Gingival tissue samples from periodontitis patients demonstrate epithelial-mesenchymal transition phenotype.

OBJECTIVE: To determine the expression of key epithelial-mesenchymal transition (EMT) markers in gingival tissue samples collected from patients with periodontitis. BACKGROUND: Epithelial-mesenchymal transition is a process responsible for shifting epithelial-phenotype to mesenchymal-phenotype leading to loss of epithelial-barrier function. Thus, EMT could be involved as a pathogenic mechanism in periodontitis as both conditions share common promoters and signalling pathways. MATERIALS AND METHODS: Gingival tissue samples were collected from patients with periodontitis (case) and healthy periodontium (control). Periodontal parameters including bleeding on probing, probing pocket depth (PPD), and clinical attachment loss were recorded. Paraffinized tissue samples were processed and immunohistochemically stained to determine the expression of key EMT markers which included E-cadherin, ß-catenin, Snail1 and vimentin. RESULTS: The majority of cases (n = 65, 72.2%) were diagnosed with periodontitis stage 3 or 4, grade b or c vs 25 (27.8%) subjects with intact healthy periodontium. Discontinuity of epithelium was detected in up to 80.9% of periodontitis cases associated with reduced number of epithelial layers as compared to controls. Immunohistochemical expression of epithelial markers (E-cadherin and ß-catenin) was significantly downregulated in periodontitis patients as compared with controls. Periodontitis cases exhibited significant upregulation of Snail1 expression. Furthermore, cytoplasmic vimentin (66.2%) and nuclear ß-catenin (27.7%) were solely expressed in periodontally diseased tissues compared with control. Epithelial markers, E-cadherin and ß-catenin, were significantly negatively correlated with increasing PPD, while vimentin showed positive correlation with this parameter. CONCLUSION: There were marked downregulation of epithelial molecules and upregulation of mesenchymal markers in gingival tissues derived from periodontitis patients, suggesting expression of the EMT phenotype in the pathological epithelial lining of periodontal pockets.

Ameloblastoma vs basal cell carcinoma: an immunohistochemical comparison.

Despite behavioral mimicry of ameloblastoma (AB) and basal cell carcinoma (BCC), they are classified at 2 extremes within pertinent WHO classifications with respect to benign and malignant designation. This study aims to appraise the current allocation of AB in the classification through an immunohistochemical comparison of some aspects of behavior with BCC. Sections from retrospectively retrieved formalin-fixed, paraffin-embedded tissue blocks of AB (n = 37) and BCC (n = 34) were comparatively examined for the immunohistochemical expression for Ki-67, Bcl-2, MMP-2, MMP-9, CD31, and D2-40 monoclonal antibodies. No statistically significant differences between the tumors were found regarding the immunoexpressions of Bcl-2 (P = .252), CD31 microvessel density (P = .895), lymphatic vessel density (P = .642), and MMP-9 stromal expression (P = .083). MMP-2 expression was significantly higher in epithelial and stromal regions of AB (P = .009 and P = .001, respectively), whereas Ki-67 and MMP-9 epithelial expressions were significantly higher in BCC (P < .000 and P = .026, respectively). Within the studied immunohistochemical attributes for tumor behavior, the study accentuated the overall behavioral mimicry of the tumors and indicated that BCCs surmount ABs by the proliferative rate only.

Correlation of amyloid and ameloblast-associated proteins to odontogenic cysts and tumors: A cross-sectional study.

Background and Aims: Odontogenic cysts and tumors often form hard and soft structures that resemble odontogenesis. It is well known that amyloid is produced in Pindborg tumors; however, it is still debatable whether it is also formed in other odontogenic tumors and cysts. This study aimed to detect the presence of amyloid in different odontogenic cysts and tumors in correlation to matrix proteins secreted during enamel formation; namely amelogenin and odontogenic ameloblast-associated protein. Methods: This study included formalin fixed paraffin embedded tissue blocks of 106 different types of odontogenic cysts and tumors. Congo red and thioflavin T were performed to confirm the presence of amyloid; immunohistochemistry was used to detect amelogenin and odontogenic ameloblast-associated protein. Results: Amyloid was detected in pindborg tumors (conventional), adenomatoid odontogenic tumors, odontogenic fibroma (Amyloid variant), follicular solid and unicystic ameloblastomas, radicular cysts, dentigerous cysts, dentinogenic ghost cell odontogenic tumor, ameloblastic fibroma, calcifying odontogenic cyst, and primordial Odontogenic tumor. Amelogenin was detected in 95.3% of the cases, while odontogenic ameloblast-associated protein was detected in 93.4% of the cases. The association between odontogenic ameloblast-associated protein and amyloid was highly significant at p < 0.01. However, there was no significant relationship between amelogenin and amyloid p > 0.05. Conclusion: Although pindborg tumor is the bonafide example of amyloid deposition in odontogenic tumors, this study concluded that amyloid may be deposited in traces to massive amounts in various odontogenic cysts and tumors, and it is significantly linked to odontogenic ameloblast-associated protein but not amelogenin matrix protein, since all amyloid cases were odontogenic ameloblast associated protein positive.

Immunohistochemical Evaluation of S100, Alpha-Smooth Muscle Actin, Podoplanin, Matrix Metalloproteinase 13, and Human Epidermal Growth Factor Receptor 2neu Markers in Basal Cell Carcinoma Variants.

Background Variants of basal cell carcinoma (BCC) appear to behave biologically differently. Several histological patterns impact the concept of low-risk (indolent) and high-risk (aggressive) types in the head and neck. This study aims to assess the biological behavior of BCC variants by immunohistochemical expression of S100, alpha-smooth muscle actin (α-SMA), podoplanin, matrix metalloproteinase 13 (MMP-13), and human epidermal growth factor receptor 2 (HER2)neu biomarkers. Methodology A total of 65 paraffin-embedded tissue blocks of BCC of the head and neck were retrieved from the collections of the Histopathology Department of the Medical City Teaching Complex and the Ghazi Al-Harerri Hospital at the University of Baghdad's College of Dentistry, spanning the years 2015 through 2021. S100, α-SMA, podoplanin, MMP-13, and HER2neu biomarkers were used to perform immunohistochemical analysis (Abcam). Results This study noticed different expressions of S100, α-SMA, podoplanin, MMP-13, and HER2neu between different variants. There was no immunohistochemical expression in perineural invasion with all cases of BCC variants. The highest expression was seen in HER2neu, MMP-13, and α-SMA with aggressive histological patterns. There was no podoplanin lymphatic vessel density immunoexpressing in all variants, while tumoral podoplanin showed a significant difference in all variants. HER2neu was correlated with all other biomarkers. Conclusions HER2neu, MMP-13, and α-SMA biomarkers can be used as diagnostic markers to predict the aggressive biological behavior of BCC tumors.

Pathogenesis of periodontitis - A potential role for epithelial-mesenchymal transition.

Epithelial mesenchymal transition (EMT) is a process comprising cellular and molecular events which result in cells shifting from an epithelial to a mesenchymal phenotype. Periodontitis is a destructive chronic disease of the periodontium initiated in response to a dysbiotic microbiome, and dominated by Gram-negative bacteria in the subgingival niches accompanied by an aberrant immune response in susceptible subjects. Both EMT and periodontitis share common risk factors and drivers, including Gram-negative bacteria, excess inflammatory cytokine production, smoking, oxidative stress and diabetes mellitus. In addition, periodontitis is characterized by down-regulation of key epithelial markers such as E-cadherin together with up-regulation of transcriptional factors and mesenchymal proteins, including Snail1, vimentin and N-cadherin, which also occur in the EMT program. Clinically, these phenotypic changes may be reflected by increases in microulceration of the pocket epithelial lining, granulation tissue formation, and fibrosis. Both in vitro and in vivo data now support the potential involvement of EMT as a pathogenic mechanism in periodontal diseases which may facilitate bacterial invasion into the underlying gingival tissues and propagation of inflammation. This review surveys the available literature and provides evidence linking EMT to periodontitis pathogenesis.

Proliferative, apoptotic and angiogenic potentials in jaws and long bones osteosarcomas: a comparative immunohistochemical study.

BACKGROUND: Osteosarcomas (OS) of the jaws are uncommon lesions that represent less than 10% of all skeletal OS. It has a behavioral pattern which is less aggressive than their long bones counterparts. This study performed an immunohistochemical comparison between jaws and long bones OS. METHODS: The study involved 15 jaws and 15 long bones OS tissue samples for the period from 1986 to 2005. Age, sex, histologic subtypes and grades were recognized. The samples were immunohistochemically stained with monoclonal antibodies to Ki-67, P53 and vascular endothelial growth factor (VEGF). RESULTS: The mean age of the patients with jaw OS was a decade higher than that of long bones OS. A slight male predominance in jaw OS was found (1.14:1), which was more pronounced in long bones OS (2:1). The chondroblastic subtype was the predominant in jaws (66.66%), whereas (60%) of long bones OS were of osteoblastic subtype. The Ki-67 labeling index and the VEGF expression were significantly higher in long bones as compared with jaws OS, whereas there was no significant difference regarding the P53 expression between jaws and long bones OS. CONCLUSIONS: Jaws and long bones OS bear a comparable cell cycle dysregulation when quantified with P53 immunostaining, whereas the long bones OS have a higher proliferative and angiogenic capacity than their jaw counterparts when evaluated with Ki-67 and VEGF immunoexpressions respectively.

Enhancement of orthodontic anchorage and retention by the local injection of strontium: An experimental study in rats.

OBJECTIVES: To examine the clinical and histological effects of locally injected strontium on the anchoring unit of a rat model of an experimental relapsed tooth movement. MATERIALS AND METHODS: Thirty-six 10-week-old male Wister rats were randomly divided into two groups of 18 animals that were then randomly divided into three subgroups of six animals corresponding to three observation periods: T1 = 1 week, T2 = 2 weeks, and T3 = 3 weeks. In the first experiment, both the right and left maxillary first molars were moved buccally with a standardized expansive spring. Strontium chloride solution was injected every 2 days into the subperiosteal area buccal to the left maxillary first molar (the experimental side). The right-sided first molar was injected with distilled water as a control. In the second experiment, maxillary first molars were moved buccally with the spring. After 3 weeks, the spring was removed. Two days before the spring removal, strontium chloride was injected into the palatal side of left-sided maxillary first molar and distilled water was injected into the palatal side of the right-sided maxillary first molar as in experiment 1. RESULTS: At the end of the experimental period, significant levels of inhibition were noted in terms of both tooth movement and relapse movement in strontium-injected sides. Histological examinations showed that strontium enhanced the number of osteoblasts and reduced the number of osteoclasts. CONCLUSION: The local injection of strontium can inhibit the degree of experimental and relapsed tooth movement in a rat model.

Immunohistochemical expression of epidermal growth factor receptor (EGFR) in oral squamous cell carcinoma in relation to proliferation, apoptosis, angiogenesis and lymphangiogenesis.

OBJECTIVES: Squamous cell carcinoma (SCC) is by far the most common malignant neoplasm of the oral cavity. A number of etiologic factors have been implicated in its development. During the past few decades, a particular focus has been placed on the investigation of valid biomarkers predictive of cancer behavior and cervical lymph node metastasis in head and neck Squamous cell carcinoma (HNSCC).The present study was designed to investigate the expression of epidermal growth factor in these tumors in relation to proliferation, apoptosis, angiogenesis and lymphangiogenesis. MATERIALS AND METHODS: Immunohistochemical (IHC) evaluation of epidermal growth factor receptor (EGFR) expression in 40 retrospective OSCC specimens and its correlation with proliferating cell nuclear antigen (PCNA), antiapoptotic antibody (P53), vascular endothelial growth factor (VEGF), and D2-40 monoclonal antibodies (Mab), in relation to the clinicopathological parameters. RESULTS: Data revealed positive EGFR immunoreactivity in 35(87.5%) cases. There was a statistically significant correlation regarding EGFR extent score with respect to intratumoral lymphatic vessel density (ILVD) (r = 0.35) as well as EGFR intensity score with respect to ILVD and peritumoral lymphatic vessel density (PLVD) (r = 0.33, r = 0.36 respectively). EGFR expression was not correlated with the clinicopathological parameters. CONCLUSIONS: EGFR is expressed by most of the cases. EGFR correlation with D2- 40 positive lymphatic vessels suggests a higher tendency of OSCC for lymphatic dissemination. Lack of correlation among the studied markers suggests their independent effect on tumor behavior.

Gingival fine needle aspiration cytology in acute leukemia.

BACKGROUND: Oral findings in acute leukemia (AL) are common and could be the presenting feature of the disease, namely, gingival enlargement, ulceration, bleeding, and infection. Gingival enlargement in AL is either due to leukemic infiltration, or due to reactive hyperplasia. To differentiate between them a biopsy is required, but being highly contraindicated, biopsy has been substituted in this study by fine needle aspiration cytology (FNAC). METHOD: Gingival FNAC was performed on different sites in the upper and lower gingiva. Each site represents an interdental papilla, which was selected according to the clinical presentation, i.e., being enlarged or not. Seventy-two adult AL patients received a cytological and clinical examination in this study, and the cases were classified and categorized according to the French-American-British (FAB) criteria. RESULTS: Twenty-one cases were diagnosed as being infiltrated, 16 with gingival enlargement, 4 with no evidence of enlargement. In one case the infiltration affected the alveolar mucosa of an edentulous patient. In six cases the ginigva was enlarged without being infiltrated (reactive hyperplasia). Leukemic gingival enlargement was seen mostly in patients with acute myeloid leukemia, particularly M4 and M5 subtypes; however, two patients with acute mixed lineage leukemia (AMLL) were both affected with leukemic infiltration. CONCLUSION: FNAC was shown to be a simple, non-traumatic and useful diagnostic procedure for screening leukemic infiltration in gingival tissues in AL patients.