Orthokeratinized odontogenic cysts: a Spanish tertiary care centre study based on HPV DNA detection.

BACKGROUND: The role of human papillomavirus (HPV) in orthokeratinized odontogenic cysts (OOCs) has rarely been studied. The objective is to describe the clinicopathological findings in a series of OOCs from a Spanish population that were investigated in relation to the possible presence of HPV. METHODS: A clinicopathological retrospective analysis followed by a molecular analysis of 28 high- and low-risk HPV genotypes was performed in OOC samples of patients seen during the last 15-years in a Spanish tertiary care center. RESULTS: Of 115 odontogenic cysts with keratinization, 16 cases of OOCs were confirmed and evaluated. OOCs occurred predominantly in the mandible of males (mean age 36.06 ± 13.16 years). Swelling of the jaw followed by pain were the most common clinical symptoms, and 56.5% of the OOC cases were associated with an unerupted tooth. After a mean post-cystectomy follow-up of 3.8 years, only one recurrent case was observed, resulting in a verrucous cystic lesion that was considered premalignant after immunohistological examination. DNA extraction was successful from 14 of the 16 OOC cases. None of the primary OCCs or the single recurrent OOC were positive for HPV in the molecular analysis. CONCLUSIONS: OOCs show a very limited potential for recurrence. Our results suggest that neither high- or low-risk HPV subtypes are likely to play a role in the etiology or neoplastic transformation of OOC, at least in the Spanish population.

Keratinizing odontogenic cysts with a spectrum of verrucoid morphology: investigation of a potential role of human papillomavirus.

OBJECTIVE: The role of human papillomavirus (HPV) in keratinizing odontogenic cysts (OC) has only rarely been studied. We describe the clinicopathologic findings in a series of OCs that had unusual keratinization patterns and were investigated for a possible HPV etiology. STUDY DESIGN: Tissue samples from 29 patients with keratinizing OCs were studied for light microscopic features suggestive of HPV infection and by an HPV DNA polymerase chain reaction assay. RESULTS: The mean age at presentation was 31.1 years; 79.3% of the OCs occurred in the mandible and 46.4% were associated with an impacted tooth. The phenotypic characteristics koilocytes, hypergranulosis, and a verrucous pattern of the cyst-lining epithelium were observed in 69%, 62.1%, and 17.2% of cases, respectively. These histomorphologic features did not, however, correlate with HPV infection. CONCLUSIONS: HPV does not appear to play a role in keratinizing OCs and is not responsible for the wart-like histomorphologic features that may be seen in these lesions.

Survivin expression in odontogenic keratocysts and correlation with cytomegalovirus infection.

OBJECTIVES: The aim of this study was to investigate the expression of survivin, an inhibitor of apoptosis, in odontogenic keratocysts and to compare it to the findings in non-neoplastic jaw cysts - periapical cysts, as well as to establish a possible relationship between survivin expression and human cytomegalovirus presence within these cysts. MATERIALS AND METHODS: Samples of 10 odontogenic keratocysts (five positive and five negative for the presence of cytomegalovirus, as determined by polymerase chain reaction) and 10 periapical cysts (five positive and five negative for the cytomegalovirus presence) were analysed. The expression of survivin was assessed by immunohistochemical methods, using monoclonal antibody that selectively recognizes the cytoplasmic form of survivin. RESULTS: All 10 odontogenic keratocysts showed immunostaining for survivin, while all 10 periapical cysts were negative for its presence. There was no correlation between cytomegalovirus presence and expression of survivin within odontogenic keratocysts. CONCLUSION: Survivin may contribute to the aggressive behavior of odontogenic keratocysts, and thus support the emerging opinion of their neoplastic nature.

Human cytomegalovirus is present in odontogenic cysts.

INTRODUCTION: Recent studies suggest that some viruses, including human cytomegalovirus (CMV), may be involved in the pathogenesis of periapical lesions. Since periapical cysts (PCs) represent the next stage in the evolution of periapical granuloma, it seemed reasonable to investigate the presence of CMV in PCs and any possible relationship between its presence and the clinical features of those cysts, as well as to compare the results obtained with corresponding findings in non-inflammatory lesions, like odontogenic keratocysts (OKCs). METHODS: Samples of 33 PCs and 10 OKCs, obtained at the time of surgery, were used for the detection of CMV DNA by polymerase chain reaction. Presence of the virus was correlated with clinical and radiographic features of the cysts. RESULTS: CMV was detected in 18 PCs (54.5%) and six OKCs (60%). The presence of CMV was more frequent in cyst samples collected from patients who reported previous episodes of acute infection. The presence of sinus tract was more frequent in CMV-positive cysts and CMV presence was less frequent in a group of cysts showing signs of acute inflammation at the time of sample collection. The mean sizes of CMV-positive and CMV-negative PCs were almost the same; CMV-positive OKCs were slightly larger than CMV-negative OKCs. None of these results proved to be statistically significant. CONCLUSION: The presence of CMV in the cystic wall is a common feature of both inflammatory and non-inflammatory odontogenic cysts. Although this study has not proved that CMV affects pathogenesis of odontogenic cysts, such a possibility could not be ruled out.

Analysis of p53 protein by PAb240, Ki-67 expression and human papillomavirus DNA detection in different types of odontogenic keratocyst.

OBJECTIVE: To investigate the possible association between alterations in the p53 system and human papillomavirus (HPV) infection in the etiology of odontogenic keratocysts (OKCs) and to study proliferation and epithelial maturation patterns by topographic analysis of Ki-67 expression. MATERIALS AND METHODS: Eighty-three OKC samples (29 cases associated with nevoid basal cell carcinoma syndrome, 29 solitary non-recurrent cases 20 solitary recurrent cases, and 5 chondroid keratocysts) were studied by immunohistochemistry to detect p53 protein (PAb 244) and Ki-67 (MIB-1) expression, and by PCR to detect HPV DNA. RESULTS: Twelve cases (14.6%) expressed p53 protein; no case showed the presence of HPV DNA; 9 cases (11%) presented with mild epithelial dysplasia. The suprabasal expression of Ki-67 was significantly more frequent than its basal expression (p < 0.001). p53 protein expression was significantly associated with the presence of epithelial dysplasia (p = 0.023). Ki-67 expression was not associated with OKC type, the presence of dysplasia, or p53 expression. CONCLUSION: HPVs do not participate in the etiology of OKC, and it appears unlikely that a p53 gene mutation mechanism plays a major role in the genesis of OKC. OKCs show proliferation and genuine maturation behavior reminiscent of benign neoplasms with local destructive capacity.

Latent infection with Epstein-Barr virus in odontogenic disorders: comparison among ameloblastoma, dentigerous cyst and odontogenic keratocyst.

In order to investigate the relationship between Epstein-Barr virus (EBV) latent infection and histogenesis of odontogenic disorders, in situ hybridization for EBV-encoded small RNA (EBER) was applied to the paraffin sections of ameloblastoma, dentigerous cyst, and odontogenic keratocyst. Eight cases (15%) of 53 ameloblastomas showed scattered signals for EBER in the parenchymal cells, whereas no reaction of EBER transcript was observed in the non-neoplastic cystic lesions. In the ameloblastoma, the follicular and plexiform types revealed the signals in the nuclei, but cystic, acanthomatous, granular, and basal cell types exhibited no reaction with EBER. The distribution of the signals without monoclonarity indicated that ameloblastoma cells may exclude EBV genomes or inactivate EBER-encoded genes. The results suggested that EBV participates as one of the transforming factors in the occurrence of ameloblastoma.