymphocytes in normal oral epithelium or in oral hairy leukoplakia is lacking (30, 33). Model 2 proposes that EBV virions produced by B lymphocytes in the oral submucosa bind submucosal EBV-specific dimeric immunoglobulin A (IgA) and enter basal oral epithelial cells by endocytosis via the polymeric Ig receptor (37), but the polymeric Ig receptor is not expressed in oral epithelium (23). Model 3 proposes that EBV virions produced by B lymphocytes in oral lymphoid tissues (26) gain access to and infect middle-and upper-layer oral epithelial cells as a result of microscopic traumatic epithelial injury, such as that which occurs during mastication. However, this model is contradicted by evidence that EBV transitions into oral epithelium as cell-associated latent infecti...

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Section: Vol 81 2007 Ebv In Pre-lc Transitions From Blood To Epithementioning

confidence: 97%

Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation

Walling

Ray²,

Nichols

et al. 2007

J Virol

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“…U našem istraživanju je 75 posto pacijenata uzimalo ciklosporin A. U 57,3 posto slučajeva ciklosporin A propisivao se u kombinaciji s blokatorima kalcijevih kanala. Veća prevalencija gingivne hiperplazije zabilježena je u komature is gingival hyperplasia while the data for other lesions are scarce and contradictory (5,9,(21)(22)(23).…”

Section: Gašpar I Surunclassified

The Oral Cavity State in Renal Transplant Recipients

Gašpar¹,

Glavina²,

Grubišić³

et al. 2015

Acta Stomatol Croat

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“…Th is condition is related to immune status and most patients are immunocompromised 30 . Hairy leukoplakia can be seen in 8%-11% of patients with KT 7,31 . Histologically, severe hyperkeratosis and acanthosis with virally infected epithelial cells can be seen.…”

Section: Hairy Leukoplakiamentioning

confidence: 99%

Oral Lesions in Kidney Transplant Recipients

Levarda-Hudolin¹,

Hudolin

Bašić‐Jukić

et al. 2016

acc

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SUMMARY -Permanent immunosuppression is necessary to prevent rejection after kidney transplantation. However, it may predispose patients to diff erent conditions and diseases including oral lesions. Th e most common benign oral lesions in kidney transplant recipients are gingival hyperplasia, oral candidiasis, hairy leukoplakia and saburral tongue. Oral form of Kaposi sarcoma, although rarely, can also be seen in kidney transplant patients. In this review, we present the incidence, etiology, clinical fi ndings, diagnosis and treatment options for these lesions. For kidney transplant recipients, it is important to maintain good oral hygiene and care, as well as regular professional control by the dentist. Th is approach can reduce the number and severity of oral lesions.

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Prevalence and risk factors associated with leukoplakia, hairy leukoplakia, erythematous candidiasis, and gingival hyperplasia in renal transplant recipients

Cited by 89 publications

References 50 publications

Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation

Epstein-Barr Virus Infection of Langerhans Cell Precursors as a Mechanism of Oral Epithelial Entry, Persistence, and Reactivation

The Oral Cavity State in Renal Transplant Recipients

Oral Lesions in Kidney Transplant Recipients

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